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1

Extravascular lung water and the pulmonary vascular permeability index may improve the definition of ARDS  

PubMed Central

The recent Berlin definition has made some improvements in the older definition of acute respiratory distress syndrome (ARDS), although the concepts and components of the definition remained largely unchanged. In an effort to improve both predictive and face validity, the Berlin panel has examined a number of additional measures that may reflect increased pulmonary vascular permeability, including extravascular lung water. The panel concluded that although extravascular lung water has improved face validity and higher values are associated with mortality, it is infeasible to mandate on the basis of availability and the fact that it does not distinguish between hydrostatic and inflammatory pulmonary edema. However, the results of a multi-institutional study that appeared in the previous issue of Critical Care show that this latter reservation may not necessarily be true. By using extravascular lung water and the pulmonary vascular permeability index, both of which are derived from transpulmonary thermodilution, the authors could successfully differentiate between patients with ARDS and other patients in respiratory failure due to either cardiogenic edema or pleural effusion with atelectasis. This commentary discusses the merits and limitations of this study in view of the potential improvement that transpulmonary thermodilution may bring to the definition of ARDS.

2013-01-01

2

Vascular permeability and neurotoxicity.  

PubMed Central

Neurotoxic substances affect the nervous system in a selective manner. One possible basis for this selectivity is blood vessel permeability. In general, the central nervous system and the peripheral nerve trunks have impermeable blood vessels, but in certain parts the capillaries are "leaky," allowing the passage of a plasma filtrate. Intravenously injected protein tracers rapidly reach nerve cells in these regions, with the implication that these nerve cells are also readily accessible to circulating neurotoxic substances. Some examples of neurotoxicity in the central nervous system show a selectivity that could be due to capillary permeability. In experimental methylmercury poisoning, cranial nerve V and sensory dorsal root ganglia, which lie in regions of vascular permeability, are particularly susceptible. A number of drug and chemically induced neuropathies are predominantly sensory, and may be due, directly or indirectly, to the accessibility of neurotoxic substances to sensory neurons. Examination of areas of potential vulnerability to circulating toxic substances may be of value in the experimental testing of substances for neurotoxicity, where pharmacological tests may be negative and clinical symptoms difficult to assess. Images FIGURE 1. (a) FIGURE 1. (b) FIGURE 1. (c) FIGURE 2. FIGURE 3. (a) FIGURE 3. (b) FIGURE 4. FIGURE 5. (a) FIGURE 5. (b) FIGURE 6. (a) FIGURE 6. (b)

Jacobs, J M

1978-01-01

3

THE GRADIENT OF VASCULAR PERMEABILITY  

PubMed Central

A mounting gradient of permeability exists along the capillaries of frog muscle. In chicken muscle on the other hand none has been demonstrated; but the close-knit vascularization is arranged in duplicate in such manner that the blood runs in opposite directions through the capillaries of nearly adjacent fibres. In a flight muscle of the pigeon there exists in addition to this artifice what appears to be a special collecting system of venous capillaries. In the mammalian diaphragm indications of such a system are also to be found, and a gradient of capillary permeability like that in the other skeletal muscles is probably present. These vascular conditions are briefly considered in terms of function.

Smith, Frederick; Rous, Peyton

1931-01-01

4

Vascular Permeability in Diabetic Retinopathy  

Microsoft Academic Search

\\u000a A hallmark of diabetic retinopathy is increased vascular permeability. The vasculature of the retina, which normally has tight\\u000a control of the fluid and blood components that enter the retina, becomes leaky in diabetes leading to increased albumin flux\\u000a into the retina, fluid accumulation, and macular edema, and over time may progress to hemorrhaging vessels. This chapter investigates\\u000a our knowledge regarding

David A. Antonetti; Heather D. VanGuilder; Cheng Mao-Lin

5

Vascular Permeability and Drug Delivery in Cancers  

PubMed Central

The endothelial barrier strictly maintains vascular and tissue homeostasis, and therefore modulates many physiological processes such as angiogenesis, immune responses, and dynamic exchanges throughout organs. Consequently, alteration of this finely tuned function may have devastating consequences for the organism. This is particularly obvious in cancers, where a disorganized and leaky blood vessel network irrigates solid tumors. In this context, vascular permeability drives tumor-induced angiogenesis, blood flow disturbances, inflammatory cell infiltration, and tumor cell extravasation. This can directly restrain the efficacy of conventional therapies by limiting intravenous drug delivery. Indeed, for more effective anti-angiogenic therapies, it is now accepted that not only should excessive angiogenesis be alleviated, but also that the tumor vasculature needs to be normalized. Recovery of normal state vasculature requires diminishing hyperpermeability, increasing pericyte coverage, and restoring the basement membrane, to subsequently reduce hypoxia, and interstitial fluid pressure. In this review, we will introduce how vascular permeability accompanies tumor progression and, as a collateral damage, impacts on efficient drug delivery. The molecular mechanisms involved in tumor-driven vascular permeability will next be detailed, with a particular focus on the main factors produced by tumor cells, especially the emblematic vascular endothelial growth factor. Finally, new perspectives in cancer therapy will be presented, centered on the use of anti-permeability factors and normalization agents.

Azzi, Sandy; Hebda, Jagoda K.; Gavard, Julie

2013-01-01

6

Tonic regulation of vascular permeability  

PubMed Central

Our major theme is that the layered structure of the endothelial barrier requires continuous activation of signaling pathways regulated by S1P and intracellular cAMP. These pathways modulate the adherens junction, continuity of tight junction strands, and the balance of synthesis and degradation of glycocalyx components. We evaluate recent evidence that baseline permeability is maintained by constant activity of mechanisms involving the small GTPases Rap1 and Rac1. In the basal state, the barrier is compromised when activities of the small GTPases are reduced by low S1P supply or delivery. With inflammatory stimulus, increased permeability can be understood in part as the action of signaling to reduce Rap1 and Rac1 activation. With the hypothesis that microvessel permeability and selectivity under both normal and inflammatory conditions are regulated by mechanisms that are continuously active it follows that when S1P or intracellular cAMP are elevated at the time of inflammatory stimulus, they can buffer changes induced by inflammatory agents and maintain normal barrier stability. When endothelium is exposed to inflammatory conditions and subsequently exposed to elevated S1P or intracellular cAMP, the same processes restore the functional barrier by first reestablishing the adherens junction, then modulating tight junctions and glycocalyx. In more extreme inflammatory conditions, loss of the inhibitory actions of Rac1 dependent mechanisms may promote expression of more inflammatory endothelial phenotypes by contributing to the up-regulation of RhoA dependent contractile mechanisms and the sustained loss of surface glycocalyx allowing access of inflammatory cells to the endothelium.

Curry, Fitz-Roy E.; Adamson, Roger H.

2014-01-01

7

The clinical usefulness of extravascular lung water and pulmonary vascular permeability index to diagnose and characterize pulmonary edema: a prospective multicenter study on the quantitative differential diagnostic definition for acute lung injury/acute respiratory distress syndrome  

PubMed Central

Introduction Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is characterized by features other than increased pulmonary vascular permeability. Pulmonary vascular permeability combined with increased extravascular lung water content has been considered a quantitative diagnostic criterion of ALI/ARDS. This prospective, multi-institutional, observational study aimed to clarify the clinical pathophysiological features of ALI/ARDS and establish its quantitative diagnostic criteria. Methods The extravascular lung water index (EVLWI) and the pulmonary vascular permeability index (PVPI) were measured using the transpulmonary thermodilution method in 266 patients with PaO2/FiO2 ratio ? 300 mmHg and bilateral infiltration on chest radiography, in 23 ICUs of academic tertiary referral hospitals. Pulmonary edema was defined as EVLWI ? 10 ml/kg. Three experts retrospectively determined the pathophysiological features of respiratory insufficiency by considering the patients' history, clinical presentation, chest computed tomography and radiography, echocardiography, EVLWI and brain natriuretic peptide level, and the time course of all preceding findings under systemic and respiratory therapy. Results Patients were divided into the following three categories on the basis of the pathophysiological diagnostic differentiation of respiratory insufficiency: ALI/ARDS, cardiogenic edema, and pleural effusion with atelectasis, which were noted in 207 patients, 26 patients, and 33 patients, respectively. EVLWI was greater in ALI/ARDS and cardiogenic edema patients than in patients with pleural effusion with atelectasis (18.5 ± 6.8, 14.4 ± 4.0, and 8.3 ± 2.1, respectively; P < 0.01). PVPI was higher in ALI/ARDS patients than in cardiogenic edema or pleural effusion with atelectasis patients (3.2 ± 1.4, 2.0 ± 0.8, and 1.6 ± 0.5; P < 0.01). In ALI/ARDS patients, EVLWI increased with increasing pulmonary vascular permeability (r = 0.729, P < 0.01) and was weakly correlated with intrathoracic blood volume (r = 0.236, P < 0.01). EVLWI was weakly correlated with the PaO2/FiO2 ratio in the ALI/ARDS and cardiogenic edema patients. A PVPI value of 2.6 to 2.85 provided a definitive diagnosis of ALI/ARDS (specificity, 0.90 to 0.95), and a value < 1.7 ruled out an ALI/ARDS diagnosis (specificity, 0.95). Conclusion PVPI may be a useful quantitative diagnostic tool for ARDS in patients with hypoxemic respiratory failure and radiographic infiltrates. Trial registration UMIN-CTR ID UMIN000003627

2012-01-01

8

Overexpression of Vascular Permeability Factor\\/Vascular Endothelial Growth Factor and its Receptors in Psoriasis  

Microsoft Academic Search

Summary Psoriatic skin is characterized by microvascular hyperpermeability and angioproliferation, but the mechanisms responsible are unknown. We report here that the hyperplastic epidermis of psoriatic skin expresses strikingly increased amounts of vascular permeability factor (VPF; vascular endothelial growth factor), a selective endothelial cell mitogen that enhances microvascular permeability. Moreover, two VPF receptors, kdr and fit-l, are overexpressed by papillary dermal

Michael Detmar; Lawrence F. Brown; Kevin P. Claffey; Kiang-Teck Yeo; Olivier Kocher; Robert W. Jackman; Brygida Berse; Harold F. Dvorak

1994-01-01

9

Granzyme B releases vascular endothelial growth factor from extracellular matrix and induces vascular permeability.  

PubMed

The formation of unstable, leaky neovessels underlies the pathogenesis of many chronic inflammatory diseases. Granzyme B (GZMB) is an immune-derived serine protease that accumulates in the extracellular matrix (ECM) during chronic inflammation and is capable of cleaving fibronectin (FN). Vascular endothelial growth factor (VEGF) is a potent vascular permeabilizing agent that is sequestered in the ECM through its interaction with FN. As GZMB levels are elevated in chronic inflammatory diseases that are associated with increased vascular permeability, the role of GZMB in the regulation of VEGF bioavailability and vascular permeability were assessed. GZMB was added to either VEGF bound to FN or VEGF bound to endothelial cell (EC)-derived ECM. Supernatants containing released VEGF were assessed to determine VEGF activity by treating EC and evaluating VEGF receptor-2 (VEGFR2) phosphorylation. GZMB released VEGF from both FN and from EC-derived matrix, whereas GZMB inhibition prevented FN cleavage and VEGF release. GZMB-mediated VEGF release resulted in significant phosphorylation of VEGFR2. The role of GZMB-mediated VEGF release in altering vascular permeability was also assessed in vivo using Miles/Evans blue permeability assay. GZMB induced a significant VEGF-dependent increase in vascular permeability in vivo that was reduced in the presence of an anti-VEGF-neutralizing antibody. Inflammatory-mediated vascular leakage was also assessed in GZMB-KO mice using a delayed-type hypersensitivity model. GZMB-KO mice exhibited reduced microvascular leakage compared with C57\\B6 controls. GZMB increases vascular permeability in part through the proteolytic release of ECM-sequestered VEGF, leading to VEGFR2 activation and increased vascular permeability in vivo. These findings present a novel role for GZMB as a modulator of vascular response during chronic inflammation. PMID:24791744

Hendel, Alon; Hsu, Ivy; Granville, David J

2014-07-01

10

Endothelial glycocalyx and coronary vascular permeability: the fringe benefit  

Microsoft Academic Search

Current concepts of vascular permeability are largely still based on the Starling principle of 1896. Starling’s contribution\\u000a to understanding vascular fluid homeostasis comes from realising that the transport of fluid to and from the interstitial\\u000a space of peripheral tissues follows the balance between opposing oncotic and hydrostatic pressures. It is presumed that in\\u000a peripheral tissues fluid is readily filtered from

Bernhard F. Becker; Daniel Chappell; Matthias Jacob

2010-01-01

11

Time-Dependent Vascular Regression and Permeability Changes in Established Human Tumor Xenografts Induced by an Anti-Vascular Endothelial Growth Factor\\/Vascular Permeability Factor Antibody  

Microsoft Academic Search

The hyperpermeability of tumor vessels to macromolecules, compared with normal vessels, is presumably due to vascular endothelial growth factor\\/vascular permeability factor (VEGF\\/VPF) released by neoplastic and\\/or host cells. In addition, VEGF\\/VPF is a potent angiogenic factor. Removal of this growth factor may reduce the permeability and inhibit tumor angiogenesis. To test these hypotheses, we transplanted a human glioblastoma (U87), a

Fan Yuan; Yi Chen; Marc Dellian; Nina Safabakhsh; Napoleone Ferrara; Rakesh K. Jain

1996-01-01

12

Effect of FGF-binding Protein 3 on Vascular Permeability*  

PubMed Central

Fibroblast growth factor-binding protein 1 (FGF-BP1 is BP1) is involved in the regulation of embryonic development, tumor growth, and angiogenesis by mobilizing endogenous FGFs from their extracellular matrix storage. Here we describe a new member of the FGF-BP family, human BP3. We show that the hBP3 protein is secreted from cells, binds to FGF2 in vitro and in intact cells, and inhibits FGF2 binding to heparin. To determine the function of hBP3 in vivo, hBP3 was transiently expressed in chicken embryos and resulted in >50% lethality within 24 h because of vascular leakage. The onset of vascular permeability was monitored by recording the extravasation kinetics of FITC-labeled 40-kDa dextran microperfused into the vitelline vein of 3-day-old embryos. Vascular permeability increased as early as 8 h after expression of hBP3. The increased vascular permeability caused by hBP3 was prevented by treatment of embryos with PD173074, a selective FGFR kinase inhibitor. Interestingly, a C-terminal 66-amino acid fragment (C66) of hBP3, which contains the predicted FGF binding domain, still inhibited binding of FGF2 to heparin similar to full-length hBP3. However, expression of the C66 fragment did not increase vascular permeability on its own, but required the administration of exogenous FGF2 protein. We conclude that the FGF binding domain and the heparin binding domain are necessary for the hBP3 interaction with endogenous FGF and the activation of FGFR signaling in vivo.

Zhang, Wentao; Chen, Yifan; Swift, Matthew R.; Tassi, Elena; Stylianou, Dora C.; Gibby, Krissa A.; Riegel, Anna T.; Wellstein, Anton

2008-01-01

13

Gap Junction Protein Connexin43 Exacerbates Lung Vascular Permeability  

PubMed Central

Increased vascular permeability causes pulmonary edema that impairs arterial oxygenation and thus contributes to morbidity and mortality associated with Acute Respiratory Distress Syndrome and sepsis. Although components of intercellular adhesive and tight junctions are critical for maintaining the endothelial barrier, there has been limited study of the roles of gap junctions and their component proteins (connexins). Since connexins can modulate inflammatory signaling in other systems, we hypothesized that connexins may also regulate pulmonary endothelial permeability. The relationships between connexins and the permeability response to inflammatory stimuli were studied in cultured human pulmonary endothelial cells. Prolonged treatment with thrombin, lipopolysaccharide, or pathological cyclic stretch increased levels of mRNA and protein for the major connexin, connexin43 (Cx43). Thrombin and lipopolysaccharide both increased intercellular communication assayed by transfer of microinjected Lucifer yellow. Although thrombin decreased transendothelial resistance in these cells, the response was attenuated by pretreatment with the connexin inhibitor carbenoxolone. Additionally, the decreases of transendothelial resistance produced by either thrombin or lipopolysaccharide were attenuated by reducing Cx43 expression by siRNA knockdown. Both carbenoxolone and Cx43 knockdown also abrogated thrombin-induced phosphorylation of myosin light chain. Taken together, these data suggest that increased lung vascular permeability induced by inflammatory conditions may be amplified via increased expression of Cx43 and intercellular communication among pulmonary endothelial cells.

O'Donnell, James J.; Birukova, Anna A.; Beyer, Eric C.; Birukov, Konstantin G.

2014-01-01

14

Strategies for improving chemotherapeutic delivery to solid tumors mediated by vascular permeability modulation  

NASA Astrophysics Data System (ADS)

An essential mode of distribution of blood-borne chemotherapeutic agents within a solid tumor is via the micro-circulation. Poor tumor perfusion, because of a lack of functional vasculature or a lack of microvessels, as well as low tumor vascular permeability, can prevent adequate deposition of even low molecular-weight agents into the tumor. The modulation of tumor vascular function and density can provides numerous strategies for improving intratumor deposition of chemotherapeutic agents. Here we investigated strategies to improve drug delivery to two tumor types that share in common poor drug delivery, but differ in the underlying cause. First, in an angiogenesis-driven brain tumor model of Glioblastoma, the vascular permeability barrier, along with poorly-functional vasculature, hinders drug delivery. A strategy of nanoparticle-based tumor 'priming' to attack the vascular permeability barrier, employing sterically stabilized liposomal doxorubicin (SSL-DXR), was investigated. Functional and histological evaluation of tumor vasculature revealed that after an initial period of depressed vascular permeability and vascular pruning 3--4 days after SSL-DXR administration, vascular permeability and perfusion were restored and then elevated after 5--7 days. As a result of tumor priming, deposition of subsequently-administered nanoparticles was enhanced, and the efficacy of temozolomide (TMZ), if administered during the window of elevated permeability, was increased. The sequenced regimen resulted in a persistent reduction of the tumor proliferative index and a 40% suppression of tumor volume, compared to animals that received both agents simultaneously. Second, in a hypovascular, pancreatic ductal adenocarcinoma model, disruption of tumor-stromal communication via sonic hedgehog (sHH) signaling pathway inhibition mediated an indirect vascular proliferation and a more than 2-fold increase in intratumor nanoparticle deposition. Enhanced delivery of SSL-DXR in tumors pre-treated with sHH-inhibitor led to a 90% lifespan extension in animals that received a single cycle of the combined regimen, and a 200% extension in animals receiving 3-cycles of treatment, compared to control animals or those receiving either of the agents alone. We surmise that direct or indirect modulation of tumor vasculature can provide new opportunities for combination therapies that could improve delivery and efficacy of both small- and large- molecular weight agents in treatment-resistant solid tumors.

Roy Chaudhuri, Tista

15

A permissive role for tumor necrosis factor in vascular endothelial growth factor-induced vascular permeability  

Microsoft Academic Search

Vascular endothelial growth factor (VEGF) induces both angiogenesis and an increase in vascular permeability, 2 processes that are considered to be important for both tumor growth and the delivery of drugs to the site of tumors. This study demonstrates that transmembrane expression of tumor necrosis factor (tmTNF) is up-regulated in the endothelium of a murine methylcholan- threne (meth A)-induced sarcoma

Matthias Clauss; Cord Sunderkotter; Baldur Sveinbjornsson; Stefan Hippenstiel; Antje Willuweit; Michael Marino; Elvira Haas; Rolf Seljelid; Peter Scheurich; Norbert Suttorp; Matthias Grell; Werner Risau

2001-01-01

16

Effect of prior statin therapy on capillary permeability in the lungs after cardiac or vascular surgery.  

PubMed

Cholesterol-lowering statins can ameliorate severe forms of vascular hyperpermeability in experimental studies, and may thereby ameliorate acute lung injury and sepsis. It is unknown whether this also applies to humans. This study aimed to define whether or not prior statin therapy reduces mild post-operative increases in pulmonary capillary protein permeability associated with acute lung injury after cardiac or major vascular surgery. A prospective observational study was performed in an intensive care unit of a university hospital on 64 patients, 37 after elective cardiac and 27 after major vascular surgery, of whom 68 and 44%, respectively, had received prior statin therapy. A mobile probe system was used to measure the pulmonary leak index (PLI), i.e. the transvascular transport rate of gallium-67-radiolabelled transferrin. For all of the patients together, the mean PLI did not differ between the statin and control groups (22.9 versus 24.4 x 10(-3) min(-1)). The prevalence of an elevated PLI was 57% in the statin and 59% in the control group. Subgroup analysis did not reveal significant differences caused by statins in the PLI of these patients. Prior statin therapy neither has an adverse effect on mildly increased pulmonary capillary permeability in patients after cardiac or major vascular surgery nor does it ameliorate this increased capillary permeability. PMID:16707397

van de Visse, E P; van der Heijden, M; Verheij, J; van Nieuw Amerongen, G P; van Hinsbergh, V W M; Girbes, A R J; Groeneveld, A B J

2006-05-01

17

Non-invasive optical modulation of local vascular permeability  

NASA Astrophysics Data System (ADS)

For a systemically administered drug to act, it first needs to cross the vascular wall. This step represents a bottleneck for drug development, especially in the brain or retina, where tight junctions between endothelial cells form physiological barriers. Here, we demonstrate that femtosecond pulsed laser irradiation focused on the blood vessel wall induces transient permeabilization of plasma. Nonlinear absorption of the pulsed laser enabled the noninvasive modulation of vascular permeability with high spatial selectivity in three dimensions. By combining this method with systemic injection, we could locally deliver molecular probes in various tissues, such as brain cortex, meninges, ear, striated muscle, and bone. We suggest this method as a novel delivery tool for molecular probes or drugs.

Choi, Myunghwan; Choi, Chulhee

2011-02-01

18

VEGF-induced vascular permeability is mediated by FAK  

PubMed Central

SUMMARY Endothelial cells (ECs) form cell-cell adhesive junctional structures maintaining vascular integrity. This barrier is dynamically regulated by vascular endothelial growth factor (VEGF) receptor signaling. We created an inducible knockin mouse model to study the contribution of the integrin-associated focal adhesion tyrosine kinase (FAK) signaling on vascular function. Here we show that genetic or pharmacological FAK inhibition in ECs prevents VEGF-stimulated permeability downstream of VEGF receptor or Src tyrosine kinase activation in vivo. VEGF promotes tension-independent FAK activation, rapid FAK localization to cell-cell junctions, binding of the FAK FERM domain to the vascular endothelial cadherin (VE-cadherin) cytoplasmic tail, and direct FAK phosphorylation of ?-catenin at tyrosine-142 (Y142) facilitating VE-cadherin-?-catenin dissociation and EC junctional breakdown. Kinase inhibited FAK is in a closed conformation that prevents VE-cadherin association and limits VEGF-stimulated ?-catenin Y142 phosphorylation. Our studies establish a role for FAK as an essential signaling switch within ECs regulating adherens junction dynamics.

Chen, Xiao Lei; Nam, Ju-Ock; Jean, Christine; Lawson, Christine; Walsh, Colin T.; Goka, Erik; Lim, Ssang-Taek; Tomar, Alok; Tanjoni, Isabelle; Uryu, Sean; Guan, Jun-Lin; Acevedo, Lisette M.; Weis, Sara M.; Cheresh, David A.; Schlaepfer, David D.

2011-01-01

19

Increased lung vascular permeability after pancreatitis and trypsin infusion.  

PubMed Central

We examined the role of proteases in mediating lung vascular injury after acute hemorrhagic pancreatitis. Studies were made in sheep in which pulmonary lymph was collected for assessment of the changes in transvascular fluid and protein exchange. The induction of pancreatitis by injection of trypsin and sodium taurocholate into the pancreas resulted in increases in pulmonary lymph flow and transvascular protein clearance (lymph flow x lymph-to-plasma protein concentration ratio). The pulmonary vascular pressures did not change significantly after pancreatitis, indicating that the increases in pulmonary lymph flow and protein clearance were due to increased pulmonary endothelial permeability. The response to pancreatitis was also characterized by decreases in concentrations of fibrinogen, platelets, and granulocytes. Pulmonary leukostasis was a common morphologic feature in this group. In another group, an intravenous infusion of trypsin, which produced decreases in antiprotease activity comparable to those observed after pancreatitis, also resulted in increases in pulmonary lymph flow and transvascular protein clearance. These increases in lymph fluxes were comparable to those observed after pancreatitis and were also associated with decreases in concentrations of fibrinogen, platelets, and granulocytes. Pulmonary leukostasis was evident in this group upon histologic examination. In a third group, pretreatment with Trasylol prevented the increases in pulmonary lymph flow and transvascular protein clearance after pancreatitis, suggesting that the pancreatitis-induced pulmonary vascular injury is the result of the release of proteases. The results indicate a common pulmonary vascular response to acute pancreatitis and trypsin infusion. The release of proteases into the circulation after acute pancreatitis may be the initiating event mediating the pulmonary vascular injury. Images Figure 7 Figure 8 Figure 9 Figure 10 Figures 11 and 12

Tahamont, M. V.; Barie, P. S.; Blumenstock, F. A.; Hussain, M. H.; Malik, A. B.

1982-01-01

20

Vascular Endothelial Growth Factor\\/Vascular Permeability Factor is an Autocrine Growth Factor for AIDS-Kaposi Sarcoma  

Microsoft Academic Search

Kaposi sarcoma (KS) is the most common tumor associated with HIV-1 infection and develops in nearly 30% of cases. The principal features of this tumor are abnormal vascularization and the proliferation of endothelial cells and spindle (tumor) cells. KS-derived spindle cells induce vascular lesions and display enhanced vascular permeability when inoculated subcutaneously in the nude mouse. This finding suggests that

Rizwan Masood; Jie Cai; Tong Zheng; D. Lynne Smith; Yathi Naidu; Parkash S. Gill

1997-01-01

21

Vascular permeability in a human tumour xenograft: molecular charge dependence  

PubMed Central

Molecular charge is one of the main determinants of transvascular transport. There are, however, no data available on the effect of molecular charge on microvascular permeability of macromolecules in solid tumours. To this end, we measured tumour microvascular permeability to different proteins having similar size but different charge. Measurements were performed in the human colon adenocarcinoma LS174T transplanted in transparent dorsal skinfold chambers in severe combined immunodeficient (SCID) mice. Bovine serum albumin (BSA) and IgG were fluorescently labelled and were either cationized by conjugation with hexamethylenediamine or anionized by succinylation. The molecules were injected i.v. and the fluorescence in tumour tissue was quantified by intravital fluorescence microscopy. The fluorescence intensity and pharmacokinetic data were used to calculate the microvascular permeability. We found that tumour vascular permeability of cationized BSA (pI-range: 8.6–9.1) and IgG (pI: 8.6–9.3) was more than two-fold higher (4.25 and 4.65 × 10?7cm s?1) than that of the anionized BSA (pI ? 2.0) and IgG (pI: 3.0–3.9; 1.11 and 1.93 × 10?7cm s?1, respectively). Our results indicate that positively charged molecules extravasate faster in solid tumours compared to the similar-sized compounds with neutral or negative charges. However, the plasma clearance of cationic molecules was ?2 × faster than that of anionic ones, indicating that the modification of proteins enhances drug delivery to normal organs as well. Therefore, caution should be exercised when such a strategy is used to improve drug and gene delivery to solid tumours. © 2000 Cancer Research Campaign

Dellian, M; Yuan, F; Trubetskoy, V S; Torchilin, V P; Jain, R K

2000-01-01

22

Effect of leukotriene receptor antagonists on vascular permeability during endotoxic shock  

SciTech Connect

Evidence has accumulated that sulfidopeptide leukotrienes are significant pathogenic mediators of certain hematologic and hemodynamic sequelae of endotoxic shock. In the present study, the effects of a selective LTD4/E4 receptor antagonist, LY171883 (LY), or a selective LTD4 receptor antagonist, SKF-104353 (SKF), were assessed on splanchnic and pulmonary localization of 99mTechnetium-labeled human serum albumin (99mTc-HSA) in acute endotoxic shock in the rat. Dynamic gamma camera imaging of heart (H), midabdominal (GI), and lung regions of interest generated time activity curves for baseline and at 5-35 min after Salmonella enteritidis endotoxin (10 mg/kg, i.v.). Slopes of GI/H and lung/H activity (permeability index, GI/H or lung/H X 10(-3)/min) provided indices of intestinal and lung localization. Rats received LY (30 mg/kg, i.v.), LY vehicle (LY Veh), SKF (10 mg/kg), or SKF vehicle (SK Veh) 10 min prior to endotoxin or endotoxin vehicle. In rats receiving the LY Veh and endotoxin (n = 8) or SKF Veh and endotoxin (n = 12), the splanchnic permeability indices to 99mTc-HSA were increased 11.2-fold and 5.1-fold, respectively (P less than 0.05) compared to vehicle control groups not given endotoxin (n = 5). Pulmonary permeability index for 99mTc-HSA was increased (P less than 0.05) to a lesser extent (3.2-fold) by endotoxin compared to vehicle controls. Pretreatment with SKF reduced the mesenteric permeability index to control levels (P less than 0.05) during the 5-35 min time interval post-endotoxin. LY reduced the mesenteric permeability index by 70%. Pulmonary relative permeability to 99mTc-HSA was not affected by LY pretreatment. Both splanchnic and lung relative permeability to the isotope was transient; at 135-225 min post-endotoxin, splanchnic localization of 99mTc-HSA (n = 4) was not significantly different from vehicle controls in these vascular beds.

Cook, J.A.; Li, E.J.; Spicer, K.M.; Wise, W.C.; Halushka, P.V. (Medical Univ. of South Carolina, Charleston (USA))

1990-11-01

23

A novel snake venom vascular endothelial growth factor (VEGF) predominantly induces vascular permeability through preferential signaling via VEGF receptor-1.  

PubMed

Vascular endothelial growth factor (VEGF)/vascular permeability factor induces both angiogenesis and vascular permeability mainly through VEGF receptor (VEGFR)-2 activation. VEGF binds VEGFR-1 as well, but the importance of VEGFR-1 signaling in vascular permeability has been largely neglected. Here, we report the purification and characterization of a novel VEGF-like protein from Trimeresurus flavoviridis Habu snake venom. The Habu snake has a venom-specific VEGF-like molecule, T. flavoviridis snake venom VEGF (TfsvVEGF), in addition to VEGF-A. TfsvVEGF has almost 10-fold less mitotic activity than VEGF(165), a predominant isoform of human VEGF-A, but a similar effect on vascular permeability. TfsvVEGF bound VEGFR-1 and induced its autophosphorylation to almost the same extent as VEGF(165), but bound VEGFR-2 weakly and induced its autophosphorylation almost 10-fold less effectively than VEGF(165). This unique binding affinity for VEGFR-1 and VEGFR-2 leads to the vascular permeability-dominant activity of TfsvVEGF. These results suggest that Habu snakes have acquired a highly purposive molecule for a toxin, which enhances the toxicity in envenomation without inducing effective angiogenesis and the following regeneration of damaged tissues, taking advantage of the difference in signaling properties involving VEGFR-1 and VEGFR-2 between vascular permeability and angiogenesis. TfsvVEGF is thus a potent inducing factor selective for vascular permeability through preferential signaling via VEGFR-1. These data strongly indicate the importance of VEGFR-1 signaling in vascular permeability. PMID:15328352

Takahashi, Hiroyuki; Hattori, Shosaku; Iwamatsu, Akihiro; Takizawa, Hajime; Shibuya, Masabumi

2004-10-29

24

Integrin v5 Regulates Lung Vascular Permeability and Pulmonary Endothelial Barrier Function  

Microsoft Academic Search

Increased lung vascular permeability is an important contributor to respiratory failure in acute lung injury (ALI). We found that a function-blocking antibody against the integrin v5 prevented development of lung vascular permeability in two different models of ALI: ischemia-reperfusion in rats (mediated by vascular endothe- lial growth factor (VEGF)) and ventilation-induced lung injury (VILI) in mice (mediated, at least in

George Su; Maki Hodnett; Nanyan Wu; Amha Atakilit; Cynthia Kosinski; Mika Godzich; Xiao Zhu Huang; Jiyeun K. Kim; James A. Frank; Michael A. Matthay; Dean Sheppard; Jean-Francois Pittet

25

The shortest isoform of human vascular endothelial growth factor/vascular permeability factor (VEGF/VPF121) produced by Saccharomyces cerevisiae promotes both angiogenesis and vascular permeability.  

PubMed

Vascular endothelial growth factor/vascular permeability factor (VEGF/VPF) is a multifunctional cytokine that is expressed as four isoforms having 206, 189, 165, and 121 amino acids in humans. We constructed a system that produces the shortest isoform of human VEGF/VPF in Saccharomyces cerevisiae (yVEGF/VPF121). Active yVEGF/VPF121 was secreted from the yeast cells as a glycosylated dimeric protein. Various biological activities of the purified yVEGF/VPF121 were examined. It bound to cell surface receptor(s) and stimulated the growth of human umbilical vein endothelial cells in culture at a dose similar to that of native VEGF/VPF. Purified yVEGF/VPF121 also induced angiogenesis in mice, and promoted the extravasation of plasma proteins from the blood vessels. These observations demonstrated that the shortest isoform of VEGF/VPF with an amino acid sequence of 121 residues contains enough information necessary to trigger both angiogenesis and the induction of vascular permeability upon binding to its cognate receptor(s). PMID:7533000

Kondo, S; Matsumoto, T; Yokoyama, Y; Ohmori, I; Suzuki, H

1995-02-23

26

The interaction of soluble Tie2 with angiopoietins and pulmonary vascular permeability in septic and nonseptic critically ill patients.  

PubMed

Circulating angiopoietin (Ang) 1 may inhibit and Ang-2 may enhance pulmonary vascular permeability in septic and nonseptic patients with or at risk for acute lung injury or acute respiratory distress syndrome. We hypothesized that the soluble form of the Ang-binding Tie2 receptor (sTie2), whose shedding may be induced by vascular endothelial growth factor (VEGF) levels, may bind circulating Angs and thereby inhibit their effects on pulmonary vascular permeability. In 24 septic and 40 nonseptic mechanically ventilated patients, sTie2, Ang-1, Ang-2, and VEGF plasma levels were measured together with the pulmonary leak index (PLI) for (67)Gallium-labeled transferrin as a measure of pulmonary vascular permeability. Soluble Tie2 and VEGF levels correlated (r = 0.53, P = 0.001). Soluble Tie2 was higher in septic than in nonseptic patients (7.43 [6.57 - 8.40] vs. 5.03 [4.57 - 5.54] ng/mL; P < 0.001). Soluble Tie2 was associated with the PLI (standardized regression coefficient [beta] = 0.26; P = 0.006) but lost its association with the PLI when the Angs were included in a multivariate model. Soluble Tie2 did not affect the association between Ang-1 or Ang-2 and the PLI (beta = -0.39, P < 0.001; beta = 0.52, P < 0.001, respectively), independently of underlying disease. Although limited to correlations and associations, the clinical data support in vivo shedding of sTie2 through VEGF signaling upon pulmonary vascular injury. However, this shedding may not prevent a direct role of Angs in pulmonary vascular permeability. PMID:19543148

van der Heijden, Melanie; van Nieuw Amerongen, Geerten P; van Hinsbergh, Victor W M; Groeneveld, A B Johan

2010-03-01

27

Isoflurane post-treatment improves pulmonary vascular permeability via upregulation of heme oxygenase-1.  

PubMed

Isoflurane (ISO) has been shown to attenuate acute lung injury (ALI). Induction of heme oxygenase-1 (HO-1) and suppression of inducible nitric oxide synthase (iNOS) expression provide cytoprotection in lung and vascular injury. The aim of this study was to investigate the effect of post-treatment with isoflurane on lung vascular permeability and the role of HO-1 in an ALI rat model induced by cecal ligation and puncture (CLP). Male Sprague-Dawley rats were randomly assigned to one of four groups: sham group, sham rats post-treated with vehicle (Sham); CLP group, CLP rats post-treated with vehicle (CLP); ISO group, CLP rats post-treated with isoflurane (ISO); and ZnPP group, CLP rats injected with zinc protoporphyrin IX (ZnPP), a competitive inhibitor of HO-1, 1 hour before the operation, and post-treated with isoflurane (ZnPP). Isoflurane (1.4%) was administered 2 hour after CLP. At 24 hour after CLP, the extent of ALI was evaluated by lung wet/dry ratio, Evans blue dye (EBD) extravasation, lung permeability index (LPI), as well as histological and immunohistochemical examinations. We also determined pulmonary iNOS and HO-1 expression. Compared with the CLP group, the isoflurane post-treatment group showed improved pulmonary microvascular permeability as detected by EBD extravasation, LPI, as well as histological and immunohistochemical examinations. Furthermore, isoflurane decreased iNOS and increased HO-1 expression in lung tissue. Pretreatment with ZnPP prevented the protective effects of isoflurane in rats. These findings indicate that the protective role of isoflurane post-conditioning against CLP-induced lung injury may be associated with its role in upregulating HO-1 in ALI. PMID:23919323

Dong, Xiang; Hu, Rong; Sun, Yu; Li, Qifang; Jiang, Hong

2013-09-01

28

Resistance of essential fatty acid-deficient rats to endotoxin-induced increases in vascular permeability  

SciTech Connect

Resistance to endotoxin in essential fatty acid-deficient (EFAD) rats is associated with reduced synthesis of certain arachidonic acid metabolites. It was hypothesized that EFAD rats would manifest decreased vascular permeability changes during endotoxemia as a consequence of reduced arachidonic acid metabolism. To test this hypothesis, changes in hematocrit (HCT) and mesenteric localization rate of technetium-labeled human serum albumin (99mTc-HSA) and red blood cells (99mTc-RBC) were assessed in EFAD and normal rats using gamma-camera imaging. Thirty minutes after Salmonella enteritidis endotoxin, EFAD rats exhibited less hemoconcentration as determined by % HCT than normal rats. Endotoxin caused a less severe change in permeability index in the splanchnic region in EFAD rats than in normal rats (1.2 +/- 0.6 x 10(-3)min-1 vs. 4.9 +/- 1.7 x 10(-3)min-1 respectively, P less than 0.05). In contrast to 99mTc-HSA, mesenteric localization of 99mTc-RBC was not changed by endotoxin in control or EFAD rats. Supplementation with ethyl-arachidonic acid did not enhance susceptibility of EFAD rats to endotoxin-induced splanchnic permeability to 99mTc-HSA. Leukotrienes have been implicated as mediators of increased vascular permeability in endotoxin shock. Since LTC3 formation has been reported to be increased in EFA deficiency, we hypothesized that LTC3 may be less potent than LTC4. Thus the effect of LTC3 on mean arterial pressure and permeability was compared to LTC4 in normal rats. LTC3-induced increases in peak mean arterial pressure were less than LTC4 at 10 micrograms/kg (39 +/- 5 mm Hg vs. 58 +/- 4 mm Hg respectively, P less than 0.05) and at 20 micrograms/kg (56 +/- 4 mm Hg vs. 75 +/- 2 mm Hg respectively, P less than 0.05). LY171883 (30 mg/kg), an LTD4/E4 receptor antagonist, attenuated the pressor effect of LTC4, LTD4, and LTC3.

Li, E.J.; Cook, J.A.; Spicer, K.M.; Wise, W.C.; Rokach, J.; Halushka, P.V. (Medical Univ. of South Carolina, Charleston (USA))

1990-06-01

29

Effect of vascular burden as measured by vascular indexes upon vascular dementia: a matched case-control study  

PubMed Central

Background Vascular dementia (VaD) is a challenging illness that affects the lives of older adults and caregivers. It is unclear how multiple vascular risk factor exposures (polyvascular disease) affect VaD. Purpose To determine the relationship between multiple vascular risk exposures, as counted on an index in cases with VaD, compared with healthy age-/gender-matched controls. Methods This was a matched case-control study of subjects living in Olmsted County, MN with documented VaD. Controls were selected by gender and age within 3 years from those who did not have dementia. The exposures included a total index (eleven exposure factors) added together, along with indexes for cerebrovascular disease (two exposures), cardiovascular disease (four exposures), vascular disease (three exposures), and lifestyle (two exposures). Analysis used matched conditional univariable logistic regression for each index. Results A total of 1736 potential subjects were identified, and 205 subjects were diagnosed with VaD. There was a significant association of the total score index with an odds ratio of 1.45 (95% confidence interval 1.21–1.74). The cerebrovascular index was also associated with VaD with an odds ratio of 12.18 (95% confidence interval 6.29–23.61). The cardiovascular and vascular indexes were also associated with VaD status. The lifestyle index was not associated with VaD. Conclusion The cumulative role of multiple vascular risk factors or diseases increased the risk of VaD, as noted by the total vascular index. The lifestyle index did not reveal any significant differences. Further work is required for evaluation of these indexes.

Takahashi, Paul Y; Caldwell, Casey R; Targonski, Paul V

2012-01-01

30

Heterogeneity of the Angiogenic Response Induced in Different Normal Adult Tissues by Vascular Permeability Factor\\/Vascular Endothelial Growth Factor  

Microsoft Academic Search

Vascular permeability factor\\/vascular endothelial growth factor (VPF\\/VEGF) is an angiogenic cytokine with potential for the treatment of tissue ischemia. To investigate the properties of the new blood vessels induced by VPF\\/VEGF, we injected an adenoviral vector engineered to express murine VPF\\/VEGF164 into several normal tissues of adult nude mice or rats. A dose-dependent angiogenic response was induced in all tissues

Anna Pettersson; Janice A Nagy; Lawrence F Brown; Christian Sundberg; Ellen Morgan; Steven Jungles; Robert Carter; Jose E Krieger; Eleanor J Manseau; V Susan Harvey; Isabelle A Eckelhoefer; Dian Feng; Ann M Dvorak; Richard C Mulligan; Harold F Dvorak

2000-01-01

31

Integrin alphavbeta5 regulates lung vascular permeability and pulmonary endothelial barrier function.  

PubMed

Increased lung vascular permeability is an important contributor to respiratory failure in acute lung injury (ALI). We found that a function-blocking antibody against the integrin alphavbeta5 prevented development of lung vascular permeability in two different models of ALI: ischemia-reperfusion in rats (mediated by vascular endothelial growth factor [VEGF]) and ventilation-induced lung injury (VILI) in mice (mediated, at least in part, by transforming growth factor-beta [TGF-beta]). Knockout mice homozygous for a null mutation of the integrin beta5 subunit were also protected from lung vascular permeability in VILI. In pulmonary endothelial cells, both the genetic absence and blocking of alphavbeta5 prevented increases in monolayer permeability induced by VEGF, TGF-beta, and thrombin. Furthermore, actin stress fiber formation induced by each of these agonists was attenuated by blocking alphavbeta5, suggesting that alphavbeta5 regulates induced pulmonary endothelial permeability by facilitating interactions with the actin cytoskeleton. These results identify integrin alphavbeta5 as a central regulator of increased pulmonary vascular permeability and a potentially attractive therapeutic target in ALI. PMID:17079779

Su, George; Hodnett, Maki; Wu, Nanyan; Atakilit, Amha; Kosinski, Cynthia; Godzich, Mika; Huang, Xiao Zhu; Kim, Jiyeun K; Frank, James A; Matthay, Michael A; Sheppard, Dean; Pittet, Jean-François

2007-03-01

32

Limitations of the permeability-limited compartment model in estimating vascular permeability and interstitial volume fraction in DCE-MRI.  

PubMed

Dynamic contrast-enhanced magnetic resonance imaging commonly uses compartment models to estimate tissue parameters in general and perfusion parameters in particular. Compartment models assume a homogeneous distribution of the injected tracer throughout the compartment volume. Since tracer distribution within a compartment cannot be assessed, the parameters obtained by means of a compartment model might differ from the actual physical values. This work systematically examines the widely used permeability-surface-limited one-compartment model to determine the reliability of the parameters obtained by comparing them with their actual values. A computer simulation was used to model spatial tracer distribution within the interstitial volume using diffusion of contrast agent in tissue. Vascular parameters were varied as well as tissue parameters. The vascular parameters used were capillary radius (4 and 12 ?m), capillary permeability (from 0.03 to 3.3 ?m/s) and intercapillary distances from 30 to 300 ?m. The tissue parameters used were tortuosity (?), porosity (?) and interstitial volume fraction (v(e)). Our results suggest that the permeability-surface-limited compartment model generally underestimates capillary permeability for capillaries with a radius of 4 ?m by factors from ?0.03 for ?=0.04, to ? 0.1 for ?=0.2, to ? 0.5 for ?=1.0. An overestimation of actual capillary permeability for capillaries with a radius of 12 ?m by a factor of ?1.3 was found for ?=1.0, while ?=0.2 yielded an underestimation by a factor of ?0.3 and ?=0.04 by a factor of ? 0.03. The interstitial volume fraction, v(e), obtained by the compartment model differed with increasing intercapillary distances and for low vessel permeability, whereas v(e) was found to be estimated approximately accurately for P=0.3 ?m/s and P=3.3 ?m/s for vessel distances <100 ?m. PMID:21546193

Carreira, Guido Correia; Gemeinhardt, Ole; Gorenflo, Rudolf; Beyersdorff, Dirk; Franiel, Tobias; Plendl, Johanna; Lüdemann, Lutz

2011-06-01

33

The effects of prostaglandin E1, bradykinin and histamine on canine synovial vascular permeability.  

PubMed Central

1 The relative effects of prostaglandin E1, bradykinin and histamine on canine synovial vascular permeability were investigated by a method based on the measurement of the amounts of radiolabelled dextran (molecular weight 20,000) leaking from the circulation into the synovial cavity. 2 Bradykinin, prostaglandin E1 and histamine in that order of potency all increased synovial vascular permeability. Threshold concentrations were 0.3 micrometer, 3 micrometer and 30 micrometer respectively. 3 The effects of infusion of prostaglandin E1 combined with either bradykinin or histamine were greater than mere summation.

Grennan, D M; Mitchel, W; Miller, W; Zeitlin, I J

1977-01-01

34

Amino-terminal fragments of laminin ?2 chain retract vascular endothelial cells and increase vascular permeability.  

PubMed

Laminin ?2 (Lm?2) chain, a subunit of laminin-332, is a typical molecular marker of invading cancer cells, and its expression correlates with poor prognosis of cancer patients. It was previously found that forced expression of Lm?2 in cancer cells promotes their invasive growth in nude mice. However, the mechanism of the tumor-promoting activity of Lm?2 remains unknown. Here we investigated the interaction between Lm?2 and vascular endothelial cells. When treated with an N-terminal proteolytic fragment of ?2 (?2pf), HUVECs became markedly retracted or shrunken. The overexpression of Lm?2 or treatment with ?2pf stimulated T-24 bladder carcinoma cells to invade into the HUVEC monolayer and enhanced their transendothelial migration in vitro. Moreover, ?2pf increased endothelial permeability in vitro and in vivo. As the possible mechanisms, ?2pf activated ERK and p38 MAPK but inactivated Akt in HUVECs. Such effects of ?2pf led to prominent actin stress fiber formation in HUVECs, which was blocked by a ROCK inhibitor. In addition, ?2pf induced delocalization of VE-cadherin and ?-catenin from the intercellular junction. As possible receptors, ?2pf interacted with heparan sulfate proteoglycans on the surface of HUVECs. Moreover, we localized the active site of ?2pf to the N-terminal epidermal growth factor-like repeat. These data suggest that the interaction between ?2pf and heparan sulfate proteoglycans induces cytoskeletal changes of endothelial cells, leading to the loss of endothelial barrier function and the enhanced transendothelial migration of cancer cells. These activities of Lm?2 seem to support the aberrant growth of cancer cells. PMID:24238220

Sato, Hiroki; Oyanagi, Jun; Komiya, Eriko; Ogawa, Takashi; Higashi, Shouichi; Miyazaki, Kaoru

2014-02-01

35

Macrophage migration inhibitory factor induced by dengue virus infection increases vascular permeability.  

PubMed

Dengue virus (DENV) infection can cause mild dengue fever or severe dengue hemorrhage fever (DHF) and dengue shock syndrome (DSS). Serum levels of the macrophage migration inhibitory factor (MIF) have been shown to be correlated with severity and mortality in DENV patients, but the pathogenic roles of MIF in DHF/DSS are still unclear. Increase in vascular permeability is an important hallmark of DHF/DSS. In this study, we found that DENV infection of the human hepatoma cell line (Huh 7) induced MIF production. Conditioned medium collected from DENV-infected Huh 7 cells enhanced the permeability of the human endothelial cell line (HMEC-1) which was reduced in the presence of a MIF inhibitor, ISO-1 or medium from DENV-infected MIF knockdown Huh 7 cells. To further identify whether MIF can alter vascular permeability, we cloned and expressed both human and murine recombinant MIF (rMIF) and tested their effects on vascular permeability both in vitro and in vivo. Indirect immunofluorescent staining showed that the tight junction protein ZO-1 of HMEC-1 was disarrayed in the presence of rMIF and partially recovered when cells were treated with ISO-1 or PI3K/MEK-ERK/JNK signaling pathway inhibitors such as Ly294002, U0126, and SP600215. In addition, ZO-1 disarray induced by MIF was also recovered when CD74 or CXCR2/4 expression of HMEC-1 were inhibited. Last but not least, the vascular permeabilities of the peritoneal cavity and dorsal cutaneous capillary were also increased in mice treated with rMIF. Taken together; these results suggest that MIF induced by DENV infection may contribute to the increase of vascular permeability during DHF/DSS. Therapeutic intervention of MIF by its inhibitor or neutralizing antibodies may prevent DENV-induced lethality. PMID:21320786

Chuang, Yung-Chun; Lei, Huan-Yao; Liu, Hsiao-Sheng; Lin, Yee-Shin; Fu, Tzu-Fun; Yeh, Trai-Ming

2011-05-01

36

Suppressions of Serotonin-Induced Increased Vascular Permeability and Leukocyte Infiltration by Bixa orellana Leaf Extract  

PubMed Central

The aim of the present study was to evaluate the anti-inflammatory activities of aqueous extract of Bixa orellana (AEBO) leaves and its possible mechanisms in animal models. The anti-inflammatory activity of the extract was evaluated using serotonin-induced rat paw edema, increased peritoneal vascular permeability, and leukocyte infiltrations in an air-pouch model. Nitric oxide (NO), indicated by the sum of nitrites and nitrates, and vascular growth endothelial growth factor (VEGF) were measured in paw tissues of rats to determine their involvement in the regulation of increased permeability. Pretreatments with AEBO (50 and 150?mg?kg?1) prior to serotonin inductions resulted in maximum inhibitions of 56.2% of paw volume, 45.7% of Evans blue dye leakage in the peritoneal vascular permeability model, and 83.9% of leukocyte infiltration in the air-pouch model. 57.2% maximum inhibition of NO and 27% of VEGF formations in rats' paws were observed with AEBO at the dose of 150?mg?kg?1. Pharmacological screening of the extract showed significant (P < 0.05) anti-inflammatory activity, indicated by the suppressions of increased vascular permeability and leukocyte infiltration. The inhibitions of these inflammatory events are probably mediated via inhibition of NO and VEGF formation and release.

Sulaiman, NurShahira; Hakim, Muhammad Nazrul; Lian, Gwendoline Ee Cheng; Zakaria, Zainul Amirudin; Othman, Fauziah; Ahmad, Zuraini

2013-01-01

37

Pulmonary vascular permeability to transferrin in the pulmonary oedema of renal failure  

Microsoft Academic Search

Thirteen patients with renal failure and pulmonary oedema were assessed for evidence of increased pulmonary vascular permeability to protein by a double isotope technique. Comparison was made with 10 patients with cardiogenic pulmonary oedema, 11 healthy volunteers, and 10 patients with the adult respiratory distress syndrome. There was no significant difference in the accumulation of a radiolabelled plasma protein (transferrin)

G M Rocker; A G Morgan; D Pearson; G S Basran; D J Shale

1987-01-01

38

Acute lung injury and pulmonary vascular permeability: use of transgenic models.  

PubMed

Acute lung injury is a general term that describes injurious conditions that can range from mild interstitial edema to massive inflammatory tissue destruction. This review will cover theoretical considerations and quantitative and semi-quantitative methods for assessing edema formation and increased vascular permeability during lung injury. Pulmonary edema can be quantitated directly using gravimetric methods, or indirectly by descriptive microscopy, quantitative morphometric microscopy, altered lung mechanics, high-resolution computed tomography, magnetic resonance imaging, positron emission tomography, or x-ray films. Lung vascular permeability to fluid can be evaluated by measuring the filtration coefficient (Kf) and permeability to solutes evaluated from their blood to lung clearances. Albumin clearances can then be used to calculate specific permeability-surface area products (PS) and reflection coefficients (?). These methods as applied to a wide variety of transgenic mice subjected to acute lung injury by hyperoxic exposure, sepsis, ischemia-reperfusion, acid aspiration, oleic acid infusion, repeated lung lavage, and bleomycin are reviewed. These commonly used animal models simulate features of the acute respiratory distress syndrome, and the preparation of genetically modified mice and their use for defining specific pathways in these disease models are outlined. Although the initiating events differ widely, many of the subsequent inflammatory processes causing lung injury and increased vascular permeability are surprisingly similar for many etiologies. PMID:23737205

Parker, James C

2011-04-01

39

Akt1 regulates pathological angiogenesis, vascular maturation and permeability in vivo  

PubMed Central

Akt kinases control essential cellular functions, including proliferation, apoptosis, metabolism and transcription, and have been proposed as promising targets for treatment of angiogenesis-dependent pathologies, such as cancer and ischemic injury. But their precise roles in neovascularization remain elusive. Here we show that Akt1 is the predominant isoform in vascular cells and describe the unexpected consequences of Akt1 knockout on vascular integrity and pathological angiogenesis. Angiogenic responses in three distinct in vivo models were enhanced in Akt1?/? mice; these enhanced responses were associated with impairment of blood vessel maturation and increased vascular permeability. Although impaired vascular maturation in Akt1?/? mice may be attributed to reduced activation of endothelial nitric oxide synthase (eNOS), the major phenotypic changes in vascular permeability and angiogenesis were linked to reduced expression of two endogenous vascular regulators, thrombospondins 1 (TSP-1) and 2 (TSP-2). Re-expression of TSP-1 and TSP-2 in mice transplanted with wild-type bone marrow corrected the angiogenic abnormalities in Akt1?/? mice. These findings establish a crucial role of an Akt-thrombospondin axis in angiogenesis.

Chen, Juhua; Somanath, Payaningal R; Razorenova, Olga; Chen, William S; Hay, Nissim; Bornstein, Paul; Byzova, Tatiana V

2006-01-01

40

Inhibition of vascular endothelial growth factor (VEGF)-induced endothelial proliferation, arterial relaxation, vascular permeability and angiogenesis by dobesilate.  

PubMed

Vascular endothelial growth factor (VEGF) is a key factor in angiogenesis and vascular permeability which is associated with many pathological processes. 2,5-hydroxybenzene sulfonate (DHBS; dobesilate) is a small molecule with anti-angiogenic activity that has been described as an inhibitor of fibroblast growth factors (FGF). The aim of the present study was to evaluate the effects of DHBS on VEGF-induced actions. The effects of DHBS were evaluated on VEGF-induced proliferation in human umbilical vein endothelial cells (HUVEC) and rat aorta relaxation, as well as on in vivo VEGF-induced skin vascular permeability and neovascularization in rats. DHBS at 50 and 100 ?M concentration significantly inhibited the proliferation of HUVEC induced by VEGF (10 ng/ml), without significantly affecting HUVEC proliferation in the absence of VEGF. Rapid VEGF-induced activation of Akt in HUVEC was also prevented by DHBS (100 ?M). Additionally, DHBS (2 ?M) specifically inhibited the relaxation of rat aorta induced by VEGF (0.1 to 30 ng/ml), but not endothelium-dependent relaxation to acetylcholine (1 nM to 10 ?M). The in vivo enhancement of vascular permeability caused by VEGF injection (50 ?l at 10 ng/ml) in rat skin was also inhibited by DHBS co-administration (200 ?M) (74.8±3.8% inhibition of dye extravasation). Administration of DHBS (200 mg/kg/day; i.p.) also reduced VEGF-induced angiogenesis in vivo. DHBS inhibits main responses elicited in vitro and in vivo by VEGF. As a dual antagonist of VEGF and FGF activities, DHBS could be of therapeutic interest in the treatment of diseases related to VEGF/FGF overproduction and excessive angiogenesis. PMID:21703259

Angulo, Javier; Peiró, Concepción; Romacho, Tania; Fernández, Argentina; Cuevas, Begoña; González-Corrochano, Rocío; Giménez-Gallego, Guillermo; de Tejada, Iñigo Sáenz; Sánchez-Ferrer, Carlos F; Cuevas, Pedro

2011-09-30

41

Latent KSHV infection increases the vascular permeability of human endothelial cells  

PubMed Central

Kaposi sarcoma–associated herpesvirus (KSHV) is associated with 3 different human malignancies: Kaposi sarcoma (KS), primary effusion lymphoma, and multicentric Castleman disease. The KS lesion is driven by KSHV-infected endothelial cells and is highly dependent on autocrine and paracrine factors for survival and growth. We report that latent KSHV infection increases the vascular permeability of endothelial cells. Endothelial cells with latent KSHV infection display increased Rac1 activation and activation of its downstream modulator, p21-activated kinase 1 (PAK1). The KSHV-infected cells also exhibit increases in tyrosine phosphorylation of vascular endothelial (VE)–cadherin and ?-catenin, whereas total levels of these proteins remained unchanged, suggesting that latent infection disrupted endothelial cell junctions. Consistent with these findings, we found that KSHV-infected endothelial cells displayed increased permeability compared with uninfected endothelial cells. Knockdown of Rac1 and inhibition of reactive oxygen species (ROS) resulted in decreased permeability in the KSHV-infected endothelial cells. We further demonstrate that the KSHV K1 protein can activate Rac1. Rac1 was also highly activated in KSHV-infected endothelial cells and KS tumors. In conclusion, KSHV latent infection increases Rac1 and PAK1 activity in endothelial cells, resulting in the phosphorylation of VE-cadherin and ?-catenin and leading to the disassembly of cell junctions and to increased vascular permeability of the infected endothelial cells.

