Wyniki wyszukiwania

1

Decreased immunoreactivity of von Willebrand factor may reflect persistent nature of the endothelial dysfunction in non-ischemic heart failure

100%

Reichman-Warmusz E., Brzozowska-Zasada M., Wojciechowska C., Dudek D., Warmusz O., Wojnicz R.

Folia Histochemica et Cytobiologica

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2021

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tom 59

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nr 2

2

Ischemic preconditioning prevents endothelial dysfunction, P-selectin expression, and neutrophil adhesion by preventing endothelin and O2-generation in the post-