Guilluy, Christophe; Zhang, Zhigang; Bhende, Prasanna M.; Sharek, Lisa; Wang, Ling; Burridge, Keith

2011-01-01

42

A Neurodegenerative Vascular Burden Index and the Impact on Cognition  

PubMed Central

A wide range of vascular burden factors has been identified to impact vascular function and structure as indicated by carotid intima–media thickness (IMT). On the basis of their impact on IMT, vascular factors may be selected and clustered in a vascular burden index (VBI). Since many vascular factors increase the risk of Alzheimer’s disease (AD), a multifactorial neurodegenerative VBI may be related to early pathological processes in AD and cognitive decline in its preclinical stages. We investigated an elderly cohort at risk for neurodegeneration (TREND study, n?=?1102) for the multifactorial influence of vascular burden factors on IMT measured by ultrasound. To create a VBI for this cohort, vascular factors and their definitions (considering medical history, medication, and/or blood marker data) were selected based on their statistical effects on IMT in multiple regressions including age and sex. The impact of the VBI on cognitive performance was assessed using the Trail-Making Test (TMT) and the consortium to establish a registry for Alzheimer’s disease (CERAD) neuropsychological battery. IMT was significantly predicted by age (standardized ??=?0.26), sex (0.09; males?>?females) and the factors included in the VBI: obesity (0.18), hypertension (0.14), smoking (0.08), diabetes (0.07), and atherosclerosis (0.05), whereas other cardiovascular diseases or hypercholesterolemia were not significant. Individuals with 2 or more VBI factors compared to individuals without had an odds ratio of 3.17 regarding overly increased IMT ( ??1.0?mm). The VBI showed an impact on executive control [log(TMT B?A), p?=?0.047] and a trend toward decreased global cognitive function (CERAD total score, p?=?0.057) independent of age, sex, and education. A VBI established on the basis of IMT may help to identify individuals with overly increased vascular burden linked to decreased cognitive function indicating neurodegenerative processes. The longitudinal study of this risk cohort will reveal the value of the VBI as prodromal marker for cognitive decline and AD.

Heinzel, Sebastian; Liepelt-Scarfone, Inga; Roeben, Benjamin; Nasi-Kordhishti, Isabella; Suenkel, Ulrike; Wurster, Isabel; Brockmann, Kathrin; Fritsche, Andreas; Niebler, Raphael; Metzger, Florian G.; Eschweiler, Gerhard W.; Fallgatter, Andreas J.; Maetzler, Walter; Berg, Daniela

2014-01-01

43

Significance of vascular endothelial growth factor/vascular permeability factor for solid tumor growth, and its inhibition by the antibody.  

PubMed

Angiogenesis is essential for successful tumor growth in vivo. There is a hypothesis that tumors secrete a putative tumor angiogenic factor (TAF) to facilitate blood vessel formations. Although several endothelial growth factors have been reported, it remains unclear whether these factors function as TAF in vivo. Vascular endothelial growth factor (VEGF)/vascular permeability factor (VPF) is a vascular endothelial mitogen that can increase blood vessel permeability. We have established a cell line (HeLa/v5), which secretes VEGF/VPF, by transfection of human VEGF/VPF cDNA. HeLa/v5 showed higher angiogenic activity, taken/planted ratio and tumor growth rate than the control transformant (HeLa/c), when they were implanted to nude mice. Administration of a polyclonal antibody, which neutralizes the mitogenic activity of VEGF/VPF in vitro, to the tumor implanted nude mice suppressed the in vivo growth of HeLa/v5. Furthermore, all 8 tumor cell lines we tested secrete VEGF/VPF into culture media. Our findings indicate that VEGF/VPF is a tumor angiogenic factor. PMID:7688963

Kondo, S; Asano, M; Suzuki, H

1993-08-16

44

Identifying tumor vascular permeability heterogeneity using reduced encoding techniques  

NASA Astrophysics Data System (ADS)

We test the hypothesis that the loss of spatial resolution to gain temporal resolution in clinical dynamic contrast enhanced (DCE) magnetic resonance mammography (MRM) causes partial volume effects that yield inaccurate permeability-surface area products (PS = Kp?t) which results in erroneous diagnostic information and we offer a potential solution using reduced encoding techniques to solve this problem. We compared the PS obtained from DCE MRI at clinical MRI resolutions (2500 x 2500 mum resolution), to that obtained from resolutions analogous to histopathological in plane resolutions (938 x 938 mum and 469 x 469 mum resolution). Secondly, we determined the accuracy of PS obtained from Keyhole, ?educed-encoding I&barbelow;maging by G&barbelow;eneralized-series ?econstruction (RIGR), and ?wo-reference RIGR (TRIGR) using high-resolution baseline data (469 x 469 mum resolution) and clinical resolution dynamic data (2500 x 2500 mum resolution). Lastly, we statistically correlated two-compartment model fitting parameters (tumor EES volume fraction, ve, tumor plasma volume fraction, vp, and PS) obtained from DCE MRI at all three resolutions to histopathologically determined tumor diagnosis. In our model, female Sprague Dawley rats with N-ethyl-N-nitrosourea (ENU) induced mammary tumors imaged with fast T1-weighted gradient echo DCE MRI following a Gd-DTPA injection, there is a window of resolutions that detects similar PS "hot spots" compared to those obtained from the clinical imager resolution. The top five PS "hot spots" obtained from 469 mum resolution FFT are statistically different from those at 938 mum resolution FFT, p = 0.0014, and 2500 mum resolution FFT, p < 0.0001. Keyhole when compared with a FFT of similar resolution does not detect PS "hot spots" of similar value, p = 0.0002. PS "hot spots" obtained from RIGR compared to those from FFT are statistically the same value, p = 0.2734, but do not statistically agree on the location of mapped values. The top five Kp?t/VT "hot spots" and their corresponding ve can statistically differentiate invasive ductal carcinoma from non-invasive papillary carcinoma for the 469 mum and 938 mum resolution, p = 0.0017 and p = 0.0047, respectively, but not for 2500 mum resolution, p = 0.9008.

Aref, Michael

45

Anatomic basis of ulnar index metacarpal reverse flow vascularized bone graft for index distal bone loss.  

PubMed

Well-known advantages of vascularized bone grafts led us to determine the anatomical basis of a metacarpal vascularized bone graft to find a solution for distal index bone loss. Seventeen adult human hands from fresh cadavers were dissected and analyzed. For each hand, we studied the second dorsal metacarpal artery, the ulnar dorsal proper digital artery of index, and the ulnar palmar proper digital artery of the index. Location, diameters, origins, and anastomoses were observed, and at the end, the vascularised bone graft was raised. The second dorsal metacarpal artery was present in all hands, always arising from the dorsal carpal arch with a 1-mm mean diameter. The ulnar dorsal proper digital artery of index was isolated on all dissections, with a subcutaneous location on the ulno-dorsal side of the proximal phalanx. The mean diameter of ulnar dorsal proper digital artery at the level of index proximal phalanx was 0.4 mm. We found anastomotic branches between the ulnar dorsal and palmar proper digital artery of index at the level of the proximal phalanx which permitted us to elevate a vascularised bone graft. We succeeded in removing the graft in all specimens. Its pivot point was always more distal than the middle of the proximal phalanx. The arc of rotation allowed the graft to reach the distal phalanx in 80% of the cases. This anatomical study has demonstrated the theoretical possibility of a reversed pedicled bone graft taken from the ulnar neck of the second metacarpal. This graft brings the following benefits: (a) the use of a minor vascular axis, (b) a surgical technique with a dorsal approach allowing the elevation and the use of the graft at the same time. It can be used on the index for failures of DIP joint arthrodesis, huge chondroma, or traumatology. PMID:20461513

Ardouin, L; Le Nen, D; Geffard, B; Hanouz, N; Vielpeau, C; Salame, E

2010-10-01

46

Corticotropin-releasing hormone induces skin vascular permeability through a neurotensin-dependent process  

PubMed Central

Many skin disorders are associated with increased numbers of activated mast cells and are worsened by stress; however, the mechanism underlying these processes is not understood. Corticotropin-releasing hormone (CRH) is secreted under stress from the hypothalamus, but also in the skin, where it induces mast cell activation and vascular permeability. We investigated the effect of CRH in a number of animal models by using i.v. Evans blue extravasation as a marker of vascular permeability. Intradermal CRH is among the most potent peptides at 100 nM, its effect being nearly comparable to that of neurotensin (NT). Pretreatment of skin injection sites with the NT receptor antagonist SR48692 blocks CRH-induced vascular permeability, which is diminished in NT?/? mice, implying that NT is necessary for the effect of CRH. CRH and NT precursor mRNA are shown to be expressed in both dorsal root ganglia and skin, whereas the latter also expresses mRNA for prohormone convertase 5, an enzyme that cleaves pro-NT into its active form. We also show that the effect of both CRH and NT is absent in W/Wv mast cell-deficient mice; however, only a fraction of skin mast cells express CRH receptors, as shown by FACS analysis of CRH receptor (CRHR) and c-kit double-positive disaggregated mouse skin mast cells. These findings suggest that CRH induces skin vascular permeability through NT acting on mast cells and that both peptides should be considered in the pathogenesis of skin disorders exacerbated by stress.

Donelan, Jill; Boucher, William; Papadopoulou, Nikoletta; Lytinas, Michael; Papaliodis, Dean; Dobner, Paul; Theoharides, Theoharis C.

2006-01-01

47

Inhibition of vascular permeability by antisense-mediated inhibition of plasma kallikrein and coagulation factor 12.  

PubMed

Hereditary angioedema (HAE) is a rare disorder characterized by recurrent, acute, and painful episodes of swelling involving multiple tissues. Deficiency or malfunction of the serine protease inhibitor C1 esterase inhibitor (C1-INH) results in HAE types 1 and 2, respectively, whereas mutations in coagulation factor 12 (f12) have been associated with HAE type 3. C1-INH is the primary inhibitor of multiple plasma cascade pathways known to be altered in HAE patients, including the complement, fibrinolytic, coagulation, and kinin-kallikrein pathways. We have selectively inhibited several components of both the kinin-kallikrein system and the coagulation cascades with potent and selective antisense oligonucleotides (ASOs) to investigate their relative contributions to vascular permeability. We have also developed ASO inhibitors of C1-INH and characterized their effects on vascular permeability in mice as an inducible model of HAE. Our studies demonstrate that ASO-mediated reduction in C1-INH plasma levels results in increased vascular permeability and that inhibition of proteases of the kinin-kallikrein system, either f12 or prekallikrein (PKK) reverse the effects of C1-INH depletion with similar effects on both basal and angiotensin converting enzyme (ACE) inhibitor-induced permeability. In contrast, inhibition of coagulation factors 11 (f11) or 7 (f7) had no effect. These results suggest that the vascular defects observed in C1-INH deficiency are dependent on the kinin-kallikrein system proteases f12 and PKK, and not mediated through the coagulation pathways. In addition, our results highlight a novel therapeutic modality that can potentially be employed prophylactically to prevent attacks in HAE patients. PMID:23582057

Bhattacharjee, Gourab; Revenko, Alexey S; Crosby, Jeffrey R; May, Chris; Gao, Dacao; Zhao, Chenguang; Monia, Brett P; MacLeod, A Robert

2013-06-01

48

Extracellular carbonic anhydrase mediates hemorrhagic retinal and cerebral vascular permeability through prekallikrein activation  

Microsoft Academic Search

Excessive retinal vascular permeability contributes to the pathogenesis of proliferative diabetic retinopathy and diabetic macular edema, leading causes of vision loss in working-age adults. Using mass spectroscopy–based proteomics, we detected 117 proteins in human vitreous and elevated levels of extracellular carbonic anhydrase-I (CA-I) in vitreous from individuals with diabetic retinopathy, suggesting that retinal hemorrhage and erythrocyte lysis contribute to the

Ben-Bo Gao; Allen Clermont; Susan Rook; Stephanie J Fonda; Vivek J Srinivasan; Maciej Wojtkowski; James G Fujimoto; Robert L Avery; Paul G Arrigg; Sven-Erik Bursell; Lloyd Paul Aiello; Edward P Feener

2007-01-01

49

Increase in vascular permeability produced in rat airways by PAF: potentiation by adrenalectomy.  

PubMed Central

1. The effect of bilateral adrenalectomy on the sensitivity of blood vessels in rat airways to mediators that increase vascular permeability was examined. 2. An increase in vascular permeability was induced by intravenous platelet activating factor (PAF, 50, 100, 500, 1000 ng kg-1) and measured by quantifying the extravasation of Evans blue dye. 3. PAF consistently increased the amount of Evans blue extravasation in the larynx, trachea, main bronchi and intrapulmonary airways in sham-operated rats. 4. The magnitude of this extravasation was significantly greater in the larynx (P less than 0.05), trachea (P less than 0.05) and main bronchi (P less than 0.05) of the adrenalectomized rats than it was in these tissues of the sham-operated rats. 5. When adrenalectomized rats were given subcutaneous dexamethasone (0.2 mg kg-1 4 h before PAF) the amount of plasma extravasation produced by PAF was decreased to the level of the sham-operated rats. 6. We conclude that adrenalectomy potentiates the increase in airway vascular permeability induced by PAF in rats and that this effect may be due to the depletion of endogenous corticosteroids.

Boschetto, P.; Musajo, F. G.; Tognetto, L.; Boscaro, M.; Mapp, C. E.; Barnes, P. J.; Fabbri, L. M.

1992-01-01

50

Intravital analysis of vascular permeability in mice using two-photon microscopy  

PubMed Central

Blood vessel endothelium forms a semi-permeable barrier and its permeability controls the traffics of plasma contents. Here we report an intravital evaluation system for vascular permeability in mice using two-photon microscopy. We used various sizes of fluorescein-conjugated dextran as a tracer and its efflux was quantified by measuring the changes of fluorescent intensity both on the blood vessel area and the interstitial space. Using this system, we demonstrated that skin blood vessels limited the passage of dextran larger than 70?kDa under homeostatic conditions. We evaluated the kinetics of vascular permeability in histamine- or IgE-induced type I allergic models and a hapten-induced type IV allergic model. In such inflammatory conditions, the hyperpermeability was selectively induced in the postcapillary venules and dextran as large as 2000-kDa leaked from the bloods. Taken together, our study provides a convenient method to characterize the skin blood vessels as a traffic barrier in physiological conditions.

Egawa, Gyohei; Nakamizo, Satoshi; Natsuaki, Yohei; Doi, Hiromi; Miyachi, Yoshiki; Kabashima, Kenji

2013-01-01

51

Intravital analysis of vascular permeability in mice using two-photon microscopy.  

PubMed

Blood vessel endothelium forms a semi-permeable barrier and its permeability controls the traffics of plasma contents. Here we report an intravital evaluation system for vascular permeability in mice using two-photon microscopy. We used various sizes of fluorescein-conjugated dextran as a tracer and its efflux was quantified by measuring the changes of fluorescent intensity both on the blood vessel area and the interstitial space. Using this system, we demonstrated that skin blood vessels limited the passage of dextran larger than 70 kDa under homeostatic conditions. We evaluated the kinetics of vascular permeability in histamine- or IgE-induced type I allergic models and a hapten-induced type IV allergic model. In such inflammatory conditions, the hyperpermeability was selectively induced in the postcapillary venules and dextran as large as 2000-kDa leaked from the bloods. Taken together, our study provides a convenient method to characterize the skin blood vessels as a traffic barrier in physiological conditions. PMID:23732999

Egawa, Gyohei; Nakamizo, Satoshi; Natsuaki, Yohei; Doi, Hiromi; Miyachi, Yoshiki; Kabashima, Kenji

2013-01-01

52

Cortactin deficiency is associated with reduced neutrophil recruitment but increased vascular permeability in vivo  

PubMed Central

Neutrophil extravasation and the regulation of vascular permeability require dynamic actin rearrangements in the endothelium. In this study, we analyzed in vivo whether these processes require the function of the actin nucleation–promoting factor cortactin. Basal vascular permeability for high molecular weight substances was enhanced in cortactin-deficient mice. Despite this leakiness, neutrophil extravasation in the tumor necrosis factor–stimulated cremaster was inhibited by the loss of cortactin. The permeability defect was caused by reduced levels of activated Rap1 (Ras-related protein 1) in endothelial cells and could be rescued by activating Rap1 via the guanosine triphosphatase (GTPase) exchange factor EPAC (exchange protein directly activated by cAMP). The defect in neutrophil extravasation was caused by enhanced rolling velocity and reduced adhesion in postcapillary venules. Impaired rolling interactions were linked to contributions of ?2-integrin ligands, and firm adhesion was compromised by reduced ICAM-1 (intercellular adhesion molecule 1) clustering around neutrophils. A signaling process known to be critical for the formation of ICAM-1–enriched contact areas and for transendothelial migration, the ICAM-1–mediated activation of the GTPase RhoG was blocked in cortactin-deficient endothelial cells. Our results represent the first physiological evidence that cortactin is crucial for orchestrating the molecular events leading to proper endothelial barrier function and leukocyte recruitment in vivo.

Schnoor, Michael; Lai, Frank P.L.; Zarbock, Alexander; Klaver, Ruth; Polaschegg, Christian; Schulte, Dorte; Weich, Herbert A.; Oelkers, J. Margit; Rottner, Klemens

2011-01-01

53

Measurements of pulmonary vascular permeability with PET and gallium-68 transferrin  

SciTech Connect

We quantified pulmonary vascular permeability with positron emission tomography (PET) and gallium-68-(/sup 68/Ga) labeled transferrin. Six dogs with oleic acid-induced lung injury confined to the left lower lobe, two normal human volunteers, and two patients with the adult respiratory distress syndrome (ARDS) were evaluated. Lung tissue-activity measurements were obtained from sequential 1-5 min PET scans collected over 60 min, after in vivo labeling of transferrin through intravenous administration of (/sup 68/Ga)citrate. Blood-activity measurements were measured from simultaneously obtained peripheral blood samples. A forward rate constant describing the movement of transferrin from pulmonary vascular to extravascular compartments, the pulmonary transcapillary escape rate (PTCER), was then calculated from these data using a two-compartment model. In dogs, PTCER was 49 +/- 18 in normal lung tissue and 485 +/- 114 10(-4) min-1 in injured lung. A repeat study in these dogs 4 hr later showed no significant change. Values in the human subjects showed similarly marked differences between normal and abnormal lung tissue. We conclude that PET will be a useful method of evaluating vascular permeability changes after acute lung injury.

Mintun, M.A.; Dennis, D.R.; Welch, M.J.; Mathias, C.J.; Schuster, D.P.

1987-11-01

54

Extracellular RNA mediates endothelial-cell permeability via vascular endothelial growth factor.  

PubMed

Cell injury leads to exposure of intracellular material and is associated with increased permeability of vessels in the vicinity of the damage. Here, we demonstrate that natural extracellular RNA as well as artificial RNA (poly-I:C), or single-stranded RNA but not DNA, significantly increased the permeability across brain microvascular endothelial cells in vitro and in vivo. RNA-induced hyperpermeability of tight monolayers of endothelial cells correlated with disintegration of tight junctions and was mediated through vascular endothelial growth factor (VEGF), reminiscent of heparin's activities. Antisense oligonucleotides against VEGF-receptor 2 (VEGF-R2) prevented the permeability-inducing activity of extracellular RNA and heparin completely. Hence, these polyanionic substances can lead to mobilization/stabilization of VEGF with the subsequent activation of VEGF-R2. In accordance with these functional data, strong binding of VEGF as well as other growth factors to RNA was demonstrable. In in vivo rat models of FeCl(3)-induced sinus sagittal is superior thrombosis and stroke/brain edema, pretreatment of animals with RNase (but not DNase) resulted in a significant reduction of vessel occlusion, infarct volume, and prevention of brain edema formation. Together, these results identify extracellular RNA as a novel natural permeability factor, upstream of VEGF, whereas counteracting RNase treatment may serve as new vessel-protective modality. PMID:17576819

Fischer, Silvia; Gerriets, Tibo; Wessels, Carina; Walberer, Maureen; Kostin, Sawa; Stolz, Erwin; Zheleva, Kirila; Hocke, Andreas; Hippenstiel, Stefan; Preissner, Klaus T

2007-10-01

55

Effect of ultrasound on the permeability of vascular wall to nano-emulsion droplets.  

PubMed

The effect of ultrasound on the permeability of blood vessels to nano-emulsion droplets was investigated using excised mouse carotid arteries as model blood vessels. Perfluorocarbon nano-droplets were formed by perfluoro-15-crown-5-ether and stabilized by poly(ethylene oxide)-co-poly(DL-lactide) block co-polymer shells. Nano-droplet fluorescence was imparted by interaction with fluorescein isothiocyanate-dextran (molecular weight = 70,000 Da). The permeability of carotid arteries to nano-droplets was studied in the presence and absence of continuous wave or pulsed therapeutic 1-MHz ultrasound. The data indicated that the application of ultrasound resulted in permeabilization of the vascular wall to nano-droplets. The effect of continuous wave ultrasound was substantially stronger than that of pulsed ultrasound of the same total energy. No effect of blood vessel pre-treatment with ultrasound was observed. PMID:23849384

Thakkar, Dhaval; Gupta, Roohi; Monson, Kenneth; Rapoport, Natalya

2013-10-01

56

Effect of sulodexide on endothelial glycocalyx and vascular permeability in patients with type 2 diabetes mellitus  

Microsoft Academic Search

Aims\\/hypothesis  Endothelial glycocalyx perturbation contributes to increased vascular permeability. In the present study we set out to evaluate\\u000a whether: (1) glycocalyx is perturbed in individuals with type 2 diabetes mellitus, and (2) oral glycocalyx precursor treatment\\u000a improves glycocalyx properties.\\u000a \\u000a \\u000a \\u000a \\u000a Methods  Male participants with type 2 diabetes (n?=?10) and controls (n?=?10) were evaluated before and after 2 months of sulodexide administration (200 mg\\/day). The glycocalyx

L. N. Broekhuizen; B. A. Lemkes; H. L. Mooij; M. C. Meuwese; H. Verberne; F. Holleman; R. O. Schlingemann; M. Nieuwdorp; E. S. G. Stroes; H. Vink

2010-01-01

57

Sphingosine-1-phosphate modulates vascular permeability and cell recruitment in acute inflammation in vivo.  

PubMed

The sphingosine kinase (SPK)/sphingosine-1-phosphate (S1P) pathway recently has been associated with a variety of inflammatory-based diseases. The majority of these studies have been performed in vitro. Here, we have addressed the relevance of the SPK/S1P pathway in the acute inflammatory response in vivo by using different well known preclinical animal models. The study has been performed by operating a pharmacological modulation using 1) L-cycloserine and DL-threo-dihydrosphingosine (DTD), S1P synthesis inhibitors or 2) 2-undecyl-thiazolidine-4-carboxylic acid (BML-241) and N-(2,6-dichloro-4-pyridinyl)-2-[1,3-dimethyl-4-(1-methylethyl)-1H-pyrazolo[3,4-b]pyridin-6-yl]-hydrazinecarboxamide (JTE-013), specific S1P(2) and S1P(3) receptor antagonists. After local injection of carrageenan in mouse paw S1P release significantly increases locally and decreases during the resolution phase. Expression of SPKs and S1P(2) and S1P(3) receptors is increased in inflamed tissues. Administration of L-cycloserine or DTD caused a significant anti-inflammatory effect. By using different animal models we have also demonstrated that the SPK/S1P pathway contributes to changes in vascular permeability and promotes cell recruitment. The S1P effect on cell recruitment results is receptor-mediated because both JTE-013 and BML-241 inhibited zymosan-induced cell chemotaxis without effect on vascular leakage. Conversely, changes in vascular permeability involve mainly SPK activity, because compound 48/80-induced vascular leakage was significantly inhibited by DTD. In conclusion, the SPK/S1P pathway is involved in acute inflammation and could represent a valuable therapeutic target for developing a new class of anti-inflammatory drugs. PMID:21421740

Roviezzo, Fiorentina; Brancaleone, Vincenzo; De Gruttola, Luana; Vellecco, Valentina; Bucci, Mariarosaria; D'Agostino, Bruno; Cooper, Dianne; Sorrentino, Raffaella; Perretti, Mauro; Cirino, Giuseppe

2011-06-01

58

Ischemia-reperfusion injury induces occludin phosphorylation/ubiquitination and retinal vascular permeability in a VEGFR-2-dependent manner.  

PubMed

Retinal ischemia-reperfusion (IR) induces neurodegenaration as well as blood-retinal barrier (BRB) breakdown causing vascular permeability. Whereas the neuronal death has been extensively studied, the molecular mechanisms related to BRB breakdown in IR injury remain poorly understood. In this study, we investigated the early changes in tight junctional (TJ) proteins in response to IR injury. Ischemia-reperfusion injury was induced in male rat retinas by increasing the intraocular pressure for 45?minutes followed by natural reperfusion. The results demonstrate that IR injury induced occludin Ser490 phosphorylation and ubiquitination within 15?minutes of reperfusion with subsequent vascular permeability. Immunohistochemical analysis revealed a rapid increase in occludin Ser490 phosphorylation and loss of Zonula occludens-1 (ZO-1) protein, particularly in arterioles. Ischemia-reperfusion injury also rapidly induced the activation and phosphorylation of vascular endothelial growth factor receptor-2 (VEGFR-2) at tyrosine 1175. Blocking vascular endothelial growth factor (VEGF) function by intravitreal injection of bevacizumab prevented VEGFR-2 activation, occludin phosphorylation, and vascular permeability. These studies suggest a novel mechanism of occludin Ser490 phosphorylation and ubiquitination downstream of VEGFR2 activation associated with early IR-induced vascular permeability. PMID:24398936

Muthusamy, Arivalagan; Lin, Cheng-Mao; Shanmugam, Sumathi; Lindner, Heather M; Abcouwer, Steven F; Antonetti, David A

2014-03-01

59

Minocycline prevents retinal inflammation and vascular permeability following ischemia-reperfusion injury  

PubMed Central

Background Many retinal diseases are associated with vascular dysfunction accompanied by neuroinflammation. We examined the ability of minocycline (Mino), a tetracycline derivative with anti-inflammatory and neuroprotective properties, to prevent vascular permeability and inflammation following retinal ischemia-reperfusion (IR) injury, a model of retinal neurodegeneration with breakdown of the blood-retinal barrier (BRB). Methods Male Sprague–Dawley rats were subjected to 45 min of pressure-induced retinal ischemia, with the contralateral eye serving as control. Rats were treated with Mino prior to and following IR. At 48 h after reperfusion, retinal gene expression, cellular inflammation, Evan’s blue dye leakage, tight junction protein organization, caspase-3 activation, and DNA fragmentation were measured. Cellular inflammation was quantified by flow-cytometric evaluation of retinal tissue using the myeloid marker CD11b and leukocyte common antigen CD45 to differentiate and quantify CD11b+/CD45low microglia, CD11b+/CD45hi myeloid leukocytes and CD11bneg/CD45hi lymphocytes. Major histocompatibility complex class II (MHCII) immunoreactivity was used to determine the inflammatory state of these cells. Results Mino treatment significantly inhibited IR-induced retinal vascular permeability and disruption of tight junction organization. Retinal IR injury significantly altered mRNA expression for 21 of 25 inflammation- and gliosis-related genes examined. Of these, Mino treatment effectively attenuated IR-induced expression of lipocalin 2 (LCN2), serpin peptidase inhibitor clade A member 3 N (SERPINA3N), TNF receptor superfamily member 12A (TNFRSF12A), monocyte chemoattractant-1 (MCP-1, CCL2) and intercellular adhesion molecule-1 (ICAM-1). A marked increase in leukostasis of both myeloid leukocytes and lymphocytes was observed following IR. Mino treatment significantly reduced retinal leukocyte numbers following IR and was particularly effective in decreasing the appearance of MHCII+ inflammatory leukocytes. Surprisingly, Mino did not significantly inhibit retinal cell death in this model. Conclusions IR induces a retinal neuroinflammation within hours of reperfusion characterized by inflammatory gene expression, leukocyte adhesion and invasion, and vascular permeability. Despite Mino significantly inhibiting these responses, it failed to block neurodegeneration.

2013-01-01

60

Agmatine induces gastric protection against ischemic injury by reducing vascular permeability in rats  

PubMed Central

AIM: To investigate the effect of administration of agmatine (AGM) on gastric protection against ischemia reperfusion (I/R) injury. METHODS: Three groups of rats (6/group); sham, gastric I/R injury, and gastric I/R + AGM (100 mg/kg, i.p. given 15 min prior to gastric ischemia) were recruited. Gastric injury was conducted by ligating celiac artery for 30 min and reperfusion for another 30 min. Gastric tissues were histologically studied and immunostained with angiopoietin 1 (Ang-1) and Ang-2. Vascular endothelial growth factor (VEGF) and monocyte chemoattractant protein-1 (MCP-1) were measured in gastric tissue homogenate. To assess whether AKt/phosphatidyl inositol-3-kinase (PI3K) mediated the effect of AGM, an additional group was pretreated with Wortmannin (WM) (inhibitor of Akt/PI3K, 15 ?g/kg, i.p.), prior to ischemic injury and AGM treatment, and examined histologically and immunostained. Another set of experiments was run to study vascular permeability of the stomach using Evan’s blue dye. RESULTS: AGM markedly reduced Evan’s blue dye extravasation (3.58 ± 0.975 ?g/stomach vs 1.175 ± 0.374 ?g/stomach, P < 0.05), VEGF (36.87 ± 2.71 pg/100 mg protein vs 48.4 ± 6.53 pg/100 mg protein, P < 0.05) and MCP-1 tissue level (29.5 ± 7 pg/100 mg protein vs 41.17 ± 10.4 pg/100 mg protein, P < 0.01). It preserved gastric histology and reduced congestion. Ang-1 and Ang-2 immunostaining were reduced in stomach sections of AGM-treated animals. The administration of WM abolished the protective effects of AGM and extensive hemorrhage and ulcerations were seen. CONCLUSION: AGM protects the stomach against I/R injury by reducing vascular permeability and inflammation. This protection is possibly mediated by Akt/PI3K.

Masri, Abeer A Al; Eter, Eman El

2012-01-01

61

Control of vascular permeability by atrial natriuretic peptide via a GEF-H1-dependent mechanism.  

PubMed

Microtubule (MT) dynamics is involved in a variety of cell functions, including control of the endothelial cell (EC) barrier. Release of Rho-specific nucleotide exchange factor GEF-H1 from microtubules activates the Rho pathway of EC permeability. In turn, pathologic vascular leak can be prevented by treatment with atrial natriuretic peptide (ANP). This study investigated a novel mechanism of vascular barrier protection by ANP via modulation of GEF-H1 function. In pulmonary ECs, ANP suppressed thrombin-induced disassembly of peripheral MT and attenuated Rho signaling and cell retraction. ANP effects were mediated by the Rac1 GTPase effector PAK1. Activation of Rac1-PAK1 promoted PAK1 interaction with the Rho activator GEF-H1, inducing phosphorylation of total and MT-bound GEF-H1 and leading to attenuation of Rho-dependent actin remodeling. In vivo, ANP attenuated lung injury caused by excessive mechanical ventilation and TRAP peptide (TRAP/HTV), which was further exacerbated in ANP(-/-) mice. The protective effects of ANP against TRAP/HTV-induced lung injury were linked to the increased pool of stabilized MT and inactivation of Rho signaling via ANP-induced, PAK1-dependent inhibitory phosphorylation of GEF-H1. This study demonstrates a novel protective mechanism of ANP against pathologic hyperpermeability and suggests a novel pharmacological intervention for the prevention of increased vascular leak via PAK1-dependent modulation of GEF-H1 activity. PMID:24352660

Tian, Xinyong; Tian, Yufeng; Gawlak, Grzegorz; Sarich, Nicolene; Wu, Tinghuai; Birukova, Anna A

2014-02-21

62

Evidence of a role for TRPC channels in VEGF-mediated increased vascular permeability in vivo.  

PubMed

Vascular endothelial growth factor (VEGF) increases vascular permeability by stimulating endothelial Ca(2+) influx. Here we provide evidence that links VEGF-mediated increased permeability and endothelial intracellular Ca(2+) concentration ([Ca(2+)](i)) with diacylglycerol (DAG)-mediated activation of the transient receptor potential channels (TRPCs). We used the Landis-Michel technique to measure changes in hydraulic conductivity (L(p)) and fluorescence photometry to quantify changes in endothelial [Ca(2+)](i) in individually perfused Rana mesenteric microvessels in vivo and transfected nonendothelial cells in vitro. The membrane-permeant DAG analog 1-oleoyl-2-acetyl-sn-glycerol (OAG, 100 microM), which is known to increase Ca(2+) influx through TRPCs, transiently increased L(p) 3.8 +/- 1.2-fold (from 1.6 +/- 0.8 to 9.8 +/- 2.7 x 10(-7) cm.s(-1).cmH(2)O(-1); P < 0.0001; n = 18). Protein kinase C inhibition by bisindolylmaleimide (1 microM) did not affect the OAG-induced increases in L(p). OAG also significantly increased microvascular endothelial [Ca(2+)](i) in vivo (n = 13; P < 0.0001), which again was not sensitive to protein kinase C inhibition. VEGF induced a transient increase in endothelial [Ca(2+)](i) in human embryonic kidney cells (HEK-293) that were cotransfected with VEGF receptor 2 and TRPC-6 but not with control, VEGF receptor 2, or TRPC-6 expression vector alone (P < 0.01; n = 9). Flufenamic acid, which has been shown to enhance activity of TRPC-6 but inhibit TRPC-3 and -7, enhanced the VEGF-mediated increase in L(p) in approximately half of the vessels tested but inhibited the response in the other half of the vessels. These data provide evidence consistent with the hypothesis that VEGF increases vascular permeability via DAG-mediated Ca(2+) entry through TRPCs. Although the exact identities of the TRPCs remain to be confirmed, TRPC-6 appears to be a likely candidate in approximately half of the vessels. PMID:14551041

Pocock, T M; Foster, R R; Bates, D O

2004-03-01

63

S-nitrosation of proteins: An emergent regulatory mechanism in microvascular permeability and vascular function.  

PubMed

Nitric oxide (NO) is a key factor in inflammation as it regulates microvascular permeability, leukocyte adhesion and wound healing. This mini-review addresses mainly spatial and temporal requirements of NO regulatory mechanisms, with special emphasis on S-nitrosation. Endothelial nitric oxide synthase (eNOS)-derived NO induces S-nitrosation of p120 and ?-catenin, particularly in response to platelet-activating factor (PAF), and through traffic and interactions at the adherens junction promotes endothelial hyperpermeability. S-nitrosation is a determinant in vascular processes such as vasodilation and leukocyte-endothelium interactions. Interestingly, NO decreases leukocytes adhesion to endothelium, but the mechanisms are unknown. Advances in NO molecular biology and regulation may serve as a basis for the development of new therapeutic strategies in the treatment of diseases characterized by inflammation such as ischemia-reperfusion injury, stroke, cancer and atherosclerosis. PMID:24665382

Sánchez, Fabiola A; Ehrenfeld, Ingrid P; Durán, Walter N

2013-01-01

64

The diaphragms of fenestrated endothelia: gatekeepers of vascular permeability and blood composition.  

PubMed

Fenestral and stomatal diaphragms are endothelial subcellular structures of unknown function that form on organelles implicated in vascular permeability: fenestrae, transendothelial channels, and caveolae. PV1 protein is required for diaphragm formation in vitro. Here, we report that deletion of the PV1-encoding Plvap gene in mice results in the absence of diaphragms and decreased survival. Loss of diaphragms did not affect the fenestrae and transendothelial channels formation but disrupted the barrier function of fenestrated capillaries, causing a major leak of plasma proteins. This disruption results in early death of animals due to severe noninflammatory protein-losing enteropathy. Deletion of PV1 in endothelium, but not in the hematopoietic compartment, recapitulates the phenotype of global PV1 deletion, whereas endothelial reconstitution of PV1 rescues the phenotype. Taken together, these data provide genetic evidence for the critical role of the diaphragms in fenestrated capillaries in the maintenance of blood composition. PMID:23237953

Stan, Radu V; Tse, Dan; Deharvengt, Sophie J; Smits, Nicole C; Xu, Yan; Luciano, Marcus R; McGarry, Caitlin L; Buitendijk, Maarten; Nemani, Krishnamurthy V; Elgueta, Raul; Kobayashi, Takashi; Shipman, Samantha L; Moodie, Karen L; Daghlian, Charles P; Ernst, Patricia A; Lee, Hong-Kee; Suriawinata, Arief A; Schned, Alan R; Longnecker, Daniel S; Fiering, Steven N; Noelle, Randolph J; Gimi, Barjor; Shworak, Nicholas W; Carrière, Catherine

2012-12-11

65

Downregulation of Connexin 43 promotes vascular cell loss and excess permeability associated with the development of vascular lesions in the diabetic retina  

PubMed Central

Purpose To determine whether downregulation of Connexin 43 (Cx43) expression promotes development of acellular capillaries (ACs), pericyte loss (PL), excess permeability, and retinal thickening in rat retinas. Methods Control rats, diabetic rats, and rats intravitreally injected with Cx43 siRNA or scrambled siRNA were used in this study to determine if acute downregulation of Cx43 expression contributes to retinal vascular cell death and excess permeability. Western blot (WB) analysis and Cx43 immunostaining were performed to assess Cx43 protein levels and distribution in the retinal vessels. Concurrently, retinal networks were subjected to terminal deoxynucleotidyl transferase-mediated uridine 5?-triphosphate-biotin nick end labeling (TUNEL) assay and counter-stained to assess the number of apoptotic cells, ACs, and PL. Assessment of fluorescein isothiocyanate-dextran (FITC-dex) extravasation from retinal capillaries and optical coherence tomography (OCT) were performed to determine retinal vascular permeability and retinal thickness, respectively. Results WB analysis indicated a significant decrease in the Cx43 protein level in the retinas of the diabetic rats and those intravitreally injected with Cx43 siRNA compared to the retinas of the control rats. Likewise, the retinal vascular cells of the diabetic rats and the Cx43 siRNA-treated rats showed a significant decrease in Cx43 immunostaining. Importantly, the number of apoptotic cells, ACs and PL, FITC-dex extravasation, and thickness increased in the retinas of the diabetic and Cx43 siRNA-treated rats compared to those of the control rats. Conclusions Results indicate that downregulation of Cx43 expression alone induces vascular cell death and promotes vascular permeability in the retina. These findings suggest that diabetes-induced downregulation of Cx43 participates in promoting retinal vascular lesions associated with diabetic retinopathy (DR).

Tien, Thomas; Muto, Tetsuya; Barrette, Kevin; Challyandra, Lucky

2014-01-01

66

Measurement of injectivity indexes in geothermal wells with two permeable zones  

SciTech Connect

Injectivity tests in wells with two permeable zones and internal flow is analyzed in order to include the usually severe thermal transient effects. A theoretical analysis is performed and a method devised to obtain information from the thermal transient, provided that temperature is measured simultaneously with pressure. The technique is illustrated with two real tests performed at Miravalles, Costa Rica. It allows to estimate total injectivity index as well as the injectivity index of each one of the two zones separately. Correct position of measuring tools and nature of spontaneous internal flow is also discussed.

Acuna, Jorge A.

1994-01-20

67

The application of fluorescein labeled serum proteins (FLSP) to the study of vascular permeability in the brain  

Microsoft Academic Search

1.Vascular permeability in normal and edematous brain tissue was studied by application of the fluorescein labeled serum proteins (FLSP) as well as by the use of free fluorescein isothiocyanate (FITC) marker.2.The electrophoretic studies demonstrated that the binding capacity of the FITC to albumin was of such degree that morphological observations made after injection of the free tracer can be considered

Igor Klatzo; Jaime Miquel; Richard Otenasek

1962-01-01

68

Neurogenic inflammation in the rat trachea. II. Identity and distribution of nerves mediating the increase in vascular permeability  

Microsoft Academic Search

Summary This study addresses the question of whether increased vascular permeability, which is a prominent feature of neurogenic inflammation in the respiratory tract, is mediated by sensory axons that end near venules in the airway mucosa. In these experiments, neurogenic inflammation was produced in the tracheal and bronchial mucosa of atropine-treated Long-Evans rats by electrical stimulation of the left or

Donald M. McDonald; Robert A. Mitchell; Giorgio Gabella; Amy Haskell

1988-01-01

69

A 3D porous media liver lobule model: the importance of vascular septa and anisotropic permeability for homogeneous perfusion.  

PubMed

The hepatic blood circulation is complex, particularly at the microcirculatory level. Previously, 2D liver lobule models using porous media and a 3D model using real sinusoidal geometries have been developed. We extended these models to investigate the role of vascular septa (VS) and anisotropic permeability. The lobule was modelled as a hexagonal prism (with or without VS) and the tissue was treated as a porous medium (isotropic or anisotropic permeability). Models were solved using computational fluid dynamics. VS inclusion resulted in more spatially homogeneous perfusion. Anisotropic permeability resulted in a larger axial velocity component than isotropic permeability. A parameter study revealed that results are most sensitive to the lobule size and radial pressure drop. Our model provides insight into hepatic microhaemodynamics, and suggests that inclusion of VS in the model leads to perfusion patterns that are likely to reflect physiological reality. The model has potential for applications to unphysiological and pathological conditions. PMID:23237543

Debbaut, Charlotte; Vierendeels, Jan; Siggers, Jennifer H; Repetto, Rodolfo; Monbaliu, Diethard; Segers, Patrick

2014-09-01

70

Vascular endothelial growth factor/vascular permeability factor is detectable in the sera of tumor-bearing mice and cancer patients.  

PubMed

We developed an enzyme-linked immunosorbent assay (ELISA) for vascular endothelial growth factor/vascular permeability factor (VEGF/VPF). The assay revealed that VEGF/VPF levels in the sera of mice were significantly increased from undetectable level by s.c. transplantation with a solid tumor. We also measured VEGF/VPF levels in serum specimens obtained from cancer patients with several types of cancers. VEGF/VPF levels in the sera from cancer patients were significantly higher than those in the sera from the individuals with no sign of cancer. PMID:8148401

Kondo, S; Asano, M; Matsuo, K; Ohmori, I; Suzuki, H

1994-03-31

71

VEGFR2 induces c-Src signaling and vascular permeability in vivo via the adaptor protein TSAd  

PubMed Central

Regulation of vascular endothelial (VE) growth factor (VEGF)–induced permeability is critical in physiological and pathological processes. We show that tyrosine phosphorylation of VEGF receptor 2 (VEGFR2) at Y951 facilitates binding of VEGFR2 to the Rous sarcoma (Src) homology 2-domain of T cell–specific adaptor (TSAd), which in turn regulates VEGF-induced activation of the c-Src tyrosine kinase and vascular permeability. c-Src was activated in vivo and in vitro in a VEGF/TSAd-dependent manner, and was regulated via increased phosphorylation at pY418 and reduced phosphorylation at pY527. Tsad silencing blocked VEGF-induced c-Src activation, but did not affect pathways involving phospholipase C?, extracellular regulated kinase, and endothelial nitric oxide. VEGF-induced rearrangement of VE–cadherin–positive junctions in endothelial cells isolated from mouse lungs, or in mouse cremaster vessels, was dependent on TSAd expression, and TSAd formed a complex with VE-cadherin, VEGFR2, and c-Src at endothelial junctions. Vessels in tsad?/? mice showed undisturbed flow and pressure, but impaired VEGF-induced permeability, as measured by extravasation of Evans blue, dextran, and microspheres in the skin and the trachea. Histamine-induced extravasation was not affected by TSAd deficiency. We conclude that TSAd is required for VEGF-induced, c-Src-mediated regulation of endothelial cell junctions and for vascular permeability.

Sun, Zuyue; Li, Xiujuan; Massena, Sara; Kutschera, Simone; Padhan, Narendra; Gualandi, Laura; Sundvold-Gjerstad, Vibeke; Gustafsson, Karin; Choy, Wing Wen; Zang, Guangxiang; Quach, My; Jansson, Leif; Phillipson, Mia; Abid, Md Ruhul; Spurkland, Anne

2012-01-01

72

VEGFR2 induces c-Src signaling and vascular permeability in vivo via the adaptor protein TSAd.  

PubMed

Regulation of vascular endothelial (VE) growth factor (VEGF)-induced permeability is critical in physiological and pathological processes. We show that tyrosine phosphorylation of VEGF receptor 2 (VEGFR2) at Y951 facilitates binding of VEGFR2 to the Rous sarcoma (Src) homology 2-domain of T cell-specific adaptor (TSAd), which in turn regulates VEGF-induced activation of the c-Src tyrosine kinase and vascular permeability. c-Src was activated in vivo and in vitro in a VEGF/TSAd-dependent manner, and was regulated via increased phosphorylation at pY418 and reduced phosphorylation at pY527. Tsad silencing blocked VEGF-induced c-Src activation, but did not affect pathways involving phospholipase C?, extracellular regulated kinase, and endothelial nitric oxide. VEGF-induced rearrangement of VE-cadherin-positive junctions in endothelial cells isolated from mouse lungs, or in mouse cremaster vessels, was dependent on TSAd expression, and TSAd formed a complex with VE-cadherin, VEGFR2, and c-Src at endothelial junctions. Vessels in tsad(-/-) mice showed undisturbed flow and pressure, but impaired VEGF-induced permeability, as measured by extravasation of Evans blue, dextran, and microspheres in the skin and the trachea. Histamine-induced extravasation was not affected by TSAd deficiency. We conclude that TSAd is required for VEGF-induced, c-Src-mediated regulation of endothelial cell junctions and for vascular permeability. PMID:22689825

Sun, Zuyue; Li, Xiujuan; Massena, Sara; Kutschera, Simone; Padhan, Narendra; Gualandi, Laura; Sundvold-Gjerstad, Vibeke; Gustafsson, Karin; Choy, Wing Wen; Zang, Guangxiang; Quach, My; Jansson, Leif; Phillipson, Mia; Abid, Md Ruhul; Spurkland, Anne; Claesson-Welsh, Lena

2012-07-01

73

Permeability  

NSDL National Science Digital Library

This web page describes the permeability of a magnetic material. A magnetization curve with hysteresis demonstrates the relation between magnetic field and magnetic flux. This is part of a large web site on the magnetic properties of materials. This item is part of a larger collection of educational resources developed by the Non-destructive Testing Resource Center.

2007-10-12

74

Preserved vascular integrity and enhanced survival following neuropilin-1 inhibition in a mouse model of CD8 T cell-initiated CNS vascular permeability  

PubMed Central

Background Altered permeability of the blood–brain barrier (BBB) is a feature of numerous neurological conditions including multiple sclerosis, cerebral malaria, viral hemorrhagic fevers and acute hemorrhagic leukoencephalitis. Our laboratory has developed a murine model of CD8 T cell-initiated central nervous system (CNS) vascular permeability in which vascular endothelial growth factor (VEGF) signaling plays a prominent role in BBB disruption. Findings In this study, we addressed the hypothesis that in vivo blockade of VEGF signal transduction through administration of peptide (ATWLPPR) to inhibit neuropilin-1 (NRP-1) would have a therapeutic effect following induction of CD8 T cell-initiated BBB disruption. We report that inhibition of NRP-1, a co-receptor that enhances VEGFR2 (flk-1) receptor activation, decreases vascular permeability, brain hemorrhage, and mortality in this model of CD8 T cell-initiated BBB disruption. We also examine the expression pattern of VEGFR2 (flk-1) and VEGFR1 (flt-1) mRNA expression during a time course of this condition. We find that viral infection of the brain leads to increased expression of flk-1 mRNA. In addition, flk-1 and flt-1 expression levels decrease in the striatum and hippocampus in later time points following induction of CD8 T cell-mediated BBB disruption. Conclusion This study demonstrates that NRP-1 is a potential therapeutic target in neuro-inflammatory diseases involving BBB disruption and brain hemorrhage. Additionally, the reduction in VEGF receptors subsequent to BBB disruption could be involved in compensatory negative feedback as an attempt to reduce vascular permeability.

2012-01-01

75

Ankle-arm blood pressure index as a marker for atherosclerotic vascular diseases in hemodialysis patients  

Microsoft Academic Search

The ankle to arm blood pressure index (AABI) has been recently found to be a strong predictor of cardiovascular and overall mortality in several populations. The test, which is a noninvasive marker for lower extremity vascular disease (when the index is <0.9), is an office procedure that is simple to perform. The purpose of this study was to evaluate the

Steven Fishbane; Sugkee Youn; Edward J. Kowalski; Gill L. Frei

1995-01-01

76

Mast cells increase vascular permeability by heparin-initiated bradykinin formation in vivo.  

PubMed

Activated mast cells trigger edema in allergic and inflammatory disease. We report a paracrine mechanism by which mast cell-released heparin increases vascular permeability in vivo. Heparin activated the protease factor XII, which initiates bradykinin formation in plasma. Targeting factor XII or kinin B2 receptors abolished heparin-triggered leukocyte-endothelium adhesion and interfered with a mast cell-driven drop in blood pressure in rodents. Intravital laser scanning microscopy and tracer measurements showed heparin-driven fluid extravasation in mouse skin microvessels. Ablation of factor XII or kinin B2 receptors abolished heparin-induced skin edema and protected mice from allergen-activated mast cell-driven leakage. In contrast, heparin and activated mast cells induced excessive edema in mice deficient in the major inhibitor of factor XII, C1 esterase inhibitor. Allergen exposure triggered edema attacks in hereditary angioedema patients, lacking C1 esterase inhibitor. The data indicate that heparin-initiated bradykinin formation plays a fundamental role in mast cell-mediated diseases. PMID:21349432

Oschatz, Chris; Maas, Coen; Lecher, Bernd; Jansen, Thomas; Björkqvist, Jenny; Tradler, Thomas; Sedlmeier, Reinhard; Burfeind, Peter; Cichon, Sven; Hammerschmidt, Sven; Müller-Esterl, Werner; Wuillemin, Walter A; Nilsson, Gunnar; Renné, Thomas

2011-02-25

77

Dissociation of cutaneous vascular permeability and the development of cutaneous late-phase allergic reactions  

SciTech Connect

Cutaneous late-phase allergic reactions (LPR) are characterized by an early, immediate hypersensitivity whealing reaction followed by persistent, localized induration that peaks 6 to 8 hours later. In this study we used rodents to examine the relationship between vascular permeability (VP) and induration during LPR. Efflux of macromolecular tracers from the vasculature into skin was measured with the use of radiolabeled albumin and neutral dextran tracers having large molecular radii. To induce LPR immunologically, we used either intradermal injections of antirat IgE or passive cutaneous sensitization with IgE antidinitrophenyl followed 24 hours later by intravenous injection of albumin-dinitrophenyl. (/sup 125/I)albumin and (/sup 3/H)dextran tracers were injected intravenously before and at various intervals after the induction of LPR. Although a marked increase in VP occurred within the first 30 minutes after induction of mast cell degranulation, analysis of radiolabeled tracer accumulation at 2, 4, 8, and 24 hours failed to demonstrate any further increase in VP. These findings indicate that the induration observed in rodent LPR is not associated with increased VP beyond the immediate hypersensitivity stage and suggest that impairment of lymphatic drainage, cellular infiltration, and/or fibrin deposition are contributing factors.

Keahey, T.M.; Indrisano, J.; Kaliner, M.A.

1989-03-01

78

Vascular permeability and axonal regeneration in skin autotransplanted into the brain.  

PubMed Central

Pieces of skin were autotransplanted from the pinna of an ear into a cerebral hemisphere in 36 albino rats. The grafts were examined 2, 4 and 6 weeks later for signs of vascular permeability and for the presence of nerve fibres. An intravenously injected fluorescent protein exuded into the connective tissue of the dermis and into the spaces between epidermal cells. Extravascular leukocytes were also seen in the dermis. Nerve fibres, derived from the caudate nucleus, corpus callosum and neocortex, were seen in nearly all the grafts, entering both the dermis and epidermis. They were more numerous after the fourth and sixth than after the second post-operative week. A few of these axons were myelinated and a few contained acetylcholinesterase. It has thus been shown that central axons can regenerate into a region in which they are surrounded by proteins and cells derived from the blood, for at least 6 weeks. This observation does not support a recently advanced hypothesis invoking autoimmunity as the cause of the failure of most axons to regenerate following severance within the central nervous system. It is tentatively suggested that the presence of plasma proteins in the extracellular fluid around the tips of axons may be necessary for the occurrence of regeneration. Images Fig. 1 Fig. 2 Fig. 3 Fig. 4 Fig. 5 Fig. 6 Fig. 7 Fig. 8 Fig. 9

Heinicke, E A; Kiernan, J A

1978-01-01

79

Selective Targeting of Angiogenic Tumor Vasculature by Vascular Endothelial-cadherin Antibody Inhibits Tumor Growth without Affecting Vascular Permeability  

Microsoft Academic Search

Vascular endothelial-cadherin (VE-cadherin) is an endothelial cell- specific adhesion molecule that is localized exclusively at cell-cell contacts referred to as adherens junctions. VE-cadherin-mediated adhesion is crucial for proper assembly of vascular structures during angiogenesis as well as for maintenance of a normal vascular integrity. We have shown previously that a monoclonal antibody (BV13) to VE-cadherin not only inhibits the formation

Fang Liao; Jacqueline F. Doody; Jay Overholser; Bridget Finnerty; Rajiv Bassi; Yan Wu; Elisabetta Dejana; Paul Kussie; Peter Bohlen; Daniel J. Hicklin

2002-01-01

80

IL8 is an essential mediator of the increased delayed-phase vascular permeability in LPS-induced rabbit pleurisy  

Microsoft Academic Search

We investigated the involvement of IL-8 in the delayed vascular permeability (VP) in rabbit lipopolysaccharide (LPS)-pleurisy. Maximal level of interleukin-8 (IL-8) was detected in pleural fluid at 2 h after LPS injection and anti-IL-8 inhibited the delayed VP by 90%. Injection of homologous IL-8 induced VP, the time-course of which pre- ceded that of LPS-induced delayed VP. Production of IL-8

Takumi Fukumoto; Akihiro Matsukawa; Teizo Yoshimura; Sunao Edamitsu; Susumu Ohkawara; Katsumasa Takagi; Masaru Yoshinaga

81

Effects of endothelin-1 on vascular permeability in the conscious rat: interactions with platelet-activating factor.  

PubMed Central

1. The objectives of the present experiments were to assess the effects of endothelin-1 on the macrovascular permeability in selected vascular beds, to study the involvement of platelet-activating factor (PAF) in vascular responses to endothelin-1 and to examine the vascular effects of combined administration of endothelin-1 and PAF in conscious rats. 2. Intravenous bolus injection of endothelin-1 (0.1-2 nmol kg-1) resulted in a dose-dependent biphasic change in mean arterial blood pressure (MABP) with initial transient hypotension followed by a prolonged pressor action. These changes were accompanied by a dose-dependent increase in haematocrit values. 3. Endothelin-1 (0.1 and 1 nmol kg-1) increased dose-dependently the vascular permeability of the trachea, upper and lower bronchi, stomach, duodenum, spleen and kidney (up to 240%) as measured by the extravasation of Evans blue dye. The permeability of pulmonary parenchyma, liver and pancreas was not affected significantly by endothelin-1 treatment. 4. Pretreatment of animals with the specific PAF receptor antagonist, WEB 2086 (1 mg kg-1, i.v.) or BN 52021 (10 mg kg-1, i.v.) reduced the endothelin-1 (1 nmol kg-1)-induced rise in haematocrit by about 50 and 30%, respectively. Both antagonists were highly effective at inhibiting protein extravasation in the stomach, duodenum and kidney. On the other hand, BN 52021, but not WEB 2086, significantly attenuated the effect of endothelin-1 on permeability in the lower bronchi and spleen. Neither WEB 2086 nor BN 52021 modified the changes in MABP evoked by endothelin-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Filep, J. G.; Sirois, M. G.; Rousseau, A.; Fournier, A.; Sirois, P.

1991-01-01

82

Vascular endothelial growth factor C is increased in endometrium and promotes endothelial functions, vascular permeability and angiogenesis and growth of endometriosis.  

PubMed

Endometriosis is an angiogenesis-dependent disease. Many studies demonstrated inhibition of angiogenesis leads to inhibition of endometriotic growth, however underlying mechanism is still not fully understood. Our previous study suggested vascular endothelial growth factor C (VEGF-C) as a target of anti-angiogenesis therapy for endometriosis. In this study, VEGF-C in endometrium and its role in angiogenesis of endometriosis were studied. Human endometrium were obtained from women with and without endometriosis for molecular studies. VEGF-A, VEGF-B, VEGF-C and VEGF-D mRNA and proteins in eutopic and ectopic endometrium were measured. Human endothelial cells were transfected with VEGF-C siRNA in vitro, effects of VEGF-C on endothelial cell migration, invasion and tube formation were investigated in vitro. Angiogenesis was inhibited in wild type mice, vascular permeability in dermal skin was determined in vivo. Transplanted endometrium were inhibited by VEGF-C siRNA in immunocompromised mice, development, growth and angiogenesis of the experimental endometriosis were compared in vivo. The results showed that VEGF-C mRNA and protein were increased in eutopic and ectopic endometrium of endometriosis patients. VEGF-C siRNA significantly inhibited endothelial cell migration and tube formation. VEGF-C siRNA significantly inhibited development and angiogenesis of the experimental endometriotic lesions in mice. Supplementation and over-expression of VEGF-C significantly reversed the inhibitory effects on the endothelial functions, vascular permeability and endometriotic growth. In conclusion, VEGF-C is increased in endometrium and it promotes endothelial functions, vascular permeability and development of experimental endometriosis. VEGF-C is important for angiogenesis in endometriosis. PMID:23334337

Xu, Hui; Zhang, Tao; Man, Gene Chi Wai; May, Katie E; Becker, Christian M; Davis, Tina N; Kung, Andrew L; Birsner, Amy E; D'Amato, Robert J; Wong, Alice Wai Yee; Wang, Chi Chiu

2013-07-01

83

Silver nanoparticles inhibit VEGF-and IL-1?-induced vascular permeability via Src dependent pathway in porcine retinal endothelial cells  

PubMed Central

The aim of this study is to determine the effects of silver nanoparticles (Ag-NP) on vascular endothelial growth factor (VEGF)-and interleukin-1 beta (IL-1?)-induced vascular permeability, and to detect the underlying signaling mechanisms involved in endothelial cells. Porcine retinal endothelial cells (PRECs) were exposed to VEGF, IL-1? and Ag-NP at different combinations and endothelial cell permeability was analyzed by measuring the flux of RITC-dextran across the PRECs monolayer. We found that VEGF and IL-1? increase flux of dextran across a PRECs monolayer, and Ag-NP block solute flux induced by both VEGF and IL-1?. To explore the signalling pathway involved VEGF- and IL-1?-induced endothelial alteration, PRECs were treated with Src inhibitor PP2 prior to VEGF and IL-1? treatment, and the effects were recorded. Further, to clarify the possible involvement of the Src pathways in endothelial cell permeability, plasmid encoding dominant negative(DN) and constitutively active(CA) form of Src kinases were transfected into PRECs, 24 h prior to VEGF and IL-1? exposure and the effects were recorded. Overexpression of DN Src blocked both VEGF-and IL-1?-induced permeability, while overexpression of CA Src rescues the inhibitory action of Ag-NP in the presence or absence of VEGF and IL-1?. Further, an in vitro kinase assay was performed to identify the presence of the Src phosphorylation at Y419. We report that VEGF and IL-1?-stimulate endothelial permeability via Src dependent pathway by increasing the Src phosphorylation and Ag-NP block the VEGF-and IL-1?-induced Src phosphorylation at Y419. These results demonstrate that Ag-NP may inhibit the VEGF-and IL-1?-induced permeability through inactivation of Src kinase pathway and this pathway may represent a potential therapeutic target to inhibit the ocular diseases such as diabetic retinopathy.

Sheikpranbabu, Sardarpasha; Kalishwaralal, Kalimuthu; Venkataraman, Deepak; Eom, Soo Hyun; Park, Jongsun; Gurunathan, Sangiliyandi

2009-01-01

84

TLR4 activation of TRPC6-dependent calcium signaling mediates endotoxin-induced lung vascular permeability and inflammation  

PubMed Central

Lung vascular endothelial barrier disruption and the accompanying inflammation are primary pathogenic features of acute lung injury (ALI); however, the basis for the development of both remains unclear. Studies have shown that activation of transient receptor potential canonical (TRPC) channels induces Ca2+ entry, which is essential for increased endothelial permeability. Here, we addressed the role of Toll-like receptor 4 (TLR4) intersection with TRPC6-dependent Ca2+ signaling in endothelial cells (ECs) in mediating lung vascular leakage and inflammation. We find that the endotoxin (lipopolysaccharide; LPS) induces Ca2+ entry in ECs in a TLR4-dependent manner. Moreover, deletion of TRPC6 renders mice resistant to endotoxin-induced barrier dysfunction and inflammation, and protects against sepsis-induced lethality. TRPC6 induces Ca2+ entry in ECs, which is secondary to the generation of diacylglycerol (DAG) induced by LPS. Ca2+ entry mediated by TRPC6, in turn, activates the nonmuscle myosin light chain kinase (MYLK), which not only increases lung vascular permeability but also serves as a scaffold to promote the interaction of myeloid differentiation factor 88 and IL-1R–associated kinase 4, which are required for NF-?B activation and lung inflammation. Our findings suggest that TRPC6-dependent Ca2+ entry into ECs, secondary to TLR4-induced DAG generation, participates in mediating both lung vascular barrier disruption and inflammation induced by endotoxin.

Tauseef, Mohammad; Knezevic, Nebojsa; Chava, Koteswara R.; Smith, Monica; Sukriti, Sukriti; Gianaris, Nicholas; Obukhov, Alexander G.; Vogel, Stephen M.; Schraufnagel, Dean E.; Dietrich, Alexander; Birnbaumer, Lutz; Malik, Asrar B.

2012-01-01

85

Superconducting artificial materials with a negative permittivity, a negative permeability, or a negative index of refraction  

NASA Astrophysics Data System (ADS)

Artificial materials are media made of inclusions such that the sizes and spacing of the inclusions is much smaller than the incident electromagnetic radiation. This allows a medium to act as an effective bulk medium to electromagnetic radiation. Artificial materials can be tailored to produce desired values of the permittivity, permeability, and index of refraction at specific frequencies. The applications of this tailoring include electromagnetic cloaking, and, theoretically, subwavelength imaging resolution. However, the success of these applications depends on their sensitivity to loss. This research uses superconducting niobium (Nb) metals to create arrays of wires, split-ring resonators, and a combination of wires and split-ring resonators, with very low loss. These arrays are used to investigate properties of a medium with an index of refraction that contains a bandwidth of frequency where the real part is negative. The Nb wire arrays produce a frequency bandwidth with a negative real part of the permittivity, while the Nb split-ring resonators produce a frequency bandwidth with a negative real part of the permeability. The combination of Nb wires and Nb split-ring resonators creates an artificial medium with a negative real part of the index of refraction. The electromagnetic transmission of the wires, split-ring resonators, and combination medium is measured in a waveguide as a function of frequency, and models of the permittivity and permeability are used to fit this data. For a single Nb split-ring resonator, the change in the resonant frequency and quality factor with temperature is measured and fit with a two-fluid model of superconductivity. The change in the resonant frequency and quality factor with an applied dc H field and applied power is also measured and compared to, respectively, magneto-optical imaging and laser scanning photoresponse measurements. Bianisotropy and perturbations in the resonant frequency are investigated, and simulated with commercial electromagnetic modeling software. The electromagnetic transmission of a single Nb split-ring resonator is compared to resonators made of YBa2Cu3O7-delta, Copper, and a Nb closed-ring resonator. Similar measurements are made with the single resonators embedded in a metallic wire array.

Ricci, Michael Christopher

86

Relationship between Cardio-Ankle Vascular Index (CAVI) and Carotid Atherosclerosis in Patients with Essential Hypertension  

Microsoft Academic Search

Aortic stiffness measured by aorta-iliac or carotid-femoral pulse wave velocity (PWV) predicts all-cause and cardiovascular mortality. Brachial-ankle PWV (baPWV) has been developed as a more convenient assessment of arterial stiffness. However, the problem with clinical use of baPWV is that the index itself is closely dependent on blood pressure. Recently, a new method, termed the cardio-ankle vascular index (CAVI), has

Takafumi Okura; Sanae Watanabe; Mie Kurata; Seiko Manabe; Mitsuko Koresawa; Jun Irita; Daijiro Enomoto; Ken-ichi Miyoshi; Tomikazu Fukuoka; Jitsuo Higaki

2007-01-01

87

Color Doppler Vascularity Index Can Predict Distant Metastasis and Survival in Colon Cancer Patients1  

Microsoft Academic Search

The purpose of this study was to investigate the clinical usefulness of the color Doppler vascularity index (CDVI) in patients with colon cancer before surgery. Forty-four patients with sonographically visible tumor mass of colon cancer were investigated. The CDVI of each tumor was determined using transabdominal color Doppler ultrasound. The CDVI was defined as the ratio of the number of

Chiung-Nien Chen; Yung-Ming Cheng; Jin-Tung Liang; Po-Huang Lee; Fon-Jou Hsieh; Ray-Hwang Yuan; Shih-Ming Wang; Mei-Fang Chang; King-Jen Chang

2000-01-01

88

Simvastatin Inhibits Leukocyte Accumulation and Vascular Permeability in the Retinas of Rats with Streptozotocin-Induced Diabetes  

PubMed Central

Leukocytes play important roles in the pathogenesis of diabetic retinopathy. Recently, 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors have been reported to exert various effects in addition to their lipid-lowering ability. We investigated the effects of simvastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, on leukocyte-induced diabetic changes in retinas. Diabetes was induced in Long-Evans rats with streptozotocin, and simvastatin administration was begun immediately after the induction of diabetes. Two weeks of treatment with simvastatin suppressed significantly the number of leukocytes adhering to retinal vessel endothelium and the number of leukocytes accumulated in the retinal tissue by 72.9% and 41.0%, respectively (P < 0.01). The expression of intercellular adhesion molecule-1 (ICAM-1) and the CD18 (the common ?-chain of ICAM-1 ligands) were both suppressed with simvastatin. The amount of vascular endothelial growth factor in the retina was attenuated in the simvastatin-treated group. To evaluate the effects of simvastatin on leukocyte-induced endothelial cell damage, vascular permeability in the retina was measured with fluorescein-labeled dextran. Treatment with simvastatin markedly reduced retinal permeability (P = 0.014). This suggests that simvastatin attenuates leukocyte-endothelial cell interactions and subsequent blood-retinal barrier breakdown via suppression of vascular endothelial growth factor-induced ICAM-1 expression in the diabetic retina. Simvastatin may thus be useful in the prevention of diabetic retinopathy.

Miyahara, Shinsuke; Kiryu, Junichi; Yamashiro, Kenji; Miyamoto, Kazuaki; Hirose, Fumitaka; Tamura, Hiroshi; Katsuta, Hideto; Nishijima, Kazuaki; Tsujikawa, Akitaka; Honda, Yoshihito

2004-01-01

89

Peripheral augmentation index as a biomarker of vascular aging: an invasive hemodynamics approach.  

PubMed

We compared two measures of vascular function obtained from digital volume waveforms with measures of target organ damage and novel invasive measures of vascular function as they relate to vascular aging. Aortic pulse pressure amplification, pulsatility, form factor and extent of coronary atherosclerosis (modified Gensini score) were obtained invasively in 59 patients undergoing left heart catheterization. Digital volume waveforms were captured via peripheral arterial tone (PAT) and used to derive augmentation index (AIx) and the pulse wave amplitude-reactive hyperemia index (PWA-RHI). AIx was associated with age (r = 0.50, p < 0.05) and aortic pulsatility (r = 0.45, p < 0.05) and inversely associated with estimated glomerular filtration rate (-0.29, p < 0.05) aortic pulse pressure amplification (r = -0.28, p < 0.05) and aortic form factor (r = -0.38, p < 0.05). AIx was slightly higher in patients with left ventricular hypertrophy (LVH) versus those without left ventricular hypertrophy (30 vs. 14%, p = 0.058). There was no association between AIx and Gensini score. PWA-RHI was not associated with age, estimated glomerular filtration rate or invasive vascular parameters and did not differ in patients with versus without LVH (p = ns). PWA-RHI was inversely associated with Gensini score (r = -0.32, p < 0.05). AIx derived from PAT is correlated with age-associated changes in vascular function and target organ damage but not coronary atherosclerotic burden. PWA-RHI is associated with coronary atherosclerotic burden but is not associated with target organ damage or other measures of vascular aging assessed in this study. Each parameter provides distinct insight into systemic vascular aging and target organ damage. PMID:22138867

Heffernan, Kevin S; Patvardhan, Eshan A; Kapur, Navin K; Karas, Richard H; Kuvin, Jeffrey T

2012-08-01

90

Changes in Vascular Permeability and Expression of Different Angiogenic Factors Following Anti-Angiogenic Treatment in Rat Glioma  

PubMed Central

Background Anti-angiogenic treatments of malignant tumors targeting vascular endothelial growth factor receptors (VEGFR) tyrosine kinase are being used in different early stages of clinical trials. Very recently, VEGFR tyrosine kinase inhibitor (Vetanalib, PTK787) was used in glioma patient in conjunction with chemotherapy and radiotherapy. However, changes in the tumor size, tumor vascular permeability, vascular density, expression of VEGFR2 and other angiogenic factors in response to PTK787 are not well documented. This study was to determine the changes in tumor size, vascular permeability, fractional plasma volume and expression of VEGFR2 in PTK787 treated U-251 glioma rat model by in vivo magnetic resonance imaging (MRI) and single photon emission computed tomography (SPECT). The findings were validated with histochemical and western blot studies. Methodologies and Principal Findings Seven days after implantation of U251 glioma cells, animals were treated with either PTK787 or vehicle-only for two weeks, and then tumor size, tumor vascular permeability transfer constant (Ktrans), fractional plasma volume (fPV) and expression of VEGFR2 and other relevant angiogenic factors were assessed by in vivo MRI and SPECT (Tc-99-HYNIC-VEGF), and by immunohistochemistry and western blot analysis. Dynamic contrast-enhanced MRI (DCE-MRI) using a high molecular weight contrast agent albumin-(GdDTPA) showed significantly increased Ktrans at the rim of the treated tumors compared to that of the central part of the treated as well as the untreated (vehicle treated) tumors. Size of the tumors was also increased in the treated group. Expression of VEGFR2 detected by Tc-99m-HYNIC-VEGF SPECT also showed significantly increased activity in the treated tumors. In PTK787-treated tumors, histological staining revealed increase in microvessel density in the close proximity to the tumor border. Western blot analysis indicated increased expression of VEGF, SDF-1, HIF-1?, VEGFR2, VEGFR3 and EGFR at the peripheral part of the treated tumors compared to that of central part of the treated tumors. Similar expression patters were not observed in vehicle treated tumors. Conclusion These findings indicate that PTK787 treatment induced over expression of VEGF as well as the Flk-1/VEGFR2 receptor tyrosine kinase, especially at the rim of the tumor, as proven by DCE-MRI, SPECT imaging, immunohistochemistry and western blot.

Babajani-Feremi, Abbas; Varma, Nadimpalli R. S.; Iskander, A. S. M.; Anagli, John; Arbab, Ali S.

2010-01-01

91

Diesel exhaust particles modulate vascular endothelial cell permeability: Implication of ZO-1 Expression  

PubMed Central

Exposure to air pollutants increases the incidence of cardiovascular disease. Recent toxicity studies revealed that ultra fine particles (UFP, dp<100–200 nm), the major portion of particulate matter (PM) by numbers in the atmosphere, induced atherosclerosis. In this study, we posited that variations in chemical composition in diesel exhausted particles (DEP) regulated endothelial cell permeability to a different extent. Human aortic endothelial cells (HAEC) were exposed to well-characterized DEP (dp<100 nm) emitted from a diesel engine in either idling mode (DEP1) or in urban dynamometer driving schedule (UDDS) (DEP2). Horse Radish Peroxidase-Streptavidin activity assay showed that DEP2 increased endothelial permeability to a greater extent than DEP1 (Control=0.077± 0.005, DEP1=0.175±0.003, DEP2=0.265±0.006, n=3, p<0.01). DEP2 also down-regulated tight junction protein, Zonular Occludin-1 (ZO-1), to a greater extent compared to DEP1. LDH and caspase-3 activities revealed that DEP-mediated increase in permeability was not due to direct cytotoxicity, and DEP-mediated ZO-1 down-regulation was not due to a decrease in ZO-1 mRNA. Hence, our findings suggest that DEP1 versus DEP2 differentially influenced the extent of endothelial permeability at the post-translational level. This increase in endothelium permeability is implicated in inflammatory cell transmigration into subendothelial layers with relevance to the initiation of atherosclerosis.

Li, Rongsong; Ning, Zhi; Cui, Jeffrey; Yu, Fei; Sioutas, Constantinos; Hsiai, Tzung

2010-01-01

92

Angiomodulin, a marker of cancer vasculature, is upregulated by vascular endothelial growth factor and increases vascular permeability as a ligand of integrin ?v?3  

PubMed Central

Angiomodulin (AGM) is a member of insulin-like growth factor binding protein (IGFBP) superfamily and often called IGFBP-rP1 or IGFBP-7. AGM was originally identified as a tumor-derived cell adhesion factor, which was highly accumulated in blood vessels of human cancer tissues. AGM is also overexpressed in cancer-associated fibroblasts (CAFs) and activates fibroblasts. However, some studies have shown tumor-suppressing activity of AGM. To understand the roles of AGM in cancer progression, we here investigated the expression of AGM in benign and invasive breast cancers and its functions in cancer vasculature. Immunohistochemical analysis showed that AGM was highly expressed in cancer vasculature even in ductal carcinoma in situ (DCIS) as compared to normal vasculature, while its expression in CAFs was more prominent in invasive carcinomas than DCIS. In vitro analyses showed that AGM was strongly induced by vascular endothelial cell growth factor (VEGF) in vascular endothelial cells. Although AGM stimulated neither the growth nor migration of endothelial cells, it supported efficient adhesion of endothelial cells. Integrin ?v?3 was identified as a novel major receptor for AGM in vascular endothelial cells. AGM retracted endothelial cells by inducing actin stress fibers and loosened their VE-cadherin-mediated intercellular junction. Consequently, AGM increased vascular permeability both in vitro and in vivo. Furthermore, AGM and integrin ?v?3 were highly expressed and colocalized in cancer vasculature. These results suggest that AGM cooperates with VEGF to induce the aberrant functions of cancer vasculature as a ligand of integrin ?v?3.

Komiya, Eriko; Sato, Hiroki; Watanabe, Naoko; Ise, Marii; Higashi, Shouichi; Miyagi, Yohei; Miyazaki, Kaoru

2014-01-01

93

Neuron-derived semaphorin 3A is an early inducer of vascular permeability in diabetic retinopathy via neuropilin-1.  

PubMed

The deterioration of the inner blood-retinal barrier and consequent macular edema is a cardinal manifestation of diabetic retinopathy (DR) and the clinical feature most closely associated with loss of sight. We provide evidence from both human and animal studies for the critical role of the classical neuronal guidance cue, semaphorin 3A, in instigating pathological vascular permeability in diabetic retinas via its cognate receptor neuropilin-1. We reveal that semaphorin 3A is induced in early hyperglycemic phases of diabetes within the neuronal retina and precipitates initial breakdown of endothelial barrier function. We demonstrate, by a series of orthogonal approaches, that neutralization of semaphorin 3A efficiently prevents diabetes-induced retinal vascular leakage in a stage of the disease when vascular endothelial growth factor neutralization is inefficient. These observations were corroborated in Tg(Cre-Esr1)/Nrp1(flox/flox) conditional knockout mice. Our findings identify a therapeutic target for macular edema and provide further evidence for neurovascular crosstalk in the pathogenesis of DR. PMID:24093675

Cerani, Agustin; Tetreault, Nicolas; Menard, Catherine; Lapalme, Eric; Patel, Chintan; Sitaras, Nicholas; Beaudoin, Felix; Leboeuf, Dominique; De Guire, Vincent; Binet, François; Dejda, Agnieszka; Rezende, Flavio A; Miloudi, Khalil; Sapieha, Przemyslaw

2013-10-01

94

Vascular permeability factor: a tumor-derived polypeptide that induces endothelial cell and monocyte procoagulant activity, and promotes monocyte migration  

PubMed Central

Systemic infusion of low concentrations of tumor necrosis factor/cachectin (TNF) into mice that bear TNF-sensitive tumors leads to activation of coagulation, fibrin formation, and occlusive thrombosis exclusively within the tumor vascular bed. To identify mechanisms underlying the localization of this vascular procoagulant response, a tumor-derived polypeptide has been purified to homogeneity from supernatants of murine methylcholanthrene A-induced fibrosarcomas that induces endothelial tissue factor synthesis and expression (half- maximal response at approximately 300 pM), and augments the procoagulant response to TNF in a synergistic fashion. This tumor- derived polypeptide was identified as the murine homologue of vascular permeability factor (VPF) based on similar mobility on SDS-PAGE, an homologous NH2-terminal amino acid sequence, and recognition by a monospecific antibody to guinea pig VPF. In addition, VPF was shown to induce monocyte activation, as evidenced by expression of tissue factor. Finally, VPF was shown to induce monocyte chemotaxis across collagen membranes and endothelial cell monolayers. Taken together, these results indicate that VPF can modulate the coagulant properties of endothelium and monocytes, and can promote monocyte migration into the tumor bed. This suggests one mechanism through which tumor-derived mediators can alter properties of the vessel wall.

1990-01-01

95

Inhibition of SUR1 Decreases the Vascular Permeability of Cerebral Metastases1  

PubMed Central

Inhibition of sulfonylurea receptor 1 (SUR1) by glyburide has been shown to decrease edema after subarachnoid hemorrhage. We investigated if inhibiting SUR1 reduces cerebral edema due to metastases, the most common brain tumor, and explored the putative association of SUR1 and the endothelial tight junction protein, zona occludens-1 (ZO-1). Nude rats were intracerebrally implanted with small cell lung carcinoma (SCLC) LX1 or A2058 melanoma cells (n = 36). Rats were administered vehicle, glyburide (4.8 µg twice, orally), or dexamethasone (0.35 mg, intravenous). Blood-tumor barrier (BTB) permeability (Ktrans) was evaluated before and after treatment using dynamic contrast-enhanced magnetic resonance imaging. SUR1 and ZO-1 expression was evaluated using immunofluorescence and Western blots. In both models, SUR1 expression was significantly increased (P < .05) in tumors. In animals with SCLC, control mean Ktrans (percent change ± standard error) was 101.8 ± 36.6%, and both glyburide (-21.4 ± 14.2%, P < .01) and dexamethasone (-14.2 ± 13.1%, P < .01) decreased BTB permeability. In animals with melanoma, compared to controls (117.1 ± 43.4%), glyburide lowered BTB permeability increase (3.2 ± 15.4%, P < .05), while dexamethasone modestly lowered BTB permeability increase (63.1 ± 22.1%, P > .05). Both glyburide (P < .001) and dexamethasone (P < .01) decreased ZO-1 gap formation. By decreasing ZO-1 gaps, glyburide was at least as effective as dexamethasone at halting increased BTB permeability caused by SCLC and melanoma. Glyburide is a safe, inexpensive, and efficacious alternative to dexamethasone for the treatment of cerebral metastasis-related vasogenic edema.

Thompson, Eric M; Pishko, Gregory L; Muldoon, Leslie L; Neuwelt, Edward A

2013-01-01

96

Isolation and characterization of neutralizing monoclonal antibodies to human vascular endothelial growth factor/vascular permeability factor121 (VEGF/VPF121).  

PubMed

We have established monoclonal antibodies (MAbs) against human vascular endothelial growth factor/vascular permeability factor121 (VEGF/VPF121). Two (MV101 and MV303) of the 28 MAbs neutralized the mitogenic activity of VEGF/VPF121 on human umbilical vein endothelial cells (HUVEC) in a dose-dependent manner. Both of the MAbs reacted to VEGF/VPF121 and also VEGF/VPF165 with somewhat different binding properties in a sandwich-type enzyme-linked immunosorbent assay (ELSIA). The binding of MV101 and MV303 to VEGF/VPF121 was competitive, but MV415, another anti-VEGF/VPF121 MAb without neutralizing activity, did not complete with either of the antibodies. MV101 and MV303 specifically recognized the native form of VEGF/VPF121 and VEGF/VPF165 in Western blotting. They did not react with VEGF/VPF when the antigens were fractionated under reducing conditions. These observations suggested that MV101 and MV303 might recognize the epitopes closely located on the configuration of VEGF/VPF121 molecule and the epitopes recognized by MV101 and MV303 may play an important role in the VEGF/VPF-receptor signal transduction. These MAbs significantly suppressed the growth of a human hepatoma, PLC/PRF/5, in vivo. PMID:8575796

Asano, M; Yukita, A; Matsumoto, T; Matsuo, K; Kondo, S; Suzuki, H

1995-10-01

97

Overexpression of vascular permeability factor (VPF/VEGF) and its endothelial cell receptors in delayed hypersensitivity skin reactions.  

PubMed

Delayed hypersensitivity (DH) is a T cell-mediated form of immune response characterized by a predominantly perivascular, mononuclear cell infiltrate. The venules in DH reactions are hyperpermeable to plasma proteins, leading to extravasation of plasma fibrinogen and its extravascular clotting to form a fibrin gel that promotes induration and angiogenesis. The mechanisms responsible for microvascular hyperpermeability in DH are unknown. Recently, a cytokine named vascular permeability factor (VPF, also known as vascular endothelial growth factor or VEGF) has been implicated in the chronic vascular hyperpermeability and angiogenesis of solid and ascites tumors, healing wounds, rheumatoid arthritis, and psoriasis. These findings suggested that VPF/VEGF might also have a role in the pathogenesis of DH. Two model systems were studied: allergic contact dermatitis to poison ivy in human volunteers and classical tuberculin hypersensitivity in rats. In both, in situ hybridization revealed that the mRNAs encoding VPF/VEGF were strikingly overexpressed in keratinocytes of the epidermis; scattered mononuclear cells infiltrating the dermis also overexpressed VPF/VEGF mRNA, to a greater extent in rat tuberculin than in human contact reactions. In contact reactions, mRNAs for two VPF/VEGF vascular endothelial cell receptors, flt-1 and KDR, were also strikingly overexpressed. Abundant fibrin deposition in both models confirmed that dermal microvessels were indeed hyperpermeable to plasma fibrinogen. These results implicate VPF/VEGF as a potentially important mediator in the pathogenesis of cell-mediated immunity and provide further evidence that products of epithelial cells may regulate the inflammatory response. PMID:7876550

Brown, L F; Olbricht, S M; Berse, B; Jackman, R W; Matsueda, G; Tognazzi, K A; Manseau, E J; Dvorak, H F; Van de Water, L

1995-03-15

98

Quantitative Evaluation of Vascular Permeability in the Gerbil Brain After Transient Ischemia Using Evans Blue Fluorescence  

Microsoft Academic Search

Summary: Mongolian gerbils were used to evaluate brain edema during restoration of flow following bilateral carotid occlusion for 1 h. We have modified the method for fluorometric measurement of Evans blue to monitor vascular protein leakage (vasogenic edema). The extraction of extravasated Evans blue was performed by homogenizing the whole brain in 50% trichloroacetic acid. The supernatant was diluted fourfold

Osamu Uyama; Nobutaka Okamura; Masahiro Yanase; Mitsuhiro Narita; Keita Kawabata; Minoru Sugita

1988-01-01

99

Characterization of vascular disruption and blood-spinal cord barrier permeability following traumatic spinal cord injury.  

PubMed

Significant vascular changes occur subsequent to spinal cord injury (SCI), which contribute to progressive pathophysiology. In the present study, we used female Wistar rats (300-350?g) and a 35-g clip-compression injury at T6 to T7 to characterize the spatial and temporal vascular changes that ensue post-SCI. Before sacrifice, animals were injected with vascular tracing dyes (2% Evans Blue (EB) or fluorescein isothiocyanate/Lycopersicon esculentum agglutinin [FITC-LEA]) to assess blood-spinal cord barrier (BSCB) integrity or vascular architecture, respectively. Spectrophotometry of EB tissue showed maximal BSCB disruption at 24?h postinjury, with significant disruption observed until 5 days postinjury (p<0.01). FITC-LEA-identified functional vasculature was dramatically reduced by 24?h. Similarly, RECA-1 immunohistochemistry showed a significant decrease in the number of vessels at 24?h postinjury, compared to uninjured animals (p<0.01), with slight increases in endogenous revascularization by 10 days postinjury. White versus gray matter (GM) quantification showed that GM vessels are more susceptible to SCI. Finally, we observed an endogenous angiogenic response between 3 and 7 days postinjury: maximal endothelial cell proliferation was observed at day 5. These data indicate that BSCB disruption and endogenous revascularization occur at specific time points after injury, which may be important for developing effective therapeutic interventions for SCI. PMID:24237182

Figley, Sarah A; Khosravi, Ramak; Legasto, Jean M; Tseng, Yun-Fan; Fehlings, Michael G

2014-03-15

100

CLINICAL SIGNIFICANCE OF THE ANKLE-BRACHIAL INDEX (ABI) AND PULSE WAVE VELOCITY (PWV) IN PATIENTS WITH RETINAL VASCULAR OCCLUSION  

Microsoft Academic Search

Purpose: To report the clinical significance of ankle-brachial index (ABI) and pulse wave velocity (PWV) in retinal vascular occlusion. Method: We measured the ABI and PWV, which are used as clinical indicators of arteriosclerosis, of 106 patients with retinal vascular occlusion (RVO) as well as hypertensive retinopathy (HR) and diabetic retinopathy (DR), and 100 age-matched healthy control subjects. Results: ABI

Hiroshi Ohguro; Ryoichi Shimokawa; Ikuyo Ohguro; Futoshi Ishikawa; Hitoshi Yamazaki; Mitsuru Nakazawa

2006-01-01

101

Cardio-ankle vascular index (CAVI) as an indicator of arterial stiffness  

PubMed Central

Arterial stiffness has been identified as an independent predictor of prognostic outcomes for patients with cardiovascular disease. Although measurement of pulse wave velocity has been a widely accepted noninvasive approach to the assessment of arterial stiffness, its accuracy is hampered by changes in blood pressure. Taking the exponential relation between intravascular pressure and arterial diameter into consideration, a stiffness parameter can be obtained by plotting the natural logarithm of systolic–diastolic pressure ratio against the arterial wall extensibility. Cardio-ankle vascular index (CAVI), which is calculated based on the stiffness parameter thus obtained, is theoretically independent of changes in blood pressure. With this distinct advantage, CAVI has been widely applied clinically to assess arterial stiffness in subjects with known cardiovascular diseases including those with diagnosed atherosclerosis, coronary heart disease, and stroke as well as those at risk, including those with hypertension, diabetes, the elderly, and the obese. Because of its enhanced sensitivity, not only has the index been used to discern subtle changes in the disease process, it has also been utilized in studying normal individuals to assess their potential risks of developing cardiovascular diseases. The primary aims of assessing arterial stiffness using CAVI are not only to aid in early detection of arteriosclerosis to allow timely treatment and change in lifestyle, but also to quantitatively evaluate the progression of disease and the effectiveness of treatment. Despite its merit of being unaffected by blood pressure, discretion in data interpretation is suggested because an elevated CAVI represents not just vascular stiffness caused by pathological changes in the arterial wall, but can also be attributed to an increased vascular tone brought about by smooth muscle contraction. Moreover, certain patient populations, such as those with an ankle-brachial index < 0.9, may give falsely low CAVI and are suggested to be excluded from study.

Sun, Cheuk-Kwan

2013-01-01

102

Association of the cardioankle vascular index and ankle-brachial index with carotid artery intima media thickness in hemodialysis patients.  

PubMed

The objectives of the present study are (1) to compare the cardioankle vascular index (CAVI), ankle-brachial index (ABI), and carotid artery intima-media thickness (CA-IMT) between HD patients with and without type 2 diabetes (T2D) or prevalence of cardiovascular (CV) disease and (2) also to evaluate the relationship of these indices with CA-IMT in these patients according to ABI levels. This study consisted of 132 HD patients with T2D and the same number of patients without T2D. The patients with diabetes or prevalence of CV disease had significantly higher CA-IMT and lower ABI values than those without diabetes or prevalence of CV disease, respectively. Although diabetic patients had higher CAVI than those without diabetes, CAVI did not differ between patients with or without prevalence of CV disease. In univariate analysis, CA-IMT was more strongly correlated with ABI than CAVI. However, the opposite was true in patients with an ABI value of more than 0.95. Both indices were significantly correlated with CA-IMT although ABI was a powerful determinant than CAVI. It appears that both indices are associated with CA-IMT in HD patients, especially with an ABI value of more than 0.95. PMID:23864949

Gohda, Tomohito; Gotoh, Hiromichi; Gotoh, Yoshikazu; Yamaguchi, Saori; Tomino, Yasuhiko

2013-01-01

103

Mechanotransduction by GEF-H1 as a novel mechanism of ventilator-induced vascular endothelial permeability  

PubMed Central

Pathological lung overdistention associated with mechanical ventilation at high tidal volumes (ventilator-induced lung injury; VILI) compromises endothelial cell (EC) barrier leading to development of pulmonary edema and increased morbidity and mortality. We have previously shown involvement of microtubule (MT)-associated Rho-specific guanine nucleotide exchange factor GEF-H1 in the agonist-induced regulation of EC permeability. Using an in vitro model of human pulmonary EC exposed to VILI-relevant magnitude of cyclic stretch (18% CS) we tested a hypothesis that CS-induced alterations in MT dynamics contribute to the activation of Rho-dependent signaling via GEF-H1 and mediate early EC response to pathological mechanical stretch. Acute CS (30 min) induced disassembly of MT network, cell reorientation, and activation of Rho pathway, which was prevented by MT stabilizer taxol. siRNA-based GEF-H1 knockdown suppressed CS-induced disassembly of MT network, abolished Rho signaling, and attenuated CS-induced stress fiber formation and EC realignment compared with nonspecific RNA controls. Depletion of GEF-H1 in the murine two-hit model of VILI attenuated vascular leak induced by lung ventilation at high tidal volume and thrombin-derived peptide TRAP6. These data show for the first time the critical involvement of microtubules and microtubule-associated GEF-H1 in lung vascular endothelial barrier dysfunction induced by pathological mechanical strain.

Fu, Panfeng; Xing, Junjie; Yakubov, Bakhtiyor; Cokic, Ivan; Birukov, Konstantin G.

2010-01-01

104

Studies of Vascular Permeability Factor derived from T Lymphocytes and Inhibitory Effect of Plasma on Its Production in Minimal Change Nephrotic Syndrome  

Microsoft Academic Search

Peripheral T lymphocytes from patients with minimal change nephrotic syndrome (MCNS) and controls were treated for their ability to produce vascular permeability factors (VPF) without concanavalin A stimulation. In vitro cultures of T lymphocytes from active MCNS produced VPF in the supernatant, whereas T lymphocytes from inactive MCNS or normal subjects did not. Furthermore, the plasma from patients with active

S. Tomizawa; K. Maruyama; N. Nagasawa; S. Suzuki; T. Kuroume

1985-01-01

105

The genesis of peritumoral vasogenic brain edema and tumor cysts: a hypothetical role for tumor-derived vascular permeability factor.  

PubMed Central

Cerebral edema and fluid-filled cysts are common accompaniments of brain tumors. They contribute to the mass effect imposed by the primary tumor and are often responsible for a patient's signs and symptoms. Cerebral edema significantly increases the morbidity associated with tumor biopsy, excision, radiation therapy, and chemotherapy. Both edema and cyst formation are thought to result from a deficiency in the blood-brain barrier, with consequent extravasation of water, electrolytes, and plasma proteins from altered tumor microvessels. The resultant expansion of the cerebral interstitial space contributes to the elevated intracranial pressure observed with brain tumors. Departure from the typical blood-brain barrier microvascular architecture may only partially explain the occurrence of edema and tumor cyst formation. Biochemical mediators have also been implicated in vascular extravasation. Vascular permeability factor or vascular endothelial growth factor (VPF/VEGF) is a protein that has recently been isolated from a variety of tumors including human brain tumors. VPFb is an extraordinarily potent inducer of both microvascular extravasation (edemagenesis) and the formation of new blood vessels (angiogenesis). Its role in tumor growth and progression would therefore appear pivotal. Herein, the author presents an updated account of the investigation of VPF. Historical and clinical perspectives of the study and treatment of tumor associated edema are provided. The efficacy of high-dose dexamethasone in the treatment of neoplastic brain edema is discussed. A hypothetical role for VPF in edemagenesis is presented and discussed. It is hoped that an expanded understanding of the mechanisms responsible for the genesis of edema will ultimately facilitate therapeutic intervention. Images Figure 1 Figure 2 Figure 3

Criscuolo, G. R.

1993-01-01

106

Dissociation of VE-PTP from VE-cadherin is required for leukocyte extravasation and for VEGF-induced vascular permeability in vivo  

PubMed Central

We have recently shown that vascular endothelial protein tyrosine phosphatase (VE-PTP), an endothelial membrane protein, associates with VE-cadherin and is required for optimal VE-cadherin function and endothelial cell contact integrity. The dissociation of VE-PTP from VE-cadherin is triggered by vascular endothelial growth factor (VEGF) and by the binding of leukocytes to endothelial cells in vitro, suggesting that this dissociation is a prerequisite for the destabilization of endothelial cell contacts. Here, we show that VE-cadherin/VE-PTP dissociation also occurs in vivo in response to LPS stimulation of the lung or systemic VEGF stimulation. To show that this dissociation is indeed necessary in vivo for leukocyte extravasation and VEGF-induced vascular permeability, we generated knock-in mice expressing the fusion proteins VE-cadherin-FK 506 binding protein and VE-PTP-FRB* under the control of the endogenous VE-cadherin promoter, thus replacing endogenous VE-cadherin. The additional domains in both fusion proteins allow the heterodimeric complex to be stabilized by a chemical compound (rapalog). We found that intravenous application of the rapalog strongly inhibited VEGF-induced (skin) and LPS-induced (lung) vascular permeability and inhibited neutrophil extravasation in the IL-1? inflamed cremaster and the LPS-inflamed lung. We conclude that the dissociation of VE-PTP from VE-cadherin is indeed required in vivo for the opening of endothelial cell contacts during induction of vascular permeability and leukocyte extravasation.

Broermann, Andre; Winderlich, Mark; Block, Helena; Frye, Maike; Rossaint, Jan; Zarbock, Alexander; Cagna, Giuseppe; Linnepe, Ruth; Schulte, Dorte; Nottebaum, Astrid Fee

2011-01-01

107

Inhibition of tumor growth and metastasis by an immunoneutralizing monoclonal antibody to human vascular endothelial growth factor/vascular permeability factor121.  

PubMed

We elucidated the relationship between vascular endothelial growth factor/vascular permeability factor (VEGF/VPF), which is a potent angiogenic factor, and the growth of primary and metastatic tumors using an immunoneutralizing monoclonal antibody against human VEGF/VPF121. The monoclonal antibody, MV303, suppressed the growth of human umbilical vein endothelial cells (HUVEC) induced by VEGF/VPF121 or VEGF/VPF165 but did not inhibit its growth induced by basic fibroblast growth factor. MV303 inhibited the binding of 125I-VEGF/VPF121 to HUVEC. We examined the effects of MV303 on tumor angiogenesis using a membrane chamber packed with the human fibrosarcoma cell line HT-1080 and implanted s.c. into BALB/c mice. The neovascularization induced by HT-1080 was inhibited by the i.v. injection of MV303 at a dose of 100 micrograms/mouse. Furthermore, the growth of solid tumors of s.c. implanted HT-1080 in BALB/c nude mice was almost completely inhibited by the i.v. and s.c. administration of MV303 ten times from day 1 at a dose of 100 micrograms/mouse (T/C values of tumor volume at day 18 were 0.20 and 0.18, respectively). Tumor growth was suppressed when MV303 was administered, even from eight days after tumor inoculation. MV303 suppressed the increase in lung weight caused by experimental metastasis with i.v. inoculation of cultured HT-1080 cells to BALB/c nude mice. The life spans of the mice treated with MV303 were significantly prolonged. These results indicated that VEGF/VPF played an important role in both primary and metastatic tumor growth as a tumor angiogenesis factor. MV303, an immunoneutralizing monoclonal antibody against VEGF/VPF, potently inhibited both primary and metastatic tumor growth with no marked side effects. PMID:7585591

Asano, M; Yukita, A; Matsumoto, T; Kondo, S; Suzuki, H

1995-11-15

108

Host endothelial S1PR1 regulation of vascular permeability modulates tumor growth.  

PubMed

Understanding vascular growth and maturation in developing tumors has important implications for tumor progression, spread, and ultimately host survival. Modulating the signaling of endothelial G protein-coupled receptors (GPCRs) in blood and lymphatic vessels can enhance or limit tumor progression. Sphingosine 1-phosphate receptor 1 (S1PR1) is a GPCR for circulating lysophospholipid S1P that is highly expressed in blood and lymphatic vessels. Using the S1PR1- enhanced green fluorescent protein (eGFP) mouse model in combination with intravital imaging and pharmacologic modulation of S1PR1 signaling, we show that boundary conditions of high and low S1PR1 signaling retard tumor progression by enhancing or destabilizing neovasculature integrity, respectively. In contrast, midrange S1PR1 signaling, achieved by receptor antagonist titration, promotes abundant growth of small, organized vessels and thereby enhances tumor progression. Furthermore, in vivo S1PR1 antagonism supports lung colonization by circulating tumor cells. Regulation of endothelial S1PR1 dynamically controls vascular integrity and maturation and thus modulates angiogenesis, tumor growth, and hematogenous metastasis. PMID:24740542

Sarkisyan, Gor; Gay, Laurie J; Nguyen, Nhan; Felding, Brunhilde H; Rosen, Hugh

2014-07-01

109

Inhibitory effect of a novel bradykinin B1 receptor antagonist, R-954, on enhanced vascular permeability in type 1 diabetic mice.  

PubMed

The morbidity and mortality associated with type 1 diabetes are essentially related to the micro- and macrovascular complications that develop over time and lead to several diabetic complications, including hypertension, atherosclerosis, and retinopathy, as well as coronary and renal failure. Normally absent in physiological conditions, the bradykinin B1 receptor (BKB1-R) was recently found to be overexpressed in pathological conditions, including type 1 diabetes. In the present study, we evaluated the effect of the new BKB1-R antagonist, R-954 (Ac-Orn-[Oic2, alpha-MePhe5, D-betaNal7, Ile8]desArg9-bradykinin, on the increase in vascular permeability in streptozotocin (STZ)-diabetic mice. The capillary permeability to albumin was measured by quantifying the extravasation of albumin-bound Evans blue dye in selected target tissues (liver, pancreas, duodenum, ileum, spleen, heart, kidney, stomach, skin, muscle, and thyroid gland). Acute single administration of R-954 (300 microg/kg, i.v.) to type 1 diabetic mice 4 weeks after STZ significantly inhibited the enhanced vascular permeability in most tissues. These data provide further experimental evidence for the implication of BKB1-R in the enhanced vascular permeability associated with type 1 diabetes. PMID:12564648

Simard, Bryan; Gabra, Bichoy H; Sirois, Pierre

2002-12-01

110

Permeability of the blood-tumor barrier is enhanced by combining vascular endothelial growth factor with papaverine.  

PubMed

This study aims to determine the effects of vascular endothelial growth factor (VEGF), papaverine (PA), and the combination of VEGF and PA on the permeability of the blood-tumor barrier (BTB) and to determine possible molecular mechanisms contributing to the effects. In the rat C6 glioma model, the extravasation of Evans blue (EB) through the BTB was increased significantly by VEGF and PA. VEGF-induced and PA-induced increase of EB extravasation was further increased after combining VEGF with PA infusion. Transmission electron microscopy (TEM) showed that the combination of VEGF and PA not only opened tight junctions (TJ) dramatically but increased the presence of pinocytotic vesicles of brain microvascular endothelial cells (BMECs) significantly. Meanwhile, the downregulation of the TJ-associated proteins occludin and claudin-5 and the upregulation of the caveolae structure proteins caveolin-1 and caveolin-2 caused by the combination of VEGF and PA were observed by Western blot and immunohistochemistry, which were more remarkable than those by the two strategies separately. In addition, after VEGF and PA infusion, the results of radioimmunoassay, Western blot, and enzyme-linked immunosorbent assay (ELISA) revealed a significant increase in expression levels of cGMP and protein kinase G-1 (PKG-1) and the activation of nuclear factor-?B (NF-?B) p65. This study demonstrates that combination of VEGF and PA can increase the permeability of the BTB by a paracellular pathway (downregulation of occludin and claudin-5) and a transcellular pathway (upregulation of caveolin-1 and caveolin-2) and that the cGMP/PKG/NF-?B signal pathway might be involved in the modulation process. © 2014 Wiley Periodicals, Inc. PMID:24523141

Yang, Zhi-Hang; Liu, Li-Bo; Zhao, Li-Ni; Liu, Yun-Hui; Xue, Yi-Xue

2014-06-01

111

Effect of hypertension and its reverse on serum nitric oxide concentration and vascular permeability in two-kidney one-clip hypertensive rats.  

PubMed

The aim of this study was to evaluate the effect of hypertension and its reverse on serum nitric oxide (NO) concentration and endothelial permeability in two-kidney one-clip (2K1C) hypertensive rats. 28 male Wistar rats were divided into four groups: 1) 2K1C for 12 weeks; 2) sham-clipped for 12 weeks; 3) 2K1C for 12 weeks and unclipped for 12 weeks; 4) sham-clipped for 12 weeks and unclipped for 12 weeks. Blood samples were taken before experiment, 12th week and 24th week (in groups 3 and 4). Coronary vascular and aortic endothelial permeability were determined by extravasation of Evans blue dye method. Serum NO level was significantly lower in hypertensive group compare with sham group (4.21 ± 1.28 vs. 9.47 ± 1.34 µmol/l, respectively). Reversal of hypertension did not improve serum NO concentration in 2K1C group (4.21 ± 1.28 vs. 4.32 ± 1.34 µmol/l). Coronary vascular and aortic endothelial permeability were not different between hypertensive and normotensive groups and reversal of hypertension did not alter endothelial permeability. Lower serum NO concentration in 2K1C hypertensive rats even after reversal of hypertension suggested that in addition to NO, other mechanisms could be involved in surgical reversal of hypertension. Hypertension and its reverse did not change endothelial permeability at least in this model of hypertension. PMID:21613665

Khazaei, Majid; Zarei, Mohammad; Sharifi, Mohammad R; Pourshanazari, Ali A

2011-06-01

112

Mitogen-Activated Protein Kinase-Activated Protein Kinase 2 Mediates Apoptosis during Lung Vascular Permeability by Regulating Movement of Cleaved Caspase 3.  

PubMed

Apoptosis is a key pathologic feature in acute lung injury. Animal studies have demonstrated that pathways regulating apoptosis are necessary in the development of acute lung injury, and that activation of p38 mitogen-activated protein kinase (MAPK) is linked to the initiation of the apoptotic cascade. In this study, we assessed the role of the MAPK-activated protein kinase (MK) 2, one of p38 MAPK's immediate downstream effectors, in the development of apoptosis in an animal model of LPS-induced pulmonary vascular permeability. Our results indicate that wild-type (WT) mice exposed to LPS demonstrate increased apoptosis, as evidenced by cleavage of caspase 3 and poly (ADP-ribose) polymerase 1 and increased deoxynucleotidyl transferase-mediated dUDP nick-end labeling staining, which is accompanied by increases in markers of vascular permeability. In contrast, MK2(-/-) mice are protected from pulmonary vascular permeability and apoptosis in response to LPS. Although there was no difference in activation of caspase 3 in MK2(-/-) compared with WT mice, interestingly, cleaved caspase 3 translocated to the nucleus in WT mice while it remained in the cytosol of MK2(-/-) mice in response to LPS. In separate experiments, LPS-induced apoptosis in human lung microvascular endothelial cells was also associated with nuclear translocation of cleaved caspase 3 and apoptosis, which were both prevented by MK2 silencing. In conclusion, our data suggest that MK2 plays a critical role in the development of apoptosis and pulmonary vascular permeability, and its effects on apoptosis are in part related to its ability to regulate nuclear translocation of cleaved caspase 3. PMID:24304496

Damarla, Mahendra; Parniani, Ahmad R; Johnston, Laura; Maredia, Hasina; Serebreni, Leonid; Hamdan, Omar; Sidhaye, Venkataramana K; Shimoda, Larissa A; Myers, Allen C; Crow, Michael T; Schmidt, Eric P; Machamer, Carolyn E; Gaestel, Matthias; Rane, Madhavi J; Kolb, Todd M; Kim, Bo S; Damico, Rachel L; Hassoun, Paul M

2014-05-01

113

New noninvasive index for evaluation of the vascular age of healthy and sick people  

NASA Astrophysics Data System (ADS)

We conducted a study on 861 healthy and sick subjects and demonstrated that some calculated parameters based on measurement of the dynamic light scattering (DLS) signal from the finger correlate highly with chronological age ranging from 1.5 to 85 years old. Measurements of DLS signals were obtained during both occlusion and nonocclusion of blood flow in the finger. For the nonocclusion case we found that the low-frequency component of the DLS signal significantly correlates with the biological age while the high-frequency component of the DLS signal resembles the arterial pulse-wave and does correlate with age. However, the most prominent correlation between the DLS characteristics and age was noted with the stasis stage measurements. We propose that the observed age-related phenomena are caused by alterations in local blood viscosity and interactions of the endothelial cells with erythrocytes. Further, a new noninvasive index based on the age-related optical characteristics was introduced. This noninvasive index may be used as a research and diagnostic tool to examine the endothelial and thrombolytic properties of the vascular system.

Fine, Ilya; Kuznik, Boris I.; Kaminsky, Alexander V.; Shenkman, Louis; Kustovsjya, Evgeniya M.; Maximova, Olga G.

2012-08-01

114

Vascular permeability in cancer and infection as related to macromolecular drug delivery, with emphasis on the EPR effect for tumor-selective drug targeting  

PubMed Central

Tumor and inflammation have many common features. One hallmark of both is enhanced vascular permeability, which is mediated by various factors including bradykinin, nitric oxide (NO), peroxynitrite, prostaglandins etc. A unique characteristic of tumors, however, is defective vascular anatomy. The enhanced vascular permeability in tumors is also distinctive in that extravasated macromolecules are not readily cleared. We utilized the enhanced permeability and retention (EPR) effect of tumors for tumor selective delivery of macromolecular drugs. Consequently, such drugs, nanoparticles or lipid particles, when injected intravenously, selectively accumulate in tumor tissues and remain there for long periods. The EPR effect of tumor tissue is frequently inhomogeneous and the heterogeneity of the EPR effect may reduce the tumor delivery of macromolecular drugs. Therefore, we developed methods to augment the EPR effect without inducing adverse effects for instance raising the systemic blood pressure by infusing angiotensin II during arterial injection of SMANCS/Lipiodol. This method was validated in clinical setting. Further, benefits of utilization of NO-releasing agent such as nitroglycerin or angiotensin-converting enzyme (ACE) inhibitors were demonstrated. The EPR effect is thus now widely accepted as the most basic mechanism for tumor-selective targeting of macromolecular drugs, or so-called nanomedicine.

MAEDA, Hiroshi

2012-01-01

115

Upregulation of Tissue Factor by Activated Stat3 Contributes to Malignant Pleural Effusion Generation via Enhancing Tumor Metastasis and Vascular Permeability in Lung Adenocarcinoma  

PubMed Central

Malignant pleural effusion (MPE) is a poor prognostic sign for patients with lung cancer. Tissue factor (TF) is a coagulation factor that participates in angiogenesis and vascular permeability and is abundant in MPE. We previously demonstrated that autocrine IL-6-activated Stat3 contributes to tumor metastasis and upregulation of VEGF, resulting in the generation of MPE in lung adenocarcinoma. In this study, we found IL-6-triggered Stat3 activation also induces TF expression. By using pharmacologic inhibitors, it was shown that JAK2 kinase, but not Src kinase, contributed to autocrine IL-6-induced TF expression. Inhibition of Stat3 activation by dominant negative Stat3 (S3D) in lung adenocarcinoma suppressed TF-induced coagulation, anchorage-independent growth in vitro, and tumor growth in vivo. Consistently, knockdown of TF expression by siRNA resulted in a reduction of anchorage-independent growth of lung adenocarcinoma cells. Inhibition of TF expression also decreased the adhesion ability of cancer cells in normal lung tissues. In the nude mouse model, both lung metastasis and MPE generation were decreased when PC14PE6/AS2-siTF cells (TF expression was silenced) were intravenously injected. PC14PE6/AS2-siTF cells also produced less malignant ascites through inhibition of vascular permeability. In summary, we showed that TF expression plays a pivotal role in the pathogenesis of MPE generation via regulating of tumor metastasis and vascular permeability in lung adenocarcinoma bearing activated Stat3.

Yeh, Hsuan-Heng; Chang, Wen-Tsan; Lu, Kuang-Chu; Lai, Wu-Wei; Liu, Hsiao-Sheng; Su, Wu-Chou

2013-01-01

116

Upregulation of tissue factor by activated Stat3 contributes to malignant pleural effusion generation via enhancing tumor metastasis and vascular permeability in lung adenocarcinoma.  

PubMed

Malignant pleural effusion (MPE) is a poor prognostic sign for patients with lung cancer. Tissue factor (TF) is a coagulation factor that participates in angiogenesis and vascular permeability and is abundant in MPE. We previously demonstrated that autocrine IL-6-activated Stat3 contributes to tumor metastasis and upregulation of VEGF, resulting in the generation of MPE in lung adenocarcinoma. In this study, we found IL-6-triggered Stat3 activation also induces TF expression. By using pharmacologic inhibitors, it was shown that JAK2 kinase, but not Src kinase, contributed to autocrine IL-6-induced TF expression. Inhibition of Stat3 activation by dominant negative Stat3 (S3D) in lung adenocarcinoma suppressed TF-induced coagulation, anchorage-independent growth in vitro, and tumor growth in vivo. Consistently, knockdown of TF expression by siRNA resulted in a reduction of anchorage-independent growth of lung adenocarcinoma cells. Inhibition of TF expression also decreased the adhesion ability of cancer cells in normal lung tissues. In the nude mouse model, both lung metastasis and MPE generation were decreased when PC14PE6/AS2-siTF cells (TF expression was silenced) were intravenously injected. PC14PE6/AS2-siTF cells also produced less malignant ascites through inhibition of vascular permeability. In summary, we showed that TF expression plays a pivotal role in the pathogenesis of MPE generation via regulating of tumor metastasis and vascular permeability in lung adenocarcinoma bearing activated Stat3. PMID:24086497

Yeh, Hsuan-Heng; Chang, Wen-Tsan; Lu, Kuang-Chu; Lai, Wu-Wei; Liu, Hsiao-Sheng; Su, Wu-Chou

2013-01-01

117

Ozone-induced bronchial hyperresponsiveness in the rat is not accompanied by neutrophil influx or increased vascular permeability in the trachea  

SciTech Connect

We determined whether ozone-induced bronchial hyperresponsiveness in the rat is accompanied by neutrophil influx or increased vascular permeability in the trachea. Three groups of female Long-Evans rats were studied. One group was exposed to 4 ppm ozone for 2 h and studied immediately thereafter, another group was similarly exposed but was not studied until 24 h after the ozone exposure, and a third group consisted of control rats that breathed room air. Increases in total pulmonary resistance caused by acetylcholine aerosol were measured to assess bronchial responsiveness in these 3 groups. In parallel studies, neutrophil influx into the tracheal mucosa was quantified by counting cells within whole mounts of tracheas that were treated histochemically to stain the myeloperoxidase in neutrophils, and tracheal vascular permeability was quantified by measuring the amount of Evans blue dye extravasated into the trachea. In the rats studied immediately after the ozone exposure, the concentration of acetylcholine required to increase total pulmonary resistance to three-fold the baseline value was only 6% of that required in the controls. In the rats studied 24 h after the ozone exposure, this provocative acetylcholine concentration was not significantly different from that of the controls. Neither the number of neutrophils in the tracheal mucosa nor the amount of Evans blue dye extravasated into the trachea was significantly different from the corresponding control values at either time. We conclude that rats exposed to ozone develop bronchial hyperresponsiveness without detectable neutrophil influx or increased vascular permeability in the trachea.

Evans, T.W.; Brokaw, J.J.; Chung, K.F.; Nadel, J.A.; McDonald, D.M.

1988-07-01

118

Negative real parts of the equivalent permittivity, permeability, and refractive index of sculptured-nanorod arrays of silver  

SciTech Connect

Thin films comprising parallel nanorods were deposited by directing silver vapor obliquely toward a plane substrate. The direction of the vapor flux was varied in two different ways to sculpture the nanorods in different shapes. The reflection and transmission coefficients of the thin films were measured at three wavelengths in the visible regime for normal-illumination conditions for two linear-polarization states, using walk-off interferometry and polarization interferometry. The authors found that sculpturing significantly affects the signs of the real parts of the equivalent permittivity, permeability, and refractive index of the silver thin films for the two polarization states at different wavelengths. Thus, vapor deposition combined with sculpturing can be useful for large-scale production of materials having different equivalent constitutive parameters with negative real parts.

Jen, Yi-Jun; Lakhtakia, Akhlesh; Yu, Ching-Wei; Wang, Yu-Hsiung [Department of Electro-Optical Engineering, National Taipei University of Technology, No. 1, Sec. 3, Chung-Hsiao E. Road, Taipei 106, Taiwan (China); Department of Engineering Science and Mechanics and Materials Research Institute, Pennsylvania State University, University Park, Pennsylvania 16802 (United States); Department of Electro-Optical Engineering, National Taipei University of Technology, No. 1, Sec. 3, Chung-Hsiao E. Road, Taipei 106, Taiwan (China)

2010-09-15

119

Doppler resistive index to reflect regulation of renal vascular tone during sepsis and acute kidney injury.  

PubMed

ABSTRACT: INTRODUCTION: Renal resistive index (RI), determined by Doppler ultrasonography, directly reveals and quantifies modifications in renal vascular resistance. The aim of this study was to evaluate if mean arterial pressure (MAP) is determinant of renal RI in septic, critically ill patients suffering or not from acute kidney injury (AKI). METHODS: This prospective observational study included 96 patients. AKI was defined according to RIFLE criteria and transient or persistent AKI according to renal recovery within 3 days. RESULTS: Median renal RIs were 0.72 (0.68-0.75) in patients without AKI and 0.76 (0.72-0.80) in patients with AKI (P=0.001). RIs were 0.75 (0.72-0.79) in transient AKI and 0.77 (0.70-0.80) in persistent AKI (P=0.84). RI did not differ in patients given norepinephrine infusion and was not correlated with norepinephrine dose. RI was correlated with MAP (?= -0.47; P=0.002), PaO2/FiO2 ratio (?= -0.33; P=0.04) and age (?=0.35; P=0.015) only in patients without AKI. CONCLUSIONS: A poor correlation between renal RI and MAP, age, or PaO2/FiO2 ratio was found in septic and critically ill patients without AKI compared to patients with AKI. These findings suggest that determinants of RI are multiple. Renal circulatory response to sepsis estimated by Doppler ultrasonography cannot reliably be predicted simply from changes in systemic hemodynamics. As many factors influence its value, the interest in a single RI measurement at ICU admission to determine optimal MAP remains uncertain. PMID:22971333

Dewitte, Antoine; Coquin, Julien; Meyssignac, Bertrand; Joannès-Boyau, Olivier; Fleureau, Catherine; Roze, Hadrien; Ripoche, Jean; Janvier, Gérard; Combe, Christian; Ouattara, Alexandre

2012-09-12

120

Macromolecular DCE-MRI detects reduced vascular permeability in a prostate cancer bone metastasis model following anti-PDGFR therapy, indicating a drop in VEGFR activation  

PubMed Central

The anti-vascular function of platelet-derived growth factor receptor (PDGFR) inhibitor imatinib combined with paclitaxel has been demonstrated by invasive immunohistochemistry. The purpose of this study was 1. to noninvasively monitor the response to anti-PDGFR treatment and 2. to understand the underlying mechanism of this response. Thus, response to treatment was studied in a prostate cancer bone metastasis model using macromolecular (biotin-BSA-GdDTPA) dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI). PC-3MM2 bone metastases that caused osteolysis and grew in neighboring muscle showed high blood volume fraction (fBV) and vascular permeability (PS) at the tumor periphery, compared to muscle tissue and intraosseous tumor. Imatinib alone or with paclitaxel significantly reduced PS by 35% (one-tailed paired t-test p=0.045) and 40% (p=0.0003) respectively, whereas paclitaxel alone or no treatment had no effect. Based on changes in PS we hypothesized that imatinib interferes with the signaling pathway of vascular endothelial growth factor (VEGF). This mechanism was verified by immunohistochemistry. It demonstrated reduced activation of both PDGFR-? and VEGFR2 in imatinib-treated mice. Our study therefore demonstrates that macromolecular DCE-MRI can be used to detect early vascular effects associated with response to therapy targeted to PDGFR and provides insight into the role played by VEGF in anti-PDGFR therapy.

Dafni, Hagit; Kim, Sun-Jin; Bankson, James A; Sankaranarayanapillai, Madhuri; Ronen, Sabrina M

2014-01-01

121

Coenzyme Q10: a novel gastroprotective effect via modulation of vascular permeability, prostaglandin E?, nitric oxide and redox status in indomethacin-induced gastric ulcer model.  

PubMed

Coenzyme Q10 is an essential cofactor in the mitochondrial electron transport pathway, and is endowed for its potent antioxidant capacity; characters that endorse its implication in several clinical practices and as a food supplement. Nevertheless, its potential gastro-protective effect, in acute models, has never been assessed, which is the objective of this study. Since indomethacin mediated gastropathy is multifaceted, including mitochondrial dysfunction and generation of reactive oxygen species, thus, the indomethacin-induced gastric injury serves as a convenient animal model for this work. Rats treated with indomethacin revealed mucosal hemorrhagic lesions, increased microvascular permeability and inhibited prostaglandin E? and mucus content. Redox imbalance was reflected by decreased mucosal glutathione (GSH), nitric oxide and glutathione peroxidase contents/activity, along with elevated lipid peroxides. Pretreatment with CoQ10 caused discernible decrease in indomethacin-induced gastric lesions, vascular permeability and lipid peroxide content. In addition, prostaglandin E? and GSH levels were restored, while those of nitric oxide and glutathione peroxidase were elevated significantly above normal; however, mucus formation was not altered significantly. The positive effects were comparable to those of sucralfate, the standard drug used herein, except for the mucus and prostaglandin E? levels that were increased above normal by sucralfate. CoQ10-mediated gastroprotective effect involves preservation of microvascular permeability, elevation of prostaglandin E?, improvement of redox status, as well as boosting of nitric oxide. Nevertheless, maintaining gastric mucus content is ruled out. PMID:20858483

El-Abhar, Hanan S

2010-12-15

122

Endothelial-like properties of claudin-low breast cancer cells promote tumor vascular permeability and metastasis.  

PubMed

The vasculature serves as the main conduit for breast tumor metastases and is a target of therapeutics in many tumor types. In this study, we aimed to determine if tumor-associated vascular properties could help to explain the differences observed in metastagenicity across the intrinsic subtypes of human breast tumors. Analysis of gene expression signatures from more than 3,000 human breast tumors found that genomic programs that measured vascular quantity, vascular proliferation, and a VEGF/Hypoxia-signature were the most highly expressed in claudin-low and basal-like tumors. The majority of the vascular gene signatures added metastasis-predictive information to immunohistochemistry-defined microvessel density scores and genomically defined-intrinsic subtype classification. Interestingly, pure claudin-low cell lines, and subsets of claudin-low-like cells within established basal-like cancer cell lines, exhibited endothelial/tube-like morphology when cultured on Matrigel. In vivo xenografts found that claudin-low tumors, but not luminal tumors, extensively perfused injected contrast agent through paracellular spaces and non-vascular tumor-lined channels. Taken together, the endothelial-like characteristics of the cancer cells, combined with both the amount and the physiologic state of the vasculature contribute to breast cancer metastatic progression. We hypothesize that the genetic signatures we have identified highlight patients that should respond most favorably to anti-vascular agents. PMID:23975155

Harrell, J Chuck; Pfefferle, Adam D; Zalles, Nicole; Prat, Aleix; Fan, Cheng; Khramtsov, Andrey; Olopade, Olufunmilayo I; Troester, Melissa A; Dudley, Andrew C; Perou, Charles M

2014-01-01

123

Bevacizumab-Induced Alterations in Vascular Permeability and Drug Delivery: A Novel Approach to Augment Regional Chemotherapy for In-Transit Melanoma  

PubMed Central

Purpose To investigate whether the systemically administered anti-VEGF monoclonal antibody bevacizumab could improve regional chemotherapy treatment of advanced extremity melanoma by enhancing delivery and tumor uptake of regionally infused melphalan (LPAM). Experimental Design After treatment with systemic bevacizumab or saline, changes in vascular permeability were determined by spectrophotometric analysis of tumors infused with Evan’s blue dye. Changes in vascular structure and tumor hemoglobin-oxygen saturation HbO2 were determined by intravital microscopy and diffuse reflectance spectroscopy, respectively. Rats bearing the low-VEGF secreting DM738 and the high-VEGF secreting DM443 melanoma xenografts underwent isolated limb infusion (ILI) with melphalan (LPAM) or saline via the femoral vessels. The effect of bevacizumab on terminal drug delivery was determined by immunohistochemical analysis of LPAM-DNA adducts in tumor tissues. Results Single-dose bevacizumab given three days before ILI with LPAM significantly decreased vascular permeability (50.3% in DM443, P < 0.01 and 35% in DM738, P < 0.01) and interstitial fluid pressure (57% in DM443, P < 0.01 and 50% in DM738, P = 0.01). HbO2 decreased from baseline in mice following treatment with bevacizumab. Systemic bevacizumab significantly enhanced tumor response to ILI with LPAM in two melanoma xenografts, DM443 and DM738, increasing quadrupling time 37% and 113%, respectively (P = 0.03). Immunohistochemical analyses of tumor specimens showed that pretreatment with systemic bevacizumab markedly increased LPAM-DNA adduct formation. Conclusions Systemic treatment with bevacizumab before regional chemotherapy increases delivery of LPAM to tumor cells and represents a novel way to augment response to regional therapy for advanced extremity melanoma.

Turley, Ryan S.; Fontanella, Andrew N.; Padussis, James C.; Toshimitsu, Hiroaki; Tokuhisa, Yoshihiro; Cho, Eugenia H.; Hanna, Gabi; Beasley, Georgia M.; Augustine, Christina K.; Dewhirst, Mark W.; Tyler, Douglas S.

2013-01-01

124

The Cytokine Response of U937-Derived Macrophages Infected through Antibody-Dependent Enhancement of Dengue Virus Disrupts Cell Apical-Junction Complexes and Increases Vascular Permeability  

PubMed Central

Severe dengue (SD) is a life-threatening complication of dengue that includes vascular permeability syndrome (VPS) and respiratory distress. Secondary infections are considered a risk factor for developing SD, presumably through a mechanism called antibody-dependent enhancement (ADE). Despite extensive studies, the molecular bases of how ADE contributes to SD and VPS are largely unknown. This work compares the cytokine responses of differentiated U937 human monocytic cells infected directly with dengue virus (DENV) or in the presence of enhancing concentrations of a humanized monoclonal antibody recognizing protein E (ADE-DENV infection). Using a cytometric bead assay, ADE-DENV-infected cells were found to produce significantly higher levels of the proinflammatory cytokines interleukin 6 (IL-6), IL-12p70, and tumor necrosis factor alpha (TNF-?), as well as prostaglandin E2 (PGE2), than cells directly infected. The capacity of conditioned supernatants (conditioned medium [CM]) to disrupt tight junctions (TJs) in MDCK cell cultures was evaluated. Exposure of MDCK cell monolayers to CM collected from ADE-DENV-infected cells (ADE-CM) but not from cells infected directly led to a rapid loss of transepithelial electrical resistance (TER) and to delocalization and degradation of apical-junction complex proteins. Depletion of either TNF-?, IL-6, or IL-12p70 from CM from ADE-DENV-infected cells fully reverted the disrupting effect on TJs. Remarkably, mice injected intraperitoneally with ADE-CM showed increased vascular permeability in sera and lungs, as indicated by an Evans blue quantification assay. These results indicate that the cytokine response of U937-derived macrophages to ADE-DENV infection shows an increased capacity to disturb TJs, while results obtained with the mouse model suggest that such a response may be related to the vascular plasma leakage characteristic of SD.

Puerta-Guardo, Henry; Raya-Sandino, Arturo; Gonzalez-Mariscal, Lorenza; Rosales, Victor H.; Ayala-Davila, Jose; Chavez-Mungia, Bibiana; Martinez-Fong, Daniel; Medina, Fernando

2013-01-01

125

Evaluation of Blood Pressure Control using a New Arterial Stiffness Parameter, Cardio-ankle Vascular Index (CAVI)  

PubMed Central

Arterial stiffness has been known to be a surrogate marker of arteriosclerosis, and also of vascular function. Pulse wave velocity (PWV) had been the most popular index and was known to be a predictor of cardiovascular events. But, it depends on blood pressure at measuring time. To overcome this problem, cardio-ankle vascular index (CAVI) is developed. CAVI is derived from stiffness parameter ? by Hayashi, and the equation of Bramwell-Hill, and is independent from blood pressure at a measuring time. Then, CAVI might reflect the proper change of arterial wall by antihypertensive agents. CAVI shows high value with aging and in many arteriosclerotic diseases and is also high in persons with main coronary risk factors. Furthermore, CAVI is decreased by an administration of ?1 blocker, doxazosin for 2-4 hours, Those results suggested that CAVI reflected the arterial stiffness composed of organic components and of smooth muscle cell contracture. Angiotensin II receptor blocker, olmesartan decreased CAVI much more than that of calcium channel antagonist, amlodipine, even though the rates of decreased blood pressure were almost same. CAVI might differentiate the blood pressure-lowering agents from the point of the effects on proper arterial stiffness. This paper reviewed the principle and rationale of CAVI, and the possibilities of clinical applications, especially in the studies of hypertension.

Shirai, Kohji; Utino, Junji; Saiki, Atsuhito; Endo, Kei; Ohira, Masahiro; Nagayama, Daiji; Tatsuno, Ichiro; Shimizu, Kazuhiro; Takahashi, Mao; Takahara, Akira

2013-01-01

126

Monitoring of peripheral vascular condition using a log-linearized arterial viscoelastic index during endoscopic thoracic sympathectomy.  

PubMed

This paper proposes a novel technique to support the monitoring of peripheral vascular conditions using biological signals such as electrocardiograms, arterial pressure values and pulse oximetry plethysmographic waveforms. In this approach, a second-order log-linearized model (referred to here as a log-linearized peripheral arterial viscoelastic model) is used to describe the non-linear viscoelastic relationship between blood pressure waveforms and photo-plethysmographic waveforms. The proposed index enables estimation of peripheral arterial wall stiffness changes induced by sympathetic nerve activity. The validity of the method is discussed here based on the results of peripheral vascular condition monitoring conducted during endoscopic thoracic sympathectomy (ETS). The results of ETS monitoring showed significant changes in stiffness variations between the periods before and during the procedures observed (p < 0.01) as well as during and after them (p < 0.01), so that it was confirmed that sympathetic nerve activity is drastically decreased in the area around the monitoring site after the thoracic sympathetic nerve trunk on the monitoring side is successfully blocked. In addition, no change was observed in the values of the proposed index during the ETS procedure on the side opposite that of the monitoring site. The experimental results obtained clearly show the proposed method can be used to assess changes in sympathetic nerve activity during ETS. PMID:24110256

Hirano, Hiroki; Horiuchi, Tetsuya; Hirano, Harutoyo; Kurita, Yuichi; Ukawa, Teiji; Nakamura, Ryuji; Saeki, Noboru; Yoshizumi, Masao; Kawamoto, Masashi; Tsuji, Toshio

2013-01-01

127

Cardioankle vascular index evaluations revealed that cotreatment of ARB Antihypertension medication with traditional Chinese medicine improved arterial functionality.  

PubMed

Qian Yang He Ji (QYHJ) is a traditional Chinese medicine composed of Digitalis purpurea, Uncaria gambir, Fructus tribuli terrestris, and Ligustrum lucidum. Here, we explored whether combining an antihypertensive angiotensin II receptor blocker (ARB) therapy with QYHJ can improve the arterial functionality of hypertensive patients. One hundred and eight hypertensive patients were randomized into 2 groups; 1 group (n = 53) was treated with ARB and the other group (n = 55) was treated with ARB combined with QYHJ. Each of the 2 groups included 3 subgroups (pure hypertension, hypertension with diabetes, and hypertension with coronary heart disease) and was further divided into patients with and without complications. The cardioankle vascular index and intima-media thickness and pulse pressure were the outcome evaluation parameter. Combined QYHJ and ARB treatment reduced the values of cardioankle vascular index, systolic blood pressure, diastolic blood pressure, and pulse pressure to significantly lower levels than ARB treatment alone did in hypertension patients after 6 months of treatment. ARB improves hypertension, but a combined QYHJ treatment can additionally ameliorate the arterial functionality not only in solely hypertensive patients but also in hypertensive patients with diabetes and coronary heart disease complications. QYHJ coapplication might be a choice to further improve the arterial functionality during an ARB hypertension treatment. PMID:23188130

Xu, Yan; Yan, Hua; Yao, Min J; Ma, Jie; Jia, Jun M; Ruan, Fen X; Yao, Zeng C; Huang, Hua M; Zheng, Jing; Chen, Ting; Lv, Hua; Endler, Alexander M

2013-05-01

128

Tiam1 and Rac1 Are Required for Platelet-activating Factor-induced Endothelial Junctional Disassembly and Increase in Vascular Permeability*  

PubMed Central

It is known that platelet-activating factor (PAF) induces severe endothelial barrier leakiness, but the signaling mechanisms remain unclear. Here, using a wide range of biochemical and morphological approaches applied in both mouse models and cultured endothelial cells, we addressed the mechanisms of PAF-induced disruption of interendothelial junctions (IEJs) and of increased endothelial permeability. The formation of interendothelial gaps filled with filopodia and lamellipodia is the cellular event responsible for the disruption of endothelial barrier. We observed that PAF ligation of its receptor induced the activation of the Rho GTPase Rac1. Following PAF exposure, both Rac1 and its guanine nucleotide exchange factor Tiam1 were found associated with a membrane fraction from which they co-immunoprecipitated with PAF receptor. In the same time frame with Tiam1-Rac1 translocation, the junctional proteins ZO-1 and VE-cadherin were relocated from the IEJs, and formation of numerous interendothelial gaps was recorded. Notably, the response was independent of myosin light chain phosphorylation and thus distinct from other mediators, such as histamine and thrombin. The changes in actin status are driven by the PAF-induced localized actin polymerization as a consequence of Rac1 translocation and activation. Tiam1 was required for the activation of Rac1, actin polymerization, relocation of junctional associated proteins, and disruption of IEJs. Thus, PAF-induced IEJ disruption and increased endothelial permeability requires the activation of a Tiam1-Rac1 signaling module, suggesting a novel therapeutic target against increased vascular permeability associated with inflammatory diseases.

Knezevic, Ivana I.; Predescu, Sanda A.; Neamu, Radu F.; Gorovoy, Matvey S.; Knezevic, Nebojsa M.; Easington, Cordus; Malik, Asrar B.; Predescu, Dan N.

2009-01-01

129

Reduced Retinal Neovascularization, Vascular Permeability, and Apoptosis in Ischemic Retinopathy in the Absence of Prolyl Hydroxylase-1 Due to the Prevention of Hyperoxia-Induced Vascular Obliteration  

PubMed Central

Purpose. Prolyl hydroxylases (PHDs) are oxygen sensors that stabilize hypoxia-inducible factors (HIFs) to induce proinflammatory, vasopermeability, and proapoptotic factors. These may be potential targets to reduce the complications of ischemic retinopathies. Methods. Oxygen-induced ischemic retinopathy (OIR) was generated as a model for retinopathy of prematurity (ROP) by placing 7-day-old mice in 75% oxygen for 5 days and returning them to the relative hypoxia of room air for 5 days. Neovascularization (NV) and avascular areas were assessed on retinal flat-mounts by image analysis. Blood-retinal barrier breakdown was assessed using 3H-mannitol as a tracer. Apoptosis was detected with TUNEL staining. HIF-1? and VEGF were quantified using Western blot analysis and ELISA. Results. PHD1-deficient mice demonstrated reduced hyperoxia-associated vascular obliteration during oxygen-induced ischemic retinopathy. This was associated with subsequent reduced avascularity, vascular leakage, and pathologic NV during the hypoxic phase, which could be accounted for by a reduced expression of HIF-1? and VEGF. Apoptosis in the retina was also reduced in PHD1-depleted mice after 2 days in hyperoxia. Conclusions. PHD1 deficiency is associated with a reduction of ischemia-induced retinal NV. The regulatory mechanism in this model appears to be: PHD1 depletion prevents HIF-1? degradation in hyperoxia, which induces VEGF, thus preventing hyperoxia-related vessel loss. Without a vessel deficiency, there would not be relative hypoxia when the mice are returned to room air and there would be no need to initiate angiogenesis signaling. Blocking PHD1 may be beneficial for ischemic retinopathies and inflammatory and neurodegenerative disorders.

Huang, Hu; Van de Veire, Sara; Dalal, Mansi; Parlier, Rachel; Semba, Richard D.; Carmeliet, Peter

2011-01-01

130

Survey of ocular irritation predictive capacity using Chorioallantoic Membrane Vascular Assay (CAMVA) and Bovine Corneal Opacity and Permeability (BCOP) test historical data for 319 personal care products over fourteen years  

Microsoft Academic Search

The Chorioallantoic Membrane Vascular Assay (CAMVA) and Bovine Corneal Opacity and Permeability (BCOP) test are widely used to predict ocular irritation potential for consumer-use products. These in vitro assays do not require live animals, produce reliable predictive data for defined applicability domains compared to the Draize rabbit eye test, and are rapid and inexpensive. Data from 304 CAMVA and\\/or BCOP

D. A. Donahue; L. E. Kaufman; J. Avalos; F. A. Simion; D. R. Cerven

2011-01-01

131

Simultaneous optical and mr imaging of tissue within implanted window chamber: System development and application in measuring vascular permeability  

NASA Astrophysics Data System (ADS)

Simultaneous optical imaging and MRI of a dorsal skin-fold window chamber mouse model is investigated as a novel methodology to study the tumor microenvironment. Simultaneous imaging with two modalities allows for cross-validation of results, integration of the capabilities of the two modalities in one study and mitigation of invasive factors, such as surgery and anesthesia, in an in-vivo experiment. To make this investigation possible, three optical imaging systems were developed that operated inside the MRI scanner. One of the developed systems was applied to estimate vascular kinetic parameters of tumors in a dorsal skin-fold window chamber mouse model with simultaneous optical and MRI imaging. The target of imaging was a molecular agent that was dual labeled with both optical and MRI contrast agents. The labeling of the molecular agent, characteristics of the developed optical systems, the methodologies of measuring vascular kinetic parameters using optical imaging and MRI data, and the obtained results are described and illustrated.

Shayegan Salek, Mir Farrokh

132

Publicações indexadas geradas a partir de resumos de congressos de angiologia e cirurgia vascular no Brasil Indexed publications generated from abstracts of angiology and vascular surgery congresses in Brazil  

Microsoft Academic Search

Background: Great part of the scientific production presented in congresses is not published. Even in developed countries, figures show an expressive difference between presentations and publications. Objective: To evaluate the number of published and indexed articles, based on available national and international databases, searching for titles and authors of papers and panels from Brazilian vascular surgery congresses held in 2001

Winston Bonetti Yoshida; Nicole França Holmo; Gabriela Tieme Corregliano; Karina Marcellino Baldon

133

Relationship between smoking and a new index of arterial stiffness, the cardio-ankle vascular index, in male workers: a cross-sectional study  

PubMed Central

Background Cigarette smoking is one of the major factors that increases arterial stiffness. The purpose of this study was to examine further the relationship between smoking status and arterial stiffness using a new index, the cardio-ankle vascular index (CAVI), in male Japanese workers. Methods This cross-sectional study included 4,729 male Japanese workers undergoing annual health checkups. CAVI was measured at the time of the annual health checkup between April 2007 and March 2008. The subjects were divided into three groups, smokers (n?=?1,913), former smokers (n?=?1,481) and non-smokers (n?=?1,348) according to their responses to a questionnaire. We compared the CAVI in the three groups after adjusting for age. Multiple regression analysis was used to examine the association between CAVI and the number of cigarettes smoked per day in order to examine whether there was a dose–response relationship between smoking and CAVI. Results The mean CAVI for each group was 7.81?±?0.02 for smokers, 7.70?±?0.02 for former smokers and 7.64?±?0.02 for non-smokers. A significant difference was observed between each group. According to the results of multiple regression analysis, the standardized ? of the number of cigarettes smoked per day was 0.09 (p?

2012-01-01

134

ICAM-2 regulates vascular permeability and N-cadherin localization through ezrin-radixin-moesin (ERM) proteins and Rac-1 signalling  

PubMed Central

Background Endothelial junctions control functions such as permeability, angiogenesis and contact inhibition. VE-Cadherin (VECad) is essential for the maintenance of intercellular contacts. In confluent endothelial monolayers, N-Cadherin (NCad) is mostly expressed on the apical and basal membrane, but in the absence of VECad it localizes at junctions. Both cadherins are required for vascular development. The intercellular adhesion molecule (ICAM)-2, also localized at endothelial junctions, is involved in leukocyte recruitment and angiogenesis. Results In human umbilical vein endothelial cells (HUVEC), both VECad and NCad were found at nascent cell contacts of sub-confluent monolayers, but only VECad localized at the mature junctions of confluent monolayers. Inhibition of ICAM-2 expression by siRNA caused the appearance of small gaps at the junctions and a decrease in NCad junctional staining in sub-confluent monolayers. Endothelioma lines derived from WT or ICAM-2-deficient mice (IC2neg) lacked VECad and failed to form junctions, with loss of contact inhibition. Re-expression of full-length ICAM-2 (IC2 FL) in IC2neg cells restored contact inhibition through recruitment of NCad at the junctions. Mutant ICAM-2 lacking the binding site for ERM proteins (IC2 ?ERM) or the cytoplasmic tail (IC2 ?TAIL) failed to restore junctions. ICAM-2-dependent Rac-1 activation was also decreased in these mutant cell lines. Barrier function, measured in vitro via transendothelial electrical resistance, was decreased in IC2neg cells, both in resting conditions and after thrombin stimulation. This was dependent on ICAM-2 signalling to the small GTPase Rac-1, since transendothelial electrical resistance of IC2neg cells was restored by constitutively active Rac-1. In vivo, thrombin-induced extravasation of FITC-labeled albumin measured by intravital fluorescence microscopy in the mouse cremaster muscle showed that permeability was increased in ICAM-2-deficient mice compared to controls. Conclusions These results indicate that ICAM-2 regulates endothelial barrier function and permeability through a pathway involving N-Cadherin, ERMs and Rac-1.

2014-01-01

135

[Relation between cardio-ankle vascular index (Cavi) and preheparin serum lipoprotein lipase mass--effect of age adjustment].  

PubMed

Many risk factors for coronary arterial diseases have been reported. Lipoprotein lipase (LPL) mass in serum has been suggested to be a new risk factor, but remains to be proven. The cardio-ankle vascular index (CAVI) was developed as a new arterial stiffness index and is considered to be a surrogate marker of arteriosclerosis. The purpose of this study was to establish the role of LPL mass in arteriosclerosis by examining the relationship between LPL mass and CAVI in patients with arteriosclerotic risk factors. We studied 216 patients who attended our diabetic center with diagnoses of diabetes, hypertension and/or dyslipidemia. CAVI was measured using VaSera1500 (Fukuda Denshi, Tokyo). Serum level of LPL mass was measured by ELISA(Sekisui Co. Ltd.). When the subjects were divided by a CAVI cutoff level of 9.0, the glucose level, glycohemoglobin A1c (HbA1c) level and systolic blood pressure level were significantly higher in the over 9.0 individuals than in the under 9.0 individuals (p < 0.05). CAVI level was significantly higher in patients with hyperglycemia and hypertension. LPL mass was lower in subjects with higher CAVI than in those with lower CAVI. CAVI level correlated inversely with LPL mass. CAVI adjusted for the age was associated significantly with LPL mass. These results suggest that decreased LPL mass may be a risk marker for arteriosclerosis as indicated by the surrogate marker CAVI. PMID:23198531

Moteki, Masashi; Murano, Takeyoshi; Kurosu, Takumi; Kataoka, Manabu; Nakano, Mizuaki; Hiruta, Nobuyuki; Shirai, Kohji

2012-08-01

136

Impact of oncogenes in tumor angiogenesis: mutant K-ras up-regulation of vascular endothelial growth factor/vascular permeability factor is necessary, but not sufficient for tumorigenicity of human colorectal carcinoma cells.  

PubMed

Targeted disruption of the single mutant K-ras allele in two human colorectal carcinoma cell lines (DLD-1 and HCT-116) leads to loss of tumorigenic competence in nude mice with retention of ability to grow indefinitely in monolayer culture. Because expression of the mutant K-ras oncogene in these cell lines is associated with marked up-regulation of vascular endothelial growth factor/vascular permeability factor (VEGF/VPF), we sought to determine whether this potent angiogenesis inducer plays a role in K-ras-dependent tumorigenic competence. Transfection of a VEGF121 antisense expression vector into DLD-1 and HCT-116 cells resulted in suppression of VEGF/VPF production by a factor of 3- to 4-fold. The VEGF/VPF-deficient sublines, unlike the parental population or vector controls, were profoundly suppressed in their ability to form tumors in nude mice for as long as 6 months after cell injection. In contrast, in vitro growth of these sublines was unaffected, thus demonstrating the critical importance of VEGF/VPF as an angiogenic factor for HCT-116 and DLD-1 cells. Transfection of a full-length VEGF121 cDNA into two nontumorigenic mutant K-ras knockout sublines resulted in a weak but detectable restoration of tumorigenic ability in vivo in a subset of the transfectants, with no consistent change in growth properties in vitro. The findings indicate that mutant ras-oncogene-dependent VEGF/VPF expression is necessary, but not sufficient, for progressive tumor growth in vivo and highlight the relative contribution of oncogenes, such as mutant K-ras, to the process of tumor angiogenesis. PMID:9520413

Okada, F; Rak, J W; Croix, B S; Lieubeau, B; Kaya, M; Roncari, L; Shirasawa, S; Sasazuki, T; Kerbel, R S

1998-03-31

137

Impact of oncogenes in tumor angiogenesis: Mutant K-ras up-regulation of vascular endothelial growth factor/vascular permeability factor is necessary, but not sufficient for tumorigenicity of human colorectal carcinoma cells  

PubMed Central

Targeted disruption of the single mutant K-ras allele in two human colorectal carcinoma cell lines (DLD-1 and HCT-116) leads to loss of tumorigenic competence in nude mice with retention of ability to grow indefinitely in monolayer culture. Because expression of the mutant K-ras oncogene in these cell lines is associated with marked up-regulation of vascular endothelial growth factor/vascular permeability factor (VEGF/VPF), we sought to determine whether this potent angiogenesis inducer plays a role in K-ras-dependent tumorigenic competence. Transfection of a VEGF121 antisense expression vector into DLD-1 and HCT-116 cells resulted in suppression of VEGF/VPF production by a factor of 3- to 4-fold. The VEGF/VPF-deficient sublines, unlike the parental population or vector controls, were profoundly suppressed in their ability to form tumors in nude mice for as long as 6 months after cell injection. In contrast, in vitro growth of these sublines was unaffected, thus demonstrating the critical importance of VEGF/VPF as an angiogenic factor for HCT-116 and DLD-1 cells. Transfection of a full-length VEGF121 cDNA into two nontumorigenic mutant K-ras knockout sublines resulted in a weak but detectable restoration of tumorigenic ability in vivo in a subset of the transfectants, with no consistent change in growth properties in vitro. The findings indicate that mutant ras-oncogene-dependent VEGF/VPF expression is necessary, but not sufficient, for progressive tumor growth in vivo and highlight the relative contribution of oncogenes, such as mutant K-ras, to the process of tumor angiogenesis.

Okada, Futoshi; Rak, Janusz W.; Croix, Brad St.; Lieubeau, Blandine; Kaya, Mitsunori; Roncari, Luba; Shirasawa, Senji; Sasazuki, Takehiko; Kerbel, Robert S.

1998-01-01

138

Novel Application of a Multiscale Entropy Index as a Sensitive Tool for Detecting Subtle Vascular Abnormalities in the Aged and Diabetic  

PubMed Central

Although previous studies have shown the successful use of pressure-induced reactive hyperemia as a tool for the assessment of endothelial function, its sensitivity remains questionable. This study aims to investigate the feasibility and sensitivity of a novel multiscale entropy index (MEI) in detecting subtle vascular abnormalities in healthy and diabetic subjects. Basic anthropometric and hemodynamic parameters, serum lipid profiles, and glycosylated hemoglobin levels were recorded. Arterial pulse wave signals were acquired from the wrist with an air pressure sensing system (APSS), followed by MEI and dilatation index (DI) analyses. MEI succeeded in detecting significant differences among the four groups of subjects: healthy young individuals, healthy middle-aged or elderly individuals, well-controlled diabetic individuals, and poorly controlled diabetic individuals. A reduction in multiscale entropy reflected age- and diabetes-related vascular changes and may serve as a more sensitive indicator of subtle vascular abnormalities compared with DI in the setting of diabetes.

Wu, Hsien-Tsai; Lo, Men-Tzung; Chen, Guan-Hong; Sun, Cheuk-Kwan; Chen, Jian-Jung

2013-01-01

139

Accuracy of Doppler-derived estimation of pulmonary vascular resistance in congenital heart disease: an index of operability.  

PubMed

Pulmonary vascular resistance (PVR) is a critical and essential parameter during the assessment and selection of modality of treatment in patients with congenital heart disease (CHD) accompanied by pulmonary arterial hypertension (PAH). Cardiac catheterization is the "gold standard" but is an invasive method for PVR measurement. A noninvasive and reliable method for estimation of PVR in children has been a major challenge and most desirable during past decades, especially for those who need repeated measurements. In a prospective study and among consecutive patients who were referred for cardiac catheterizations, PVR was calculated as the ratio of the transpulmonary pressure gradient (?P) to the amount of the pulmonary flow (QP) accordingly for 20 patients with CHD and high PAH. Subsequently and noninvasively, PVR was assessed for these patients by a Doppler echocardiography-derived index defined as the ratio of the tricuspid regurgitation velocity (TRV(m/s)) to the velocity time integral (VTI(cm)) of the right-ventricular outflow tract (RVOT). There was a good correlation between PVR measured at catheterization (PVR(cath)) and TRV/VTI(m) ratio; the mean of three measurements of VTI (VTI(m)) with R (2) = 0.53 (p = 0.008). In addition, a TRV/VTI(m) value of 0.2 provided a sensitivity of 71.4% and a specificity of 100% for PVR >6 Woods units (WU) as well as sensitivity of 90% and specificity of 90% for a PVR equal to 8 WU. PVR value between 6 and 8 WU by catheterization has been considered as a cut-off point for intervention in children with left-to-right shunts and PAH. In conclusion, Doppler-derived TRV/VTI(m) ratio is a reliable index that may be helpful as a supplementary diagnostic tool for the selection of modality of treatment and follow-up of patients with PAH and increased PVR. PMID:21779967

Ajami, Gholam Hossein; Cheriki, Sirous; Amoozgar, Hamid; Borzouee, Mohammad; Soltani, Manoucher

2011-12-01

140

Blood pressure-independent effect of candesartan on cardio-ankle vascular index in hypertensive patients with metabolic syndrome  

PubMed Central

Angiotensin receptor blockers (ARBs) are known to reduce the cardiovascular risk in hypertensive patients. This study was designed to examine the effect of an ARB candesartan on subclinical atherosclerosis assessed by cardio-ankle vascular index (CAVI) in comparison with calcium channel blockers (CCBs) alone in hypertensive patients with metabolic syndrome (MetS). A total of 53 consecutive hypertensive patients with MetS were randomly assigned to the candesartan group, in which candesartan was added on, or the CCBs group, in which CCBs were added on. Clinical and biological parameters were obtained before and after the 12-month treatment period. The primary measure of efficacy was the %change in CAVI. When treated with candesartan, but not CCBs, CAVI significantly decreased from 8.7 to 7.7 by 11%. Blood pressure (BP) significantly decreased with both treatments, but the differences between groups were not significant. The changes in other parameters remained unchanged in both the groups. Analysis of covariance found that both the BP reduction and the therapy difference contributed to the decrease in CAVI, but the BP reduction was not involved in the decrease in CAVI caused by the difference in the therapy. Candesartan may be a better antihypertensive drug than CCBs to improve subclinical atherosclerosis of patients with MetS.

Bokuda, Kanako; Ichihara, Atsuhiro; Sakoda, Mariyo; Mito, Asako; Kinouchi, Kenichiro; Itoh, Hiroshi

2010-01-01

141

Sarpogrelate hydrochloride decreases cardio-ankle vascular index accompanied by increased serum lipoprotein lipase mass in type 2 diabetic patients.  

PubMed

The 5-hydroxytryptamine2A receptor antagonist sarpogrelate hydrochloride exerts its effect not only by inhibition of platelet aggregation, but also by some pleiotropic effects. We have reported that a low serum lipoprotein lipase (LPL) mass level reflects insulin resistance and may be a risk factor for atherosclerotic diseases. The aim of this prospective study was to clarify the effect of sarpogrelate on serum LPL mass and cardio-ankle vascular index (CAVI) as a marker related to arterial stiffness.Thirty-five type 2 diabetic patients (21 males and 14 females) with ankle brachial indices higher than 0.90 received sarpogrelate hydrochloride 300 mg/day for 6 months. Serum LPL mass and CAVI were measured during the study.After 6 months of sarpogrelate hydrochloride treatment, CAVI decreased significantly (10.11 ± 0.92 to 9.87 ± 0.97, P < 0.05) and serum LPL mass increased significantly (58.2 ± 17.5 to 63.5 ± 21.4, P < 0.05). A negative correlation between change in CAVI and change in serum LPL mass was observed (r = -0.34, P < 0.05). Multiple regression analysis identified a change in serum LPL mass as a significant independent predictor for change in CAVI.We demonstrated that sarpogrelate hydrochloride decreased CAVI accompanied by increased serum LPL mass in type 2 diabetic patients. This result suggests that sarpogrelate hydrochloride improves arterial stiffness and is a potential treatment for diabetic angiopathy. PMID:24898600

Nagayama, Daiji; Ohira, Masahiro; Saiki, Atsuhito; Shirai, Kohji; Tatsuno, Ichiro

2014-07-10

142

Measurement of absolute cell volume, osmotic membrane water permeability, and refractive index of transmembrane water and solute flux by digital holographic microscopy.  

PubMed

A dual-wavelength digital holographic microscope to measure absolute volume of living cells is proposed. The optical setup allows us to reconstruct two quantitative phase contrast images at two different wavelengths from a single hologram acquisition. When adding the absorbing dye fast green FCF as a dispersive agent to the extracellular medium, cellular thickness can be univocally determined in the full field of view. In addition to the absolute cell volume, the method can be applied to derive important biophysical parameters of living cells including osmotic membrane water permeability coefficient and the integral intracellular refractive index (RI). Further, the RI of transmembrane flux can be determined giving an indication about the nature of transported solutes. The proposed method is applied to cultured human embryonic kidney cells, Chinese hamster ovary cells, human red blood cells, mouse cortical astrocytes, and neurons. PMID:23487181

Boss, Daniel; Kühn, Jonas; Jourdain, Pascal; Depeursinge, Christian; Magistretti, Pierre J; Marquet, Pierre

2013-03-01

143

Catalase and Superoxide Dismutase Conjugated with Platelet-Endothelial Cell Adhesion Molecule Antibody Distinctly Alleviate Abnormal Endothelial Permeability Caused by Exogenous Reactive Oxygen Species and Vascular Endothelial Growth Factor  

PubMed Central

Reactive oxygen species (ROS) superoxide anion (O2?) and hydrogen peroxide (H2O2) produced by activated leukocytes and endothelial cells in sites of inflammation or ischemia cause endothelial barrier dysfunction that may lead to tissue edema. Antioxidant enzymes (AOEs) catalase and superoxide dismutase (SOD) conjugated with antibodies to platelet-endothelial cell adhesion molecule-1 (PECAM-1) specifically bind to endothelium, quench the corresponding ROS, and alleviate vascular oxidative stress and inflammation. In the present work, we studied the effects of anti-PECAM/catalase and anti-PECAM/SOD conjugates on the abnormal permeability manifested by transendothelial electrical resistance decline, increased fluorescein isothiocyanate-dextran influx, and redistribution of vascular endothelial-cadherin in human umbilical vein endothelial cell (HUVEC) monolayers. Anti-PECAM/catalase protected HUVEC monolayers against H2O2-induced endothelial barrier dysfunction. Polyethylene glycol-conjugated catalase exerted orders of magnitude lower endothelial uptake and no protective effect, similarly to IgG/catalase. Anti-PECAM/catalase, but not anti-PECAM/SOD, alleviated endothelial hyperpermeability caused by exposure to hypoxanthine/xanthine oxidase, implicating primarily H2O2 in the disruption of the endothelial barrier in this model. Thrombin-induced endothelial permeability was not affected by treatment with anti-PECAM/AOEs or the NADPH oxidase inhibitor apocynin or overexpression of AOEs, indicating that the endogenous ROS play no key role in thrombin-mediated endothelial barrier dysfunction. In contrast, anti-PECAM/SOD, but not anti-PECAM/catalase, inhibited a vascular endothelial growth factor (VEGF)-induced increase in endothelial permeability, identifying a key role of endogenous O2? in the VEGF-mediated regulation of endothelial barrier function. Therefore, AOEs targeted to endothelial cells provide versatile molecular tools for testing the roles of specific ROS in vascular pathology and may be translated into remedies for these ROS-induced abnormalities.

Han, Jingyan; Shuvaev, Vladimir V.

2011-01-01

144

Relationship between coronary artery stenosis and cardio-ankle vascular index (CAVI) in patients undergoing cardiovascular surgery  

PubMed Central

Background The cardio-ankle vascular index (CAVI) was developed as an indicator of arterial wall stiffness, and it is less influenced by blood pressure (BP). We investigated the relationship between the CAVI and coronary artery disease (CAD), and evaluated the effects of rapid changes in BP induced by anesthetics on CAVI. Materials and methods We measured the CAVI in 76 patients before and after the administration of anesthetics for elective cardiovascular surgery. The patients were assigned to groups with or without CAD (0VD). The CAD group was then divided into 3 subgroups based on the number of stenotic vessels (1VD, 2VD, and 3VD). We compared the CAVI between CAD and 0VD, and changes in BP during the induction of anesthesia. All data were analyzed using Stat View 5.0 software. Results Systolic BP significantly decreased from 145 ± 21 to 107 ± 20 mmHg, whereas CAVI was not altered after the administration of intravenous anesthetics. Changes in BP and in pre-anesthetic CAVI (pre-CAVI) did not correlate. The pre- and post-anesthetic values for the CAVI (post-CAVI) in the 0VD and CAD groups were 8.34 ± 1.01 and 8.44 ± 1.39, and 9.95 ± 1.22 and 10.12 ± 1.56, respectively. Both values were higher in the CAD, than in the 0VD group (P < 0.05). Conclusion The CAVI is independent of BP and reproducible regardless of the induction of anesthesia and is significantly higher in patients with CAD. The CAVI might be able to predict atherosclerosis and coronary artery stenosis in patients undergoing cardiovascular surgery.

Kanamoto, Masafumi; Matsumoto, Naoki; Shiga, Tatsuya; Kunimoto, Fumio; Saito, Shigeru

2013-01-01

145

Abnormal peripheral circulation in type 2 diabetic patients with normal ankle-brachial index associates with coronary atherosclerosis, large artery stiffness, and peripheral vascular resistance  

Microsoft Academic Search

We tested the hypothesis that impaired peripheral circulation in diabetes arises from different aspects of vascular abnormalities even when accompanied by a normal ankle-brachial index (ABI>0.9). One hundred fourteen type 2 diabetic patients with normal ABI and 33 age-matched non-diabetic subjects consecutively admitted to our hospital were enrolled. The Agatston coronary artery calcium score (CACS), as a marker of coronary

Masanobu Tsuchiya; Eiji Suzuki; Katsuya Egawa; Yoshihiko Nishio; Hiroshi Maegawa; Shigehiro Morikawa; Toshiro Inubushi; Atsunori Kashiwagi

2005-01-01

146

Prevalence of subclinic peripheral vascular disease assessed by ankle:arm blood pressure index in essential hypertensive patients  

Microsoft Academic Search

The ankle:arm blood pressure index (ABI) is a simple and usefulness test for detecting lower extremity arterial disease (LEAD). This test has a fair value when arterial estenosis of lower limb arteries are equal o higher to 50% (sensitibity >90% and specificity >98%). Some studies have demonstrated that ABI predicts future coronary heart disease and total cardiovascular morbidity and mortality.

Julian Segura; Carlos Campo; Lucia Guerrero; Luisa Fernandez; Luis M. Ruilope

2002-01-01

147

Changes of blood flow, oxygen tension, action potential and vascular permeability induced by arterial ischemia or venous congestion on the spinal cord in canine model.  

PubMed

It is generally considered that the genesis of myelopathy associated with the degenerative conditions of the spine may result from both mechanical compression and circulatory disturbance. Many references about spinal cord tissue ischemic damage can be found in the literature, but not detailed studies about spinal cord microvasculature damage related to congestion or blood permeability. This study investigates the effect of ischemia and congestion on the spinal cord using an in vivo model. The aorta was clamped as an ischemia model of the spinal cord and the inferior vena cava was clamped as a congestion model at the 6th costal level for 30?min using forceps transpleurally. Measurements of blood flow, partial oxygen pressure, and conduction velocity in the spinal cord were repeated over a period of 1?h after release of clamping. Finally, we examined the status of blood-spinal cord barrier under fluorescence and transmission electron microscope. Immediately after clamping of the inferior vena cava, the central venous pressure increased by about four times. Blood flow, oxygen tension and action potential were more severely affected by the aorta clamping; but this ischemic model did not show any changes of blood permeability in the spinal cord. The intramedullar edema was more easily produced by venous congestion than by arterial ischemia. In conclusions, venous congestion may be a preceding and essential factor of circulatory disturbance in the compressed spinal cord inducing myelopathy. PMID:22912247

Kobayashi, Shigeru; Yoshizawa, Hidezo; Shimada, Seiichiro; Guerrero, Alexander Rodríguez; Miyachi, Masaya

2013-01-01

148

Myocardial performance index is sensitive to changes in cardiac contractility, but is also affected by vascular load condition.  

PubMed

Myocardial performance index (MPI), or Tei index, is measured by Doppler echocardiography in clinical practice. MPI has been shown to be useful in evaluating left ventricular (LV) performance and predicting prognosis in cardiac patients. However, the effects of LV load and contractile states on MPI remain to be thoroughly investigated. In 14 anesthetized dogs, we obtained LV pressure-volume relationship with use of sonomicrometry and catheter-tip manometry. MPI was determined from the time derivative of LV volume and pressure. LV end-systolic pressure-volume ratio (Ees'), effective arterial elastance (Ea) and LV end-diastolic volume (Ved) were used as indices of LV contractility, afterload and preload, respectively. Hemodynamic conditions were varied over wide ranges [heart rate (HR), 66-192 bpm; mean arterial pressure, 71-177 mmHg] by infusing cardiovascular agents, by inducing ischemic heart failure and by electrical atrial pacing. Multiple linear regression analysis of pooled data (66 data sets) indicated that MPI (0.6-1.8) significantly correlated with Ees' [1.5-17.5 mmHg·ml(-1), p<0.0001, standard partial regression coefficient (?) =-0.66], Ea (3.6-21.9 mmHg·ml(-1), p<0.001, ? = 0.4) and Ved (11-100 ml, p<0.0001, ? = -0.69). MPI directly correlated with the time constant of isovolumic relaxation (19-66 ms, p<0.05), but not with HR or LV diastolic-stiffness (all p>0.1). Theoretical analysis also indicated that MPI decreases following the increases in LV contractility and in preload, while it increases in response to an increase in LV afterload. We conclude that MPI sensitively detects changes in LV contractility. However, MPI is also affected by changes in LV afterload and preload. PMID:24109782

Uemura, Kazunori; Kawada, Toru; Zheng, Can; Li, Meihua; Shishido, Toshiaki; Sugimachi, Masaru

2013-01-01

149

Association of bilateral brachial-ankle pulse wave velocity difference with peripheral vascular disease and left ventricular mass index.  

PubMed

Unequal arterial stiffness had been associated with cardiovascular risks. We investigated whether an association existed between unequal arterial stiffness indicated by bilateral brachial-ankle pulse wave velocity (baPWV) difference and ankle-brachial index (ABI), baPWV, echocardiographic parameters and interarm and interankle systolic blood pressure (BP) differences. A total of 1111 patients referred for echocardiographic examination were included in this study. The BPs, ABI and baPWV were measured simultaneously by an ABI-form device. The ?baPWV was defined as absolute value of difference between bilateral baPWV. We performed three multivariate analyses for determining the factors associated with a ?baPWV ? 185 cm/s (90 percentile of ?baPWV) (model 1: significant variables in univariate analysis and ABI <0.9 and baPWV; model 2: significant variables in univariate analysis and left ventricular mass index [LVMI]; model 3: significant variables in univariate analysis and interankle systolic BP difference ? 15 mmHg). The ABI <0.9 and high baPWV (both P<0.001) in model 1, high LVMI (P = 0.021) in model 2 and an interankle systolic BP difference ? 15 mmHg (P = 0.026) in model 3 were associated with a ?baPWV ? 185 cm/s, but the interarm systolic BP difference ? 10 mmHg was not (P = NS). Our study demonstrated ABI <0.9, high baPWV, high LVMI and an interankle systolic BP difference ? 15 mmHg were associated with unequal arterial stiffness. PMID:24551090

Su, Ho-Ming; Lin, Tsung-Hsien; Hsu, Po-Chao; Lee, Wen-Hsien; Chu, Chun-Yuan; Chen, Szu-Chia; Lee, Chee-Siong; Voon, Wen-Chol; Lai, Wen-Ter; Sheu, Sheng-Hsiung

2014-01-01

150

Hyperemia-Related Changes in Arterial Stiffness: Comparison between Pulse Wave Velocity and Stiffness Index in the Vascular Reactivity Assessment  

PubMed Central

Carotid-to-radial pulse wave velocity (PWVcr) has been proposed to evaluate endothelial function. However, the measurement of PWVcr is not without limitations. A new simple approach could have wide application. Stiffness index (SI) is obtained by analysis of the peripheral pulse wave and gives reproducible information about stiffness of large arteries. This study assessed the effects of hyperemia on SI and compared it with PWVcr in 14 healthy subjects. Both were measured at rest and during 8 minutes after ischemia. SI temporal course was determined. At 1 minute, SI and PWVcr decreased (5.58 ± 0.24 to 5.34 ± 0.23?m/s, P < 0.05; 7.8 ± 1.0 to 7.2 ± 0.9?m/s; P < 0.05, resp.). SI was positively related to PWVcr in baseline (r = 0.62 , P < 0.05), at 1 minute (r = 0.79, P < 0.05), and during the whole experimental session (r = 0.52, P < 0.05). Conclusion. Hyperemia significantly decreases SI in healthy subjects. SI was related to PWVcr and could be used to facilitate the evaluation of hyperemia-related changes in arterial stiffness.

Torrado, Juan; Bia, Daniel; Zocalo, Yanina; Farro, Ignacio; Farro, Federico; Armentano, Ricardo L.

2012-01-01

151

Associations of Candidate Biomarkers of Vascular Disease with the Ankle-Brachial Index and Peripheral Arterial Disease  

PubMed Central

BACKGROUND The use of multiple biomarkers representing various etiologic pathways of atherosclerosis may improve the prediction of interindividual variation in the ankle–brachial index (ABI). To this end, we investigated associations of 47 candidate biomarkers with the ABI and presence of peripheral arterial disease (PAD) in African–Americans (AAs) and non-Hispanic whites (NHWs). METHODS Study participants included 1,291 AAs (71.1% women, mean age, 63.4±9.3 years) and 1,152 NHWs (57.5% women, mean age 58.5±10.1 years) belonging to hypertensive sibships. Peripheral arterial disease was defined as an ABI ? 0.90. Circulating levels of 47 candidate biomarkers were log-transformed before analysis because of skewed distribution. Multivariate regression analyses were used to identify biomarkers associated with ABI or PAD independently of age, sex, conventional risk factors, and medication use. RESULTS After adjustment for covariates, higher levels of nine biomarkers were associated with a lower ABI in AAs (all P ? 0.005); these biomarkers were C-reactive protein (CRP), interleukin-6, tumor necrosis factor receptor-II (TNF-R II), lipoprotein(a), N-terminal pro-brain natriuretic peptide (NT-proBNP), pro-atrial natriuretic peptide, C-terminal pro-arginine vasopressin, osteoprotegerin, and fibrinogen. Three biomarkers - myeloperoxidase, NT-proBNP, and D-dimer - were associated with ABI in NHWs (all P ? 0.01). C-reactive protein, interleukin-6, TNF-R II, lipoprotein(a), NT-proBNP, pro-atrial natriuretic peptide, D-dimer, and fibrinogen were associated with PAD (all P ? 0.005) in AAs after adjustment for covariates. None of the biomarkers were independently associated with PAD in NHWs. CONCLUSION A multimarker approach improved the prediction of interindividual variation in the ABI in AAs and NHWs, and improved prediction of the presence of PAD in AAs.

2013-01-01

152

Peritoneal Permeability and Drug Enhancement in Uremia.  

National Technical Information Service (NTIS)

The first year of study of peritoneal permeability has expanded the observations that peritoneal clearances of urea 19.3 and creatinine 14.5 ml/min decrease with vascular disease to 13.9 and 8.3, consistent with decreased permeability, a phenomenon that w...

J. F. Maher D. C. Hohnadel

1976-01-01

153

The percentage flow-mediated dilation index: a large-sample investigation of its appropriateness, potential for bias and causal nexus in vascular medicine.  

PubMed

The percentage flow-mediated dilation index (FMD%) scales the increase in arterial diameter (Ddiff) as a constant proportion of baseline artery diameter (Dbase). We have demonstrated, albeit with small samples, that the scaling properties of FMD% can lead to biased inferences on endothelial dysfunction. Therefore, we aimed to investigate the underlying rationale and potential bias of FMD% using a selection of new examples from the large (n = 3499) and diverse Multi-Ethnic Study of Atherosclerosis (MESA). In this dataset, we found that smaller values of Ddiff are associated with larger values of Dbase, which contradicts the scaling properties of FMD%. Consequently, FMD% 'over-scales' and naturally generates an even stronger negative correlation between itself and Dbase. Using a data simulation, we show that this FMD%-Dbase correlation can be a statistical artefact due to inappropriate scaling. The new examples we present from MESA indicate that FMD% biases the differences in flow-mediated response between men and women, Framingham risk score categories, and diseased and healthy people. We demonstrate how FMD%, as an exposure for predicting cardiovascular disease, is confounded by its dependency on Dbase, which itself could be clinically important. This critical review, incorporating an allometric analysis of a large dataset, suggests that the FMD% index has a less-than-clear rationale, can itself generate the Dbase-dependency problem, provides biased estimates of differences in the flow-mediated response, complicates the interpretation of the flow-mediated protocol and clouds the causal pathway to vascular disease. These interpretative problems can be resolved by applying accepted allometric principles to the flow-mediated response. PMID:24172228

Atkinson, Greg; Batterham, Alan M

2013-12-01

154

Vascular Endothelial Growth Factor-C, a Potential Paracrine Regulator of Glomerular Permeability, Increases Glomerular Endothelial Cell Monolayer Integrity and Intracellular Calcium  

PubMed Central

We have previously reported expression of vascular endothelial growth factor (VEGF)-A and -C in glomerular podocytes and actions of VEGF-A on glomerular endothelial cells (GEnC) that express VEGF receptor-2 (VEGFR-2). Here we define VEGFR-3 expression in GEnC and investigate the effects of the ligand VEGF-C. Renal cortex and cultured GEnC were examined by microscopy, and both cell and glomerular lysates were assessed by Western blotting. VEGF-C effects on trans-endothelial electrical resistance and albumin flux across GEnC monolayers were measured. The effects of VEGF-C156S, a VEGFR-3-specific agonist, and VEGF-A were also studied. VEGF-C effects on intracellular calcium ([Ca2+]i) were measured using a fluorescence technique, receptor phosphorylation was examined by immunoprecipitation assays, and phosphorylation of myosin light chain-2 and VE-cadherin was assessed by blotting with phospho-specific antibodies. GEnC expressed VEGFR-3 in tissue sections and culture, and VEGF-C increased trans-endothelial electrical resistance in a dose-dependent manner with a maximal effect at 120 minutes of 6.8 ? whereas VEGF-C156S had no effect. VEGF-C reduced labeled albumin flux by 32.8%. VEGF-C and VEGF-A increased [Ca2+]i by 15% and 39%, respectively. VEGF-C phosphorylated VEGFR-2 but not VEGFR-3, myosin light chain-2, or VE-cadherin. VEGF-C increased GEnC monolayer integrity and increased [Ca2+]i, which may be related to VEGF-C-S particular receptor binding and phosphorylation induction characteristics. These observations suggest that podocytes direct GEnC behavior through both VEGF-C and VEGF-A.

Foster, Rebecca R.; Slater, Sadie C.; Seckley, Jaqualine; Kerjaschki, Dontscho; Bates, David O.; Mathieson, Peter W.; Satchell, Simon C.

2008-01-01

155

Permeability Test  

NSDL National Science Digital Library

This resource from the Indian Institute of Technology Kanpur provides an outline of constant head and falling head permeability tests of soil. This is a great resource for anyone studying geology and soil science.

2008-05-16

156

Permeable Pavement  

NSDL National Science Digital Library

Students investigate how different riparian ground covers, such as grass or pavement, affect river flooding. They learn about permeable and impermeable materials through the measurement how much water is absorbed by several different household materials in a model river. Students use what they learn to make recommendations for engineers developing permeable pavement. Also, they consider several different limitations for design in the context of a small community.

Integrated Teaching And Learning Program

157

Impact of Cardiovascular Risk Factors on Progression of Arteriosclerosis in Younger Patients: Evaluation by Carotid Duplex Ultrasonography and Cardio-Ankle Vascular Index(CAVI).  

PubMed

Aim: To evaluate progression of arteriosclerosis using cardio-ankle vascular index(CAVI) and carotid duplex ultrasonography(DUS) in young and adolescent patients considered to be at risk of cardiovascular disease. Methods: We evaluated the progression of arteriosclerosis using CAVI and carotid DUS in 240 young and adolescent patients. Dyslipidemia(DL), hypertension(HT), and diabetes mellitus(DM) were major cardiovascular risk factors. Patients were divided to 4 groups according to number of risk factors. Results: In terms of risk factors, CAVI and CAVI difference(CAVI-D) were elevated only in the HT group(p=0.0290, p=0.0243 vs. no risk respectively). CAVI-D was positively associated with diastolic blood pressure(DBP). Mean IMT was positively associated with LDL-C or systolic blood pressure, and negatively with HDL-C. Plaque score was associated with LDL-C or DBP. In patients with the 3 risk factors, CAVI, CAVI-D and mean intima-media thickness(IMT) were significantly higher than in those without risk(p=0.0009, p=0.0042 and p=0.0151 respectively), and CAVI and CAVID were higher than in those with 1 risk(p=0.0204 and p=0.0231). Carotid plaque develops from around 30 years of age in Japan. Despite numbers of risk factors, there were no differences in CAVI, CAVI-D, mean IMT or plaque score between smoker and non-smoker groups. Conclusion: In conclusion, an increase in the number of risk factors also results in progression of arteriosclerosis in young and adolescent patients. HT was the most important risk factor for arteriosclerosis in these patients. PMID:24521982

Suzuki, Jun; Kurosu, Takumi; Kon, Tokuo; Tomaru, Takanobu

2014-06-25

158

Survey of ocular irritation predictive capacity using Chorioallantoic Membrane Vascular Assay (CAMVA) and Bovine Corneal Opacity and Permeability (BCOP) test historical data for 319 personal care products over fourteen years.  

PubMed

The Chorioallantoic Membrane Vascular Assay (CAMVA) and Bovine Corneal Opacity and Permeability (BCOP) test are widely used to predict ocular irritation potential for consumer-use products. These in vitro assays do not require live animals, produce reliable predictive data for defined applicability domains compared to the Draize rabbit eye test, and are rapid and inexpensive. Data from 304 CAMVA and/or BCOP studies (319 formulations) were surveyed to determine the feasibility of predicting ocular irritation potential for various formulations. Hair shampoos, skin cleansers, and ethanol-based hair styling sprays were repeatedly predicted to be ocular irritants (accuracy rate=0.90-1.00), with skin cleanser and hair shampoo irritation largely dependent on surfactant species and concentration. Conversely, skin lotions/moisturizers and hair styling gels/lotions were repeatedly predicted to be non-irritants (accuracy rate=0.92 and 0.82, respectively). For hair shampoos, ethanol-based hair stylers, skin cleansers, and skin lotions/moisturizers, future ocular irritation testing (i.e., CAMVA/BCOP) can be nearly eliminated if new formulations are systematically compared to those previously tested using a defined decision tree. For other tested product categories, new formulations should continue to be evaluated in CAMVA/BCOP for ocular irritation potential because either the historical data exhibit significant variability (hair conditioners and mousses) or the historical sample size is too small to permit definitive conclusions (deodorants, make-up removers, massage oils, facial masks, body sprays, and other hair styling products). All decision tree conclusions should be made within a conservative weight-of-evidence context, considering the reported limitations of the BCOP test for alcohols, ketones, and solids. PMID:21147215

Donahue, D A; Kaufman, L E; Avalos, J; Simion, F A; Cerven, D R

2011-03-01

159

Mechanisms of Tumor Vascular Priming by a Nanoparticulate Doxorubicin Formulation  

PubMed Central

Purpose Tumor vascular normalization by antiangiogenic agents may increase tumor perfusion but reestablish vascular barrier properties in CNS tumors. Vascular priming via nanoparticulate carriers represents a mechanistically distinct alternative. This study investigated mechanisms by which sterically-stabilized liposomal doxorubicin (SSL-DXR) modulates tumor vascular properties. Methods Functional vascular responses to SSL-DXR were investigated in orthotopic rat brain tumors using deposition of fluorescent permeability probes and dynamic contrast-enhanced magnetic resonance imaging. Microvessel density and tumor burden were quantified by immunohistochemistry (CD-31) and quantitative RT-PCR (VE-cadherin). Results Administration of SSL-DXR (5.7 mg/kg iv) initially (3–4 days post-treatment) decreased tumor vascular permeability, ktrans (vascular exchange constant), vascular endothelial cell content, microvessel density, and deposition of nanoparticulates. Tumor vasculature became less chaotic. Permeability and perfusion returned to control values 6–7 days post-treatment, but intratumor SSL-DXR depot continued to effect tumor vascular endothelial compartment 7–10 days post-treatment, mediating enhanced permeability. Conclusions SSL-DXR ultimately increased tumor vascular permeability, but initially normalized tumor vasculature and decreased tumor perfusion, permeability, and nanoparticulate deposition. These temporal changes in vascular integrity resulting from a single SSL-DXR dose have important implications for the design of combination therapies incorporating nanoparticle-based agents for tumor vascular priming.

Chaudhuri, Tista Roy; Arnold, Robert D.; Yang, Jun; Turowski, Steven G.; Qu, Yang; Spernyak, Joseph A.; Mazurchuk, Richard; Mager, Donald E.

2013-01-01

160

Significance of plasma D-dimer in relation to the severity of atherosclerosis among patients evaluated by non-invasive indices of cardio-ankle vascular index and carotid intima-media thickness  

Microsoft Academic Search

The aim of this study is to elucidate the usefulness of plasma D-dimer for the prediction of thrombotic events in highly atherosclerotic\\u000a patients. The severity of atherosclerosis was measured by non-invasive methods including cardio-ankle vascular index (CAVI)\\u000a and carotid intima-media thickness (IMT) in 100 patients with atherosclerosis aged 72.1 years on average. CAVI was significantly\\u000a correlated with the levels of D-dimer,

Shigeru Hayashi

2010-01-01

161

Microvascular albumin permeability in isolated perfused lung: effects of EDTA  

Microsoft Academic Search

The authors examined the effects of decreases in perfusate concentrations of calcium and magnesium on the pulmonary vascular permeability in the isolated perfused rabbit lung. The albumin permeability-surface area product (PS) and the albumin reflection coefficient (sigma) were determined in the same lung using ¹²⁵I- and ¹³¹I-labeled albumin tracers. Decreases in vascular Ca\\/sup 2 +\\/ and Mg\\/sup 2 +\\/ concentrations

D. F. Kern; A. B. Malik

1985-01-01

162

Corticosteroids inhibit the expression of the vascular endothelial growth factor gene in human vascular smooth muscle cells  

Microsoft Academic Search

The vascular endothelial growth factor (VEGF) is a specific mitogen for vascular endothelial cells and enhances vascular permeability and edemagenesis. VEGF is also a major regulator of angiogenesis and may be a key target for inhibiting angiogenesis in angiogenesis-associated diseases. Among the extensively studied angiostatic compounds are several corticosteroids when used alone or in combination with heparin. In this study

Markus Nauck; George Karakiulakis; André P Perruchoud; Eleni Papakonstantinou; Michael Roth

1998-01-01

163

Capsaicin stimulation of the cochlea and electric stimulation of the trigeminal ganglion mediate vascular permeability in cochlear and vertebro-basilar arteries: a potential cause of inner ear dysfunction in headache  

Microsoft Academic Search

Trigeminal neurogenic inflammation is one explanation for the development of vascular migraine. The triggers for this inflammation and pain are not well understood, but are probably vasoactive components acting on the blood vessel wall. Migraine-related inner ear symptoms like phonophobia, tinnitus, fluctuation in hearing perception and increased noise sensitivity provide indirect evidence that cochlear blood vessels are also affected by

Z Vass; P. S Steyger; A. J Hordichok; D. R Trune; G Jancsó; A. L Nuttall

2001-01-01

164

EPA Permeable Surface Research  

EPA Science Inventory

EPA recognizes permeable surfaces as an effective post-construction infiltration-based Best Management Practice to mitigate the adverse effects of stormwater runoff. The professional user community conceptually embraces permeable surfaces as a tool for making runoff more closely...

165

Spatial and Phenotypic Characterization of Vascular Remodeling in a Mouse Model of Asthma  

Microsoft Academic Search

Asthma is a chronic inflammatory disease characterized by airway wall remodeling in which vascular remodeling is thought to be a main contributor. Vascular endothelial growth factor (VEGF) is known as a major regulator of angiogenesis and enhancer of vascular permeability. Here, we define the spatial nature of vascular remodeling and the role of VEGF and its receptors (Flt-1 and Flk-1)

Xinming Su; Namiko Taniuchi; Enjing Jin; Masakazu Fujiwara; Lei Zhang; Mohammad Ghazizadeh; Hiroyuki Tashimo; Naomi Yamashita; Ken Ohta; Oichi Kawanami

2008-01-01

166

Vascular Arterial Compression Syndromes  

Microsoft Academic Search

Opinion statement  Vascular arterial compression syndromes are uncommon disorders due to dynamic anatomic compression of an artery resulting\\u000a in significant ischemia in the supplied territories with ensuing symptoms. The diagnosis of these disorders requires heightened\\u000a awareness and a high index of suspicion by the clinician. These diagnoses should be particularly suspected in young patients\\u000a with typical symptoms but without underlying cardiovascular

Veerendra Chadachan; Robert T. Eberhardt

2011-01-01

167

An in vivo assay to test blood vessel permeability.  

PubMed

This method is based on the intravenous injection of Evans Blue in mice as the test animal model. Evans blue is a dye that binds albumin. Under physiologic conditions the endothelium is impermeable to albumin, so Evans blue bound albumin remains restricted within blood vessels. In pathologic conditions that promote increased vascular permeability endothelial cells partially lose their close contacts and the endothelium becomes permeable to small proteins such as albumin. This condition allows for extravasation of Evans Blue in tissues. A healthy endothelium prevents extravasation of the dye in the neighboring vascularized tissues. Organs with increased permeability will show significantly increased blue coloration compared to organs with intact endothelium. The level of vascular permeability can be assessed by simple visualization or by quantitative measurement of the dye incorporated per milligram of tissue of control versus experimental animal/tissue. Two powerful aspects of this assay are its simplicity and quantitative characteristics. Evans Blue dye can be extracted from tissues by incubating a specific amount of tissue in formamide. Evans Blue absorbance maximum is at 620 nm and absorbance minimum is at 740 nm. By using a standard curve for Evans Blue, optical density measurements can be converted into milligram dye captured per milligram of tissue. Statistical analysis should be used to assess significant differences in vascular permeability. PMID:23524912

Radu, Maria; Chernoff, Jonathan

2013-01-01

168

Streptococcus pneumoniae Induces Secretion of Vascular Endothelial Growth Factor by Human Neutrophils  

Microsoft Academic Search

Infection by pneumococci causes an acute inflammatory response associated with neutrophil influx, in- creased vascular permeability, and edema. Vascular endothelial growth factor (VEGF) is one of the most potent regulators of endothelial permeability. In vitro stimulation of neutrophils showed that pneumococci and purified pneumococcal cell wall induce VEGF secretion, independent of the presence of pneumolysin or polysaccharide capsule. The results

MICHIEL VAN DER FLIER; FRANK COENJAERTS; JAN L. L. KIMPEN; ANDY M. HOEPELMAN; SIBYL P. M. GEELEN

2000-01-01

169

Permeability and relative permeability in rocks  

SciTech Connect

Important features of the topology of the pore space of rocks can be usefully quantified by analyzing digitized images of rock cross sections. One approach computes statistical correlation functions using modern image processing techniques. These correlation functions contain information about porosity, specific surface area, tortuosity, formation factor, and elastic constants, as well as the fluid permeability and relative permeability. The physical basis of this approach is discussed and examples of the results for various sandstones are presented. The analysis shows that Kozeny-Carman relations and Archie's empirical laws must be modified to account for finite percolation thresholds in order to avoid unphysical behavior in the calculated relative permeabilities. 33 refs., 4 figs., 1 tab.

Blair, S.C.; Berryman, J.G.

1990-10-01

170

Importance of the Terminal alpha -Amino Group of Bradykinin and Some Kynins on Capillary Permeability Increase.  

National Technical Information Service (NTIS)

A simple and reliable method is described for the quantitative evaluation of vascular permeability increase induced by vasoactive drugs with Evans blue labelled with iodine-125 or 131. By using this method the importance of alpha -amino group of bradykini...

S. Sugavara

1979-01-01

171

Permeability of Dentine  

PubMed Central

This is an update on the present integrated knowledge regarding dentine permeability that assumed a role in dentine sensitivity and contribute clinically to the effective bonding properties of restorative dental materials. This paper will attempt to refer to in vivo and in vitro studies of dentine permeability and the various interrelated factors governing it.

Ghazali, Farid Bin Che

2003-01-01

172

A SIMPLE TECHNIQUE FOR ESTIMATING THE COEFFICIENT OF PERMEABILITY OF UNSATURATED SOILS  

Microsoft Academic Search

A simple technique is proposed in this paper to estimate the coefficient of permeability of unsaturated soils based solely on conventional soil properties; namely, the saturated coefficient of permeability, degree of saturation (or water content), and the plasticity index, Ip of the soil. The technique is developed based on a relationship derived between the relative coefficient of permeability, krel (defined

J. P. Lobbezoo; S. K. Vanapalli

173

Management of Vascular Defects in Digital Replantation  

Microsoft Academic Search

207 cases of digital amputation (261 digits) with vascular defects were replantated during the past two decades. The vascular defect was managed with various methods. 240 digits (92%) survived with good post-operative circulation and recovery of function. The methods of management of arterial defects were as follows: 1) Digital artery transfer from adjacent digits in 25 thumbs and three index

Z. Y. Ren; C. Q. Wang; Q. S. Fan; G. F. Shen; H. Yan; Z. T. Wang

1995-01-01

174

Effects of inflation volume during lung preservation on pulmonary capillary permeability  

Microsoft Academic Search

The degree of lung allograft inflation during harvest and storage may affect posttransplantation function. High volume ventilation causes pulmonary vascular injury and increased pulmonary capillary permeability. However, the effect of lung inflation on pulmonary capillary permeability after hypothermic flush and storage is unknown. The current study was designed to examine the effects of hyperinflation and hypoinflation during preservation on pulmonary

Masayuki Haniuda; Seiki Hasegawa; Takeshi Shiraishi; Carolyn M. Dresler; Joel D. Cooper; G. Alexander Patterson

1996-01-01

175

Vascular ring  

MedlinePLUS

... following tests can help diagnose vascular ring: Chest x-ray Computed tomography (CT) scan of the heart Camera down the throat to examine the airways (bronchoscopy) Magnetic resonance imaging ... of heart X-ray of blood vessels (angiography) X-ray of the ...

176

Vascular Proliferation  

NSDL National Science Digital Library

This FlashTM animation depicts vascularization of the early germ disc. It is shown in the context of a transverse section through a trilaminar germ disc and yolk sac. Clicking shows the cardiogenic field developing into the heart tube, along with vasculogenesis of the major vessels. Clicking again shows angiogenesis of peripheral vessels throughout the developing embryo and yolk sac.

PhD Jack D Thatcher (West Virginia School of Osteopathic Medicine Structural Biology)

2009-11-20

177

Vascular Caliber  

Microsoft Academic Search

Many aspects of vascular caliber can be accounted for on the basis of interactions between the frictional drag generated by the stream, and the sensitivity of the endothelial cells to this force. When the drag force on endothelial cells is at its critical set-point, these lining cells are at rest with respect to factors that affect caliber. An increase in

Simon Rodbard

1975-01-01

178

ConcepTest: Permeability  

NSDL National Science Digital Library

Three similar containers were filled with flour, rice or Cheerios. If you were to pour water into each container, how would they rank in terms of permeability (from highest to lowest)? a. Flour, Rice, Cheerios b. ...

179

Mechanosensing at the vascular interface.  

PubMed

Mammals are endowed with a complex set of mechanisms that sense mechanical forces imparted by blood flow to endothelial cells (ECs), smooth muscle cells, and circulating blood cells to elicit biochemical responses through a process referred to as mechanotransduction. These biochemical responses are critical for a host of other responses, including regulation of blood pressure, control of vascular permeability for maintaining adequate perfusion of tissues, and control of leukocyte recruitment during immunosurveillance and inflammation. This review focuses on the role of the endothelial surface proteoglycan/glycoprotein layer-the glycocalyx (GCX)-that lines all blood vessel walls and is an agent in mechanotransduction and the modulation of blood cell interactions with the EC surface. We first discuss the biochemical composition and ultrastructure of the GCX, highlighting recent developments that reveal gaps in our understanding of the relationship between composition and spatial organization. We then consider the roles of the GCX in mechanotransduction and in vascular permeability control and review the prominent interaction of plasma-borne sphingosine-1 phosphate (S1P), which has been shown to regulate both the composition of the GCX and the endothelial junctions. Finally, we consider the association of GCX degradation with inflammation and vascular disease and end with a final section on future research directions. PMID:24905872

Tarbell, John M; Simon, Scott I; Curry, Fitz-Roy E

2014-07-11

180

Reduction of high glucose and phorbol-myristate-acetate-induced endothelial cell permeability by protein kinase C inhibitors LY379196 and hypocrellin A  

Microsoft Academic Search

Endothelial barrier dysfunction plays a pivotal role in the pathogenesis of diabetic vascular complications. Although recent studies have established a link between protein kinase C (PKC) pathway and hyperglycaemic-induced vascular permeability, it is unclear which PKC isoforms involve increased endothelial cell permeability. In the present study, we investigated whether high glucose induced endothelial hyperpermeability via distinct PKC isoforms in human

Lei Dang; J. Paul Seale; Xianqin Qu

2004-01-01

181

Endothelial contractile cytoskeleton and microvascular permeability  

PubMed Central

Microvascular barrier dysfunction represents a significant problem in clinical conditions associated with trauma, burn, sepsis, acute respiratory distress syndrome, ischemia-reperfusion injury, and diabetic retinopathy. An important cellular mechanism underlying microvascular leakage is the generation of contractile force from the endothelial cytoskeleton, which counteracts cell–cell and cell–matrix adhesions leading to paracellular hyperpermeability. In this review, we present recent experimental evidence supporting the critical role of MLCK-activated, RhoA/ROCK-regulated contractile cytoskeleton in endothelial permeability response to inflammatory and thrombotic stimuli arising from thermal injury, activated neutrophils, vascular endothelial growth factor, and fibrinogen degradation products. Further understanding the molecular basis of microvascular barrier structure and function would contribute to the development of novel therapeutic targets for treating circulatory disorders and vascular injury.

Shen, Qiang; Wu, Mack H; Yuan, Sarah Y

2010-01-01

182

Seismic waves increase permeability.  

PubMed

Earthquakes have been observed to affect hydrological systems in a variety of ways--water well levels can change dramatically, streams can become fuller and spring discharges can increase at the time of earthquakes. Distant earthquakes may even increase the permeability in faults. Most of these hydrological observations can be explained by some form of permeability increase. Here we use the response of water well levels to solid Earth tides to measure permeability over a 20-year period. At the time of each of seven earthquakes in Southern California, we observe transient changes of up to 24 degrees in the phase of the water level response to the dilatational volumetric strain of the semidiurnal tidal components of wells at the Piñon Flat Observatory in Southern California. After the earthquakes, the phase gradually returns to the background value at a rate of less than 0.1 degrees per day. We use a model of axisymmetric flow driven by an imposed head oscillation through a single, laterally extensive, confined, homogeneous and isotropic aquifer to relate the phase response to aquifer properties. We interpret the changes in phase response as due to changes in permeability. At the time of the earthquakes, the permeability at the site increases by a factor as high as three. The permeability increase depends roughly linearly on the amplitude of seismic-wave peak ground velocity in the range of 0.21-2.1 cm s(-1). Such permeability increases are of interest to hydrologists and oil reservoir engineers as they affect fluid flow and might determine long-term evolution of hydrological and oil-bearing systems. They may also be interesting to seismologists, as the resulting pore pressure changes can affect earthquakes by changing normal stresses on faults. PMID:16810253

Elkhoury, Jean E; Brodsky, Emily E; Agnew, Duncan C

2006-06-29

183

Vascular dementia  

PubMed Central

The epidemic grow of dementia causes great concern for the society. It is customary to consider Alzheimer’s disease (AD) as the most common cause of dementia, followed by vascular dementia (VaD). This dichotomous view of a neurodegenerative disease as opposed to brain damage caused by extrinsic factors led to separate lines of research in these two entities. Indeed, accumulated data suggest that the two disorders have additive effects and probably interact; however it is still unknown to what degree. Furthermore, epidemiological studies have shown “vascular” risk factors to be associated with AD. Therefore, a clear distinction between AD and VaD cannot be made in most cases, and is furthermore unhelpful. In the absence of efficacious treatment for the neurodegenerative process, special attention must be given to vascular component, even in patients with presumed mixed pathology. Symptomatic treatment of VaD and AD are similar, although the former is less effective. For prevention of dementia it is important to treat aggressively all factors, even in stroke survivors who do not show evidence of cognitive decline,. In this review, we will give a clinical and pathological picture of the processes leading to VaD and discuss it interaction with AD.

Korczyn, Amos D; Vakhapova, Veronika; Grinberg, Lea T

2012-01-01

184

Resistin increases monolayer permeability of human coronary artery endothelial cells.  

PubMed

Resistin has been linked to obesity, insulin resistance, atherosclerosis, and the development of cardiovascular disease. Nevertheless, the effects and the molecular mechanisms of resistin on endothelial permeability, a key event in the development of atherosclerosis, inflammation, and vascular disease, are largely unknown. In order to determine the effect of resistin on endothelial permeability, human coronary artery endothelial cells (HCAECs) were treated with clinically relevant concentrations of resistin and the endothelial permeability was measured using the Transwell system with a Texas-Red-labeled dextran tracer. The permeability of HCAEC monolayers treated with resistin (80 ng/mL) was 51% higher than the permeability of control monolayers (P<0.05). The mRNA levels of tight junction proteins zonula occludens-1 (ZO-1) and occludin in resistin-treated cells were 37% and 42% lower, respectively, than the corresponding levels in untreated cells. The protein levels of these molecules in resistin-treated cells were significantly reduced by 35% and 37%, respectively (P<0.05), as shown by flow cytometry and Western blot analysis. Superoxide dismutase (SOD) mimetic MnTBAP effectively blocked the resistin-mediated reduction of ZO-1 and occludin levels in HCAECs. In addition, superoxide anion production was increased from 21% (untreated cells) to 55% (cells treated with 40 ng/mL resistin), and 64% (resistin, 80 mg/mL) (P<0.05). The natural antioxidant Ginkgolide A effectively inhibited resistin-induced increase in permeability and the increase in superoxide anion production in HCAECs. Furthermore, resistin treatment significantly activated p38 MAPK, but not ERK1/2. Pretreatment of HCAECs with a p38 inhibitor effectively blocked resistin-induced permeability. These results provide new evidence that resistin may contribute to the vascular lesion formation via increasing endothelial permeability through the mechanism of oxidative stress and the activation of p38 MAPK. PMID:24386395

Jamaluddin, Md Saha; Yan, Shaoyu; Lü, Jianming; Liang, Zhengdong; Yao, Qizhi; Chen, Changyi

2013-01-01

185

Resistin Increases Monolayer Permeability of Human Coronary Artery Endothelial Cells  

PubMed Central

Resistin has been linked to obesity, insulin resistance, atherosclerosis, and the development of cardiovascular disease. Nevertheless, the effects and the molecular mechanisms of resistin on endothelial permeability, a key event in the development of atherosclerosis, inflammation, and vascular disease, are largely unknown. In order to determine the effect of resistin on endothelial permeability, human coronary artery endothelial cells (HCAECs) were treated with clinically relevant concentrations of resistin and the endothelial permeability was measured using the Transwell system with a Texas-Red-labeled dextran tracer. The permeability of HCAEC monolayers treated with resistin (80 ng/mL) was 51% higher than the permeability of control monolayers (P<0.05). The mRNA levels of tight junction proteins zonula occludens-1 (ZO-1) and occludin in resistin-treated cells were 37% and 42% lower, respectively, than the corresponding levels in untreated cells. The protein levels of these molecules in resistin-treated cells were significantly reduced by 35% and 37%, respectively (P<0.05), as shown by flow cytometry and Western blot analysis. Superoxide dismutase (SOD) mimetic MnTBAP effectively blocked the resistin-mediated reduction of ZO-1 and occludin levels in HCAECs. In addition, superoxide anion production was increased from 21% (untreated cells) to 55% (cells treated with 40 ng/mL resistin), and 64% (resistin, 80 mg/mL) (P<0.05). The natural antioxidant Ginkgolide A effectively inhibited resistin-induced increase in permeability and the increase in superoxide anion production in HCAECs. Furthermore, resistin treatment significantly activated p38 MAPK, but not ERK1/2. Pretreatment of HCAECs with a p38 inhibitor effectively blocked resistin-induced permeability. These results provide new evidence that resistin may contribute to the vascular lesion formation via increasing endothelial permeability through the mechanism of oxidative stress and the activation of p38 MAPK.

Jamaluddin, Md Saha; Yan, Shaoyu; Lu, Jianming; Liang, Zhengdong; Yao, Qizhi; Chen, Changyi

2013-01-01

186

Effect of polycaprolactone scaffold permeability on bone regeneration in vivo.  

PubMed

Successful bone tissue engineering depends on the scaffold's ability to allow nutrient diffusion to and waste removal from the regeneration site, as well as provide an appropriate mechanical environment. Since bone is highly vascularized, scaffolds that provide greater mass transport may support increased bone regeneration. Permeability encompasses the salient features of three-dimensional porous scaffold architecture effects on scaffold mass transport. We hypothesized that higher permeability scaffolds will enhance bone regeneration for a given cell seeding density. We manufactured poly-?-caprolactone scaffolds, designed to have the same internal pore design and either a low permeability (0.688×10(-7)m(4)/N-s) or a high permeability (3.991×10(-7)m(4)/N-s), respectively. Scaffolds were seeded with bone morphogenic protein-7-transduced human gingival fibroblasts and implanted subcutaneously in immune-compromised mice for 4 and 8 weeks. Micro-CT evaluation showed better bone penetration into high permeability scaffolds, with blood vessel infiltration visible at 4 weeks. Compression testing showed that scaffold design had more influence on elastic modulus than time point did and that bone tissue infiltration increased the mechanical properties of the high permeability scaffolds at 8 weeks. These results suggest that for polycaprolactone, a more permeable scaffold with regular architecture is best for in vivo bone regeneration. This finding is an important step toward the end goal of optimizing a scaffold for bone tissue engineering. PMID:21395465

Mitsak, Anna G; Kemppainen, Jessica M; Harris, Matthew T; Hollister, Scott J

2011-07-01

187

Amifostine reduces lung vascular permeability via suppression of inflammatory signaling  

PubMed Central

Multiple events are involved in the development of acute inflammation and injury in the lungs. A progressive rise of oxidative stress due to altered reduction-oxidation (redox) homeostasis appears to be one of the hallmarks of lung pathologies such as injury, inflammation and ischemia/reperfusion. However, despite the growing evidence that alteration of the redox balance in the lungs, antioxidant therapy may attenuate acute lung injury and inflammation. We studied the effect of thiol antioxidant compound, amifostine, on acute lung dysfunction and pulmonary endothelial barrier compromise induced by gram-negative bacterial wall lypopolysacharide (LPS). In vitro, LPS as well as other producers of reactive oxygen spices (ROS), interleukin-6 (IL-6) and hydrogen peroxide (H2O2), induced significant reorganization of actin cytoskeleton accompanied by formation of stress fibers and paracellular gaps and associated with decreased transendothelial electrical resistance, a hallmark of endothelial barrier dysfunction. These disruptive effects were inhibited by pretreatment of endothelial monolayer with amifostine. Moreover, amifostine inhibited LPS-mediated ROS production and significantly suppressed LPS-, IL-6-, and H2O2-induced activation of redox sensitive signaling mechanisms including p38 and Erk1/2 MAP kinases, and NF?B pathway. In the murine model of LPS-induced acute lung injury, intraperitoneal administration of amifostine reduced LPS-induced oxidative stress and neutrophil recruitment to the lungs. These studies demonstrate for the first time that amifostine dramatically reduces endothelial cell barrier dysfunction and acute lung injury caused by bacterial products via inhibition of oxidative stress and redox-sensitive inflammatory pathways, and may therefore be considered for therapeutic treatment of lung inflammation.

Fu, Panfeng; Birukova, Anna A.; Sammani, Saad; Burdette, Dylan; Murley, Jeffrey S.; Garcia, Joe G.N.; Grdina, David J.; Birukov, Konstantin G.

2013-01-01

188

Anti-VEGF Agents for Ocular Angiogenesis and Vascular Permeability  

PubMed Central

We review articles describing intravitreal injection of anti-VEGF drug trials, while discussing the mechanisms of the action of anti-VEGF antibodies, and also evaluating their outcomes. Intraocular injections of anti-VEGF drug are considered to be an effective treatment for macular edema after retinal vein occlusion, however, recurrent/persistent edema is common. The recent reports may lead to a shift in treatment paradigm for DME, from laser photocoagulation, to newer approaches using anti-VEGF drugs. There have been several well-publicized prospective, randomized studies that demonstrated the efficacy of intravitreal injection of anti-VEGF drugs for patients with AMD. Adjuvant bevacizumab for neovascular glaucoma may prevent further PAS formation, and it is likely to open up a therapeutic window for a panretinal photocoagulation and trabeculectomy. Intravitreal injection of bevacizumab (IVB) results in a substantial decrease in bleeding from the retinal vessels or new vessels during a standard vitrectomy. IVB has also been reported to be effective for inducing the regression of new vessels in proliferative diabetic retinopathy. The use of bevacizumab in stage 4 or 5 retinopahty of permaturity (ROP) is to reduce the plus sign to help reduce hemorrhage during the subsequent vitrectomy. Some authors reported cases of resolution of stage 4?A ROP after bevacizumab injection.

Kimoto, Kenichi; Kubota, Toshiaki

2012-01-01

189

[Vascular ultrasonography].  

PubMed

Vascular ultrasound plays an important role in the visual depiction of arteries, veins, and changes of tissue in lymphatic diseases. In the case of arteries, this ranges from endothelial dysfunction over measuring the increase of intima media thickness to the detection of stenoses, occlusion, or aneurysm. Ultrasound helps to differentiate in functional arterial diseases such as primary and secondary Raynaud's syndrome as well as arterial compression syndromes like entrapment syndrome of different arterial regions or the chronic exceptional compartment syndrome of the lower leg. Ultrasound plays a central role in the diagnosis of rare arterial diseases like large vessel vasculitis, arterial dissection, cystic adventitial degeneration, and the differentiation of vascular malformation especially in children, thus, permitting ultrasound-guided intervention and follow-up controls. In venous thrombosis, sonography is the primary imaging method, while follow-up controls help in the prediction of recurrent venous thrombosis. Ultrasound is a tool to determine the cause and severity of chronic venous insufficiency and allows different therapeutic procedures for the treatment of varicose veins to be visually monitored. PMID:22358939

Stiegler, H

2012-03-01

190

The epidermal permeability barrier  

Microsoft Academic Search

The permeability barrier of the skin which prevents transcutaneous water loss and penetration of harmful drugs from the environment is localized in the horny layer of the epidermis. Multiple lipid bilayers obstructing the intercellular space of the stratum corneum fulfill this function. In contrast to cellular membranes consisting predominantly of phospholipids, these lamellae contain mostly ceramides, cholesterol and free fatty

Lukas Landmann

1988-01-01

191

Intestinal permeability: An overview  

Microsoft Academic Search

The noninvasive assessment of intestinal permeability in humans has a 20-year history. Because the tests are increasingly used in clinical practice and research and because there is much controversy, we reviewed the literature and outlined the potential and possible shortcomings of these procedures. Data was obtained from personal files and from a systemic search through MEDLINE and EMBASE. The principle

Ingvar Bjarnason; Andrew Macpherson; Daniel Hollander

1995-01-01

192

The Ability of Permeability  

NSDL National Science Digital Library

In this activity (page 11 of the PDF), learners investigate how quickly water moves through various materials. They measure and compare the permeability of gravel, sand, and soil. Although this was created as a post-visit activity for a workshop about earth processes, it also makes an excellent stand alone activity.

Cosi

2009-01-01

193

Scales of rock permeability  

NASA Astrophysics Data System (ADS)

Permeability is a transport property which is currently measured in Darcy units. Although this unit is very convenient for most purposes, its use prevents from recognizing that permeability has units of length squared. Physically, the square root of permeability can thus be seen as a characteristic length or a characteristic pore size. At the laboratory scale, the identification of this characteristic length is a good example of how experimental measurements and theoretical modelling can be integrated. Three distinct identifications are of current use, relying on three different techniques: image analysis of thin sections, mercury porosimetry and nitrogen adsorption. In each case, one or several theoretical models allow us to derive permeability from the experimental data (equivalent channel models, statistical models, effective media models, percolation and network models). Permeability varies with pressure and temperature and this is a decisive point for any extrapolation to crustal conditions. As far as pressure is concerned, most of the effect is due to cracks and a model which does not incorporate this fact will miss its goal. Temperature induced modifications can be the result of several processes: thermal cracking (due to thermal expansion mismatch and anisotropy, or to fluid pressure build up), and pressure solution are the two main ones. Experimental data on pressure and temperature effects are difficult to obtain but they are urgently needed. Finally, an important issue is: up to which point are these small scale data and models relevant when considering formations at the oil reservoir scale, or at the crust scale? At larger scales the identification of the characteristic scale is also a major goal which is examined.

Guéguen, Y.; Gavrilenko, P.; Le Ravalec, M.

1996-05-01

194

Indexing Images.  

ERIC Educational Resources Information Center

Focuses on access to digital image collections by means of manual and automatic indexing. Contains six sections: (1) Studies of Image Systems and their Use; (2) Approaches to Indexing Images; (3) Image Attributes; (4) Concept-Based Indexing; (5) Content-Based Indexing; and (6) Browsing in Image Retrieval. Contains 105 references. (AEF)

Rasmussen, Edie M.

1997-01-01

195

EPA Permeable Surface Research - Poster  

EPA Science Inventory

EPA recognizes permeable surfaces as an effective post-construction infiltration-based Best Management Practice to mitigate the adverse effects of stormwater runoff. The professional user community conceptually embraces permeable surfaces as a tool for making runoff more closely...

196

Vascular cells.  

PubMed

Embryonic stem (ES) cells are cells derived from the inner cell mass of a blastocyst stage embryo. These self-renewing multipotent cells are able to differentiate to the three embryonic germ layers, the endoderm, ectoderm, and mesoderm, and are thus able to produce virtually all cell types. The ES cell capacity to generate various cell types has been studied extensively, and exploitation of ES cell characteristics allowed the production of several differentiated cell types of multiple tissues. Moreover, the process of ES cell differentiation provides a unique opportunity to observe early embryonic developmental events that are unattainable in the embryo itself. This chapter addresses the in vitro differentiation procedure of endothelial and vascular smooth muscle cells from human ES cells, with reference to similar studies performed in mouse and nonhuman primate ES cells, and provides several tools for the detailed characterization of differentiated cells. PMID:17141040

Goldberg-Cohen, Ilana; Beck, Gilad; Ziskind, Anna; Itskovitz-Eldor, Joseph

2006-01-01

197

Induction of permeability across endothelial cell monolayers by tumor necrosis factor (TNF) occurs via a tissue factor-dependent mechanism: relationship between the procoagulant and permeability effects of TNF  

Microsoft Academic Search

Tumor necrosis factor (TNF) has marked effects on permeability and procoagulant activity on tumor-associated neovascula- ture when used in isolation perfusion, the latter effect primarily mediated via induction of cell surface expression of tissue factor (TF) on endothelial tissue. However, the cel- lular events that result in rapid alterations in endothelial cell (EC) permeability after intra- vascular TNF administration in

Josef Friedl; Markus Puhlmann; David L. Bartlett; Steven K. Libutti; Ewa N. Turner; Michael F. X. Gnant; H. Richard Alexander

2002-01-01

198

Hemodynamics analysis of patient-specific carotid bifurcation: a CFD model of downstream peripheral vascular impedance.  

PubMed

The study of cardiovascular models was presented in this paper based on medical image reconstruction and computational fluid dynamics. Our aim is to provide a reality platform for the purpose of flow analysis and virtual intervention outcome predication for vascular diseases. By connecting two porous mediums with transient permeability at the downstream of the carotid bifurcation branches, a downstream peripheral impedance model was developed, and the effect of the downstream vascular bed impedance can be taken into consideration. After verifying its accuracy with a healthy carotid bifurcation, this model was implemented in a diseased carotid bifurcation analysis. On the basis of time-averaged wall shear stress, oscillatory shear index, and the relative residence time, fractions of abnormal luminal surface were highlighted, and the atherosclerosis was assessed from a hemodynamic point of view. The effect of the atherosclerosis on the transient flow division between the two branches because of the existence of plaque was also analysed. This work demonstrated that the proposed downstream peripheral vascular impedance model can be used for computational modelling when the outlets boundary conditions are not available, and successfully presented the potential of using medical imaging and numerical simulation to provide existing clinical prerequisites for diagnosis and therapeutic treatment. PMID:23345076

Dong, Jingliang; Wong, Kelvin K L; Tu, Jiyuan

2013-04-01

199

What Is Vascular Disease?  

MedlinePLUS

... DVT) Peripheral Artery Disease (PAD) Pulmonary Embolism Stroke Varicose Veins Diabetes and Vascular Disease Kidney Failure and Vascular ... vein thrombosis (DVT), chronic venous insufficiency (CVI), and varicose veins. Everyone is at risk of vascular disease , and ...

200

Liquid-permeable electrode  

DOEpatents

Electrodes for use in an electrolytic cell, which are liquid-permeable and have low electrical resistance and high internal surface area are provided of a rigid, porous, carbonaceous matrix having activated carbon uniformly embedded throughout. The activated carbon may be catalyzed with platinum for improved electron transfer between electrode and electrolyte. Activated carbon is mixed with a powdered thermosetting phenolic resin and compacted to the desired shape in a heated mold to melt the resin and form the green electrode. The compact is then heated to a pyrolyzing temperature to carbonize and volatilize the resin, forming a rigid, porous structure. The permeable structure and high internal surface area are useful in electrolytic cells where it is necessary to continuously remove the products of the electrochemical reaction.

Folser, George R. (Lower Burrell, PA)

1980-01-01

201

Intraocular Hemorrhage Causes Retinal Vascular Dysfunction via Plasma Kallikrein  

PubMed Central

Purpose. Retinal hemorrhages occur in a variety of sight-threatening conditions including ocular trauma, high altitude retinopathy, and chronic diseases such as diabetic and hypertensive retinopathies. The goal of this study is to investigate the effects of blood in the vitreous on retinal vascular function in rats. Methods. Intravitreal injections of autologous blood, plasma kallikrein (PK), bradykinin, and collagenase were performed in Sprague-Dawley and Long-Evans rats. Retinal vascular permeability was measured using vitreous fluorophotometry and Evans blue dye permeation. Leukostasis was measured by fluorescein isothiocyanate–coupled concanavalin A lectin and acridine orange labeling. Retinal hemorrhage was examined on retinal flatmounts. Primary cultures of bovine retinal pericytes were cultured in the presence of 25 nM PK for 24 hours. The pericyte-conditioned medium was collected and the collagen proteome was analyzed by tandem mass spectrometry. Results. Intravitreal injection of autologous blood induced retinal vascular permeability and retinal leukostasis, and these responses were ameliorated by PK inhibition. Intravitreal injections of exogenous PK induced retinal vascular permeability, leukostasis, and retinal hemorrhage. Proteomic analyses showed that PK increased collagen degradation in pericyte-conditioned medium and purified type IV collagen. Intravitreal injection of collagenase mimicked PK's effect on retinal hemorrhage. Conclusions. Intraocular hemorrhage increases retinal vascular permeability and leukostasis, and these responses are mediated, in part, via PK. Intravitreal injections of either PK or collagenase, but not bradykinin, induce retinal hemorrhage in rats. PK exerts collagenase-like activity that may contribute to blood–retinal barrier dysfunction.

Liu, Jia; Clermont, Allen C.; Gao, Ben-Bo; Feener, Edward P.

2013-01-01

202

Vascular Endothelial (VE)Cadherin: Only an Intercellular Glue?  

Microsoft Academic Search

Data collected during the past years indicate that AJ- and more specifically VE-cadherin play an important role in endothelial cell biology. VE-cadherin may transfer information intracellularly through interaction with a complex network of cytoskeletal and signaling molecules. Expression of VE-cadherin is required for the control of vascular permeability and vascular integrity. In addition, the molecule may exert a morphogenetic role

Elisabetta Dejana; Gianfranco Bazzoni; Maria Grazia Lampugnani

1999-01-01

203

Glucose degradation product methylglyoxal enhances the production of vascular endothelial growth factor in peritoneal cells: role in the functional and morphological alterations of peritoneal membranes in peritoneal dialysis  

Microsoft Academic Search

Peritoneal membrane permeability deteriorates in peritoneal dialysis (PD) patients. We test whether glucose degradation products (GDPs) in PD fluids, glyoxal, methylglyoxal and 3-deoxyglucosone, stimulate the production of vascular endothelial growth factor (VEGF), a factor known to enhance vascular permeability and angiogenesis. VEGF increased in cultured rat mesothelial and human endothelial cells exposed to methylglyoxal, but not to glyoxal or 3-deoxyglucosone.

Reiko Inagi; Toshio Miyata; Takashi Yamamoto; Daisuke Suzuki; Ken-ichi Urakami; Akira Saito; Charles van Ypersele de Strihou; Kiyoshi Kurokawa

1999-01-01

204

Endothelial precursors in vascular repair.  

PubMed

The endothelium is an essential component of the cardiovascular system, playing a vital role in blood vessel formation, vascular homeostasis, permeability and the regulation of inflammation. The integrity of the endothelial monolayer is also critical in the prevention of atherogenesis and as such, restoration of the monolayer is essential following damage or cell death. Over the past decade, data has suggested that progenitor cells from different origins within the body are released into the circulation and contribute to re-endothelialisation. These cells, termed endothelial progenitor cells (EPCs), also gave rise to the theory of new vessel formation within adults (vasculogenesis) without proliferation and migration of mature endothelial cells (angiogenesis). As such, intense research has been carried out identifying how these cells may be mobilised and contribute to vascular repair, either encouraging vasculogenesis into regions of ischemia or the re-endothelialisation of vessels with a dysfunctional endothelium. However, classification and isolation procedures have been a major problem in this area of research and beneficial use for therapeutic application has been controversial. In the present review we focus on the role of EPCs in vascular repair. We also provide an update on EPC classification and discuss autologous stem cell-derived endothelial cell (EC) as a functional source for therapy. PMID:20184904

Kirton, John Paul; Xu, Qingbo

2010-05-01

205

Automatic indexing  

SciTech Connect

Automatic indexing has been a critical technology as more full-text data becomes available online. The paper discusses issues for automatic indexing of different types of full-text and also presents a survey of much of the current research into new techniques for automatic indexing.

Harman, D.

1992-09-01

206

Microvascular albumin permeability in isolated perfused lung: effects of EDTA  

SciTech Connect

The authors examined the effects of decreases in perfusate concentrations of calcium and magnesium on the pulmonary vascular permeability in the isolated perfused rabbit lung. The albumin permeability-surface area product (PS) and the albumin reflection coefficient (sigma) were determined in the same lung using /sup 125/I- and /sup 131/I-labeled albumin tracers. Decreases in vascular Ca/sup 2 +/ and Mg/sup 2 +/ concentrations were induced by adding ethylenediaminetetraacetic acid (EDTA) to the perfusate. Decreases in the concentration of these cations resulted in an increase in the PS from a control value of 1.18 +/- 0.13 X 10(-3) to 7.69 +/- 0. 75 X 10(-3) cm3 X min-1 X g wet lung wt-1 and a decrease in the sigma from 0.96 +/- 0.01 to 0.74 +/- 0.02. The decrease in sigma suggests an increase in the calculated equivalent pore radius from 44 to 63 A. The results indicate that Ca/sup 2 +/ and Mg/sup 2 +/ play a role in the maintenance of normal pulmonary vascular permeability to proteins.

Kern, D.F.; Malik, A.B.

1985-02-01

207

Changes in mast cells and in permeability of mesenteric microvessels under the effect of immobilization and electrostimulation  

NASA Technical Reports Server (NTRS)

It was shown that a reduction in the amount of mast cells in the mesentery and an increase in their degranulation was accompanied by an increase in vascular permeability of rat mesentery. It is supposed that immobilization and electrostimulation causing degranulation of mast cells prompted histamine and serotonin release from them, thus increasing the permeability of the venular portion of the microvascular bed. Prophylactic use of esculamin preparation with P-vitaminic activity decreased mast cell degranulation, which apparently prolonged the release of histamine and serotonin from them and normalized vascular permeability.

Gorizontova, M. P.

1980-01-01

208

A Computer Numerical Simulation Study Considering Starting Up Pressure Gradient for Low Permeability Reservoir  

Microsoft Academic Search

According to the fact that starting up pressure gradient exists when fluids flow in low permeability reservoir, a nondarcy flow mathematical model is established, in which the factor of starting up pressure gradient is included for low permeability reservoir. Software, by solving the partial differential equations by difference method, is developed, and is used to calculate development index and the

Daiyin Yin; Weiming Huang

2009-01-01

209

Wave propagation in media having negative permittivity and permeability  

Microsoft Academic Search

Wave propagation in a double negative (DNG) medium, i.e., a medium having negative permittivity and negative permeability, is studied both analytically and numerically. The choices of the square root that leads to the index of refraction and the wave impedance in a DNG medium are determined by imposing analyticity in the complex frequency domain, and the corresponding wave properties associated

Richard W. Ziolkowski; Ehud Heyman

2001-01-01

210

Permeability identification of a weakly permeable partially saturated porous rock  

Microsoft Academic Search

The present paper deals with the determination of permeability in partially saturated conditions for weakly permeable porous\\u000a continua such as argillites or deep clayey formations. The permeability can be deduced from measurements of transient weight\\u000a loss of a sample submitted to a laboratory drying test: a decrease of relative humidity is imposed by saline solution in an\\u000a hermetic chamber. Assumptions

Albert Giraud; Richard Giot; Françoise Homand; Amine Koriche

2007-01-01

211

Biodiesel permeability in polyethylene  

NASA Astrophysics Data System (ADS)

This paper reports solubility, diffusivity and permeability data for soy and rapeseed methyl esters in polyethylene together with comparisons with methyl oleate and linoleate. The solubility was estimated on the order of 5% in weight at room temperature and increased up to more than 10% at 75°C. Diffusion kinetics obeys Fick's law and measured diffusion coefficient increased from 10-13 at room temperature to 5.10-11 m2 s-1 at 75°C. No significant difference was observed between all methyl esters under study. These data were used to discuss the reliability of predictive models for diffusion and solubility of additive type molecules into semi-crystalline thermoplastic polymers.

Richaud, Emmanuel; Fayolle, Bruno; Flaconnèche, Bruno; Verdu, Jacques

2012-07-01

212

Gas permeability of shocked chondrites  

NASA Astrophysics Data System (ADS)

The gas permeability of 11 ordinary chondrites was measured at various gas pressures (0.5-2.5 bars) under confining pressures up to 120 bars. The gas permeability ranges from less than a nanodarcy to a few millidarcies. There is a positive correlation between the permeability and the porosity. The permeabilithy decreased by as much as 50 percent when the confining pressure was increased from 10 to 100 bars, suggesting that the permeability of some chondrites is partly due to cracks. A linear relation between gas flow pressure dependence and confining pressure dependence of the gas permeability is observed, suggesting that on average, crack apertures are larger than pore spaces. The permeabilithy of heavily-shocked chondrites is less than of mildly shocked chondrites. Using the measured permeability data the size of a possible shocked-chondrite precursor body is estimated.

Matsui, T.; Sugiura, N.; Brar, N. S.

1986-03-01

213

Expression of Vascular Endothelial Growth Factor and Its Receptors in Hematopoietic Malignancies1  

Microsoft Academic Search

Vascular endothelial growth factor (VEGF) plays an important role in angiogenesis by acting as a potent inducer of vascular permeability as well as serving as a specific endothelial cell mitogen. The importance of angio- genic factors such as VEGF, although clearly established in solid tumors, has not been fully elucidated in human hematopoietic neoplasms. We examined the expression of mRNA

William T. Bellamy; Lynne Richter; Yvette Frutiger; Thomas M. Grogan

1999-01-01

214

Vascular endothelial growth factor gene and protein: strong expression in thyroiditis and thyroid carcinoma  

Microsoft Academic Search

Angiogenesis is implicated in several pathological con- ditions, such as inflammation and tumor growth. Vascular endothelial growth factor (VEGF), also known as vascular permeability factor, is a potent stimulator of endothelial cell proliferation in vitro and in vivo. The present work aimed to compare VEGF expression in human normal thyroid glands, thyroiditis tissue and thyroid carcinomas using immunohistochemistry and in

M Klein; E Picard; J-M Vignaud; B Marie; L Bresler; B Toussaint; G Weryha; A Duprez; J Lecler

1999-01-01

215

Permeability of narrow permalloy stripes  

Microsoft Academic Search

The effective permeability between 1 MHz and 100 MHz was measured for 1-3 ?m thick permalloy(80Ni- 20Fe) films in 2-3 cm diameter sheets and compared with the effective permeability for the same films after etching them into 51?m wide stripes on 127?m centers. Solid permalloy films show a 15%-40% loss of effective permeability at all frequencies after having been etched

J. Feng; D. Thompson

1977-01-01

216

Plant Vascular Biology 2013: vascular trafficking.  

PubMed

About 200 researchers from around the world attended the Third International Conference on Plant Vascular Biology (PVB 2013) held in July 2013 at the Rantapuisto Conference Center, in Helsinki, Finland (http://www.pvb2013.org). The plant vascular system, which connects every organ in the mature plant, continues to attract the interest of researchers representing a wide range of disciplines, including development, physiology, systems biology, and computational biology. At the meeting, participants discussed the latest research advances in vascular development, long- and short-distance vascular transport and long-distance signalling in plant defence, in addition to providing a context for how these studies intersect with each other. The meeting provided an opportunity for researchers working across a broad range of fields to share ideas and to discuss future directions in the expanding field of vascular biology. In this report, the latest advances in understanding the mechanism of vascular trafficking presented at the meeting have been summarized. PMID:24431156

Ursache, Robertas; Heo, Jung-Ok; Helariutta, Ykä

2014-04-01

217

Sensitive chemiluminescence enzyme immunoassay for vascular endothelial growth factor/vascular permeability factor in human serum.  

PubMed

A sandwich chemiluminescence enzyme immunoassay for measuring the level of VEGF/VPF in serum was constructed. The detectability of the assay is very low (1.0 pg/ml) and the measurable range of the assay was very wide (1-1000 pg/ml). The assay showed that the average level of VEGF/VPF in human sera from healthy blood donors was approximately 19 pg/ml. PMID:8534992

Hanatani, M; Tanaka, Y; Kondo, S; Ohmori, I; Suzuki, H

1995-10-01

218

Complexity in the vascular permeability factor\\/vascular endothelial growth factor (VPF\\/VEGF)-receptors signaling  

Microsoft Academic Search

The adult vasculature results from a network of vessels that is originally derived in the embryo by vasculogenesis, a process whereby vessels are formed de novo from endothelial cell (EC) precursors, known as angioblasts. During vasculogenesis, angioblasts proliferate and come together to form an initial network of vessels, also known as the primary capillary plexus. Sprouting and branching of new

Debabrata Mukhopadhyay; Huiyan Zeng; Resham Bhattacharya

2005-01-01

219

Design and development of multilayer vascular graft  

NASA Astrophysics Data System (ADS)

Vascular graft is a widely-used medical device for the treatment of vascular diseases such as atherosclerosis and aneurysm as well as for the use of vascular access and pediatric shunt, which are major causes of mortality and morbidity in this world. Dysfunction of vascular grafts often occurs, particularly for grafts with diameter less than 6mm, and is associated with the design of graft materials. Mechanical strength, compliance, permeability, endothelialization and availability are issues of most concern for vascular graft materials. To address these issues, we have designed a biodegradable, compliant graft made of hybrid multilayer by combining an intimal equivalent, electrospun heparin-impregnated poly-epsilon-caprolactone nanofibers, with a medial equivalent, a crosslinked collagen-chitosan-based gel scaffold. The intimal equivalent is designed to build mechanical strength and stability suitable for in vivo grafting and to prevent thrombosis. The medial equivalent is designed to serve as a scaffold for the activity of the smooth muscle cells important for vascular healing and regeneration. Our results have shown that genipin is a biocompatible crosslinker to enhance the mechanical properties of collagen-chitosan based scaffolds, and the degradation time and the activity of smooth muscle cells in the scaffold can be modulated by the crosslinking degree. For vascular grafting and regeneration in vivo, an important design parameter of the hybrid multilayer is the interface adhesion between the intimal and medial equivalents. With diametrically opposite affinities to water, delamination of the two layers occurs. Physical or chemical modification techniques were thus used to enhance the adhesion. Microscopic examination and graft-relevant functional characterizations have been performed to evaluate these techniques. Results from characterization of microstructure and functional properties, including burst strength, compliance, water permeability and suture strength, showed that the multilayer graft possessed properties mimicking those of native vessels. Achieving these FDA-required functional properties is essential because they play critical roles in graft performances in vivo such as thrombus formation, occlusion, healing, and bleeding. In addition, cell studies and animal studies have been performed on the multilayer graft. Our results show that the multilayer graft support mimetic vascular culture of cells and the acellular graft serves as an artery equivalent in vivo to sustain the physiological conditions and promote appropriate cellular activity. In conclusion, the newly-developed hybrid multilayer graft provides a proper balance of biomechanical and biochemical properties and demonstrates the potential for the use of vascular tissue engineering and regeneration.

Madhavan, Krishna

220

Endogenous endothelial cell signaling systems maintain vascular stability  

PubMed Central

The function of the endothelium is to provide a network to allow delivery of oxygen and nutrients to tissues throughout the body. This network is comprised of adjacent endothelial cells which utilize adherens junction proteins such as vascular endothelial cadherin (VE-cadherin) to maintain the appropriate level of vascular permeability. The disruption of VE-cadherin interactions during pathologic settings can lead to excessive vascular leak with adverse effects. Endogenous cell signaling systems have been defined that help to maintain the proper level of vascular stability. Perhaps the best described system is Angiopoietin-1 (Ang-1). Ang-1 acting through its receptor Tie2 generates a well described set of signaling events ultimately leading to enhanced vascular stability. In this review we will focus on what is known about additional endogenous cell signaling systems that stabilize the vasculature, and using Ang-1/Tie2 as a model, we will address where our understanding of these additional systems is lacking.

London, Nyall R.; Whitehead, Kevin J.; Li, Dean Y.

2009-01-01

221

Functional vascular endothelium derived from human induced pluripotent stem cells.  

PubMed

Vascular endothelium is a dynamic cellular interface that displays a unique phenotypic plasticity. This plasticity is critical for vascular function and when dysregulated is pathogenic in several diseases. Human genotype-phenotype studies of endothelium are limited by the unavailability of patient-specific endothelial cells. To establish a cellular platform for studying endothelial biology, we have generated vascular endothelium from human induced pluripotent stem cells (iPSCs) exhibiting the rich functional phenotypic plasticity of mature primary vascular endothelium. These endothelial cells respond to diverse proinflammatory stimuli, adopting an activated phenotype including leukocyte adhesion molecule expression, cytokine production, and support for leukocyte transmigration. They maintain dynamic barrier properties responsive to multiple vascular permeability factors. Importantly, biomechanical or pharmacological stimuli can induce pathophysiologically relevant atheroprotective or atheroprone phenotypes. Our results demonstrate that iPSC-derived endothelium possesses a repertoire of functional phenotypic plasticity and is amenable to cell-based assays probing endothelial contributions to inflammatory and cardiovascular diseases. PMID:24052946

Adams, William J; Zhang, Yuzhi; Cloutier, Jennifer; Kuchimanchi, Pranati; Newton, Gail; Sehrawat, Seema; Aird, William C; Mayadas, Tanya N; Luscinskas, Francis W; García-Cardeña, Guillermo

2013-01-01

222

Sphingolipids affect fibrinogen-induced caveolar transcytosis and cerebrovascular permeability.  

PubMed

Inflammation-induced vascular endothelial dysfunction can allow plasma proteins to cross the vascular wall, causing edema. Proteins may traverse the vascular wall through two main pathways, the paracellular and transcellular transport pathways. Paracellular transport involves changes in endothelial cell junction proteins, while transcellular transport involves caveolar transcytosis. Since both processes are associated with filamentous actin formation, the two pathways are interconnected. Therefore, it is difficult to differentiate the prevailing role of one or the other pathway during various pathologies causing an increase in vascular permeability. Using a newly developed dual-tracer probing method, we differentiated transcellular from paracellular transport during hyperfibrinogenemia (HFg), an increase in fibrinogen (Fg) content. Roles of cholesterol and sphingolipids in formation of functional caveolae were assessed using a cholesterol chelator, methyl-?-cyclodextrin, and the de novo sphingolipid synthesis inhibitor myriocin. Fg-induced formation of functional caveolae was defined by association and colocalization of Na(+)-K(+)-ATPase and plasmalemmal vesicle-associated protein-1 with use of Förster resonance energy transfer and total internal reflection fluorescence microscopy, respectively. HFg increased permeability of the endothelial cell layer mainly through the transcellular pathway. While M?CD blocked Fg-increased transcellular and paracellular transport, myriocin affected only transcellular transport. Less pial venular leakage of albumin was observed in myriocin-treated HFg mice. HFg induced greater formation of functional caveolae, as indicated by colocalization of Na(+)-K(+)-ATPase with plasmalemmal vesicle-associated protein-1 by Förster resonance energy transfer and total internal reflection fluorescence microscopy. Our results suggest that elevated blood levels of Fg alter cerebrovascular permeability mainly by affecting caveolae-mediated transcytosis through modulation of de novo sphingolipid synthesis. PMID:24829496

Muradashvili, Nino; Khundmiri, Syed Jalal; Tyagi, Reeta; Gartung, Allison; Dean, William L; Lee, Menq-Jer; Lominadze, David

2014-07-15

223

Pyrotechnic deflagration velocity and permeability  

Microsoft Academic Search

Particle size, porosity, and permeability of the reactive material have long been considered to be important factors in propellant burning rates and the deflagration-to-detonation transition in explosives. It is reasonable to assume that these same parameters will also affect the deflagration velocity of pyrotechnics. This report describes an experimental program that addresses the permeability of porous solids (particulate beds), in

D. R. Begeal; P. L. Stanton

1982-01-01

224

Measurements on stress dependent permeability  

NASA Astrophysics Data System (ADS)

Hydrostatic loading is the conventional test procedure to determine the stress dependence of permeability. However, hydrostatic tests do not truly reflect the deviatoric stress state that exists in most reservoirs. The main objective of the present project was to study permeability changes under deviatoric stresses, like encountered in standard triaxial tests. However in measuring permeability in a triaxial cell, end effects may be important. The friction between the axial steel pistons and the sample may cause stress concentrations and thereby a non-homogeneous strain pattern towards the sample ends. To overcome this problem, the cell was modified to have pressure outlets from the mid-section of the sample, with the pressure tubes connected to the outside of the cell for pressure recording. The cell was designed for 1.5 in plugs with plug lengths of about 80 mm. Tests have been performed on two types of high porosity outcrop chalk: Liège chalk with porosity around 40 percent and permeability 1-2 millidarcy, and Aalborg chalk with porosity around 45 percent and permeability in the range 3-5 millidarcy. Methanol was used as saturating fluid for the chalks. In addition some sandstone samples from core material were included. The porosity values were rather high, around 30 percent, and the permeability ranged from around 50 millidarcy to over one Darcy. Synthetic oil was used as saturating fluid for the sandstone samples, to avoid any reactions with clay minerals. The results so far can be summarized as follows:(1) In almost all the tests, the permeability calculated by the overall pressure drop is smaller than the mid-section permeability. The reduction could typically be around 20 percent. This means that end-effects play an important role.(2) The permeability generally decrease with increasing hydrostatic stresses. This is in agreement with observations from other sources.(3) During deviatoric phases the average stress level is increasing, but the changes in permeability are rather small, even if the tests are run beyond yield. The mid-section permeability seems to show a small increasing trend with increasing deviatoric stresses after yield. But the yield point does not seem to have any drastic effect on the permeability.(4) The overall permeability seems in general to show a decreasing trend under deviatoric stresses. The results indicate that permeability changes with pressure depletion under reservoir conditions may be much less than expected from hydrostatic tests or tests uncorrected for end-effects.

Risnes, R.; Faldaas, I.; Korsnes, R. I.; Norland, T.

2003-04-01

225

Soluble receptor for advanced glycation end products as an indicator of pulmonary vascular injury after cardiac surgery  

PubMed Central

Background Cardiac surgery is frequently complicated by an acute vascular lung injury and this may be mediated, at least in part, by the (soluble) receptor for advanced glycation end products (sRAGE). Methods In two university hospital intensive care units, circulating sRAGE was measured together with the 68Gallium-transferrin pulmonary leak index (PLI), a measure of pulmonary vascular permeabiliy, in 60 consecutive cardiac surgery patients stratified by the amount of blood transfusion, within 3 hours of admission to the intensive care. Results Cardiac surgery resulted in elevated plasma sRAGE levels compared to baseline (315?±?181 vs 110?±?55 pg/ml, P?=?0.001). In 37 patients the PLI was elevated 50% above normal. The PLI correlated with sRAGE (r2?=?0.11, P?=?0.018). Plasma sRAGE discriminated well between those with an elevated PLI and those with a normal PLI (area under the operator curve 0.75; P?=?0.035; 95% CI 0.55-0.95), with 91% sensitivity but low specificity of 36% at a cutoff value of 200 pg/mL. Blood transfusion did not influence sRAGE levels. Conclusions sRAGE is elevated in plasma after cardiac surgery and indicates increased pulmonary vascular permeability. The level of sRAGE is not affected by transfusion.

2013-01-01

226

Vascular Access for Hemodialysis  

MedlinePLUS

... Kidney Failure Series : Vascular Access for Hemodialysis Vascular Access for Hemodialysis On this page: What is an ... Top ] What is a venous catheter for temporary access? If your kidney disease has progressed quickly, you ...

227

Vascular Disease Foundation  

MedlinePLUS

... vascular eye openers ? TYPES of VASCULAR DISEASE Abdominal Aortic Aneurysm (AAA) Abdominal Aortic Aneurysms (AAA) are caused by progressive ... when a blood vessel bursts. Learn More Thoracic Aortic Aneurysm Aneurysms of the aorta can occur in the ...

228

Gas permeability of carbon aerogels  

SciTech Connect

Carbon aerogels are synthesized via the aqueous polycondensation of resorcinol with formaldehyde, followed by supercritical drying and subsequent pyrolysis at 1050 [degree]C. As a result of their interconnected porosity, ultrafine cell/pore size, and high surface area, carbon aerogels have many potential applications such as supercapacitors, battery electrodes, catalyst supports, and gas filters. The performance of carbon aerogels in the latter two applications depends on the permeability or gas flow conductance in these materials. By measuring the pressure differential across a thin specimen and the nitrogen gas flow rate in the viscous regime, the permeability of carbon aerogels was calculated from equations based upon Darcy's law. Our measurements show that carbon aerogels have permeabilities on the order of 10[sup [minus]12] to 10[sup [minus]10] cm[sup 2] over the density range from 0.05--0.44 g/cm[sup 3]. Like many other aerogel properties, the permeability of carbon aerogels follows a power law relationship with density, reflecting differences in the average mesopore size. Comparing the results from this study with the permeability of silica aerogels reported by other workers, we found that the permeability of aerogels is governed by a simple universal flow equation. This paper discusses the relationship between permeability, pore size, and density in carbon aerogels.

Kong, F.; LeMay, J.D.; Hulsey, S.S.; Alviso, C.T.; Pekala, R.W. (Chemistry and Materials Science Department, Lawrence Livermore National Laboratory, Livermore, California 94550 (United States))

1993-12-01

229

Permeable membrane experiment  

NASA Technical Reports Server (NTRS)

The purpose of the Permeable Membrane Experiment is to gather flight data on three areas of membrane performance that are influenced by the presence of gravity. These areas are: (1) Liquid/gas phase separation, (2) gas bubble interference with diffusion through porous membranes and (3) wetting characteristics of hydrophilic membrane surfaces. These data are important in understaning the behavior of membrane/liquid/gas interfaces where surface tension forces predominate. The data will be compared with 1-g data already obtained and with predicted micrograviity behavior. The data will be used to develop designs for phase separation and plant nutrient delivery systems and will be available to the life support community for use in developing technologies which employ membranes. A conceptual design has been developed to conduct three membrane experiments, in sequence, aboard a single Complex Autonomous Payload (CAP) carrier to be carried in the Shuttle Orbiter payload bay. One experiment is conducted for each of the three membrane performance areas under study. These experiments are discussed in this paper.

Slavin, Thomas J.; Cao, Tuan Q.; Kliss, Mark H.

1993-01-01

230

Vascular endothelial growth factor in bacterial meningitis: detection in cerebrospinal fluid and localization in postmortem brain.  

PubMed

Vascular endothelial growth factor (VEGF) is a potent vascular permeability factor and a mediator of brain edema. To assess the role of VEGF during bacterial meningitis, VEGF was measured in cerebrospinal fluid (CSF) and blood of 37 patients with bacterial meningitis and 51 control patients, including 16 patients with viral meningitis. Circulating VEGF levels were similar in bacterial meningitis patients and control patients. VEGF(CSF) was detected in 11 (30%) of 37 of bacterial meningitis patients (range, <25-633 pg/mL) but in none of the control patients. The median VEGF index was 6.2 (range, 0.6-42), indicating intrathecal production. Median CSF cell counts, protein levels, and CSF: serum albumin ratios were higher for patients with detectable VEGF(CSF), although the difference was not statistically significant. VEGF immunoreactivity in autopsy brain specimens was found in the inflammatory infiltrate of patients with bacterial meningitis. These results indicate that inflammatory cells secrete VEGF during bacterial meningitis and that VEGF may contribute to blood-brain barrier disruption. PMID:11106541

van der Flier, M; Stockhammer, G; Vonk, G J; Nikkels, P G; van Diemen-Steenvoorde, R A; van der Vlist, G J; Rupert, S W; Schmutzhard, E; Gunsilius, E; Gastl, G; Hoepelman, A I; Kimpen, J L; Geelen, S P

2001-01-01

231

Relative Permeability of Fractured Rock  

SciTech Connect

Contemporary understanding of multiphase flow through fractures is limited. Different studies using synthetic fractures and various fluids have yielded different relative permeability-saturation relations. This study aimed to extend the understanding of multiphase flow by conducting nitrogen-water relative permeability experiments on a naturally-fractured rock from The Geysers geothermal field. The steady-state approach was used. However, steady state was achieved only at the endpoint saturations. Several difficulties were encountered that are attributed to phase interference and changes in fracture aperture and surface roughness, along with fracture propagation/initiation. Absolute permeabilities were determined using nitrogen and water. The permeability values obtained change with the number of load cycles. Determining the absolute permeability of a core is especially important in a fractured rock. The rock may change as asperities are destroyed and fractures propagate or st rain harden as the net stresses vary. Pressure spikes occurred in water a solute permeability experiments. Conceptual models of an elastic fracture network can explain the pressure spike behavior. At the endpoint saturations the water relative permeabilities obtained are much less than the nitrogen gas relative permeabilities. Saturations were determined by weighing and by resistivity calculations. The resistivity-saturation relationship developed for the core gave saturation values that differ by 5% from the value determined by weighing. Further work is required to complete the relative permeability curve. The steady-state experimental approach encountered difficulties due to phase interference and fracture change. Steady state may not be reached until an impractical length of time. Thus, unsteady-state methods should be pursued. In unsteady-state experiments the challenge will be in quantifying rock fracture change in addition to fluid flow changes.

Mark D. Habana

2002-06-30

232

Permeability of oxidized phosphatidylcholine liposomes.  

PubMed

Permeability of liposomes made from mixtures of unoxidized and singlet oxygen oxidized phosphatidylcholine has been related to the degree of lipid oxidation expressed as hydroperoxide moiety content in the lipids. The effect of oxidation on the liposomes permeability has been studied by fluorometry using calcein as a fluorescent probe that undergoes self quenching when highly concentrated inside liposomes. The liposomes containing 73% and 5% of hydroperoxides retain respectively 64.5 and 96.3% of calcein with respect to that retained by the liposomes made from unoxidized phosphatidylcholine. The fluorescence data show a linear relationship between the liposome permeability and the oxidation degree of lipids. PMID:2775263

Tanfani, F; Bertoli, E

1989-08-30

233

Tetraspanins and vascular functions  

PubMed Central

Tetraspanins are multiple membrane-spanning proteins that likely function as the organizers of membrane microdomains. Tetraspanins associate with other membrane-bound molecules such as cell-adhesion proteins, growth factor receptors, and Ig superfamily members and regulate key cellular processes such as adhesion, migration, and fusion. Tetraspanins are widely expressed in vascular and haematopoietic cells and are involved in both physiological and pathological processes related to angiogenesis, vascular injury, thrombosis, and haemostasis. A wide body of evidence suggests that tetraspanins directly regulate the development and functions of the vascular system and the pathogenesis of vascular diseases. This article reviews current understanding of the roles of tetraspanins in vascular functions.

Zhang, Feng; Kotha, Jayaprakash; Jennings, Lisa K.; Zhang, Xin A.

2009-01-01

234

Initiation of vascular development.  

PubMed

The initiation of vascular development occurs during embryogenesis and the development of lateral organs, such as lateral roots and leaves. Understanding the mechanism underlying the initiation of vascular development has been an important goal of plant biologists. Auxin flow is a crucial factor involved in the initiation of vascular development. In addition, recent studies have identified key factors that regulate the establishment of vascular initial cells in embryos and roots. In this review, we summarize the recent findings in this field and discuss the initiation of vascular development. PMID:24111590

Ohashi-Ito, Kyoko; Fukuda, Hiroo

2014-06-01

235

Numerical simulation of the effect of permeability on the hydrodynamics in a parallel-plate coculture flow chamber.  

PubMed

To study the effect of the porous membrane permeability on the hydrodynamics in a parallel-plate coculture flow chamber (PPcFC), we demonstrated the permeability of the porous membrane as a function of some parameters, such as porosity, membrane thickness, pore size and shape of the membrane. The effect of permeability on the flow in the PPcFC was analysed using the commercial software - Fluent. Results showed that the permeability was directly proportional to the thickness, the porosity and the pore size of the membrane, and inversely proportional to the surface shape factor. To ensure the best flow pattern, the inlet velocity range was limited by the membrane permeability and fluid viscosity, and then restricted the available magnitudes of shear rate on the permeable membrane. Our findings are helpful in designing and preparing the biomaterials that have adequate mechanical properties for the functional vascular grafts production, and in using of the flow chamber in various investigations. PMID:22994242

Zeng, Ye; Yao, Xing-Hong; Liu, Xiao-Heng

2014-01-01

236

Brachial artery low-flow-mediated constriction is increased early after coronary intervention and reduces during recovery after acute coronary syndrome: characterization of a recently described index of vascular function  

PubMed Central

Aims The endothelium plays a role in regulating vascular tone. Acute and dynamic changes in low-flow-mediated constriction (L-FMC) and how it changes with regard to traditional flow-mediated dilatation (FMD) have not been described. We aimed to investigate the changes in brachial artery L-FMC following percutaneous coronary intervention (PCI) and during recovery from non-ST-segment elevation myocardial infarction (NSTEMI). Methods and results FMD was performed in accordance with a previously described technique in patients before and after PCI and in the recovery phase of NSTEMI, but in addition, L-FMC data were acquired from the last 30 s of cuff inflation. About 135 scans were performed in 96 participants (10 healthy volunteers and 86 patients). Measurement of brachial L-FMC was reproducible over hours. L-FMC was greater among patients with unstable vs. stable coronary atherosclerosis (?1.33 ±1.09% vs. ?0.03 ± 1.26%, P < 0.01). Following PCI, FMD reduced (4.43 ± 2.93% vs. 1.66 ± 2.16%, P < 0.01) and L-FMC increased (?0.33 ± 0.76% vs. ?1.63 ± 1.15%, P = 0.02). Furthermore, during convalescence from NSTEMI, L-FMC reduced (?1.37 ± 1.19% vs. 0.01 ± 0.82%, P = 0.02) in parallel with improvements in FMD (2.54 ± 2.19% vs. 5.15 ± 3.07%, P < 0.01). Conclusion Brachial L-FMC can be measured reliably. Differences were observed between patients with stable and unstable coronary disease. L-FMC was acutely increased following PCI associated with reduced FMD and, in the recovery from NSTEMI, L-FMC reduced associated with increased FMD. These novel findings characterize acute and subacute variations in brachial L-FMC. The pathophysiological and clinical implications of these observations require further study.

Spiro, Jonathan R.; Digby, Janet E.; Ghimire, Gopal; Mason, Mark; Mitchell, Andrew G.; Ilsley, Charles; Donald, Ann; Dalby, Miles C.D.; Kharbanda, Rajesh K.

2011-01-01

237

Thrombin and vascular inflammation.  

PubMed

Vascular endothelium is a key regulator of homeostasis. In physiological conditions it mediates vascular dilatation, prevents platelet adhesion, and inhibits thrombin generation. However, endothelial dysfunction caused by physical injury of the vascular wall, for example during balloon angioplasty, acute or chronic inflammation, such as in atherothrombosis, creates a proinflammatory environment which supports leukocyte transmigration toward inflammatory sites. At the same time, the dysfunction promotes thrombin generation, fibrin deposition, and coagulation. The serine protease thrombin plays a pivotal role in the coagulation cascade. However, thrombin is not only the key effector of coagulation cascade; it also plays a significant role in inflammatory diseases. It shows an array of effects on endothelial cells, vascular smooth muscle cells, monocytes, and platelets, all of which participate in the vascular pathophysiology such as atherothrombosis. Therefore, thrombin can be considered as an important modulatory molecule of vascular homeostasis. This review summarizes the existing evidence on the role of thrombin in vascular inflammation. PMID:21858738

Popovi?, Milan; Smiljani?, Katarina; Dobutovi?, Branislava; Syrovets, Tatiana; Simmet, Thomas; Isenovi?, Esma R

2012-01-01

238

Doxycycline induces membrane expression of VE-cadherin on endothelial cells and prevents vascular hyperpermeability.  

PubMed

The endothelium lining blood vessels serves as a barrier against vascular hyperpermeability, and its maintenance is critical to organ health. Inflammatory mediators evoke tissue edema by disrupting the expression of membrane junctional proteins, which mediate binding between endothelial cell membranes. Endothelial cell-cell junctions form a diffusion barrier between the intravascular and interstitial space. To prevent the morbidity and mortality caused by exaggerated vascular permeability associated with pathological states (e.g., inflammatory and hypersensitivity disorders, pulmonary edema, traumatic lung injury, cerebral edema resulting from stroke, and others), it is important to develop therapeutic approaches to stabilize these interendothelial junctions. Vascular endothelial growth factor (VEGF), a potent proangiogenic cytokine, was first described as vascular permeability factor (VPF). Doxycycline, a tetracycline derivative, has been shown to inhibit angiogenesis in both humans and animal models. We now report that oral doxycycline prevents VPF/VEGF-induced vascular permeability, interleukin-2-induced pulmonary edema, and delayed-type hypersensitivity (DTH) in mice. Remarkably, doxycycline also inhibits tumor growth and tumor-associated vascular hyperpermeability. Finally, we show that doxycycline targets the adherens junction in vascular endothelial cells by inducing the total amount of VE-cadherin expression while decreasing the degree of its phosphorylation. The potential of doxycyline as a therapeutic inhibitor of vascular hyperpermeability in human clinical conditions is promising and warrants further studies. PMID:18606869

Fainaru, Ofer; Adini, Irit; Benny, Ofra; Bazinet, Lauren; Pravda, Elke; D'Amato, Robert; Folkman, Judah

2008-10-01

239

Opening the flood-gates: how neutrophil-endothelial interactions regulate permeability  

PubMed Central

Many diseases have an inflammatory component, where neutrophil interactions with the vascular endothelium lead to barrier dysfunction and increased permeability. Neutrophils increase permeability through secreted products like the chemokines CXCL1, 2, 3 and 8, through adhesion-dependent processes like ?2 integrins interacting with endothelial ICAM-1, and combinations, where ?2 integrin engagement leads to degranulation and secretion of heparin-binding protein (HBP), which in turn increases permeability. Some neutrophil products like arachidonic acid or leukotriene (LT)A4 are further processed by endothelial enzymes through transcellular metabolism before the resulting products thromboxane A2, LTB4 or LTC4 can activate their cognate receptors. Neutrophils also generate reactive oxygen species that induce vascular leakage. This review focuses on the mechanisms of neutrophil-mediated leakage.

DiStasi, Matthew R.; Ley, Klaus

2009-01-01

240

VEGFR2 and Src kinase inhibitors suppress Andes virus-induced endothelial cell permeability.  

PubMed

Hantaviruses predominantly infect human endothelial cells and, in the absence of cell lysis, cause two diseases resulting from increased vascular permeability. Andes virus (ANDV) causes a highly lethal acute pulmonary edema termed hantavirus pulmonary syndrome (HPS). ANDV infection enhances the permeability of endothelial cells in response to vascular endothelial growth factor (VEGF) by increasing signaling responses directed by the VEGFR2-Src-VE-cadherin pathway, which directs adherens junction (AJ) disassembly. Here we demonstrate that inhibiting pathway-specific VEGFR2 and Src family kinases (SFKs) blocks ANDV-induced endothelial cell permeability. Small interfering RNA (siRNA) knockdown of Src within ANDV-infected endothelial cells resulted in an ?70% decrease in endothelial cell permeability compared to that for siRNA controls. This finding suggested that existing FDA-approved small-molecule kinase inhibitors might similarly block ANDV-induced permeability. The VEGFR2 kinase inhibitor pazopanib as well as SFK inhibitors dasatinib, PP1, bosutinib, and Src inhibitor 1 dramatically inhibited ANDV-induced endothelial cell permeability. Consistent with their kinase-inhibitory concentrations, dasatinib, PP1, and pazopanib inhibited ANDV-induced permeability at 1, 10, and 100 nanomolar 50% inhibitory concentrations (IC(50)s), respectively. We further demonstrated that dasatinib and pazopanib blocked VE-cadherin dissociation from the AJs of ANDV-infected endothelial cells by >90%. These findings indicate that VEGFR2 and Src kinases are potential targets for therapeutically reducing ANDV-induced endothelial cell permeability and, as a result, capillary permeability during HPS. Since the functions of VEGFR2 and SFK inhibitors are already well defined and FDA approved for clinical use, these findings rationalize their therapeutic evaluation for efficacy in reducing HPS disease. Endothelial cell barrier functions are disrupted by a number of viruses that cause hemorrhagic, edematous, or neurologic disease, and as a result, our findings suggest that VEGFR2 and SFK inhibitors should be considered for regulating endothelial cell barrier functions altered by additional viral pathogens. PMID:21177802

Gorbunova, Elena E; Gavrilovskaya, Irina N; Pepini, Timothy; Mackow, Erich R

2011-03-01

241

Pyrotechnic Deflagration Velocity and Permeability.  

National Technical Information Service (NTIS)

Particle size, porosity, and permeability of the reactive material have long been considered to be important factors in propellant burning rates and the deflagration-to-detonation transition in explosives. It is reasonable to assume that these same parame...

D. R. Begeal P. L. Stanton

1982-01-01

242

Consolidation and compaction as a means to prevent settlement of bentonite\\/sandy silt mixes for use in waste disposal sites. [Low permeability mixture for caps and lining of waste disposal sites  

Microsoft Academic Search

The texture of the local Los Alamos tuff is that of a sandy silt with a high hydraulic conductivity. The permeability is dramatically decreased by addition of small amounts of bentonite. The coefficient of consolidation for bentonite\\/sandy silt ratios decreases inversely proportional with the square of that ratio, whereas the compression index, the swelling index, and the permeability change index

Abeele

1985-01-01

243

Fibrin endothelial interaction increases pulmonary endothelial permeability in vitro  

SciTech Connect

Fibrin has been implicated in the genesis of lung vascular injury. They examined the effect of adherence of fibrin to endothelial cells on endothelial permeability to protein. Bovine pulmonary arterial endothelial cells (EC) were grown to confluence on a gelatinized polycarbonate micropore filter and mounted in a chamber in which the luminal and abluminal media could be sampled. Fibrin was deposited on the endothelium by adding sheep fibrinogen (0.5 mg/ml) in Dulbecco's Modified Eagle Medium (DMEM) to the luminal surface of the endothelium, and then clotting the fibrinogen with 1 U/ml ..cap alpha..-thrombin. The fibrin was kept in contact with the endothelium for 3 hrs in an incubator at 37/sup 0/C plus 5% CO/sub 2/. The endothelial permeability to albumin was assessed by measurement of /sup 125/I-albumin clearance after removal of the fibrin clot from the endothelium. Therefore, fibrin contact with the endothelium independently induces an increase in endothelial permeability to albumin. The reversibility implies a transient change in the permeability dependent on the fibrin endothelial interaction.

Lo, S.K.; Del Vecchio, P.J.; Malik, A.B.

1986-03-05

244

Structural mechanisms of acute VEGF effect on microvessel permeability.  

PubMed

To investigate the ultrastructural mechanisms of acute microvessel hyperpermeability by vascular endothelial growth factor (VEGF), we combined a mathematical model (J Biomech Eng 116: 502-513, 1994) with experimental data of the effect of VEGF on microvessel hydraulic conductivity (L(p)) and permeability of various-sized solutes. We examined the effect of VEGF on microvessel permeability to a small solute (sodium fluorescein, Stokes radius 0.45 nm), an intermediate solute (alpha-lactalbumin, Stokes radius 2.01 nm), and a large solute [albumin (BSA), Stokes radius 3.5 nm]. Exposure to 1 nM VEGF transiently increased apparent permeability to 2.3, 3.3, and 6.2 times their baseline values for sodium fluorescein, alpha-lactalbumin, and BSA, respectively, within 30 s, and all returned to control within 2 min. On the basis of L(p) (DO Bates and FE Curry. Am J Physiol Heart Circ Physiol 271: H2520-H2528, 1996) and permeability data, the prediction from the model suggested that the most likely structural changes in the interendothelial cleft induced by VEGF would be a approximately 2.5-fold increase in its opening width and partial degradation of the surface glycocalyx. PMID:12560209

Fu, Bingmei M; Shen, Shang

2003-06-01

245

Small intestinal permeability in older adults.  

PubMed

Abstract It is not yet clear whether intestinal mucosal permeability changes with advancing age in humans. This question is of high importance for drug and nutrition approaches for older adults. Our main objective was to answer the question if small intestinal barrier integrity deteriorates with healthy aging. We conducted a cross-sectional study including the pooled data of 215 nonsmoking healthy adults (93 female/122 male), 84 of whom were aged between 60 and 82 years. After a 12-h fast, all participants ingested 10 g of lactulose and 5 g of mannitol. Urine was collected for 5 h afterwards and analyzed for test sugars. The permeability index (PI = lactulose/mannitol) was used to assess small intestinal permeability. Low-grade inflammation defined by high-sensitivity C-reactive protein ?1 mL/L and kidney function (estimated glomerular filtration rate) were determined in the older age group. The PI was similar in older compared to younger adults (P = 0.887). However, the urinary recovery of lactulose and mannitol was lower in the older adults and this change was neither associated with urinary volume nor glomerular filtration rate. The PI was not significantly correlated with low-grade inflammation or presence of noninsulin-dependent type 2 diabetes. However, it significantly deteriorated in the copresence of both conditions compared to low-grade inflammation alone (P = 0.043) or type 2 diabetes alone (P = 0.015). Small intestinal mucosal barrier does not deteriorate with age per se. But low-grade inflammation coupled with minor disease challenges, such as type 2 diabetes, can compromise the small intestinal barrier. PMID:24771689

Valentini, Luzia; Ramminger, Sara; Haas, Verena; Postrach, Elisa; Werich, Martina; Fischer, André; Koller, Michael; Swidsinski, Alexander; Bereswill, Stefan; Lochs, Herbert; Schulzke, Jörg-Dieter

2014-01-01

246

Small intestinal permeability in older adults  

PubMed Central

Abstract It is not yet clear whether intestinal mucosal permeability changes with advancing age in humans. This question is of high importance for drug and nutrition approaches for older adults. Our main objective was to answer the question if small intestinal barrier integrity deteriorates with healthy aging. We conducted a cross?sectional study including the pooled data of 215 nonsmoking healthy adults (93 female/122 male), 84 of whom were aged between 60 and 82 years. After a 12?h fast, all participants ingested 10 g of lactulose and 5 g of mannitol. Urine was collected for 5 h afterwards and analyzed for test sugars. The permeability index (PI = lactulose/mannitol) was used to assess small intestinal permeability. Low?grade inflammation defined by high?sensitivity C?reactive protein ?1 mL/L and kidney function (estimated glomerular filtration rate) were determined in the older age group. The PI was similar in older compared to younger adults (P =0.887). However, the urinary recovery of lactulose and mannitol was lower in the older adults and this change was neither associated with urinary volume nor glomerular filtration rate. The PI was not significantly correlated with low?grade inflammation or presence of noninsulin?dependent type 2 diabetes. However, it significantly deteriorated in the copresence of both conditions compared to low?grade inflammation alone (P =0.043) or type 2 diabetes alone (P =0.015). Small intestinal mucosal barrier does not deteriorate with age per se. But low?grade inflammation coupled with minor disease challenges, such as type 2 diabetes, can compromise the small intestinal barrier.

Valentini, Luzia; Ramminger, Sara; Haas, Verena; Postrach, Elisa; Werich, Martina; Fischer, Andre; Koller, Michael; Swidsinski, Alexander; Bereswill, Stefan; Lochs, Herbert; Schulzke, Jorg-Dieter

2014-01-01

247

Loss of the Endothelial Glycocalyx Links Albuminuria and Vascular Dysfunction  

PubMed Central

Patients with albuminuria and CKD frequently have vascular dysfunction but the underlying mechanisms remain unclear. Because the endothelial surface layer, a meshwork of surface-bound and loosely adherent glycosaminoglycans and proteoglycans, modulates vascular function, its loss could contribute to both renal and systemic vascular dysfunction in proteinuric CKD. Using Munich-Wistar-Fromter (MWF) rats as a model of spontaneous albuminuric CKD, multiphoton fluorescence imaging and single-vessel physiology measurements revealed that old MWF rats exhibited widespread loss of the endothelial surface layer in parallel with defects in microvascular permeability to both water and albumin, in both continuous mesenteric microvessels and fenestrated glomerular microvessels. In contrast to young MWF rats, enzymatic disruption of the endothelial surface layer in old MWF rats resulted in neither additional loss of the layer nor additional changes in permeability. Intravenous injection of wheat germ agglutinin lectin and its adsorption onto the endothelial surface layer significantly improved glomerular albumin permeability. Taken together, these results suggest that widespread loss of the endothelial surface layer links albuminuric kidney disease with systemic vascular dysfunction, providing a potential therapeutic target for proteinuric kidney disease.

Ferguson, Joanne K.; Burford, James L.; Gevorgyan, Haykanush; Nakano, Daisuke; Harper, Steven J.; Bates, David O.; Peti-Peterdi, Janos

2012-01-01

248

Permeabilities of Subduction Zone Sediments  

NASA Astrophysics Data System (ADS)

Permeabilities of subseafloor sediments control fluid expulsion from sediments as they are subducted or accreted and thus, compaction state, fluid overpressures, and deformation. We compare results from Integrated Ocean Drilling Program samples to compare to previously-developed permeability-porosity relationships for subduction zone sediments. Hemipelagic clay samples obtained from the incoming plate Kumano transect of the Nankai Trough (NanTroSEIZE) yield slightly lower permeability for a given porosity than previously reported results from Nankai Trough's Muroto transect and are lower than clay-rich sediments from the upper plate of CRISP offshore the Osa Peninsula of Costa Rica (CRISP). Samples from the Pacific Equatorial Transect (PEAT) and the South Pacific Gyre provide further insight to permeability behavior of sediments deposited in the Pacific basin. South Pacific Gyre sediments consist of slowly deposited pelagic clay with little biogenic or coarse clastic input. Measured permeabilities for given porosities are consistently lower than values reported for clay-rich sediments of Nankai and Costa Rica. PEAT samples comprise biogenic oozes and yield inconsistent results, with some of the highest permeabilities (10-14 m2) as well as some results similar to clay-rich sediments.

Screaton, E.; Gamage, K. R.; Daigle, H.; Harris, R. N.

2013-12-01

249

Complex vascular anomalies.  

PubMed

The classification system for vascular anomalies now used by experts worldwide comprises two distinct disease entities that differ in their biologic and pathologic features: vascular tumors and vascular malformations. Vascular tumors include infantile and congenital hemangiomas, tufted angiomas, and kaposiform hemangioendotheliomas. Infantile hemangiomas, the most common vascular anomaly, generally have a predetermined life cycle (proliferation and subsequent involution). GLUT-1, a glucose transporter, is a marker for these specific lesions during all phases of development. Vascular malformations are classified according to their vascular tissue of origin and include capillary, venous, arteriovenous, lymphatic, and mixed malformations. Complex lymphatic malformations and complex mixed malformations, which may have most vascular components, are the most difficult vascular malformations to successfully treat. These lesions are present at birth and often expand or grow in response to trauma, infection, or hormonal changes. Imaging advancements have enabled more accurate assessments and improved management of vascular anomalies. In addition, many lesions are now being managed with targeted pharmacologic therapy. Propranolol and steroids are used for complex or disfiguring tumors, and new anti-angiogenesis inhibitors such as sirolimus are selectively used to treat lymphatic and venous lymphatic malformations that are poorly responsive to sclerotherapy, embolization, and surgical excision. Multimodal therapies are often essential for complex lesions and require the combined expertise of an interdisciplinary team. PMID:23989523

Azizkhan, Richard G

2013-10-01

250

Geochemistry Index  

NSDL National Science Digital Library

This site is the index of a book used in a geochemistry course taught by W. M. White at Cornell University. There are 15 chapters and a table of contents available. All of the chapters are large PDF files and take some time to download. Figures and exercises accompany the text.

White, William M.; Department Of Earth And Atmospheric Sciences, Cornell U.

251

Cerebrospinal fluid and serum vascular endothelial growth factor and nitric oxide levels in newborns with hypoxic ischemic encephalopathy  

Microsoft Academic Search

Excitatory amino acids, cytokines and nitric oxide (NO) have been studied in the etiology and pathogenesis of hypoxic ischemic encephalopathy (HIE) of the newborn. Vascular endothelial growth factor (VEGF) is a known mediator of angiogenesis and has been shown to induce vascular proliferation and permeability via NO-mediated mechanism during hypoxia. The objective of this study was to investigate the cerebrospinal

Ebru Ergenekon; K?v?lc?m Gücüyener; Deniz Erba?; Sema Aral; Esin Koç; Y?ld?z Atalay

2004-01-01

252

Population Index  

NSDL National Science Digital Library

Two excellent bibliographic resources for population studies are the "Population Index" from the Office of Population Research at Princeton University, and "Population Organizations: Finder's Guide" from the Center for Demography and Ecology at the University of Wisconsin-Madison. "Population Index" is a quarterly publication that has been available since 1935. It "covers all fields of interest to demographers, including fertility, mortality, population size and growth, migration, nuptiality and the family, research methodology, projections and predictions, historical demography, and demographic and economic interrelations. Input is derived from original publications including monographs, journal articles, other serial publications, working papers, doctoral dissertations, machine-readable data files, and relevant acquisitions lists and bibliographies." About 3,500 citations are produced annually. Full text for the Index is available at the "Population Index" Web site for 1986-present (Vol. 52-present). Indexes can be searched by author, subject matter, geographical region, or publication year. There is now an experimental free text search capability for the 1994-present issues. "Population Organizations: Finder's Guide" is a no frills "practical tool for population professionals who need a single source for the quick location of organizations that publish and distribute or post population or family planning documents." It contains hundreds of citations, providing organization addresses, phone and FAX numbers, and Internet addresses when available. The Guide is updated every six months and is maintained by Ruth Sandor, Director of the Library of the Center for Demography and Ecology. Office of Population Research, Princeton University: http://opr.princeton.edu/ "Population Organizations: Finder's Guide": gopher://cde2.ssc.wisc.edu:70/00/addazlis gopher to: cde2.ssc.wisc.edu select: Population Organizations: Finder's Guide Center for Demography and Ecology, University of Wisconsin-Madison: http://www.ssc.wisc.edu/cde/

1986-01-01

253

Lung Vascular Cell Heterogeneity  

PubMed Central

The pulmonary circulation represents a unique vascular bed, receiving 100% of the cardiac output while maintaining low blood pressure. Multiple different cell types, including endothelium, smooth muscle, and fibroblasts, contribute to normal vascular function, and to the vascular response to injury. Our understanding of the basic cell biology of these various cell types, and the roles they play in vascular homeostasis and disease, remains quite limited despite several decades of study. Recent advances in approaches that enable the mapping of cell origin and the study of the molecular basis of structure and function have resulted in a rapid accumulation of new information that is essential to vascular biology. A recent National Institutes of Health workshop was held to discuss emerging concepts in lung vascular biology. The findings of this workshop are summarized in this article.

Stevens, Troy; Phan, Sem; Frid, Maria G.; Alvarez, Diego; Herzog, Erica; Stenmark, Kurt R.

2008-01-01

254

Neuroimaging of vascular dementia.  

PubMed

When atrophy is seen on imaging in adult patients, it does not necessarily represent Alzheimer disease. Many cases of dementia or cognitive decline could be caused by reversible or preventable diseases, such as vascular dementia. This article familiarizes the physician with various types of vascular lesions leading to dementia and cognitive decline and their imaging appearances. Neuroimaging plays an important role in identifying vascular lesions of the brain early, even before the clinical manifestation of the cognitive decline symptoms and, thus, can help to prevent or delay the symptoms related to the various vascular pathologic conditions. PMID:24582345

Kanekar, Sangam; Poot, Jeffrey D

2014-03-01

255

[Pulmonary vascular disease].  

PubMed

This review article discusses three topics related to pulmonary vascular disease: 1) pulmonary vascular changes associated with portal hypertension, 2) ANCA-associated pulmonary vasculitis, and 3) Takayasu's arteritis. Hepatopulmonary syndrome and pulmonary hypertension have recently been reported as pulmonary vascular changes accompanied with portal hypertension. Endogenous vasoactive agents that reach the pulmonary circulation through porto-systemic shunt vessels are thought to contribute to these vascular changes. In ANCA-associated vasculitis, hemorrhage, interstitial pneumonitis, and nodular lesions are common manifestations in the lung. In Takayasu's arteritis, CT occasionally demonstrates mosaic attenuation owing to pulmonary arteritis and peripheral reticulolinear changes probably due to thromboembolism. PMID:11321813

Takahashi, K

2001-03-01

256

The effects of elongation on the permeability and conduction characteristics of peripheral nerve  

SciTech Connect

The present studies analyze the effects of quasi-static tensile loading on the conduction and permeability characteristics of mouse sciatic nerve. Mechanical evaluations of nerve and roots were made via force and photographic records taken during elongation. Using strains to the proportional limit, functional properties of nerve were investigated. Recording of compound action potentials (CAP) during stretch yielded reductions in CAP velocity, slope, and area. Increments were observed in rise time, fall time, and duration. Vascular permeability was investigated for identical strains. SDS-PAGE analyses of nerve proteins yielded minimal changes in albumin concentration with stretch. Paper chromatography analyses of endoneurial fluid showed increments in amino acid concentrations during stretch. Perineurium permeability was studied using radiolabel techniques. Nerve stretch resulted in increased {sup 14}C-dextran accumulation at higher strains with additional accumulation during relaxation. Perineurial permeability increases were attributed to expansion of perineurial holes during stretch.

Beel, J.A.

1989-01-01

257

Paranodal permeability in `myelin mutants'  

PubMed Central

Fluorescent dextran tracers of varying sizes have been used to assess paranodal permeability in myelinated sciatic nerve fibers from control and three `myelin mutant' mice, Caspr-null, cst-null and shaking. We demonstrate that in all of these the paranode is permeable to small tracers (3kDa, 10kDa), which penetrate most fibers, and to larger tracers (40kDa, 70kDa), which penetrate far fewer fibers and move shorter distances over longer periods of time. Despite gross diminution in transverse bands in the Caspr-null and cst-null mice, the permeability of their paranodal junctions is equivalent to that in controls. Thus, deficiency of transverse bands in these mutants does not increase the permeability of their paranodal junctions to the dextrans we used, moving from the perinodal space through the paranode to the internodal periaxonal space. In addition, we show that the shaking mice, which have thinner myelin and shorter paranodes, show increased permeability to the same tracers despite the presence of transverse bands. We conclude that the extent of penetration of these tracers does not depend on the presence or absence of transverse bands but does depend on the length of the paranode and, in turn, on the length of `pathway 3', the helical extracellular pathway that passes through the paranode parallel to the lateral edge of the myelin sheath.

Shroff, S.; Mierzwa, A.; Scherer, S.S.; Peles, E.; Arevalo, J.C.; Chao, M.V.; Rosenbluth, J.

2011-01-01

258

Pyrotechnic deflagration velocity and permeability  

SciTech Connect

Particle size, porosity, and permeability of the reactive material have long been considered to be important factors in propellant burning rates and the deflagration-to-detonation transition in explosives. It is reasonable to assume that these same parameters will also affect the deflagration velocity of pyrotechnics. This report describes an experimental program that addresses the permeability of porous solids (particulate beds), in terms of particle size and porosity, and the relationship between permeability and the behavior of pyrotechnics and explosives. The experimental techniques used to acquire permeability data and to characterize the pyrotechnic burning are discussed. Preliminary data have been obtained on the burning characteristics of titanium hydride/potassium perchlorate (THKP) and boron/calcium chromate (BCCR). With THKP, the velocity of a pressure wave (from hot product gases) in the unburned region shows unsteady behavior which is related to the initial porosity or permeability. Simultaneous measurements with pressure gauges and ion gauges reveal that the pressure wave precedes the burn front. Steady burning of BCCR was observed with pressure gauge diagnostics and with a microwave interferometry technique.

Begeal, D R; Stanton, P L

1982-01-01

259

Rk1, a Ginsenoside, Is a New Blocker of Vascular Leakage Acting through Actin Structure Remodeling  

PubMed Central

Endothelial barrier integrity is essential for vascular homeostasis and increased vascular permeability and has been implicated in many pathological processes, including diabetic retinopathy. Here, we investigated the effect of Rk1, a ginsenoside extracted from sun ginseng, on regulation of endothelial barrier function. In human retinal endothelial cells, Rk1 strongly inhibited permeability induced by VEGF, advanced glycation end-product, thrombin, or histamine. Furthermore, Rk1 significantly reduced the vessel leakiness of retina in a diabetic mouse model. This anti-permeability activity of Rk1 is correlated with enhanced stability and positioning of tight junction proteins at the boundary between cells. Signaling experiments revealed that Rk1 induces phosphorylation of myosin light chain and cortactin, which are critical regulators for the formation of the cortical actin ring structure and endothelial barrier. These findings raise the possibility that ginsenoside Rk1 could be exploited as a novel prototype compound for the prevention of human diseases that are characterized by vascular leakage.

Maeng, Yong-Sun; Maharjan, Sony; Kim, Jeong-Hun; Park, Jeong-Hill; Suk Yu, Young; Kim, Young-Myoung; Kwon, Young-Guen

2013-01-01

260

Vascular ring diagnosis following respiratory arrest.  

PubMed

Vascular rings can present with non-specific respiratory and/or oesophageal symptoms. Early diagnosis requires a high index of suspicion. This case report describes an uncommon acute presentation of a vascular ring. We report a thriving 14-month-old child with a long history of recurrent wheeze and 'noisy breathing'. He presented acutely with food bolus impaction in the oesophagus which led to a respiratory arrest. Oesophagoscopy and bronchoscopy suggested vascular ring anomaly. A contrast-enhanced CT scan demonstrated a right-sided aortic arch with left ligamentum arteriosum encircling the oesophagus and airway. The ligament was ligated and divided. At follow-up 6?months later, the infant had mild persistent stridor but was otherwise well. PMID:24895385

Robson, Evie Alexandra; Scott, Alison; Chetcuti, Philip; Crabbe, David

2014-01-01

261

The role of dispersive magnetic permeability in ultrashort electromagnetic pulse propagation in nonlinear metamaterials  

Microsoft Academic Search

Compared to the non-magnetic ordinary dielectrics, the negative-index metamaterials have not only a dispersive electric permittivity but also a dispersive magnetic permeability. The purpose of this paper is to identify the role of dispersive magnetic permeability in nonlinear propagation of ultrashort electromagnetic pulses in metamaterials. Firstly, we derived a generalized system of coupled three-dimensional nonlinear Schroedinger equations suitable for few-cycle

Shuangchun Wen; Qiang Lv; Xi Cheng; Leyong Jiang; Wenhua Su

2007-01-01

262

Vascular Plant Image Gallery  

NSDL National Science Digital Library

Texas A&M University's Bioinformatics Working Group offers this no-nonsense botany teaching resource. Vascular plants are arranged alphabetically by family from Acanthaceae to Zygophyllaceae and users simply click for the images. Brief descriptions are provided (which may indicate the popular name of the plant). The site is searchable. Familiarity with vascular plant taxonomic nomenclature is assumed.

Manhart, James R.

263

Vascular Microenvironment in Gliomas  

Microsoft Academic Search

Structural and functional abnormalities of the vascular microenvironment determine pathophysiological characteristics of gliomas, such as loss of blood–brain barrier function, tumor cell invasiveness, or permselectivity for large molecules. Moreover, the effectiveness of various therapeutic strategies critically depends upon the successful transvascular delivery of molecules. In order to shed more light on the vascular microenvironment in gliomas, a variety of experimental

Peter Vajkoczy; Michael D. Menger

2000-01-01

264

Perspectives for vascular genomics  

Microsoft Academic Search

Diseases of the vascular system result from a complex mixture of genetic and environmental factors. Data sets, technologies and strategies emanating from the human genome programme have been applied to the analysis of both rare single-gene and common multigenic vascular disorders. Genomic approaches including inter- and intraspecies sequence comparisons, genotyping with dense marker sets spanning the genome, large-scale mutagenesis screens

Alan Tall; Edward M. Rubin

2000-01-01

265

Thromboxane A{sub 2} increases endothelial permeability through upregulation of interleukin-8  

SciTech Connect

Thromboxane A{sub 2} (TXA{sub 2}), a major prostanoid formed from prostaglandin H{sub 2} by thromboxane synthase, is involved in the pathogenesis of a variety of vascular diseases. In this study, we report that TXA{sub 2} mimetic U46619 significantly increases the endothelial permeability both in vitro and in vivo. U46619 enhanced the expression and secretion of interleukin-8 (IL-8), a major inducer of vascular permeability, in endothelial cells. Promoter analysis showed that the U46619-induced expression of IL-8 was mainly regulated by nuclear factor-{kappa}B (NF-{kappa}B). U46619 induced the activation of NF-{kappa}B through I{kappa}B kinase (IKK) activation, I{kappa}B phosphorylation and NF-{kappa}B nuclear translocation. Furthermore, the inhibition of IL-8 or blockade of the IL-8 receptor attenuated the U46619-induced endothelial cell permeability by modulating the cell-cell junctions. Overall, these results suggest that U46619 promotes vascular permeability through the production of IL-8 via NF-{kappa}B activation in endothelial cells.

Kim, Su-Ryun [School of Dentistry and Research Institute for Oral Biotechnology, Pusan National University, Yangsan 626-870 (Korea, Republic of) [School of Dentistry and Research Institute for Oral Biotechnology, Pusan National University, Yangsan 626-870 (Korea, Republic of); Medical Research Center for Ischemic Tissue Regeneration and School of Medicine, Pusan National University, Yangsan 626-870 (Korea, Republic of); Bae, Soo-Kyung [Medical Research Center for Ischemic Tissue Regeneration and School of Medicine, Pusan National University, Yangsan 626-870 (Korea, Republic of)] [Medical Research Center for Ischemic Tissue Regeneration and School of Medicine, Pusan National University, Yangsan 626-870 (Korea, Republic of); Park, Hyun-Joo; Kim, Mi-Kyoung [School of Dentistry and Research Institute for Oral Biotechnology, Pusan National University, Yangsan 626-870 (Korea, Republic of)] [School of Dentistry and Research Institute for Oral Biotechnology, Pusan National University, Yangsan 626-870 (Korea, Republic of); Kim, Koanhoi [Medical Research Center for Ischemic Tissue Regeneration and School of Medicine, Pusan National University, Yangsan 626-870 (Korea, Republic of)] [Medical Research Center for Ischemic Tissue Regeneration and School of Medicine, Pusan National University, Yangsan 626-870 (Korea, Republic of); Park, Shi-Young [Department of Molecular Biology, Pusan National University, Pusan 609-735 (Korea, Republic of)] [Department of Molecular Biology, Pusan National University, Pusan 609-735 (Korea, Republic of); Jang, Hye-Ock; Yun, Il [School of Dentistry and Research Institute for Oral Biotechnology, Pusan National University, Yangsan 626-870 (Korea, Republic of)] [School of Dentistry and Research Institute for Oral Biotechnology, Pusan National University, Yangsan 626-870 (Korea, Republic of); Kim, Yung-Jin; Yoo, Mi-Ae [Department of Molecular Biology, Pusan National University, Pusan 609-735 (Korea, Republic of)] [Department of Molecular Biology, Pusan National University, Pusan 609-735 (Korea, Republic of); Bae, Moon-Kyoung, E-mail: mkbae@pusan.ac.kr [School of Dentistry and Research Institute for Oral Biotechnology, Pusan National University, Yangsan 626-870 (Korea, Republic of)] [School of Dentistry and Research Institute for Oral Biotechnology, Pusan National University, Yangsan 626-870 (Korea, Republic of)

2010-07-02

266

Energy Characteristics of Permeable Thermoelements  

NASA Astrophysics Data System (ADS)

The construction of a permeable thermoelement that uses heat fluxes carried by a gas or liquid is presented. A method for thermoelement design on the basis of mathematical optimal control theory and computer simulation techniques is described. The results of research into a permeable planar thermoelement fabricated from Bi-Te-Se-Sb semiconductor materials are presented. The data obtained demonstrate the possibility of obtaining the desired temperature range for the optimal conditions, with energy efficiency exceeding that of conventional thermoelements by 8% to 17%. The basic theoretical principles and computer simulation results have been confirmed experimentally.

Cherkez, R. G.

2013-07-01

267

Preoperative cardiac testing before major vascular surgery  

Microsoft Academic Search

Conclusions  Preoperative risk assessment with a noninvasive stress test (MPS or DSE) is necessary only in high-risk patients without unnecessary\\u000a delay for vascular surgery. High-risk patients can easily be selected through the risk score index. Prophylactic revascularization\\u000a should only be performed in those with unstable coronary artery disease. The optimal perioperative medical treatment, especially\\u000a tight heart-rate control, is essential for decreasing

Sanne E. Hoeks; Olaf Schouten; Maureen J. van der Vlugt; Don Poldermans

2007-01-01

268

Iloprost attenuates the increased permeability in skeletal muscle after ischemia and reperfusion  

SciTech Connect

Increased vascular permeability is an early and sensitive indicator of ischemic muscle injury, occurring before significant histologic or radionuclide changes are evident. We investigated the effect of iloprost, a stable prostacyclin analog, on microvascular permeability in a rat striated muscle model. In six control and six experimental animals the cremaster muscle was dissected, placed in a closed-flow acrylic chamber, and suffused with a bicarbonate buffer solution. Dextran labeled with fluorescein was injected intravenously as a macromolecular tracer, and microvascular permeability was determined on the basis of clearance of the fluorescent tracer. Two hours of ischemia were followed by 2 hours of reperfusion. In the experimental group iloprost (0.5 microgram/kg/min) was given in a continuous intravenous infusion. Microvascular permeability increased significantly during reperfusion in both control and experimental animals (p less than 0.0001). Treatment with iloprost, however, significantly attenuated this response compared to the control group, 4.8 +/- 0.3 versus 7.3 +/- 0.5 microliters/gm/min, respectively (p less than 0.0001). Iloprost decreases the rise in vascular permeability after ischemia and reperfusion. Experimental clinical use of iloprost under controlled conditions in the treatment of patients with acute skeletal muscle ischemia appears justified.

Blebea, J.; Cambria, R.A.; DeFouw, D.; Feinberg, R.N.; Hobson, R.W. 2d.; Duran, W.N. (Univ. of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark (USA))

1990-12-01

269

VEGF Is Involved in the Increase of Dermal Microvascular Permeability Induced by Tryptase  

PubMed Central

Tryptases are predominantly mast cell-specific serine proteases with pleiotropic biological activities and play a critical role in skin allergic reactions, which are manifested with rapid edema and increases of vascular permeability. The exact mechanisms of mast cell tryptase promoting vascular permeability, however, are unclear and, therefore, we investigated the effect and mechanism of tryptase or human mast cells (HMC-1) supernatant on the permeability of human dermal microvascular endothelial cells (HDMECs). Both tryptase and HMC-1 supernatant increased permeability of HDMECs significantly, which was resisted by tryptase inhibitor APC366 and partially reversed by anti-VEGF antibody and SU5614 (catalytic inhibitor of VEGFR). Furthermore, addition of tryptase to HDMECs caused a significant increase of mRNA and protein levels of VEGF and its receptors (Flt-1 and Flk-1) by Real-time RT-PCR and Western blot, respectively. These results strongly suggest an important role of VEGF on the permeability enhancement induced by tryptase, which may lead to novel means of controlling allergic reaction in skin.

Bai, Qianming; Li, Xiaobo; Wang, Xinhong; Xu, Yali; Wang, Li; Zhang, Qingyong; Yin, Lianhua

2012-01-01

270

Heterogeneous Blood-Tumor Barrier Permeability Determines Drug Efficacy in Experimental Brain Metastases of Breast Cancer  

PubMed Central

Purpose Brain metastases of breast cancer appear to be increasing in incidence, confer significant morbidity, and threaten to compromise gains made in systemic chemotherapy. The blood-tumor barrier (BTB) is compromised in many brain metastases, however, the extent to which this influences chemotherapeutic delivery and efficacy is unknown. Herein, we answer this question by measuring BTB passive integrity, chemotherapeutic drug uptake, and anticancer efficacy in vivo in two breast cancer models that metastasize preferentially to brain. Experimental Design Experimental brain metastasis drug uptake and BTB permeability were simultaneously measured using novel fluorescent and phosphorescent imaging techniques in immune compromised mice. Drug-induced apoptosis and vascular characteristics were assessed using immunofluorescent microscopy. Results Analysis of >2000 brain metastases from two models (human 231-BR-Her2 and murine 4T1-BR5) demonstrated partial BTB permeability compromise in >89% lesions, varying in magnitude within and between metastases. Brain metastasis uptake of 14C- paclitaxel and 14C- doxorubicin was generally greater than normal brain but <15% of that of other tissues or peripheral metastases, and only reached cytotoxic concentrations in a small subset (~10%) of the most permeable metastases. Neither drug significantly decreased the experimental brain metastatic ability of 231-BR-Her2 tumor cells. BTB permeability was associated with vascular remodeling and correlated with over expression of the pericyte protein, desmin. Conclusions This work demonstrates that the BTB remains a significant impediment to standard chemotherapeutic delivery and efficacy in experimental brain metastases of breast cancer. New brain permeable drugs will be needed. Evidence is presented for vascular remodeling in BTB permeability alterations.

Lockman, Paul R.; Mittapalli, Rajendar K.; Taskar, Kunal S.; Rudraraju, Vinay; Gril, Brunilde; Bohn, Kaci A.; Adkins, Chris E.; Roberts, Amanda; Thorsheim, Helen R.; Gaasch, Julie A.; Huang, Suyun; Palmieri, Diane; Steeg, Patricia S.; Smith, Quentin R.

2010-01-01

271

Water permeability of phospholipid vesicles  

Microsoft Academic Search

Summary The water permeability of phospholipid vesicles 0.5 to 10 µ in diameter bounded by one or by several lipid bilayers was measured by following the change in turbidity of a suspension after mixing in a stopped flow apparatus. A semi-empirical formulation for evaluating volume changes of vesicles with a broad size range by measurement of turbidity is developed. The

J. P. Reeves; R. M. Dowben

1970-01-01

272

Microwave Silicon Permeable Base Transistor.  

National Technical Information Service (NTIS)

Silicon permeable base transistors (SiPBTs) have been fabricated, exhibiting a maximum available gain at 2 GHz of 11 dB and a 6 dB/octave decrement leading to a maximum frequency of oscillation (fmax) of 10 GHz. These SiPBTs differ in structural detail fr...

D. D. Rathman N. P. Economou D. J. Silversmith R. W. Mountain S. M. Cabral

1982-01-01

273

Permeable Pavement Research ? Edison, NJ  

EPA Science Inventory

This presentation gives the rationale behind NRMRL?s decision to construct and test a permeable surface parking lot the Edison Environmental Center. It also describes the monitoring program and gives preliminary results. The presentation is being given at the request of the New...

274

Measurement of braided preform permeability  

Microsoft Academic Search

Permeability is an important parameter in the simulation of resin transfer moulding (RTM) process. This is particularly so in the case of 3D braided preform reinforced composites, which have no distinct layers and consequently generally have higher levels of structural integrity than traditional laminated composites. Such braided preforms have the potential for widespread application in aerospace, marine, civil construction structures.

Xiaoqing Wu; Jialu Li; R. Ajit Shenoi

2006-01-01

275

Tumor necrosis factor alpha-induced pulmonary vascular endothelial injury.  

PubMed Central

Tumor necrosis factor alpha (TNF-alpha) mediates components of the acute-phase response, stimulates granulocyte metabolism, and induces endothelial cell surface changes. We studied whether human recombinant TNF-alpha (rTNF-alpha) could increase pulmonary edema formation and pulmonary vascular permeability. Rabbits preinfused with 125I-albumin were administered rTNF-alpha or saline. Animals were sacrificed, and lung wet/dry weight ratios as well as bronchoalveolar lavage fluid and plasma 125I activities were determined. rTNF-alpha increased lung wet/dry weight ratios by 151% (P less than 0.02) and bronchoalveolar lavage fluid/plasma 125I activity ratios by 376% (P less than 0.01) compared with values for saline controls. Electron microscopy of lung sections demonstrated endothelial injury, perivascular edema, and extravasation of an ultrastructural permeability tracer. To demonstrate that rTNF-alpha could directly increase pulmonary vascular endothelial permeability in vitro, we studied albumin transfer across cultured porcine pulmonary artery endothelial cell monolayers. rTNF-alpha induced time-dependent dose-response increments in transendothelial albumin flux in the absence of granulocyte effector cells. These observations suggest that rTNF-alpha can provoke acute pulmonary vascular endothelial injury in vivo as well as in vitro. Images

Goldblum, S E; Hennig, B; Jay, M; Yoneda, K; McClain, C J

1989-01-01

276

Vascular Access in Children  

SciTech Connect

Establishment of stable vascular access is one of the essential and most challenging procedures in a pediatric hospital. Many clinical specialties provide vascular service in a pediatric hospital. At the top of the 'expert procedural pyramid' is the pediatric interventional radiologist, who is best suited and trained to deliver this service. Growing awareness regarding the safety and high success rate of vascular access using image guidance has led to increased demand from clinicians to provide around-the-clock vascular access service by pediatric interventional radiologists. Hence, the success of a vascular access program, with the pediatric interventional radiologist as the key provider, is challenging, and a coordinated multidisciplinary team effort is essential for success. However, there are few dedicated pediatric interventional radiologists across the globe, and also only a couple of training programs exist for pediatric interventions. This article gives an overview of the technical aspects of pediatric vascular access and provides useful tips for obtaining vascular access in children safely and successfully using image guidance.

Krishnamurthy, Ganesh, E-mail: krishnamurthy@email.chop.edu; Keller, Marc S. [Children's Hospital of Philadelphia, Department of Radiology (United States)

2011-02-15

277

Vascular-Leukocyte Interactions  

PubMed Central

Transformation of uterine spiral arteries is critical for healthy human pregnancy. We recently proposed a role for maternal leukocytes in decidual spiral artery remodeling and suggested that matrix metalloprotease (MMP) activity contributed to the destruction of the arterial wall. In the current study we used our first trimester placental-decidual co-culture (PDC) model to define the temporal relationship and test the mechanistic aspects of this process. PDC experiments were assessed by image analysis over a six-day time-course for degree of vascular transformation and leukocyte distribution around progressively remodeled arterioles. We observed rapid transformation in PDCs associated with loss of vascular smooth muscle cells, widening of the vessel lumen, and significant accumulation of uterine Natural Killer cells and macrophages within the vascular wall (P < 0.001) before trophoblast presence in the vessel lumens. These events did not occur in decidua-only cultures. Active MMP-9 was detected in leukocytes and vascular cells of remodeling arterioles, and inhibition of MMP-2/9 activity in PDC resulted in failure of decidual vascular remodeling compared with vehicle-treated PDCs. Apoptosis of vascular cells, macrophage-mediated phagocytosis, and vascular smooth muscle cell dedifferentiation contributed to the remodeling observed. The PDC model indicates that placental presence is required to initiate decidual spiral artery remodeling but that uterine Natural Killer cells and macrophages mediate the early stages of this process at the cellular level.

Hazan, Aleah D.; Smith, Samantha D.; Jones, Rebecca L.; Whittle, Wendy; Lye, Stephen J.; Dunk, Caroline E.

2010-01-01

278

Nanomedicine for drug targeting: strategies beyond the enhanced permeability and retention effect  

PubMed Central

The growing research interest in nanomedicine for the treatment of cancer and inflammatory-related pathologies is yielding encouraging results. Unfortunately, enthusiasm is tempered by the limited specificity of the enhanced permeability and retention effect. Factors such as lack of cellular specificity, low vascular density, and early release of active agents prior to reaching their target contribute to the limitations of the enhanced permeability and retention effect. However, improved nanomedicine designs are creating opportunities to overcome these problems. In this review, we present examples of the advances made in this field and endeavor to highlight the potential of these emerging technologies to improve targeting of nanomedicine to specific pathological cells and tissues.

Nehoff, Hayley; Parayath, Neha N; Domanovitch, Laura; Taurin, Sebastien; Greish, Khaled

2014-01-01

279

Vascular regrowth following photodynamic therapy in the chicken embryo chorioallantoic membrane  

Microsoft Academic Search

Photodynamic therapy (PDT) induces damage to the endothelium, which can lead to increased vascular permeability and, under\\u000a intensive PDT conditions, even to platelet aggregation, vasoconstriction, and blood flow stasis. Eventually, ischemia, hypoxia,\\u000a and inflammation can occur, resulting in angiogenesis. We studied the sequence of the vascular events after Visudyne®-PDT in the chicken chorioallantoic membrane (CAM) at day 11 of development.

Patrycja Nowak-SliwinskaJudy; Judy R. van Beijnum; Maaike van Berkel; Hubert van den Bergh; Arjan W. Griffioen

2010-01-01

280

Expression of vascular endothelial growth factor in primary non-small cell lung carcinoma  

Microsoft Academic Search

Objective: Tumor growth depends on angiogenesis. The aim of this paper is to clarify the relationship between the expression\\u000a of vascular endothelial growth factor (VEGF)\\/vascular permeability factor (VPF) and the angiogenesis, or growth, or invasion\\u000a and prognostic value in Non-Small Cell Lung Cancer (NSCLC). Methods: Microvessel quantification and expression of VEGF was\\u000a performed immunohistochemically, using multiclonal antibodies against endothelial protein

Zhang Lijian; Yang Guoli; Xie Yuquan; Xu Weiguo

1999-01-01

281

Vascular endothelial growth factor and its receptors in normal human testicular tissue  

Microsoft Academic Search

Expression of vascular endothelial growth factor (VEGF), also known as vascular permeability factor (VPF), and its receptors Flt-1 and KDR (Flk-1 in mouse) and their localization in the human testis were analyzed by means of reverse transcriptase-polymerase chain reaction (RT-PCR), Western blotting and immunohistochemistry. VEGF mRNA was detected in the human testicular tissue and in fragments of seminiferous tubules by

S Ergün; N Kiliç; W Fiedler; A. K Mukhopadhyay

1997-01-01

282

Dissolution-Driven Permeability Reduction of a Fractured Carbonate Caprock  

SciTech Connect

Geochemical reactions may alter the permeability of leakage pathways in caprocks, which serve a critical role in confining CO{sub 2} in geologic carbon sequestration. A caprock specimen from a carbonate formation in the Michigan sedimentary Basin was fractured and studied in a high-pressure core flow experiment. Inflowing brine was saturated with CO{sub 2} at 40°C and 10?MPa, resulting in an initial pH of 4.6, and had a calcite saturation index of ?0.8. Fracture permeability decreased during the experiment, but subsequent analyses did not reveal calcite precipitation. Instead, experimental observations indicate that calcite dissolution along the fracture pathway led to mobilization of less soluble mineral particles that clogged the flow path. Analyses of core sections via electron microscopy, synchrotron-based X-ray diffraction imaging, and the first application of microbeam Ca K-edge X-ray absorption near edge structure, provided evidence that these occlusions were fragments from the host rock rather than secondary precipitates. X-ray computed tomography showed a significant loss of rock mass within preferential flow paths, suggesting that dissolution also removed critical asperities and caused mechanical closure of the fracture. The decrease in fracture permeability despite a net removal of material along the fracture pathway demonstrates a nonintuitive, inverse relationship between dissolution and permeability evolution in a fractured carbonate caprock.

Ellis, Brian R.; Fitts, Jeffrey P.; Bromhal, Grant S.; McIntyre, Dustin L.; Tappero, Ryan; Peters, Catherine

2013-04-01

283

Vascular inflammation and endothelial dysfunction in fracture healing.  

PubMed

Angiogenesis is an important step in bone fracture healing. In this article, we report on the healing of long bone fractures, and the involvement of the vascular and the inflammatory systems in the process. We conducted a prospective study of 20 healthy adults with traumatic long bone fracture. One week after fracture, and then 1 month later, we evaluated markers of inflammation: vascular responsiveness (brachial endothelial function and ankle brachial index) and inflammatory and cytokine levels osteopontin [OPN], E-selectin, and vascular endothelial growth factor [VEGF]). Long bone fractures caused intense vascular and inflammatory responses, represented by high levels of OPN, Eselectin, and VEGF. In vivo measurements demonstrated severe endothelial dysfunction, which could support the idea that the vascular system is recruited to build new blood vessels that support bone regeneration. PMID:22482094

Blum, Arnon; Zarqh, Oleg; Peleg, Aviva; Sirchan, Rizak; Blum, Nava; Salameh, Yosef; Ganaem, Maged

2012-02-01

284

Endothelial Fli1 Deficiency Impairs Vascular Homeostasis  

PubMed Central

Systemic sclerosis or scleroderma (SSc) is a complex autoimmune connective tissue disease characterized by obliterative vasculopathy and tissue fibrosis. The molecular mechanisms underlying SSc vasculopathy are largely unknown. Friend leukemia integration factor 1 (Fli1), an important regulator of immune function and collagen fibrillogenesis, is expressed at reduced levels in endothelial cells in affected skin of patients with SSc. To develop a disease model and to investigate the function of Fli1 in the vasculature, we generated mice with a conditional deletion of Fli1 in endothelial cells (Fli1 CKO). Fli1 CKO mice showed a disorganized dermal vascular network with greatly compromised vessel integrity and markedly increased vessel permeability. We show that Fli1 regulates expression of genes involved in maintaining vascular homeostasis including VE-cadherin, platelet endothelial cell adhesion molecule 1, type IV collagen, matrix metalloproteinase 9, platelet-derived growth factor B, and S1P1 receptor. Accordingly, Fli1 CKO mice are characterized by down-regulation of VE-cadherin and platelet endothelial cell adhesion molecule 1, impaired development of basement membrane, and a decreased presence of ?-smooth muscle actin-positive cells in dermal microvessels. This phenotype is consistent with a role of Fli1 as a regulator of vessel maturation and stabilization. Importantly, vascular characteristics of Fli1 CKO mice are recapitulated by SSc microvasculature. Thus, persistently reduced levels of Fli1 in endothelial cells may play a critical role in the development of SSc vasculopathy.

Asano, Yoshihide; Stawski, Lukasz; Hant, Faye; Highland, Kristin; Silver, Richard; Szalai, Gabor; Watson, Dennis K.; Trojanowska, Maria

2010-01-01

285

Permeable Wall Effects on Poiseuille Flow.  

National Technical Information Service (NTIS)

The effects of permeable walls on Poiseuille flow were investigated. Due to the transfer of forward momentum across the permeable interface, a very thin boundary layer region is induced within the porous material adjacent to the interface. The boundary la...

P. L. F. Liu

1979-01-01

286

Radiation Effects on the Cytoskeleton of Endothelial Cells and Endothelial Monolayer Permeability  

SciTech Connect

Purpose: To investigate the effects of radiation on the endothelial cytoskeleton and endothelial monolayer permeability and to evaluate associated signaling pathways, which could reveal potential mechanisms of known vascular effects of radiation. Methods and Materials: Cultured endothelial cells were X-ray irradiated, and actin filaments, microtubules, intermediate filaments, and vascular endothelial (VE)-cadherin junctions were examined by immunofluorescence. Permeability was determined by the passage of fluorescent dextran through cell monolayers. Signal transduction pathways were analyzed using RhoA, Rho kinase, and stress-activated protein kinase-p38 (SAPK2/p38) inhibitors by guanosine triphosphate-RhoA activation assay and transfection with RhoAT19N. The levels of junction protein expression and phosphorylation of myosin light chain and SAPK2/p38 were assessed by Western blotting. The radiation effects on cell death were verified by clonogenic assays. Results: Radiation induced rapid and persistent actin stress fiber formation and redistribution of VE-cadherin junctions in microvascular, but not umbilical vein endothelial cells, and microtubules and intermediate filaments remained unaffected. Radiation also caused a rapid and persistent increase in microvascular permeability. RhoA-guanosine triphosphatase and Rho kinase were activated by radiation and caused phosphorylation of downstream myosin light chain and the observed cytoskeletal and permeability changes. SAPK2/p38 was activated by radiation but did not influence either the cytoskeleton or permeability. Conclusion: This study is the first to show rapid activation of the RhoA/Rho kinase by radiation in endothelial cells and has demonstrated a link between this pathway and cytoskeletal remodeling and permeability. The results also suggest that the RhoA pathway might be a useful target for modulating the permeability and other effects of radiation for therapeutic gain.

Gabrys, Dorota [Department of Radiation Oncology, Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Gliwice Branch, Gliwice (Poland); Greco, Olga [Cancer Research UK Tumour Microcirculation Group, Academic Unit of Surgical Oncology, University of Sheffield, School of Medicine and Biomedical Sciences, Sheffield (United Kingdom); Patel, Gaurang; Prise, Kevin M. [Centre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast, Northern Ireland (United Kingdom); Tozer, Gillian M. [Cancer Research UK Tumour Microcirculation Group, Academic Unit of Surgical Oncology, University of Sheffield, School of Medicine and Biomedical Sciences, Sheffield (United Kingdom); Kanthou, Chryso [Cancer Research UK Tumour Microcirculation Group, Academic Unit of Surgical Oncology, University of Sheffield, School of Medicine and Biomedical Sciences, Sheffield (United Kingdom)], E-mail: C.Kanthou@sheffield.ac.uk

2007-12-01

287

Vascular adaptation to a dysfunctional endothelium as a consequence of Shb deficiency  

PubMed Central

Vascular endothelial growth factor (VEGF)-A regulates angiogenesis, vascular morphology and permeability by signaling through its receptor VEGFR-2. The Shb adapter protein has previously been found to relay certain VEGFR-2 dependent signals and consequently vascular physiology and structure was assessed in Shb knockout mice. X-ray computed tomography of vessels larger than 24 ?m diameter (micro-CT) after contrast injection revealed an increased frequency of 48–96 ?m arterioles in the hindlimb calf muscle in Shb knockout mice. Intravital microscopy of the cremaster muscle demonstrated a less regular vasculature with fewer branch points and increased vessel tortuosity, changes that led to an increased blood flow velocity. Reduced in vivo angiogenesis was observed in Shb knockout Matrigel™ plugs. Unlike the wild-type situation, VEGF-A did not provoke a dissociation of VE-cadherin from adherens junctions in Shb knockout venules. The reduced angiogenesis and altered properties of junctions had consequences for two patho-physiological responses to arterial occlusion: vascular permeability was reduced in the Shb knockout cremaster muscle after ligation of one supplying artery and heat-induced blood flow determined by Laser-Doppler measurements was decreased in the hindlimb after ligation of the femoral artery. Consequently, the Shb knockout mouse exhibited structural and functional (angiogenesis and vascular permeability) vascular abnormalities that have implications for understanding the function of VEGF-A under physiological conditions.

Christoffersson, Gustaf; Zang, Guangxiang; Zhuang, Zhen W.; Vagesjo, Evelina; Simons, Michael; Phillipson, Mia

2014-01-01

288

Vascular adaptation to a dysfunctional endothelium as a consequence of Shb deficiency.  

PubMed

Vascular endothelial growth factor (VEGF)-A regulates angiogenesis, vascular morphology and permeability by signaling through its receptor VEGFR-2. The Shb adapter protein has previously been found to relay certain VEGFR-2 dependent signals and consequently vascular physiology and structure was assessed in Shb knockout mice. X-ray computed tomography of vessels larger than 24 ?m diameter (micro-CT) after contrast injection revealed an increased frequency of 48-96 ?m arterioles in the hindlimb calf muscle in Shb knockout mice. Intravital microscopy of the cremaster muscle demonstrated a less regular vasculature with fewer branch points and increased vessel tortuosity, changes that led to an increased blood flow velocity. Reduced in vivo angiogenesis was observed in Shb knockout Matrigel™ plugs. Unlike the wild-type situation, VEGF-A did not provoke a dissociation of VE-cadherin from adherens junctions in Shb knockout venules. The reduced angiogenesis and altered properties of junctions had consequences for two patho-physiological responses to arterial occlusion: vascular permeability was reduced in the Shb knockout cremaster muscle after ligation of one supplying artery and heat-induced blood flow determined by Laser-Doppler measurements was decreased in the hindlimb after ligation of the femoral artery. Consequently, the Shb knockout mouse exhibited structural and functional (angiogenesis and vascular permeability) vascular abnormalities that have implications for understanding the function of VEGF-A under physiological conditions. PMID:22562363

Christoffersson, Gustaf; Zang, Guangxiang; Zhuang, Zhen W; Vågesjö, Evelina; Simons, Michael; Phillipson, Mia; Welsh, Michael

2012-09-01

289

Heart and vascular services  

MedlinePLUS

... Coronary angiography CT angiography (CTA) and magnetic resonance angiography (MRA) Echocardiogram PET scan of the heart Stress tests (many different types exist) Vascular ultrasound, such as carotid ultrasound Venous ultrasound of the arms and legs ...

290

On the permeability of fractal tube bundles  

Microsoft Academic Search

The permeability of a porous medium is strongly affected by its local geometry and connectivity, the size distribution of the solid inclusions and the pores available for flow. Since direct measurements of the permeability are time consuming and require experiments that are not always possible, the reliable theoretical assessment of the permeability based on the medium structural characteristics alone is

I. Zinovik; D. Poulikakos

2011-01-01

291

Vapor-liquid phase separator permeability results  

NASA Technical Reports Server (NTRS)

Continued studies are described in the area of vapor-liquid phase separator work with emphasis on permeabilities of porous sintered plugs (stainless steel, nominal pore size 2 micrometer). The temperature dependence of the permeability has been evaluated in classical fluid using He-4 gas at atmospheric pressure and in He-2 on the basis of a modified, thermosmotic permeability of the normal fluid.

Yuan, S. W. K.; Frederking, T. H. K.

1981-01-01

292

Review of hydrogen isotope permeability through materials  

SciTech Connect

This report is the first part of a comprehensive summary of the literature on hydrogen isotope permeability through materials that do not readily form hydrides. While we mainly focus on pure metals with low permeabilities because of their importance to tritium containment, we also give data on higher-permeability materials such as iron, nickel, steels, and glasses.

Steward, S.A.

1983-08-15

293

[Complex vascular access].  

PubMed

Availability of a proper vascular access is a basic condition for a proper extracorporeal replacement in end-stage chronic renal failure. However, biological factors, management and other problems, may variously condition their middle-long term survival. Therefore, personal experience of over 25 years has been critically reviewed in order to obtain useful information. In particular "hard" situations necessitating complex procedures have been examined but, if possible, preserving the peripherical vascular features. PMID:9578652

Mangiarotti, G; Cesano, G; Thea, A; Hamido, D; Pacitti, A; Segoloni, G P

1998-03-01

294

Vascular endothelium in cancer  

Microsoft Academic Search

The vascular endothelium plays an essential role during organogenesis and in tissue homeostasis. Growing evidence also supports\\u000a its essential and complex role in tumour biology and cancer progression. In particular, excessive proliferation and transformation\\u000a or dysfunction of endothelial cells leads to pathological (lymph)angiogenesis or vascular malfunctions, which are hallmarks\\u000a of neoplastic and malignant disorders. Reciprocal interactions between endothelial cells and

Leonid L. Nikitenko

2009-01-01

295

Mediterranean Diet, Alzheimer Disease, and Vascular Mediation  

PubMed Central

Objectives To examine the association between the Mediterranean diet (MeDi) and Alzheimer disease (AD) in a different AD population and to investigate possible mediation by vascular pathways. Design, Setting, Patients, and Main Outcome Measures A case-control study nested within a community-based cohort in New York, NY. Adherence to the MeDi (0- to 9-point scale with higher scores indicating higher adherence) was the main predictor of AD status (194 patients with AD vs 1790 nondemented subjects) in logistic regression models that were adjusted for cohort, age, sex, ethnicity, education, apolipoprotein E genotype, caloric intake, smoking, medical comorbidity index, and body mass index (calculated as weight in kilograms divided by height in meters squared). We investigated whether there was attenuation of the association between MeDi and AD when vascular variables (stroke, diabetes mellitus, hypertension, heart disease, lipid levels) were simultaneously introduced in the models (which would constitute evidence of mediation). Results Higher adherence to the MeDi was associated with lower risk for AD (odds ratio, 0.76; 95% confidence interval, 0.67–0.87; P<.001). Compared with subjects in the lowest MeDi tertile, subjects in the middle MeDi tertile had an odds ratio of 0.47 (95% confidence interval, 0.29–0.76) and those at the highest tertile an odds ratio of 0.32 (95% confidence interval, 0.17–0.59) for AD (P for trend <.001). Introduction of the vascular variables in the model did not change the magnitude of the association. Conclusions We note once more that higher adherence to the MeDi is associated with a reduced risk for AD. The association does not seem to be mediated by vascular comorbidity. This could be the result of either other biological mechanisms (oxidative or inflammatory) being implicated or measurement error of the vascular variables.

Scarmeas, Nikolaos; Stern, Yaakov; Mayeux, Richard; Luchsinger, Jose A.

2011-01-01

296

Iatrogenic vascular trauma.  

PubMed

With the increasing performance of percutaneous transluminal angioplasty and insertion of an increasing number of intravascular devices, the size of arterial punctures has been increasing. A consistent minority of these procedures will result in vascular injuries requiring treatment. At the same time, the regionalized nature of trauma care in the United States has resulted in a large number of vascular surgeons who are exposed to vascular trauma only when iatrogenic. The most common injuries observed are caused by percutaneous vascular instrumentation and include hemorrhage and pseudoaneurysm that may compress adjacent structures, fistula, acute occlusion, and embolization. Injuries unique to balloon angioplasty/stenting include arterial rupture and dissection. Indwelling intravascular devices are another common source of iatrogenic vascular injury ranging from arterial rupture to thrombosis and embolization. Much less common injuries are observed in orthopedic and abdominal/laparoscopic operations but show reproducible causes/patterns. Finally, pediatric iatrogenic vascular trauma is relatively common because of the small size of the vasculature, but the natural history and management is markedly different from that in adults. PMID:9876035

Nehler, M R; Taylor, L M; Porter, J M

1998-12-01

297

Deformational characteristics of rock in low permeable reservoir and their effect on permeability  

Microsoft Academic Search

In the development of oil and gas the pressure in the rocks of reservoir changes constantly and rocks are compressed and deformed. So their permeability reduces. And the production capacity of oil and gas well is affected by the permeability. This paper deals with the deformational characteristics of rocks in low permeable reservoir and their effect on the permeability. The

Hong-Xing Wang; Guan Wang; Ron C. K. Wong

2010-01-01

298

Changes in Mast Cells and in Permeability of Mesenteric Microvessels under the Effect of Immobilization and Electrostimulation.  

National Technical Information Service (NTIS)

It was shown that a reduction in the amount of mast cells in the mesentery and an increase in their degranulation was accompanied by an increase in vascular permeability of rat mesentery. It is supposed that immobilization and electrostimulation causing d...

M. P. Gorizontova

1980-01-01

299

Vascular Cognitive Deterioration and Stroke  

Microsoft Academic Search

Vascular cognitive impairment, the recent modification of the terminology related to vascular burden of the brain, reflects the all-encompassing effects of vascular disease or lesions on cognition. It incorporates the complex interactions between vascular aetiologies, risk factors and cellular changes within the brain and cognition. The concept covers the frequent poststroke cognitive impairment and dementia, as well as cerebrovascular disease

Timo Erkinjuntti

2007-01-01

300

Permeability enhancement using explosive techniques  

SciTech Connect

In situ recovery methods for many of our hydrocarbon and mineral resources depend on the ability to create or enhance permeability in the resource bed to allow uniform and predictable flow. To meet this need, a new branch of geomechanics devoted to computer prediction of explosive rock breakage and permeability enhancement has developed. The computer is used to solve the nonlinear equations of compressible flow, with the explosive behavior and constitutive properties of the medium providing the initial/boundary conditions and material response. Once the resulting computational tool has been verified and calibrated with appropriate large-scale field tests, it can be used to develop and optimize commercially useful explosive techniques for in situ resource recovery.

Adams, T.F.; Schmidt, S.C.; Carter, W.J.

1980-01-01

301

Experimental Volcanology: Fragmentation and Permeability  

NASA Astrophysics Data System (ADS)

An increasing number of scientists design new experiments to analyse processes that control the dynamics of explosive eruptions. There research is mostly coupled to numerical models and aims toward its controlling parameters. The fragmentation process, its threshold and the speed of the fragmentation wave as well as the energy consumed by the fragmentation are some hot spots of the experimental volcanology. Analysing the fragmentation behaviour of volcaniclastics as close to the natural system as possible, we found a number of physical constrains. Identifying the porosity as determining factor of the threshold, we realised that neither threshold nor the speed of the fragmentation process are solely controlled by the rock density. The later results of the shock tube type apparatus lead to the analysis of the specific surface area and permeability as direct links to textural features. Permeability analysis performed in a modified shock tube type apparatus, show two clear, distinct trends for dome rock and pyroclastic samples. The specific surface determined by Argon sorbtion (BET) as well as textural features of pumices from Campi Flegrei, Montserrat and Krakatoa (1883) give in contrary evidence of a more complex story. Large spherical, or ellipsoidal bubbles around fractured crystals prove that the high permeability of the pumice has partially developed after the fixing of the bubble size distribution. This puts up the question, if permeability measurements on pyroclastic samples reveal relevant numbers! The surface tension controlled 'self sealing' behaviour of surfaces from foaming obsidian hinders in situ measurements. Close textural investigations will have to clarify how the 'post process' samples deviate from the syneruptive conduit filling.

Spieler, O.

2005-12-01

302

Permeable barriers for groundwater remediation  

Microsoft Academic Search

Because of the limitations of conventional pump-and-treat systems in treating groundwater contaminants, permeable barriers are potentially more cost-effective than pump-and-treat systems for treating dissolved chlorinated solvent plumes, which may persist in the saturated zone for several decades. Other contaminants, such as chromium or other soluble heavy metals, can also be treated with this technology. The authors discuss the types of

A. R. Gavaskar; N. Gupta; B. Sass; R. Janosy

1998-01-01

303

Ascorbic Acid Prevents Increased Endothelial Permeability Caused by Oxidized Low Density Lipoprotein  

PubMed Central

Mildly oxidized low density lipoprotein (mLDL) acutely increases the permeability of the vascular endothelium to molecules that would not otherwise cross the barrier. We have shown that ascorbic acid tightens the permeability barrier in endothelial barrier in cells, so in this work we tested whether it might prevent the increase in endothelial permeability due to mLDL. Treatment of EA.hy926 endothelial cells with mLDL decreased intracellular GSH and activated the cells to further oxidize the mLDL. mLDL also increased endothelial permeability over 2 h to both inulin and ascorbate in cells cultured on semi-permeable filters. This effect was blocked by microtubule and microfilament inhibitors, but not by chelation of intracellular calcium. Intracellular ascorbate both prevented and reversed the mLDL-induced increase in endothelial permeability, an effect mimicked by other cell-penetrant antioxidants. These results suggest a role for endothelial cell ascorbate in ameliorating an important facet of endothelial dysfunction caused by mLDL.

May, James M.; Qu, Zhi-chao

2013-01-01

304

Effect of perfusate hematocrit on urea permeability-surface area in isolated dog lung  

SciTech Connect

Seven dog lower left lung lobes were statically inflated and perfused at a constant rate for each lobe with a perfusate in which the hematocrit was altered over a wide range. The permeability-surface area of urea was calculated from multiple indicator dilution curves using two separate injectates for each hematocrit level. One injectate contained only /sup 125/I-albumin as the vascular reference tracer and the other contained both /sup 51/Cr-erythrocytes and /sup 125/I-albumin as the vascular reference tracers; both contained (/sup 14/C)urea as the permeating tracer. The results strongly indicate that the phenomenon of erythrocyte trapping of urea does not affect the calculation of urea permeability-surface area product provided the appropriate albumin-erythrocyte composite reference tracer is utilized in its calculation.

Parker, R.E.; Roselli, R.J.; Haselton, F.R.; Harris, T.R.

1986-10-01

305

Endothelial cell permeability and adherens junction disruption induced by junín virus infection.  

PubMed

Junín virus (JUNV) is endemic to the fertile Pampas of Argentina, maintained in nature by the rodent host Calomys musculinus, and the causative agent of Argentine hemorrhagic fever (AHF), which is characterized by vascular dysfunction and fluid distribution abnormalities. Clinical as well as experimental studies implicate involvement of the endothelium in the pathogenesis of AHF, although little is known of its role. JUNV has been shown to result in productive infection of endothelial cells (ECs) in vitro with no visible cytopathic effects. In this study, we show that direct JUNV infection of primary human ECs results in increased vascular permeability as measured by electric cell substrate impedance sensing and transwell permeability assays. We also show that EC adherens junctions are disrupted during virus infection, which may provide insight into the role of the endothelium in the pathogenesis of AHF and possibly, other viral hemorrhagic fevers. PMID:24710609

Lander, Heather M; Grant, Ashley M; Albrecht, Thomas; Hill, Terence; Peters, Clarence J

2014-06-01

306

Oxidized LDL Regulates Vascular Endothelial Growth Factor Expression in Human Macrophages and Endothelial Cells Through Activation of Peroxisome Proliferator-Activated Receptor-g  

Microsoft Academic Search

Vascular endothelial growth factor (VEGF) has been recognized as an angiogenic factor that induces endothelial proliferation and vascular permeability. Recent studies have also suggested that VEGF can promote macrophage migration, which is critical for atherosclerosis. We have reported that VEGF is remarkably expressed in activated macrophages, endothelial cells, and smooth muscle cells within human coronary atherosclerotic lesions, and we have

Mayumi Inoue; Hiroshi Itoh; Tokuji Tanaka; Tae-Hwa Chun; Kentaro Doi; Yasutomo Fukunaga; Naoki Sawada; Jun Yamshita; Ken Masatsugu; Takatoshi Saito; Satsuki Sakaguchi; Masakatsu Sone; Ken-ichi Yamahara; Takami Yurugi; Kazuwa Nakao

307

Permeability equipment for porous friction surfaces  

NASA Astrophysics Data System (ADS)

Hydroplaning is the loss of traction between tires and pavement due to the presence of a layer of water. This loss of traction can result in loss of vehicle control. A porous friction surface (PFS) applied over an existing pavement permits the water to drain laterally and vertically away from the tire path, effectively lowering hydroplaning potential. Equipment used to measure pavement drainage (permeability) is discussed with respect to usage on porous friction surface. Background information on hydroplaning, flow theory, and PFS field performance as they are affected by permeability are also presented. Two dynamic test devices and four static devices are considered for measuring PFS permeability. Permeability tests are recommended to measure PFS permeability for maintenance purposes and construction control. Dynamic devices cited could possibly estimate hydroplaning potential; further research must be done to determine this. Permeability devices cannot be used to accurately estimate friction of a pavement surface, however, decreased permeability of a pavement infers a decrease in friction.

Standiford, D. L.; Graul, R. A.; Lenke, L. R.

1985-04-01

308

p38 Mitogen-Activated Protein Kinase Mediates Sidestream Cigarette Smoke-Induced Endothelial Permeability  

Microsoft Academic Search

Second-hand smoke is associated with increased risk of cardiovascular diseases. So far, little is known about the signaling mechanisms of second-hand smoke-induced vascular dysfunction. Endothelial junctions are fundamental structures important for maintaining endo- thelial barrier function. Our study showed that sidestream cigarette smoke (SCS), a major component of second-hand smoke, was able to disrupt endothelial junctions and increase endothelial permeability.

Brad Low; Mei Liang; Jian Fu

2007-01-01

309

Src family kinases as mediators of endothelial permeability: effects on inflammation and metastasis  

Microsoft Academic Search

Src family kinases (SFKs) are signaling enzymes that have long been recognized to regulate critical cellular processes such\\u000a as proliferation, survival, migration, and metastasis. Recently, considerable work has elucidated mechanisms by which SFKs\\u000a regulate normal and pathologic processes in vascular biology, including endothelial cell proliferation and permeability. Further,\\u000a when inappropriately activated, SFKs promote pathologic inflammatory processes and tumor metastasis, in

M. P. Kim; S. I. Park; S. Kopetz; G. E. Gallick

2009-01-01

310

Inhibition by beraprost sodium of thrombin-induced increase in endothelial macromolecular permeability  

Microsoft Academic Search

Effect of beraprost sodium (BPS), a long-acting and orally active stable analogue of PGI2, on the macromolecular permeability of cultured vascular endothelial cells (HUVEC) was detected by the transport of FITC-albumin. Thrombin treatment resulted in induction of FITC-albumin transport across the endothelial cell monolayer. The albumin transport induced by thrombin was not accompanied by any damage to the cells. BPS

R. Imai-Sasaki; M. Kainoh; Y. Ogawa; E. Ohmori; Y. Asai; T. Nakadate

1995-01-01

311

Numerical simulation of imbibition oil recovery for low permeability fractured reservoir  

Microsoft Academic Search

Based on mechanism of imbibition oil recovery in low permeability fractured reservoir , a mathematical model of dual porosity and dual2permibility imbibition oil recovery is established , and numerical solution method and the acquiring2value method of flow coefficient are presented. Through the verification of practical example , the corresponding water2cut index , which is calculated by this method , meets

YIN Dai; PU Hui; WU Ying

312

Screening for peripheral vascular disease with a simple oscillometric blood pressure equipment  

Microsoft Academic Search

The aim of the study was to test if an automated blood pressure measuring device could be used as a simple screening test for peripheral vascular disease. Blood pressure at the ankle level is a good predictor of vascular disease in the lower limbs. The ankle\\/arm index (AAI), i.e. the ratio between the ankle systolic blood pressure and arm (brachial)

Niels Wiinberg; Jesper Mehlsen

2001-01-01

313

Beaches: Profiles, processes and permeability  

NASA Astrophysics Data System (ADS)

The problems involved in the interaction between waves and beaches are complex and it is not yet possible to predict on empirical grounds, let alone theoretical grounds, the shape of a beach after it is subjected to given wave conditions. This investigation began as a study of the use of crushed coal as a model beach material to represent natural beaches of quartz sand but subsequently developed into a more general study of the processes which determine the shape of beach profiles formed in beach materials with different permeabilities.

Gourlay, M. R.

1980-06-01

314

Mechanisms of Microgravity Effect on Vascular Function  

NASA Technical Reports Server (NTRS)

The overall goal of the project is to characterize the effects of simulated microgravity on vascular function. Microgravity is simulated using the hindlimb unweighted (HU) rat, and the following vessels are removed from HU and paired control rats for in vitro analysis: abdominal aorta, carotid and femoral arteries, jugular and femoral veins. These vessels are cut into 3 mm long rings and mounted in tissue baths for the measurement of either isometric contraction, or relaxation of pre- contracted vessels. The isolated mesenteric vascular bed is perfused for the measurement of changes in perfusion pressure as an index of arteriolar constriction or dilation. This report presents, in addition to the statement of the overall goal of the project, a summary list of the specific hypotheses to be tested. These are followed by sections on results, conclusions, significance and plans for the next year.

Purdy, Ralph E.

1995-01-01

315

Permeability Properties of Rickettsia mooseri  

PubMed Central

The passive permeability properties of Rickettsia mooseri to both inorganic and organic solutes have been examined. Visual observations by phase-contrast microscopy of rickettsiae in macerated yolk sacs taken directly from heavily infected eggs revealed plasmolysis with hypertonic NaCl and KCl as well as with sucrose solutions. In contrast, similar visual studies of rickettsiae which had been subjected to freezing or to a purification process, or both, were plasmolyzed by hypertonic sucrose but not by hypertonic NaCl and KCl. These primary observations were extended to a variety of solutes and were placed on a quantitative basis by use of optical density and radioisotope dilution methods. Intracellular Na+ and K+ concentrations in processed rickettsiae, measured by flame photometry, closely paralleled the concentration of these ions in the suspending medium. It was concluded that R. mooseri appears to possess an osmotically active, functional, and structural membrane distinct from the cell wall, located at the surface of a structure analogous to the bacterial protoplast. In the intact organism, this membrane is passively impermeable to sucrose, NaCl, and KCl. However, altered permeability properties, especially to inorganic electrolytes, may be expected in rickettsiae which have been stored in the frozen state and subjected to a lengthy purification process.

Myers, W. F.; Provost, P. J.; Wisseman, C. L.

1967-01-01

316

OBESITY AND VASCULAR DYSFUNCTION  

PubMed Central

One of the most profound challenges facing public health and public health policy in Western society is the increased incidence and prevalence of both overweight and obesity. While this condition can have significant consequences for patient mortality and quality of life, it can be further exacerbated as overweight/obesity can be a powerful stimulus for the development of additional risk factors for a negative cardiovascular outcome, including increased insulin resistance, dyslipidemia and hypertension. This manuscript will present the effects of systemic obesity on broad issues of vascular function in both afflicted human populations and in the most relevant animal models. Among the topics that will be covered are alterations to vascular reactivity (both dilator and constrictor responses), adaptations in microvascular network and vessel wall structure, and alterations to the patterns of tissue/organ perfusion as a result of the progression of the obese condition. Additionally, special attention will be paid to the contribution of chronic inflammation as a contributor to alterations in vascular function, as well as the role of perivascular adipose tissue in terms of impacting vessel behavior. When taken together, it is clearly apparent that the development of the obese condition can have profound, and frequently difficult to predict, impacts on integrated vascular function. Much of this complexity appears to have its basis in the extent to which other co-morbidities associated with obesity (e.g., insulin resistance) are present and exert contributing effects.

Stapleton, Phoebe A.; James, Milinda E.; Goodwill, Adam G.; Frisbee, Jefferson C.

2008-01-01

317

Vascular pathology and osteoarthritis  

Microsoft Academic Search

There is mounting evidence that vascular pathology plays a role in the initiation and\\/or progression of the major disease of joints: osteoarthritis (OA). Potential mechanisms are: episodically reduced blood flow through the small vessels in the subchondral bone at the ends of long bones, and related to this, reduced interstitial fluid flow in subchondral bone. Blood flow may be reduced

D. M. Findlay

2007-01-01

318

Amputation in vascular disease.  

PubMed Central

The management of vascular amputees in the Roehampton Limb Surgery Unit since its opening in 1975 is outlined and the results in 167 cases presented. Of the 35 patients over the age of 80, 57% were walking independently at the time of their discharge from the unit. Images Fig. 1 Fig. 2 Fig. 3 Fig. 4

Robinson, K.

1980-01-01

319

Synthetic vascular prostheses.  

PubMed

Polyethyleneterephthalate (PET), and to a lesser extent Teflon have become the major synthetic grafting material. Unlike nylon, Ivalon, and Vinyon-N which lose their tensile strength after implantation, PET and Teflon remain essentially unchanged even after long periods. TRICOMED S.A. produces the family of the knitted vascular implants Dallon made from PET fibres including: Dallon, Dallon H, Tricogel. Both Dallon and Dallon H are manufactured in a form of double (external and internal) velour surface using multifilament yarn and having optimal graft design (a variety of sizes and lengths). The velour surface gives the surface a velvety, plush texture, which improves tissue in--growth. Moreover, Dallon H is a unique vascular prostheses showing the increase in the blood susceptibility that is useful for 4 times less blood demand during preclotting as compared with standard prosthesis. Tricogel graft is made of thin-wall prostheses sealed with the porcine gelatin that provides intraoperative tightness (without preclotting) and the optimal healing process. Hydrophilic behavior of the graft is observed as an instant moistening of the surface with patient's blood and as sweating. The blood stream does not dissolve nor washes away the gelatin but causes the gelatin film to swell, which makes a better tightness. The work will describe the properties of manmade vascular grafts as well as their applications in the vascular surgery. PMID:12391780

Struszczyk, Marcin H; Bednarek, Pawe?; Raczy?ski, Krzysztof

2002-01-01

320

Pathogenesis of Vascular Anomalies  

PubMed Central

Vascular anomalies are localized defects of vascular development. Most of them occur sporadically, i.e. there is no familial history of lesions, yet in a few cases clear inheritance is observed. These inherited forms are often characterized by multifocal lesions that are mainly small in size and increase in number with patient’s age. On the basis of these inherited forms, molecular genetic studies have unraveled a number of inherited mutations giving direct insight into the pathophysiological cause and the molecular pathways that are implicated. Genetic defects have been identified for hereditary haemorrhagic telangiectasia (HHT), inherited cutaneomucosal venous malformation (VMCM), glomuvenous malformation (GVM), capillary malformation - arteriovenous malformation (CM-AVM), cerebral cavernous malformation (CCM) and some isolated and syndromic forms of primary lymphedema. We focus on these disorders, the implicated mutated genes and the underlying pathogenic mechanisms. We also call attention to the concept of Knudson’s double-hit mechanism to explain incomplete penetrance and the large clinical variation in expressivity of inherited vascular anomalies. This variability renders the making of correct diagnosis of the rare inherited forms difficult. Yet, the identification of the pathophysiological causes and pathways involved in them has had an unprecedented impact on our thinking of their etiopathogenesis, and has opened the doors towards a more refined classification of vascular anomalies. It has also made it possible to develop animal models that can be tested for specific molecular therapies, aimed at alleviating the dysfunctions caused by the aberrant genes and proteins.

Boon, Laurence M.; Ballieux, Fanny; Vikkula, Miikka

2010-01-01

321

Lasers for vascular lesions.  

PubMed

Recent developments in laser technology have revolutionized the treatment of various cutaneous disorders. Lasers provide effective and safe treatment of many conditions for which previous therapy was either unavailable, ineffective, or unacceptable. Basic laser principles, laser safety, available laser systems for treatment vascular lesions, clinical applications, preoperative considerations, anesthesia, postoperative changes, side effects/complications, nursing measures, and patient education are described. PMID:10670327

Alora, M B; Dover, J S; Arndt, K A

1999-04-01

322

Riqueza de plantas vasculares  

Microsoft Academic Search

Vascular plant diversity (excluding pteridophytes) was analyzed for the countries of Ecuador, Peru, and Bolivia from information available in TROPICOS. A total of 34,286 species were registered for the three countries, distributed in 256 families and 3,309 genera. Peru is the most diverse of the three countries. Orchidaceae, Asteraceae and Fabaceae were the three most diverse families of the region.

Peter M. Jørgensen; Carmen Ulloa; Carla Maldonado

323

Predicting skin permeability from complex chemical mixtures  

SciTech Connect

Occupational and environmental exposure to topical chemicals is usually in the form of complex chemical mixtures, yet risk assessment is based on experimentally derived data from individual chemical exposures from a single, usually aqueous vehicle, or from computed physiochemical properties. We present an approach using hybrid quantitative structure permeation relationships (QSPeR) models where absorption through porcine skin flow-through diffusion cells is well predicted using a QSPeR model describing the individual penetrants, coupled with a mixture factor (MF) that accounts for physicochemical properties of the vehicle/mixture components. The baseline equation is log k {sub p} = c + mMF + a{sigma}{alpha} {sub 2} {sup H} + b{sigma}{beta} {sub 2} {sup H} + s{pi} {sub 2} {sup H} + rR {sub 2} + vV {sub x} where {sigma}{alpha} {sub 2} {sup H} is the hydrogen-bond donor acidity, {sigma}{beta} {sub 2} {sup H} is the hydrogen-bond acceptor basicity, {pi} {sub 2} {sup H} is the dipolarity/polarizability, R {sub 2} represents the excess molar refractivity, and V {sub x} is the McGowan volume of the penetrants of interest; c, m, a, b, s, r, and v are strength coefficients coupling these descriptors to skin permeability (k {sub p}) of 12 penetrants (atrazine, chlorpyrifos, ethylparathion, fenthion, methylparathion, nonylphenol, {rho}-nitrophenol, pentachlorophenol, phenol, propazine, simazine, and triazine) in 24 mixtures. Mixtures consisted of full factorial combinations of vehicles (water, ethanol, propylene glycol) and additives (sodium lauryl sulfate, methyl nicotinate). An additional set of 4 penetrants (DEET, SDS, permethrin, ricinoleic acid) in different mixtures were included to assess applicability of this approach. This resulted in a dataset of 16 compounds administered in 344 treatment combinations. Across all exposures with no MF, R{sup 2} for absorption was 0.62. With the MF, correlations increased up to 0.78. Parameters correlated to the MF include refractive index, polarizability and log (1/Henry's Law Constant) of the mixture components. These factors should not be considered final as the focus of these studies was solely to determine if knowledge of the physical properties of a mixture would improve predicting skin permeability. Inclusion of multiple mixture factors should further improve predictability. The importance of these findings is that there is an approach whereby the effects of a mixture on dermal absorption of a penetrant of interest can be quantitated in a standard QSPeR model if physicochemical properties of the mixture are also incorporated.

Riviere, Jim E. [Center for Chemical Toxicology Research and Pharmacokinetics, 4700 Hillsborough Street, North Carolina State University, Raleigh, NC 27606 (United States)]. E-mail: Jim_Riviere@ncsu.edu; Brooks, James D. [Center for Chemical Toxicology Research and Pharmacokinetics, 4700 Hillsborough Street, North Carolina State University, Raleigh, NC 27606 (United States)

2005-10-15

324

Clamshell excavation of a permeable reactive barrier  

Microsoft Academic Search

Nowadays, permeable reactive barriers (PRB) are one of the most widespread techniques for the remediation of contaminated aquifers. Over the past 10 years, the use of iron-based PRBs has evolved from innovative to accepted standard practice for the treatment of a variety of groundwater contaminants (ITRC in: Permeable reactive barriers: lessons learned\\/new directions. The Interstate Technology and Regulatory Council, Permeable Reactive

Antonio Di Molfetta; Rajandrea Sethi

2006-01-01

325

Permeability hysterisis of limestone during isotropic compression.  

PubMed

The evolution of permeability hysterisis in Indiana Limestone during application of isotropic confining pressures up to 60 MPa was measured by conducting one-dimensional constant flow rate tests. These tests were carried out either during monotonic application of the confining pressure or during loading-partial unloading cycles. Irreversible permeability changes occurred during both monotonic and repeated incremental compression of the limestone. Mathematical relationships are developed for describing the evolution of path-dependent permeability during isotropic compression. PMID:18181870

Selvadurai, A P S; G?owacki, A

2008-01-01

326

Coexistence of pheochromocytoma with uncommon vascular lesions  

PubMed Central

Background: Pheochromocytoma/paragangliomas have been described to be associated with rare vascular abnormalities like renal artery stenosis. Coexistence of physiologically significant renal artery lesions is a compounding factor that alters management and prognosis of pheochromocytoma patients. Apart from individual case reports, data on such association in Indian population is not available. The aim of this study is to find the nature and prevalence of associated vascular abnormalities. Materials and Methods: From 1990 to 2010, a total of 50 patients were diagnosed with pheochromocytoma/paragangliomas. Hospital charts of these patients were reviewed retrospectively to identify those with unusual vascular abnormalities. Available literature was also reviewed. Results: Of the 50 patients with pheochromocytoma, 7 (14%) had coexisting vascular lesions including renal artery stenosis in 4, aortoarteritis in 1, aortic aneurysm in 1 and inferior vena cava thrombosis in 1. Pheochromocytoma was adrenal in 42 and extra adrenal in 8. Laparoscopic adrenalectomy was done in the patients. One patient with renal artery stenosis due to intimal fibrosis was subjected to percutaneous balloon angioplasty; the other three improved after adrenalectomy and lysis of fibrous adhesive bands. The patient with aortoarteritos was treated with oral steroids. Inferior vena cava thrombosis was reversed with anticoagulants. The patient with abdominal aortic aneurysm was advised for annual follow-up on account of its size of 4.5 cm and asymptomatic presentation. Conclusion: There are multiple mechanisms that can lead to renal artery stenosis and other vascular abnormalities in a case of pheochromocytoma. A high index of suspicion is necessary to enable both entities to be diagnosed preoperatively and allow proper planning of surgical therapy. Incomplete diagnosis may lead to persistent hypertension postoperatively in a case of associated renal artery stenosis.

Kota, Sunil Kumar; Kota, Siva Krishna; Meher, Lalit Kumar; Jammula, Sruti; Panda, Sandip; Modi, Kirtikumar D.

2012-01-01

327

Indexing Consistency and Quality.  

ERIC Educational Resources Information Center

A measure of indexing consistency is developed based on the concept of 'fuzzy sets'. It assigns a higher consistency value if indexers agree on the more important terms than if they agree on less important terms. Measures of the quality of an indexer's work and exhaustivity of indexing are also proposed. Experimental data on indexing consistency…

Zunde, Pranas; Dexter, Margaret E.

328

Permeability of the Suberized Mestome Sheath in Winter Rye 1  

PubMed Central

Mestome sheath cells of winter rye (Secale cereale L. cv Puma) deposit suberized lamellae in their secondary cell walls. Histochemical tests including acid digestion and staining with Sudan IV and Chelidonium majus root extract were used to detect the presence of suberin in the primary cell wall. There was no evidence of a Casparian band between adjacent mestome sheath cells. Fluorescent dye techniques were used to trace solute movement through the rye leaf apoplast. Calcofluor white M2R, a fluorescent dye which binds to cell walls as it moves apoplastically, proved to be too limited in its mobility in leaves to test mestome sheath permeability. Trisodium 3-hydroxy-5,8,10 pyrene trisulfonate, a fluorescent dye which is mobile in the apoplast, moved easily up the vascular bundles in the transpiration stream, and diffused outward from the veins to the epidermal cell walls within minutes of reaching a particular level in the leaf. We conclude that the suberized mestome sheath of rye leaves is freely permeable to solutes moving apoplastically through radial primary cell walls. Images Fig. 1 Fig. 2 Fig. 3 Fig. 4 Fig. 5

Peterson, Carol A.; Griffith, Marilyn; Huner, Norman P. A.

1985-01-01

329

Permeability of the suberized mestome sheath in winter rye.  

PubMed

Mestome sheath cells of winter rye (Secale cereale L. cv Puma) deposit suberized lamellae in their secondary cell walls. Histochemical tests including acid digestion and staining with Sudan IV and Chelidonium majus root extract were used to detect the presence of suberin in the primary cell wall. There was no evidence of a Casparian band between adjacent mestome sheath cells. Fluorescent dye techniques were used to trace solute movement through the rye leaf apoplast. Calcofluor white M2R, a fluorescent dye which binds to cell walls as it moves apoplastically, proved to be too limited in its mobility in leaves to test mestome sheath permeability. Trisodium 3-hydroxy-5,8,10 pyrene trisulfonate, a fluorescent dye which is mobile in the apoplast, moved easily up the vascular bundles in the transpiration stream, and diffused outward from the veins to the epidermal cell walls within minutes of reaching a particular level in the leaf. We conclude that the suberized mestome sheath of rye leaves is freely permeable to solutes moving apoplastically through radial primary cell walls. PMID:16663999

Peterson, C A; Griffith, M; Huner, N P

1985-01-01

330

Dynamic permeability of the lacunar-canalicular system in human cortical bone.  

PubMed

A new method for the experimental determination of the permeability of a small sample of a fluid-saturated hierarchically structured porous material is described and applied to the determination of the lacunar-canalicular permeability [Formula: see text] in bone. The interest in the permeability of the lacunar-canalicular pore system (LCS) is due to the fact that the LCS is considered to be the site of bone mechanotransduction due to the loading-driven fluid flow over cellular structures. The permeability of this space has been estimated to be anywhere from [Formula: see text] to [Formula: see text]. However, the vascular pore system and LCS are intertwined, rendering the permeability of the much smaller-dimensioned LCS challenging to measure. In this study, we report a combined experimental and analytical approach that allowed the accurate determination of the [Formula: see text] to be on the order of [Formula: see text] for human osteonal bone. It was found that the [Formula: see text] has a linear dependence on loading frequency, decreasing at a rate of [Formula: see text]/Hz from 1 to 100 Hz, and using the proposed model, the porosity alone was able to explain 86 % of the [Formula: see text] variability. PMID:24146291

Benalla, M; Palacio-Mancheno, P E; Fritton, S P; Cardoso, L; Cowin, S C

2014-08-01

331

Vascular Protection in Brain Ischemia  

Microsoft Academic Search

Vascular damage occurring after cerebral ischemia may lead to a worse outcome in patients with ischemic stroke, as it facilitates edema formation and hemorrhagic transformation. There are several phases in the development of vascular injury (acute, subacute and chronic) and different mediators act in each one. Therapeutic options to avoid vascular injury must be focused on acting in each phase.

Manuel Rodríguez-Yáñez; Mar Castellanos; Miguel Blanco; Esther Mosquera; José Castillo

2006-01-01

332

The Effect of Stress and Pore Pressure on Formation Permeability of Ultra-Low-Permeability Reservoir  

Microsoft Academic Search

Low-permeability reservoirs have attracted increased attention from most oil companies due to increased demand and limited reserves in conventional reservoirs. Most scholars agree that worldwide hydrocarbon production decline from conventional reservoirs will be compensated for by the development of low-permeability reservoirs to satisfy growing demand. During the production life cycle of a low-permeability reservoir, permeability at any given location may

F. Ma; S. He; H. Zhu; Q. Xie; C. Jiao

2012-01-01

333

The Vascular Depression Hypothesis: Mechanisms Linking Vascular Disease with Depression  

PubMed Central

The ‘Vascular Depression’ hypothesis posits that cerebrovascular disease may predispose, precipitate, or perpetuate some geriatric depressive syndromes. This hypothesis stimulated much research that has improved our understanding of the complex relationships between late-life depression (LLD), vascular risk factors, and cognition. Succinctly, there are well-established relationships between late-life depression, vascular risk factors, and cerebral hyperintensities, the radiological hallmark of vascular depression. Cognitive dysfunction is common in late-life depression, particularly executive dysfunction, a finding predictive of poor antidepressant response. Over time, progression of hyperintensities and cognitive deficits predicts a poor course of depression and may reflect underlying worsening of vascular disease. This work laid the foundation for examining the mechanisms by which vascular disease influences brain circuits and influences the development and course of depression. We review data testing the vascular depression hypothesis with a focus on identifying potential underlying vascular mechanisms. We propose a disconnection hypothesis, wherein focal vascular damage and white matter lesion location is a crucial factor influencing neural connectivity that contributes to clinical symptomatology. We also propose inflammatory and hypoperfusion hypotheses, concepts that link underlying vascular processes with adverse effects on brain function that influence the development of depression. Testing such hypotheses will not only inform the relationship between vascular disease and depression but also provide guidance on the potential repurposing of pharmacological agents that may improve late-life depression outcomes.

Taylor, Warren D.; Aizenstein, Howard J.; Alexopoulos, George S.

2013-01-01

334

Negative index metamaterial combining magnetic resonators with metal films  

Microsoft Academic Search

We present simulation results of a design for negative index materials that\\u000auses magnetic resonators to provide negative permeability and metal film for\\u000anegative permittivity. We also discuss the possibility of using semicontinuous\\u000ametal films to achieve better manufacturability and enhanced impedance\\u000amatching.

Uday K. Chettiar; Alexander V. Kildishev; Thomas A. Klar; Vladimir M. Shalaev

2006-01-01

335

Noncontact monitoring of vascular lesion phototherapy efficiency by RGB multispectral imaging  

NASA Astrophysics Data System (ADS)

A prototype low-cost RGB imaging system consisting of a commercial RGB CMOS sensor, RGB light-emitting diode ring light illuminator, and a set of polarizers was designed and tested for mapping the skin erythema index, in order to monitor skin recovery after phototherapy of vascular lesions, such as hemangiomas and telangiectasias. The contrast of erythema index (CEI) was proposed as a parameter for quantitative characterization of vascular lesions. Skin recovery was characterized as a decrease of the CEI value relative to the value before the treatment. This approach was clinically validated by examining 31 vascular lesions before and after phototherapy.

Jakovels, Dainis; Kuzmina, Ilona; Berzina, Anna; Valeine, Lauma; Spigulis, Janis

2013-12-01

336

Noncontact monitoring of vascular lesion phototherapy efficiency by RGB multispectral imaging.  

PubMed

A prototype low-cost RGB imaging system consisting of a commercial RGB CMOS sensor, RGB light-emitting diode ring light illuminator, and a set of polarizers was designed and tested for mapping the skin erythema index, in order to monitor skin recovery after phototherapy of vascular lesions, such as hemangiomas and telangiectasias. The contrast of erythema index (CEI) was proposed as a parameter for quantitative characterization of vascular lesions. Skin recovery was characterized as a decrease of the CEI value relative to the value before the treatment. This approach was clinically validated by examining 31 vascular lesions before and after phototherapy. PMID:24362928

Jakovels, Dainis; Kuzmina, Ilona; Berzina, Anna; Valeine, Lauma; Spigulis, Janis

2013-12-01

337

Novel role of stathmin in microtubule-dependent control of endothelial permeability  

PubMed Central

Microtubule (MT) dynamics in vascular endothelium are modulated by vasoactive mediators and are critically involved in the control of endothelial cell (EC) permeability via Rho GTPase-dependent crosstalk with the actin cytoskeleton. However, the role of regulators in MT stability in these mechanisms remains unclear. This study investigated the involvement of the MT-associated protein stathmin in the mediation of agonist-induced permeability in EC cultures and vascular leak in vivo. Thrombin treatment of human pulmonary ECs induced rapid dephosphorylation and activation of stathmin. Inhibition of stathmin activity by small interfering RNA-based knockdown or cAMP-mediated phosphorylation abrogated thrombin-induced F-actin remodeling and Rho-dependent EC hyperpermeability, while expression of a phosphorylation-deficient stathmin mutant exacerbated thrombin-induced EC barrier disruption. Stathmin suppression preserved the MT network against thrombin-induced MT disassembly and release of Rho-specific guanine nucleotide exchange factor, GEF-H1. The protective effects of stathmin knockdown were observed in vivo in the mouse 2-hit model of ventilator-induced lung injury and were linked to MT stabilization and down-regulation of Rho signaling in the lung. These results demonstrate the mechanism of stathmin-dependent control of MT dynamics, Rho signaling, and permeability and suggest novel potential pharmacological interventions in the prevention of increased vascular leak via modulation of stathmin activity.—Tian, X., Tian, Y., Sarich, N., Wu, T., Birukova, A. A. Novel role of stathmin in microtubule-dependent control of endothelial permeability.

Tian, Xinyong; Tian, Yufeng; Sarich, Nicolene; Wu, Tinghuai; Birukova, Anna A.

2012-01-01

338

Overexpression of VEGF165b in Podocytes Reduces Glomerular Permeability  

PubMed Central

The observation that therapeutic agents targeting vascular endothelial growth factor-A (VEGF-A) associate with renal toxicity suggests that VEGF plays a role in the maintenance of the glomerular filtration barrier. Alternative mRNA splicing produces the VEGFxxxb family, which consists of antiangiogenic peptides that reduce permeability and inhibit tumor growth; the contribution of these peptides to normal glomerular function is unknown. Here, we established and characterized heterozygous and homozygous transgenic mice that overexpress VEGF165b specifically in podocytes. We confirmed excess production of glomerular VEGF165b by reverse transcriptase–PCR, immunohistochemistry, and ELISA in both heterozygous and homozygous animals. Macroscopically, the mice seemed normal up to 18 months of age, unlike the phenotype of transgenic podocyte-specific VEGF164-overexpressing mice. Animals overexpressing VEGF165b, however, had a significantly reduced normalized glomerular ultrafiltration fraction with accompanying changes in ultrastructure of the glomerular filtration barrier on the vascular side of the glomerular basement membrane. These data highlight the contrasting properties of VEGF splice variants and their impact on glomerular function and phenotype.

Qiu, Yan; Ferguson, Joanne; Oltean, Sebastian; Neal, Chris R.; Kaura, Amit; Bevan, Heather; Wood, Emma; Sage, Leslie M.; Lanati, Silvia; Nowak, Dawid G.; Salmon, Andy H.J.; Bates, David

2010-01-01

339

Taxol alleviates 2-methoxyestradiol-induced endothelial permeability  

PubMed Central

We have previously shown that the anti-cancer agent 2-methoxyestradiol (2ME) induces hyperpermeability across endothelial monolayers. Here, we show that both microtubule disruptor, 2ME, and microtubule stabilizer, paclitaxel (taxol), increase vascular lung permeability in vitro and in vivo. Simultaneous application of 2ME and taxol alleviates 2ME-induced endothelial barrier dysfunction, which is evident by the decreased Evans Blue Dye accumulation in lung tissue and increased transendothelial resistance across monolayers. 2ME significantly increases the level of p38 and MLC phosphorylation in both endothelial monolayers and murine lungs; this increase is suppressed in the presence of taxol. Taxol treatment leads to an immediate and sustained increase in tubulin acetylation in human pulmonary artery endothelial cells (HPAEC). Surprisingly, 2ME treatment also increases tubulin acetylation; however, the on-set of this process is delayed and co-insides with the stage of a partial barrier restoration in HPAEC monolayer. Inhibition of histone deacetylase 6 (HDAC6) with tubacin increases tubulin acetylation level, suppresses 2ME-induced HSP27 and MLC phosphorylation, and decreases 2ME-induced barrier dysfunction, suggesting barrier-protective and/or barrier-restorative role for tubulin acetylation in vascular endothelium.

Gorshkov, Boris A.; Zemskova, Marina A.; Verin, Alexander D.; Bogatcheva, Natalia V.

2011-01-01

340

Fibrinogen-induced increased pial venular permeability in mice  

PubMed Central

Elevated blood level of Fibrinogen (Fg) is commonly associated with vascular dysfunction. We tested the hypothesis that at pathologically high levels, Fg increases cerebrovascular permeability by activating matrix metalloproteinases (MMPs). Fibrinogen (4?mg/mL blood concentration) or equal volume of phosphate-buffered saline (PBS) was infused into male wild-type (WT; C57BL/6J) or MMP-9 gene knockout (MMP9?/?) mice. Pial venular leakage of fluorescein isothiocyanate-bovine serum albumin to Fg or PBS alone and to topically applied histamine (10?5?mol/L) were assessed. Intravital fluorescence microscopy and image analysis were used to assess cerebrovascular protein leakage. Pial venular macromolecular leakage increased more after Fg infusion than after infusion of PBS in both (WT and MMP9?/?) mice but was more pronounced in WT compared with MMP9?/? mice. Expression of vascular endothelial cadherin (VE-cadherin) was less and plasmalemmal vesicle-associated protein-1 (PV-1) was greater in Fg-infused than in PBS-infused both mice groups. However, in MMP9?/? mice, VE-cadherin expression was greater and PV-1 expression was less than in WT mice. These data indicate that at higher levels, Fg compromises microvascular integrity through activation of MMP-9 and downregulation of VE-cadherin and upregulation of PV-1. Our results suggest that elevated blood level of Fg could have a significant role in cerebrovascular dysfunction and remodeling.

Muradashvili, Nino; Qipshidze, Natia; Munjal, Charu; Givvimani, Srikanth; Benton, Richard L; Roberts, Andrew M; Tyagi, Suresh C; Lominadze, David

2012-01-01

341

[Vascular proliferations of the spleen].  

PubMed

Vascular proliferations of the spleen reflect the variability of vascular structures occurring in the normal spleen. Besides haemangiomas, there is a spleen-specific vascular neoplasm, littoral cell angioma, that often occurs as a paraneoplastic lesion and thus may require the differential diagnostic delineation of metastases to the spleen in patients with known neoplasms. The most common malignant vascular tumours of the spleen are angiosarcomas. A recently described vascular lesion of unknown pathogenesis, sclerosing angiomatoid nodular transformation (SANT) of the spleen, usually is an incidental finding detected in the course of imaging studies. PMID:18214485

Hartmann, M; Marx, A; Geissinger, E; Müller-Hermelink, H K; Rüdiger, T

2008-03-01

342

Minimally Invasive Vascular Techniques  

PubMed Central

The recent and continuing developments in radiotherapy, gene therapy, and the technologies of imaging, materials, and devices, as well as the techniques for their implementation, have expanded the options available for the treatment of peripheral vascular disease. Though long-term data are still lacking, percutaneous transluminal angioplasty (PTA) has developed into a treatment modality in its own right and continues to be an adjuvant treatment to traditional surgical revascularization. Numerous stents and grafts are currently available for the treatment of arterial lesions and aneurysms, while the testing of many more continues. In addition to these new devices, developments in gene therapy and brachytherapy have brought several new minimally invasive options to the treatment of peripheral vascular disease.

Lepore, Michael R.; Yoselevitz, Moises; Sternbergh, W. Charles; Money, Samuel R.

2000-01-01

343

Neurobiology of Vascular Dementia  

PubMed Central

Vascular dementia is, in its current conceptual form, a distinct type of dementia with a spectrum of specific clinical and pathophysiological features. However, in a very large majority of cases, these alterations occur in an already aged brain, characterized by a milieu of cellular and molecular events common for different neurodegenerative diseases. The cell signaling defects and molecular dyshomeostasis might lead to neuronal malfunction prior to the death of neurons and the alteration of neuronal networks. In the present paper, we explore some of the molecular mechanisms underlying brain malfunction triggered by cerebrovascular disease and risk factors. We suggest that, in the age of genetic investigation and molecular diagnosis, the concept of vascular dementia needs a new approach.

Enciu, Ana-Maria; Constantinescu, Stefan N.; Popescu, Laurentiu M.; Muresanu, Dafin F.; Popescu, Bogdan O.

2011-01-01

344

SOIL-AIR PERMEABILITY METHOD EVALUATION  

EPA Science Inventory

The feasibility of soil vapor extraction (SVE) is, in part, based on vadose zone soil-air permeability. ield, laboratory and empirical correlation methods for estimating soil-air permeability have been reviewed for their appropriateness in determining SVE feasibility, and the dev...

345

Porosity and Permeability of Tight Sands  

Microsoft Academic Search

Detailed analyses of more than 50 core samples of western tight sands have resulted in several unanticipated observations that are set forth in this paper. Core analyses performed under stress representative of producing conditions provided data on porosity, pore volume compressibility, stress dependence of permeability to gas, and slope of the Klinkenberg plot (permeability at constant net stress vs. the

P. L. Randolph; D. J. Soeder; Prasan Chowdiah

1984-01-01

346

Influence of fiber packing structure on permeability  

NASA Technical Reports Server (NTRS)

The study on the permeability of an aligned fiber bundle is the key building block in modeling the permeability of advanced woven and braided preforms. Available results on the permeability of fiber bundles in the literature show that a substantial difference exists between numerical and analytical calculations on idealized fiber packing structures, such as square and hexagonal packing, and experimental measurements on practical fiber bundles. The present study focuses on the variation of the permeability of a fiber bundle under practical process conditions. Fiber bundles are considered as containing openings and fiber clusters within the bundle. Numerical simulations on the influence of various openings on the permeability were conducted. Idealized packing structures are used, but with introduced openings distributed in different patterns. Both longitudinal and transverse flow are considered. The results show that openings within the fiber bundle have substantial effect on the permeability. In the longitudinal flow case, the openings become the dominant flow path. In the transverse flow case, the fiber clusters reduce the gap sizes among fibers. Therefore the permeability is greatly influenced by these openings and clusters, respectively. In addition to the porosity or fiber volume fraction, which is commonly used in the permeability expression, another fiber bundle status parameter, the ultimate fiber volume fraction, is introduced to capture the disturbance within a fiber bundle.

Cai, Zhong; Berdichevsky, Alexander L.

1993-01-01

347

Porosity and Permeability Determinations of Chondritic Materials  

NASA Astrophysics Data System (ADS)

We describe results of porosity and permeability determinations of chondritic meteorites of low petrologic grade (1-3). The porosity results are comparable to those for chondritic interplanetary dust particles. Permeabilities of CM2 chondrites are slightly higher than those for CV3s.

Corrigan, C. M.; Zolensky, M. E.; Long, M.; Sapp, C. A.; Dahl, J. M.

1996-03-01

348

Permeability-porosity data sets for sandstones  

USGS Publications Warehouse

Due to the variable nature of permeability-porosity relations, core should be obtained and permeability (k) and porosity (??) should be determined on core plugs in the laboratory for the formation of interest. A catalog of k versus (??) data sets is now available on the Web. Examples from the catalog are considered to illustrate some aspects of k versus ?? dependencies in siliciclastic reservoirs.

Nelson, P. H.

2004-01-01

349

Spontaneous Imbibition in Low Permeability Carbonates  

Microsoft Academic Search

Spontaneous imbibition is important in oil recovery from fractured and low permeability tight gas reservoirs. Gas-water spontaneous imbibition experiments were conducted using low permeability heterogeneous limestone core plugs. The interfacial tension was changed by adding differing amounts of alcohol to water. It was observed that the true residual saturation of gas is very small for all cases. A much larger

Can Ulas Hatiboglu; Ugur Karaaslan; Serhat Akin

2005-01-01

350

Groundwater Flow in Low-Permeability Environments  

Microsoft Academic Search

Certain geologic media are known to have small permeability; subsurface environments composed of these media and lacking well developed secondary permeability have groundwater flow sytems with many distinctive characteristics. Moreover, groundwater flow in these environments appears to influence the evolution of certain hydrologic, geologic, and geochemical systems, may affect the accumulation of pertroleum and ores, and probably has a role

C. E. Neuzil

1986-01-01

351

Flow Characteristics in Permeable Reactive Barrier Affected by Biological Clogging  

Microsoft Academic Search

Permeable reactive barriers (PRB) are becoming popular for the in situ remediation of contaminated groundwater. The efficiency of the PRB is affected by permeability of the reactive zone, because when permeability decreases contaminants can bypass the reactive zone without degraded. One of the factors affecting permeability of the permeable reactive zone is biological clogging of soil pore, i.e., biomass buildup

K. Seki; J. Hanada; T. Miyazaki

2004-01-01

352

Vascular Thoracic Outlet Syndrome  

Microsoft Academic Search

  Abstract\\u000a \\u000a The surgical treatment of 30 cases of vascular thoracic outlet syndrome (TOS) in 25 patients is presented. Patients included\\u000a 17 women and 8 men with average age of 26.1 years. The causes of compression were cervical rib (n = 16), soft tissue anomalies (n = 12), and scar tissue after clavicle fracture (n = 2). Ten subclavian artery aneurysms

Lazar B. Davidovic; Dusan M. Kostic; Nenad S. Jakovljevic; Ilija L. Kuzmanovic; Tijana M. Simic

2003-01-01

353

Neurocutaneous vascular syndromes  

Microsoft Academic Search

There have been significant recent advances in the past several years in the field of neurocutaneous vascular syndromes, including\\u000a the development of more stringent diagnostic criteria for PHACE syndrome, the renaming of macrocephaly-cutis marmorata telangiectatica\\u000a congenita to macrocephaly-capillary malformation to accurately reflect the true nature of the syndrome, and discovery of new\\u000a genetic mutations such as RASA-1. There have also

Katherine B. Puttgen; Doris D. M. Lin

2010-01-01

354

Lipids in vascular function  

Microsoft Academic Search

Physiological and pathological vascular responses depend on the action of numerous intercellular mediators, ranging from hormones\\u000a to gases like nitric oxide, proteins, and lipids. The last group consists not only of the different types of lipoproteins,\\u000a but also includes a broad array of other lipophilic signaling molecules such as fatty acids, eicosanoids, phospholipids and\\u000a their derivatives, sphingolipids and isoprenoids. Due

Alois Sellmayer; Nina Hrboticky; Peter C. Weber

1999-01-01

355

Reticuloendothelial Clearance of Blood-borne Particulates: Relevance to Experimental Lung Microembolization and Vascular Injury  

PubMed Central

The rapid increase in sheep lung vascular permeability observed during Pseudomonas aeruginosa bacteremia may be due to embolization of the pulmonary microvasculature by bloodborne particulates. Since alterations in lung microvascular permeability during mild septicemia in sheep may reflect inefficient RES phagocytic clearance of bacteria as well as products of bacterial induced intravascular coagulation, the opsonic and phagocytic aspects of RES function in sheep (30-50 kg) were compared to other species. RES function was evaluated by both the clearance and relative organ uptake of gelatinized I131 RE test lipid emulsion and gelatinized colloidal carbon. Immunoreactive opsonic a2SB glycoprotein levels were determined by electroimmunoassay. The phagocytic index for RES clearance of the gelatinized (500 mg/kg) test lipid in sheep was 0.019 ± 0.002 corresponding to a half-time of 16.65 ± 1.74 minutes. With colloidal carbon (64 mg/kg), the phagocytic index in sheep was 0.080 ± 0.026, corresponding to a half-time of 6.16 ± 1.99 minutes. The per cent of injected lipid emulsion (%ID) in major RE organs, on a total organ basis (TO), was: liver = 15.69 ± 1.65%; spleen = 2.09 ± 0.78%. Localization in the lung = 31.39 ± 6.2%. The per cent of carbon localized in major RE organs (%ID/TO) was: liver = 21.37 ± 1.9%; spleen = 1.95 ± 0.55%. Localization in the lung = 32.70 ± 4.55%. In contrast, clearance and organ distribution of the blood-borne test microparticles in rats and dogs at the same relative challenging dose revealed a much more intense and rapid liver and spleen RES uptake with minimal lung localization (1-2%). Immunoreactive opsonic protein concentrations varied greatly with species and directly correlated with efficiency of RES function. Levels observed were: dog = 1285 ± 135 µg/ml; mouse = 1077 ± 67 µg/ml; rat = 400 ± 31 µg/ml; human = 297 ± 10 µg/ml; and sheep = 184 ± 13 µg/ml. After intravenous particulate challenge, circulating immunoreactive opsonic protein in the sheep was depleted (p < 0.05) rapidly with partial recovery at 24 hours and mild rebound hyperopsonemia at 48 hours. This pattern is in contrast to the rapid restoration seen in dog and rat within three to six hours postchallenge. Thus, in sheep, the extensive pulmonary localization of blood-borne microparticles appears related to inefficient RES clearance function mediated by a relative deficiency of circulating opsonic protein (plasma fibronectin).

Niehaus, Gary D.; Schumacker, Paul R.; Saba, Thomas M.

1980-01-01

356

Composites with tuned effective magnetic permeability  

NASA Astrophysics Data System (ADS)

Pendry et al. [J. B. Pendry, A. J. Holden, D. J. Robbins, and W. J. Stewart, IEEE Trans. Microwave Theory Tech. 47, 2075 (1999)] and Smith et al. [D. R. Smith, W. J. Padilla, D. C. Vier, S. C. Nemat-Nasser, and S. Schultz, Phys. Rev. Lett. 84, 4184 (2000)] have shown that the effective magnetic permeability, ?, of free space can be rendered negative over a certain frequency range by a periodic arrangement of very thin conductors with suitable magnetic resonance properties, the so-called split-ring resonators. Because of its rather bulky architecture, this structure does not lend itself to a proper integration into a reasonably thin real composite structural panel. To remedy this fundamental barrier, we invented a new magnetic resonator consisting of very thin folded plates that are suitably nested within one another to form folded-doubled resonators (FDRs) that can be integrated into an actual composite panel. Measurements, using a focused beam electromagnetic characterization system combined with time-domain numerical simulations of the reflection and transmission coefficients of such a composite slab have revealed that indeed the composite has a negative ? over a frequency range of about 9.1-9.35 GHz [S. Nemat-Nasser, S. C. Nemat-Nasser, T. A. Plaisted, A. Starr, and A. Vakil Amirkhizi, in Biomimetics: Biologically Inspired Technologies, edited by Y. Bar Cohen (CRC Press, Boca Raton, FL, 2006)]. Thus, it has become possible to construct a structural composite panel with negative index of refraction by simultaneously creating negative effective ? and ? [V. G. Veselago, Sov. Phys. Usp. 10, 509 (1968); R. A. Shelby, D. R. Smith, and S. Schultz, Science 292, 77 (2001); A. F. Starr, P. M. Rye, D. R. Smith, and S. Nemat-Nasser, Phys. Rev. B 70, 113102 (2004)].

Amirkhizi, Alireza V.; Nemat-Nasser, Sia

2007-07-01

357

Nitrogen gas permeability tests at Avery Island  

SciTech Connect

Several nitrogen gas permeability tests have been performed at the Avery Island field site. These included a preliminary suite of tests performed at various locations around the site, tests performed in conjunction with the brine movement studies, and a series of extended permeability measurements. As a result of the preliminary tests and the brine movement tests, further tests were justified to refine the measurement technique and resolve observed anomalies. This report presents data acquired during the extended permeability measurements at Avery Island, analysis of the data, and comparison of the data with a finite-element simulation. Permeabilities were found as low as 4 x 10/sup -20/ ft/sup 2/ and as high as 6 x 10/sup -17/ ft/sup 2/ with a tendency of permeability decreasing as temperatures increased.

Blankenship, D.A.; Stickney, R.G.

1983-04-01

358

Glycoconjugates and Related Molecules in Human Vascular Endothelial Cells  

PubMed Central

Vascular endothelial cells (ECs) form the inner lining of blood vessels. They are critically involved in many physiological functions, including control of vasomotor tone, blood cell trafficking, hemostatic balance, permeability, proliferation, survival, and immunity. It is considered that impairment of EC functions leads to the development of vascular diseases. The carbohydrate antigens carried by glycoconjugates (e.g., glycoproteins, glycosphingolipids, and proteoglycans) mainly present on the cell surface serve not only as marker molecules but also as functional molecules. Recent studies have revealed that the carbohydrate composition of the EC surface is critical for these cells to perform their physiological functions. In this paper, we consider the expression and functional roles of endogenous glycoconjugates and related molecules (galectins and glycan-degrading enzymes) in human ECs.

Toyoda, Masashi

2013-01-01

359

Roles of alphav integrins in vascular biology and pulmonary pathology.  

PubMed

The five integrins that contain the alphav subunit are widely expressed and their expression is tightly regulated. However, most tissues in mice lacking the alphav subunit, and thus deficient in all five integrins, develop normally, suggesting that nearly all of the critical steps in development and cellular differentiation can occur in the absence of these integrins. Studies over the past few years have identified highly specialized roles for specific alphav integrins in preventing inappropriate vascular growth and in control of vascular permeability. Two members of this family, alphavbeta6 and alphavbeta8, play novel roles in activating latent complexes of the growth factor TGFbeta (transforming growth factor beta). Studies in mice lacking the beta6 subunit have identified unexpected roles for alphavbeta6-mediated TGFbeta activation in models of pulmonary and renal fibrosis, acute lung injury and pulmonary emphysema. PMID:15363806

Sheppard, Dean

2004-10-01

360

Phosphodiesterase 4 inhibition attenuates atrial natriuretic peptide-induced vascular hyperpermeability and loss of plasma volume  

PubMed Central

Inhibition of phosphodiesterase 4 (PDE4) to increase endothelial cAMP and stabilize the endothelial barrier attenuates acute inflammatory increases in vascular permeability. We extended this approach to attenuate physiological increases in vascular permeability in response to atrial natriuretic peptide (ANP), which acts with the kidney to regulate plasma volume. We measured blood-to-tissue albumin clearance and changes in plasma volume in isoflurane-anaesthetized mice (C57BL/6J) pre-treated with rolipram (8 mg kg?1i.p., 30 min). Rolipram significantly reduced albumin permeability, measured using a dual-label fluorescence method, in skin and skeletal muscle compared with ANP alone (500 ng kg?1 min?1). Skin and muscle tissue accounted for 70% of the reduction in whole body albumin clearance taking into account albumin clearance in gastrointestinal (GI) tissue, heart and kidney. The action of ANP and rolipram to modify albumin clearances in duodenum and jejunum could be accounted for by local increases in vascular perfusion to increase surface area for exchange. ANP increased haematocrit from 40.6% to 46.8%, corresponding to an average loss of 22% plasma fluid volume (227 ?l), and this was almost completely reversed with rolipram. Renal water excretion accounted for less than 30% of plasma fluid loss indicating that reduced albumin permeability and reduced filtration into vasodilated GI tissue were the predominant actions of PDE4 inhibition. Similar fluid retention was measured in mice with endothelial-restricted deletion of the guanylyl cyclase-A receptor for ANP. Stabilizing the endothelial barrier to offset ANP-induced increases in vascular permeability may be part of a strategy to maintain plasma volume.

Lin, Yueh-Chen; Samardzic, Haris; Adamson, Roger H; Renkin, Eugene M; Clark, Joyce F; Reed, Rolf K; Curry, Fitz-Roy E

2011-01-01

361

Role of small GTPases and alphavbeta5 integrin in Pseudomonas aeruginosa-induced increase in lung endothelial permeability.  

PubMed

Pseudomonas aeruginosa is an opportunistic pathogen that can cause severe pneumonia associated with airspace flooding with protein-rich edema in critically ill patients. The type III secretion system is a major virulence factor and contributes to dissemination of P. aeruginosa. However, it is still unknown which particular bacterial toxin and which cellular pathways are responsible for the increase in lung endothelial permeability induced by P. aeruginosa. Thus, the first objective of this study was to determine the mechanisms by which this species causes an increase in lung endothelial permeability. The results showed that ExoS and ExoT, two of the four known P. aeruginosa type III cytotoxins, were primarily responsible for bacterium-induced increases in protein permeability across the lung endothelium via an inhibition of Rac1 and an activation of the RhoA signaling pathway. In addition, inhibition of the alphavbeta5 integrin, a central regulator of lung vascular permeability, prevented these P. aeruginosa-mediated increases in albumin flux due to endothelial permeability. Finally, prior activation of the stress protein response or adenoviral gene transfer of the inducible heat shock protein Hsp72 also inhibited the damaging effects of P. aeruginosa on the barrier function of lung endothelium. Taken together, these results demonstrate the critical role of the RhoA/alphavbeta5 integrin pathway in mediating P. aeruginosa-induced lung vascular permeability. In addition, activation of the stress protein response with pharmacologic inhibitors of Hsp90 may protect lungs against P. aeruginosa-induced permeability changes. PMID:18703797

Ganter, Michael T; Roux, Jérémie; Su, George; Lynch, Susan V; Deutschman, Clifford S; Weiss, Yoram G; Christiaans, Sarah C; Myazawa, Byron; Kipnis, Eric; Wiener-Kronish, Jeanine P; Howard, Marybeth; Pittet, Jean-François

2009-01-01

362

Indexing Consistency and Quality.  

ERIC Educational Resources Information Center

Proposed is a measure of indexing consistency based on the concept of "fuzzy sets." By this procedure a higher consistency value is assigned if indexers agree on the more important terms than if they agree on less important terms. Measures of the quality of an indexer's work and exhaustivity of indexing are also proposed. Experimental data on…

Zunde, Pranas; Dexter, Margaret E.

363

Nucleic acid indexing  

DOEpatents

A restriction site indexing method for selectively amplifying any fragment generated by a Class II restriction enzyme includes adaptors specific to fragment ends containing adaptor indexing sequences complementary to fragment indexing sequences near the termini of fragments generated by Class II enzyme cleavage. A method for combinatorial indexing facilitates amplification of restriction fragments whose sequence is not known.

Guilfoyle, Richard A. (Madison, WI) [Madison, WI; Guo, Zhen (Bellevue, WA) [Bellevue, WA

1999-01-01

364

Nucleic acid indexing  

DOEpatents

A restriction site indexing method for selectively amplifying any fragment generated by a Class II restriction enzyme includes adaptors specific to fragment ends containing adaptor indexing sequences complementary to fragment indexing sequences near the termini of fragments generated by Class II enzyme cleavage. A method for combinatorial indexing facilitates amplification of restriction fragments whose sequence is not known.

Guilfoyle, Richard A. (Madison, WI) [Madison, WI; Guo, Zhen (Bellevue, WA) [Bellevue, WA

2001-01-01

365

21 CFR 886.5916 - Rigid gas permeable contact lens.  

Code of Federal Regulations, 2010 CFR

... 2010-04-01 false Rigid gas permeable contact lens. 886.5916 Section...Therapeutic Devices § 886.5916 Rigid gas permeable contact lens. (a) Identification. A rigid gas permeable contact lens is a device...

2010-04-01

366

21 CFR 886.5916 - Rigid gas permeable contact lens.  

Code of Federal Regulations, 2010 CFR

... 2009-04-01 false Rigid gas permeable contact lens. 886.5916 Section...Therapeutic Devices § 886.5916 Rigid gas permeable contact lens. (a) Identification. A rigid gas permeable contact lens is a device...

2009-04-01

367

21 CFR 886.5916 - Rigid gas permeable contact lens.  

Code of Federal Regulations, 2013 CFR

...2013-04-01 false Rigid gas permeable contact lens. 886.5916 Section 886.5916...Devices § 886.5916 Rigid gas permeable contact lens. (a) Identification. A rigid gas permeable contact lens is a device intended to...

2013-04-01

368

Opposing Effects of the Angiopoietins on the Thrombin-Induced Permeability of Human Pulmonary Microvascular Endothelial Cells  

PubMed Central

Background Angiopoietin-2 (Ang-2) is associated with lung injury in ALI/ARDS. As endothelial activation by thrombin plays a role in the permeability of acute lung injury and Ang-2 may modulate the kinetics of thrombin-induced permeability by impairing the organization of vascular endothelial (VE-)cadherin, and affecting small Rho GTPases in human pulmonary microvascular endothelial cells (HPMVECs), we hypothesized that Ang-2 acts as a sensitizer of thrombin-induced hyperpermeability of HPMVECs, opposed by Ang-1. Methodology/Principal Findings Permeability was assessed by measuring macromolecule passage and transendothelial electrical resistance (TEER). Angiopoietins did not affect basal permeability. Nevertheless, they had opposing effects on the thrombin-induced permeability, in particular in the initial phase. Ang-2 enhanced the initial permeability increase (passage, P?=?0.010; TEER, P?=?0.021) in parallel with impairment of VE-cadherin organization without affecting VE-cadherin Tyr685 phosphorylation or increasing RhoA activity. Ang-2 also increased intercellular gap formation. Ang-1 preincubation increased Rac1 activity, enforced the VE-cadherin organization, reduced the initial thrombin-induced permeability (TEER, P?=?0.027), while Rac1 activity simultaneously normalized, and reduced RhoA activity at 15 min thrombin exposure (P?=?0.039), but not at earlier time points. The simultaneous presence of Ang-2 largely prevented the effect of Ang-1 on TEER and macromolecule passage. Conclusions/Significance Ang-1 attenuated thrombin-induced permeability, which involved initial Rac1 activation-enforced cell-cell junctions, and later RhoA inhibition. In addition to antagonizing Ang-1, Ang-2 had also a direct effect itself. Ang-2 sensitized the initial thrombin-induced permeability accompanied by destabilization of VE-cadherin junctions and increased gap formation, in the absence of increased RhoA activity.

van der Heijden, Melanie; van Nieuw Amerongen, Geerten P.; van Bezu, Jan; Paul, Marinus A.; Groeneveld, A. B. Johan; van Hinsbergh, Victor W. M.

2011-01-01

369

Characterization of tumor microvascular structure and permeability: comparison between magnetic resonance imaging and intravital confocal imaging  

NASA Astrophysics Data System (ADS)

Solid tumors are characterized by abnormal blood vessel organization, structure, and function. These abnormalities give rise to enhanced vascular permeability and may predict therapeutic responses. The permeability and architecture of the microvasculature in human osteosarcoma tumors growing in dorsal window chambers in athymic mice were measured by confocal laser scanning microscopy (CLSM) and dynamic contrast enhanced magnetic resonance imaging (DCE-MRI). Dextran (40 kDa) and Gadomer were used as molecular tracers for CLSM and DCE-MRI, respectively. A significant correlation was found between permeability indicators. The extravasation rate Ki as measured by CLSM correlated positively with DCE-MRI parameters, such as the volume transfer constant Ktrans and the initial slope of the contrast agent concentration-time curve. This demonstrates that these two techniques give complementary information. Extravasation was further related to microvascular structure and was found to correlate with the fractal dimension and vascular density. The structural parameter values that were obtained from CLSM images were higher for abnormal tumor vasculature than for normal vessels.

Reitan, Nina Kristine; Thuen, Marte; Goa, Pa?L. Erik; de Lange Davies, Catharina

2010-05-01

370

Glioblastoma Cell-Secreted Interleukin-8 Induces Brain Endothelial Cell Permeability via CXCR2  

PubMed Central

Glioblastoma constitutes the most aggressive and deadly of brain tumors. As yet, both conventional and molecular-based therapies have met with limited success in treatment of this cancer. Among other explanations, the heterogeneity of glioblastoma and the associated microenvironment contribute to its development, as well as resistance and recurrence in response to treatments. Increased vascularity suggests that tumor angiogenesis plays an important role in glioblastoma progression. However, the molecular crosstalk between endothelial and glioblastoma cells requires further investigation. To examine the effects of glioblastoma-derived signals on endothelial homeostasis, glioblastoma cell secretions were collected and used to treat brain endothelial cells. Here, we present evidence that the glioblastoma secretome provides pro-angiogenic signals sufficient to disrupt VE-cadherin-mediated cell-cell junctions and promote endothelial permeability in brain microvascular endothelial cells. An unbiased angiogenesis-specific antibody array screen identified the chemokine, interleukin-8, which was further demonstrated to function as a key factor involved in glioblastoma-induced permeability, mediated through its receptor CXCR2 on brain endothelia. This underappreciated interface between glioblastoma cells and associated endothelium may inspire the development of novel therapeutic strategies to induce tumor regression by preventing vascular permeability and inhibiting angiogenesis.

Dwyer, Julie; Hebda, Jagoda K.; Le Guelte, Armelle; Galan-Moya, Eva-Maria; Smith, Sherri S.; Azzi, Sandy; Bidere, Nicolas; Gavard, Julie

2012-01-01

371

Radiation effects on the fibrinolytic system and their relation to hemorrhagic diathesis and increased endothelial permeability  

SciTech Connect

This study was designed to investigate the effects of wholebody X-irradiation on the fibrinolytic system, the causes of radiation-induced changes in plasmin (fibrinolytic) activity, and the contribution of increased plasmin activity to increased capillary (endothelial) permeability and hemorrhagic diathesis. The parameters evaluated using adult, male, Rochester ex-Wistar rats were: (1) plasmin, plasminogen, and plasminogen activator levels in plasma within one month after 425, 655, or 885 rad and at 3.5, 7 and 12 months after 425 rad, by a modified caseinolytic method; (2) tissue plasminogen activator activity (TPAA) in heart, kidneys, lungs, liver, pancreas and spleen, by a fibrin plate method (885 rad); (3) vascular permeability, by a radioisotopic method (885 rad); and (4) gross hemorrhagic response, scored for severity. The dose-dependent changes described in plasmin, plasminogen and plasminogen activator were multi-phasic. Epsilon-amino-caproic acid (0.3 gm/kg body weight) prevented the immediate and early radiation effects on these fibrinolytic components, and partially inhibited the later effects (within one month) whether administered only as a single injection before irradiation or maintained by daily water intake thereafter. The kidneys, spleen and pancreas were markedly susceptible to radiation-induced changes in TPAA. The lungs and liver showed significant changes in capillary permeability, which correlated positively with changes in vascular volume and blood plasmin and plasminogen activator levels. Increased plasmin (fibrinolytic) activity, superimposed on a hemostatic apparatus already impaired because of thrombocytopenia, contributed to hemorrhagic diathesis in acute radiation sickness.

Ballelos, E.E.

1982-01-01

372

Non-invasive vascular imaging: assessing tumour vascularity  

Microsoft Academic Search

.   Non-invasive assessment of vascularity is a new diagnostic approach to characterise tumours. Vascular assessment is based\\u000a on the pathophysiology of tumour angiogenesis and its diagnostic implications for tumour biology, prognosis and therapy response.\\u000a Two current techniques investigating vascular features in addition to morphology are Doppler ultrasonography and contrast-enhanced\\u000a MRI. Diagnostic differentiation has been shown to be possible with Doppler,

S. Delorme; M. V. Knopp

1998-01-01

373

Vascular Inflammation in Obesity and Sleep Apnea  

PubMed Central

Background Unrecognized obstructive sleep apnea (OSA) is highly prevalent in obesity. Both obesity and OSA are associated with vascular endothelial inflammation and increased risk for cardiovascular diseases. We investigated directly whether endothelial alterations that are commonly attributed to obesity are in fact related to OSA. Methods and Results Seventy-one subjects with body mass index (BMI) ranging from normal to obese underwent attended polysomnography. To assess directly vascular inflammation and oxidative stress, we quantified expression of nuclear factor kappa B (NF?B) and nitrotyrosine by immunofluorescence in freshly harvested venous endothelial cells. To evaluate basal endothelial nitric oxide (NO) production and activity, we quantified expression of endothelial NO synthase (eNOS) and phosphorylated eNOS (P-eNOS). Vascular reactivity was measured by brachial artery flow-mediated dilation (FMD). Expression of eNOS and P-eNOS and FMD were significantly lower whereas expression of nitrotyrosine was significantly greater in OSA patients (n=38) than in OSA-free subjects (n=33) regardless of central adiposity. Expression of NF?B was greater in obese OSA patients than in obese OSA-free subjects (p=0.004). Protein expression and FMD were not significantly affected by increasing BMI or central obesity in OSA patients and in OSA-free subjects. After 4 weeks of continuous positive airway pressure (CPAP) therapy, FMD and expression of eNOS and P-eNOS significantly increased whereas expression of nitrotyrosine and NF?B significantly decreased in OSA patients who adhered with CPAP?4 hours daily. Conclusions Untreated OSA rather than obesity is a major determinant of vascular endothelial dysfunction, inflammation and elevated oxidative stress in obese patients.

Jelic, Sanja; Lederer, David J.; Adams, Tessa; Padeletti, Margherita; Colombo, Paolo C.; Factor, Phillip H.; Le Jemtel, Thierry H.

2010-01-01

374

Anisotropy of permeability in faulted porous sandstones  

NASA Astrophysics Data System (ADS)

Studies of fault rock permeabilities advance the understanding of fluid migration patterns around faults and contribute to predictions of fault stability. In this study a new model is proposed combining brittle deformation structures formed during faulting, with fluid flow through pores. It assesses the impact of faulting on the permeability anisotropy of porous sandstone, hypothesising that the formation of fault related micro-scale deformation structures will alter the host rock porosity organisation and create new permeability pathways. Core plugs and thin sections were sampled around a normal fault and oriented with respect to the fault plane. Anisotropy of permeability was determined in three orientations to the fault plane at ambient and confining pressures. Results show that permeabilities measured parallel to fault dip were up to 10 times higher than along fault strike permeability. Analysis of corresponding thin sections shows elongate pores oriented at a low angle to the maximum principal palaeo-stress (?1) and parallel to fault dip, indicating that permeability anisotropy is produced by grain scale deformation mechanisms associated with faulting. Using a soil mechanics 'void cell model' this study shows how elongate pores could be produced in faulted porous sandstone by compaction and reorganisation of grains through shearing and cataclasis.

Farrell, N. J. C.; Healy, D.; Taylor, C. W.

2014-06-01

375

Potential vascular damage from radiation in the space environment  

NASA Astrophysics Data System (ADS)

Cultured endothelial cells of blood vessels have a Do of 2 Gy for X-rays. A dose of 0.5 Gy of X-rays has an acute effect on vessel diameter. The vessels may show other acute effects such as change in permeability including a change in the blood brain barrier. Changes occurring from late effects of chronic exposure in vascular architecture include telangiectasia and decrease in vascular density. Changes in the perivascular connective tissue particularly collagen may play a role in these changes. After charged particle exposure of 15 and 30 Gy, radiation changes in the blood brain barrier and vascular changes are noted in the nervous system. These long term changes are recorded by PET, MRI, and CT imaging. Chronic exposure to alpha particles causes vascular damage in compact bone resulting in bone infarcts. Using tandem scanning confocal microscopy in-situ imaging of the capillaries and collagen of the papillary dermis provides a non-invasive method of serial recording of changes in irradiated microvasculature.

Griem, M. L.; Robotewskyj, A.; Nagel, R. H.

1994-10-01

376

Inflammation and Vascular Injury  

PubMed Central

The invited special lecture at the 76th Annual Scientific Meeting of the Japanese Circulation Society focused on the central role of inflammation in vascular injury and repair. Early studies pioneered the concept that mechanical injury, such as balloon angioplasty and endovascular stent deployment, elicits an inflammatory response from the vessel wall. This hypothesis was developed and substantiated at a time when the prevailing dogma viewed restenosis following angioplasty as a primarily proliferative smooth muscle cell disease. Antibody targeting of Mac-1 reduced leukocyte accumulation and limited neointimal formation following balloon injury or stent implantation. Genetic absence of Mac-1 resulted in diminished leukocyte accumulation and neointimal thickening after carotid artery injury in mice. In the course of those studies, our laboratory made fundamental discoveries regarding the mechanism of leukocyte recruitment at sites of vascular injury and identified platelet glycoprotein (GP) Ib?, a component of the GPIb-IX-V complex, as the previously unknown platelet counter-receptor for Mac-1. Follow-on studies have focused extensively on the structure, function, and signaling of the leukocyte integrin Mac-1. The binding site for GPIb? in Mac-1 has been mapped and subsequently showed that leukocyte engagement of platelet GPIb? via Mac-1 is critical not only for the biological response to vascular injury, but also for thrombosis, vasculitis, glomerulonephritis, and multiple sclerosis, thereby advancing the hypothesis that virtually all inflammation is platelet-dependent. Furthermore, ligand engagement of Mac-1 initiates a novel gene program that promotes inflammation by activating NF?B and downregulating the expression of the forkhead transcription factor Foxp1 that controls monocyte differentiation. Small molecule inhibitors of Mac-1 function have been pursued, including targeting of Mac-1-GPIb? binding or the downstream tyrosine kinase spleen tyrosine kinase. Drs Teruo Inoue, Koichi Node, Tatsuya Fukotomi, Masashi Sakuma, Toshifumi Morooka, and Kohsuke Nakajima, valued Japanese collaborators and post-doctoral fellows, have contributed enormously to these discoveries.

Simon, Daniel I.

2014-01-01

377

DIABETES AND VASCULAR DISEASE  

PubMed Central

Two-thirds of American adults are overweight or obese, 75 million have hypertension and another 25 million have diabetes. Cardiovascular disease is the leading cause of morbidity and mortality and a major driver of health care costs in patients with type 2 diabetes. Observational studies suggest that insulin resistance, hypertension and hyperglycemia independently predict cardiovascular disease and chronic kidney disease. Indeed, coexisting hypertension appears to be a most powerful determinant of cardiovascular disease risk in diabetic patients. This update explores recent investigation which sheds light on our understanding of various metabolic and hemodynamic factors which promote vascular disease, as well as strategies to lessen cardiovascular disease in patients with diabetes.

Sowers, James R.

2013-01-01

378

Fibronectins in Vascular Morphogenesis  

PubMed Central

Fibronectin is an extracellular matrix protein found only in vertebrate organisms containing endothelium-lined vasculature and is required for cardiovascular development in fish and mice. Fibronectin and its splice variants containing EIIIA and EIIIB domains are highly upregulated around newly developing vasculature during embryogenesis and in pathological conditions including atherosclerosis, cardiac hypertrophy and tumorigenesis, however, their molecular roles in these processes are not entirely understood. We review genetic studies examining functions of fibronectin and its splice variants during embryonic cardiovascular development, and discuss potential roles of fibronectins in vascular disease and tumor angiogenesis.

Astrof, Sophie; Hynes, Richard O.

2009-01-01

379

Microfluidic technology in vascular research.  

PubMed

Vascular cell biology is an area of research with great biomedical relevance. Vascular dysfunction is involved in major diseases such as atherosclerosis, diabetes, and cancer. However, when studying vascular cell biology in the laboratory, it is difficult to mimic the dynamic, three-dimensional microenvironment that is found in vivo. Microfluidic technology offers unique possibilities to overcome this difficulty. In this review, an overview of the recent applications of microfluidic technology in the field of vascular biological research will be given. Examples of how microfluidics can be used to generate shear stresses, growth factor gradients, cocultures, and migration assays will be provided. The use of microfluidic devices in studying three-dimensional models of vascular tissue will be discussed. It is concluded that microfluidic technology offers great possibilities to systematically study vascular cell biology with setups that more closely mimic the in vivo situation than those that are generated with conventional methods. PMID:19911076

van der Meer, A D; Poot, A A; Duits, M H G; Feijen, J; Vermes, I

2009-01-01

380

Microfluidic Technology in Vascular Research  

PubMed Central

Vascular cell biology is an area of research with great biomedical relevance. Vascular dysfunction is involved in major diseases such as atherosclerosis, diabetes, and cancer. However, when studying vascular cell biology in the laboratory, it is difficult to mimic the dynamic, three-dimensional microenvironment that is found in vivo. Microfluidic technology offers unique possibilities to overcome this difficulty. In this review, an overview of the recent applications of microfluidic technology in the field of vascular biological research will be given. Examples of how microfluidics can be used to generate shear stresses, growth factor gradients, cocultures, and migration assays will be provided. The use of microfluidic devices in studying three-dimensional models of vascular tissue will be discussed. It is concluded that microfluidic technology offers great possibilities to systematically study vascular cell biology with setups that more closely mimic the in vivo situation than those that are generated with conventional methods.

van der Meer, A. D.; Poot, A. A.; Duits, M. H. G.; Feijen, J.; Vermes, I.

2009-01-01

381

Laser therapy of vascular lesions.  

PubMed

Since the first construction of a laser by Maiman in 1960 and the first clinical application of a laser in the therapy of skin lesions by Leon Goldman, laser therapy has become an important therapeutic modality in dermatology. Various lasers can be used for the treatment of different vascular and non-vascular lesions. According to our results, vascular lesions constitute the most important indication for laser therapy in dermatology. PMID:17100741

Landthaler, M; Hohenleutner, U

2006-12-01

382

Vascular tumors of the orbit  

Microsoft Academic Search

Eighty-five vascular lesions of the orbit examined and treated between 1963–1993 were reviewed retrospectively to reveal the types of vascular tumors, age and sex distribution, clinical characteristics, treatment options and prognosis. Capillary hemangioma was the most frequent orbital vascular tumor accounting for 37 of 85 cases making up 43.5% of the entire orbital masses. Cavernous hemangioma accounted for 35 cases

Ilhan Günalp; Kaan Gündüz

1995-01-01

383

Cyclic AMP response element-binding protein prevents endothelial permeability increase through transcriptional controlling p190RhoGAP expression  

PubMed Central

Increased endothelial permeability contributes to the morbidity and mortality associated with chronic inflammatory diseases, including acute lung injury. Cyclic AMP response element-binding protein (CREB) transcriptional factor induces genes that regulate inflammation and vascular remodeling. However, the role of CREB in regulating endothelial barrier function is unknown. Here, we demonstrate that CREB maintains basal endothelial barrier function and suppresses endothelial permeability increase by diverse agonists such as thrombin, lipopolysaccharide, histamine, and VEGF. We show that CREB transcriptionally controls the expression of p190RhoGAP-A, a GTPase-activating protein that inhibits small GTPase RhoA. Impairing CREB function using small interfering RNA or dominant-negative (dn)–CREB mutant (dn-CREB) markedly suppressed p190RhoGAP-A expression, increased RhoA activity, induced actin stress fiber formation, and produced an amplified and protracted increase in endothelial permeability in response to thrombin. Rescuing p190RhoGAP-A expression restored the permeability defect in dn-CREB–transducing endothelial cells. These findings were recapitulated in vivo because dn-CREB expression in mice vasculature increased basal lung microvessel permeability and exaggerated permeability increase induced by thrombin and lipopolysaccharide. Inhibiting RhoA signaling restored endothelial barrier dysfunction in the dn-CREB–expressing lung microvasculature. These results uncover a pivotal role of CREB in regulating endothelial barrier function by restricting RhoA signaling through controlling p190RhoGAP-A expression.

Chava, Koteswara Rao; Tauseef, Mohammad; Sharma, Tiffany

2012-01-01

384

Role of intracellular calcium and reactive oxygen species in microbubble-mediated alterations of endothelial layer permeability.  

PubMed

Drugs will be delivered to diseased tissue more efficiently if the vascular endothelial permeability is increased. Ultrasound in combination with an ultrasound contrast agent is known to increase the permeability of the endothelial layer, but the mechanism is not known. The goal of this study was to elucidate whether intracellular calcium ions, [Ca(2+)]i, and reactive oxygen species (ROS) are part of the mechanism that leads to an increased endothelial layer permeability following ultrasound and microbubble treatment. Human umbilical vein endothelial cells (HUVECs) treated for 2 min with ultrasound-activated microbubbles (1 MHz, 210 kPa, 10 000 cycles, 20 Hz repetition rate) had an increased permeability that lasted up to 12 h. Recovery of permeability after 2 h was only found when HUVECs were preincubated with the [Ca(2+)]i chelator BAPTA-AM or the antioxidant butylated hydroxytoluene (BHT). This suggests that both [Ca(2+)]i and ROS play an important role in the mechanism of increased permeability following ultrasound in combination with microbubble treatment. PMID:24658714

Kooiman, Klazina; van der Steen, Antonius F W; de Jong, Nico

2013-09-01

385

Quantifying Glomerular Permeability of Fluorescent Macromolecules Using 2-Photon Microscopy in Munich Wistar Rats  

PubMed Central

Kidney diseases involving urinary loss of large essential macromolecules, such as serum albumin, have long been thought to be caused by alterations in the permeability barrier comprised of podocytes, vascular endothelial cells, and a basement membrane working in unison. Data from our laboratory using intravital 2-photon microscopy revealed a more permeable glomerular filtration barrier (GFB) than previously thought under physiologic conditions, with retrieval of filtered albumin occurring in an early subset of cells called proximal tubule cells (PTC)1,2,3. Previous techniques used to study renal filtration and establishing the characteristic of the filtration barrier involved micropuncture of the lumen of these early tubular segments with sampling of the fluid content and analysis4. These studies determined albumin concentration in the luminal fluid to be virtually non-existent; corresponding closely to what is normally detected in the urine. However, characterization of dextran polymers with defined sizes by this technique revealed those of a size similar to serum albumin had higher levels in the tubular lumen and urine; suggesting increased permeability5. Herein is a detailed outline of the technique used to directly visualize and quantify glomerular fluorescent albumin permeability in vivo. This method allows for detection of filtered albumin across the filtration barrier into Bowman's space (the initial chamber of urinary filtration); and also allows quantification of albumin reabsorption by proximal tubules and visualization of subsequent albumin transcytosis6. The absence of fluorescent albumin along later tubular segments en route to the bladder highlights the efficiency of the retrieval pathway in the earlier proximal tubule segments. Moreover, when this technique was applied to determine permeability of dextrans having a similar size to albumin virtually identical permeability values were reported2. These observations directly support the need to expand the focus of many proteinuric renal diseases to included alterations in proximal tubule cell reclamation.

Sandoval, Ruben M.; Molitoris, Bruce A.

2013-01-01

386

Microvascular Pressure Is the Principal Driving Force for Interstitial Hypertension in Solid Tumors: Implications for Vascular Collapse1  

Microsoft Academic Search

The interstitial fluid pressure (IFF) has been found to be as high as 20 to 50 mm Hg in both experimental and human solid tumors. While the IFF is an important determinant of the delivery of therapeutic agents to neoplastic cells in vivo,the mechanisms responsible for inter stitial hypertension are not completely understood. The high vascular permeability of tumor blood

Rakesh K. Jain

1992-01-01

387

[Late detection of vascular injuries].  

PubMed

Generally recognizing of traumatical vascular injuries isn't difficult since clinical signs and symptoms show them unambiguously. For some time-mainly in case of blunt and shot wounds-lacking unanimous signs the vascular injuries can't be diagnosed. Later on appearing symptoms as complications raise the chance of existence of an earlier vascular injury. In case of three patients the elapsing time between the vascular injury and its diagnosis was 4 weeks, 3 years and more than 50 years. PMID:11300065

Gergely, M; Halmos, F; Behek, S; Szabolcsi, T; Lukács, A

2000-08-01

388

Angiotensin II and Vascular Injury.  

PubMed

Vascular injury, characterized by endothelial dysfunction, structural remodelling, inflammation and fibrosis, plays an important role in cardiovascular diseases. Cellular processes underlying this include altered vascular smooth muscle cell (VSMC) growth/apoptosis, fibrosis, increased contractility and vascular calcification. Associated with these events is VSMC differentiation and phenotypic switching from a contractile to a proliferative/secretory phenotype. Inflammation, associated with macrophage infiltration and increased expression of redox-sensitive pro-inflammatory genes, also contributes to vascular remodelling. Among the many factors involved in vascular injury is Ang II. Ang II, previously thought to be the sole biologically active downstream peptide of the renin-angiotensin system (RAS), is converted to smaller peptides, [Ang III, Ang IV, Ang-(1-7)], that are functional and that modulate vascular tone and structure. The actions of Ang II are mediated via signalling pathways activated upon binding to AT1R and AT2R. AT1R activation induces effects through PLC-IP3-DAG, MAP kinases, tyrosine kinases, tyrosine phosphatases and RhoA/Rho kinase. Ang II elicits many of its (patho)physiological actions by stimulating reactive oxygen species (ROS) generation through activation of vascular NAD(P)H oxidase (Nox). ROS in turn influence redox-sensitive signalling molecules. Here we discuss the role of Ang II in vascular injury, focusing on molecular mechanisms and cellular processes. Implications in vascular remodelling, inflammation, calcification and atherosclerosis are highlighted. PMID:24760441

Montezano, Augusto C; Nguyen Dinh Cat, Aurelie; Rios, Francisco J; Touyz, Rhian M

2014-06-01

389

Defining Vascular Stem Cells  

PubMed Central

Mesenchymal stem cells (MSCs) exist in most adult tissues and have been located near or within blood vessels. Although “perivascular” has been commonly used to describe such locations, increasing evidence points at the vessel wall as the exact location. Thus, “vascular stem cells (VSCs)” is recommended as a more accurate term for MSCs. Furthermore, 2 cell populations, namely pericytes and adventitial progenitor cells (APCs), are the likely VSCs. The pericyte evidence relies on the so-called pericyte-specific markers, but none of these markers is pericyte specific. In addition, pericytes appear to be too functionally diverse and sophisticated to have a large differentiation capacity. On the other hand, APCs are more naïve functionally and, therefore, more akin to being VSCs. In vitro, these cells spontaneously differentiate into pericytes, and can be induced to differentiate into vascular cells (endothelial and smooth muscle cells) and mesenchymal cells (eg, bone, cartilage, and fat). In vivo, indirect evidence also points to their ability to differentiate into mesenchymal cells of their native tissue (eg, fat). Moreover, they possess a large paracrine capacity and, therefore, can help maintain tissue homeostasis by encouraging the replication and differentiation of mesenchymal cells locally. These proposed in vivo functions are areas of interest for future research on VSCs.

Lue, Tom F.

2013-01-01

390

Neurocutaneous vascular syndromes.  

PubMed

There have been significant recent advances in the past several years in the field of neurocutaneous vascular syndromes, including the development of more stringent diagnostic criteria for PHACE syndrome, the renaming of macrocephaly-cutis marmorata telangiectatica congenita to macrocephaly-capillary malformation to accurately reflect the true nature of the syndrome, and discovery of new genetic mutations such as RASA-1. There have also been advances in the understanding and management of Sturge-Weber syndrome.PHACE syndrome is a constellation of neurologic, arterial, cardiac, ophthalmologic, and sternal abnormalities associated with infantile hemangiomas. PHACE is an acronym for Posterior fossa malformation, Hemangioma, Arterial anomalies, Coarctation of the aorta, Eye abnormalities. Some authors include an "S" for PHACE(S) to denote the association of ventral defects including Sternal clefting and Supraumbilical raphe.The accurate diagnosis and work-up of these patients require coordination of care across multiple disciplines, including neuroradiology, radiology, dermatology, neurology, surgery, and interventional radiology, among others.This paper is meant to update clinicians and researchers about important advances in these rare, important vascular syndromes, to improve care, and lay the foundation for future directions for research. PMID:20582592

Puttgen, Katherine B; Lin, Doris D M

2010-10-01

391

Tumoral and Choroidal Vascularization  

PubMed Central

An adequate balance between serine proteases and their plasminogen activator inhibitor-1 (PAI-1) is critical for pathological angiogenesis. PAI-1 deficiency in mice is associated with impaired choroidal neovascularization (CNV) and tumoral angiogenesis. In the present work, we demonstrate unexpected differences in the contribution of bone marrow (BM)-derived cells in these two processes regulated by PAI-1. PAI-1?/? mice grafted with BM-derived from wild-type mice were able to support laser-induced CNV formation but not skin carcinoma vascularization. Engraftment of irradiated wild-type mice with PAI-1?/? BM prevented CNV formation, demonstrating the crucial role of PAI-1 delivered by BM-derived cells. In contrast, the transient infiltration of tumor transplants by local PAI-1-producing host cells rather than by BM cells was sufficient to rescue tumor growth and angiogenesis in PAI-1-deficient mice. These data identify PAI-1 as a molecular determinant of a local permissive soil for tumor angiogenesis. Altogether, the present study demonstrates that different cellular mechanisms contribute to PAI-1-regulated tumoral and CNV. PAI-1 contributes to BM-dependent choroidal vascularization and to BM-independent tumor growth and angiogenesis.

Jost, Maud; Maillard, Catherine; Lecomte, Julie; Lambert, Vincent; Tjwa, Marc; Blaise, Pierre; Alvarez Gonzalez, Maria-Luz; Bajou, Khalid; Blacher, Silvia; Motte, Patrick; Humblet, Chantal; Defresne, Marie Paule; Thiry, Marc; Frankenne, Francis; Gothot, Andre; Carmeliet, Peter; Rakic, Jean-Marie; Foidart, Jean-Michel; Noel, Agnes

2007-01-01

392

CENDI Indexing Workshop  

NASA Technical Reports Server (NTRS)

The CENDI Indexing Workshop held at NASA Headquarters, Two Independence Square, 300 E Street, Washington, DC, on September 21-22, 1994 focused on the following topics: machine aided indexing, indexing quality, an indexing pilot project, the MedIndEx Prototype, Department of Energy/Office of Scientific and Technical Information indexing activities, high-tech coding structures, category indexing schemes, and the Government Information Locator Service. This publication consists mostly of viewgraphs related to the above noted topics. In an appendix is a description of the Government Information Locator Service.

1994-01-01

393

AGU index terms updated  

NASA Astrophysics Data System (ADS)

AGU has just completed a major revision of its Index Terms. The last major revision of the Index Terms was conducted in 1995. AGU Index Terms are used for classification of both AGU publications and meetings programs. The new Index Terms will be available for use by the AGU community on 17 December (http://www.agu.org/pubs/indexterms).A 15-person working group, representing various disciplinary groups across the AGU, was established by, and reports to, the Publications Committee. The Index Committee members consulted with their constituencies and considered term-by-term usage of the old Index Term list in creating the new list.

Kodama, Kenneth P.

2004-12-01

394

How indexes have changed  

SciTech Connect

The accompanying table compares refinery construction and operating wages monthly for the years 1992 and 1993. The Nelson-Farrar refinery construction cost indexes are inflation indexes, while the operating indexes incorporate a productivity which shows improvement with experience and the increasing size of operations. The refinery construction wage indexes in the table show a steady advance over the 2-year period. Common labor indexes moved up faster than skilled indexes. Refinery operating wages showed a steady increase, while productivities averaged higher near the end of the period. Net results is that labor costs remained steady for the period.

Farrar, G.L.

1994-04-04

395

Peritoneal Permeability and Drug Enhancement in Uremia.  

National Technical Information Service (NTIS)

To investigate factors that influence peritoneal permeability, seeking augmented mass transport during peritoneal dialysis, the authors measured clearances in patients and rabbits. Reduced clearances of urea and creatinine (12.8 and 7.5 ml/min, respective...

J. F. Maher D. C. Hohnadel

1977-01-01

396

Flexible Sandwich Diaphragms Are Less Permeable  

NASA Technical Reports Server (NTRS)

Diaphragms for use in refrigerator compressors made as laminates of commercially available elastomers and metals. Diaphragms flexible, but less permeable by chlorofluorocarbon refrigerant fluids than diaphragms made of homogeneous mixtures of materials.

Michalovic, John G.; Vassallo, Franklin A.

1993-01-01

397

Lunar electrical conductivity and magnetic permeability  

NASA Technical Reports Server (NTRS)

Improved analytical techniques are applied to a large Apollo magnetometer data set to yield values of electroconductivity, temperature, magnetic permeability, and iron abundance. Average bulk electroconductivity of the moon is calculated to be .0007 mho/m; a rapid increase with depth to about .003 mho/m within 250 km is indicated. The temperature profile, obtained from the electroconductivity profile for olivine, indicates high lunar temperatures at relatively shallow depths. Magnetic permeability of the moon relative to its environment is calculated to be 1.008 plus or minus .005; a permeability relative to free space of 1.012 plus 0.011, minus 0.008 is obtained. Lunar iron abundances corresponding to this permeability value are 2.5 plus 2.3, minus 1.7 wt% free iron and 5.0-13.5 wt% total iron for a moon composed of a combination of free iron, olivine, and orthopyroxene.

Dyal, P.; Parkin, C. W.; Daily, W. D.

1975-01-01

398

Permeability After Impact Testing of Composite Laminates  

NASA Technical Reports Server (NTRS)

Since composite laminates are beginning to be identified for use in reusable launch vehicle propulsion systems, an understanding of their permeance is needed. A foreign object impact event can cause a localized area of permeability (leakage) in a polymer matrix composite and it is the aim of this study to assess a method of quantifying permeability-after-impact results. A simple test apparatus is presented and variables that could affect the measured values of permeability-after-impact were assessed. Once it was determined that valid numbers were being measured, a fiber/resin system was impacted at various impact levels and the resulting permeability measured, first with a leak check solution (qualitative) then using the new apparatus (quantitative). The results showed that as the impact level increased, so did the measured leakage. As the pressure to the specimen was increased, the leak rate was seen to increase in a non-linear fashion for almost all of the specimens tested.

Nettles, Alan T.

2003-01-01

399

Permeability After Impact Testing of Composite Laminates  

NASA Technical Reports Server (NTRS)

Since composite laminates are beginning to be identified for use in reusable launch vehicle propulsion systems, an understanding of their permeance is needed. A foreign object impact event can cause a localized area of permeability (leakage) in a polymer matrix composite and it is the aim of this study to assess a method of quantifying permeability-after-impact results. A simple test apparatus is presented and variables that could affect the measured values of permeability-after-impact were assessed. Once it was determined that valid numbers were being measured, a fiber/resin system was impacted at various impact levels and the resulting permeability measured, first with a leak check solution (qualitative) then using the new apparatus (quantitative). The results showed that as the impact level increased, so did the measured leakage. As the pressure to the specimen was increased, the leak rate was seen to increase in a non-linear fashion for almost all of the specimens tested.

Nettles, A.T.; Munafo, Paul (Technical Monitor)

2002-01-01

400

Water Vapor Permeability of Plastic Fast Packs.  

National Technical Information Service (NTIS)

The objective of this investigation was to perform nondestructive tests that quantitatively measured the water vapor permeability of a plastic (high density polyethylene) Type I Fast Pack design. The water vapor transmission rate (WVTR) of the new pack de...

J. A. Hincks

1978-01-01

401

Permeability of protective coatings to tritium.  

National Technical Information Service (NTIS)

The permeability of four protective coatings to tritium gas and tritiated water was investigated. The coatings, including two epoxies, one vinyl and one urethane, were selected for their suitability in CANDU plant service in Ontario Hydro. Sorption rates ...

J. M. Braun

1987-01-01

402

PERMEABILITY OF POLYMERIC MEMBRANE LINING MATERIALS  

EPA Science Inventory

Permeabilities to three gases (carbon dioxide, methane, and nitrogen),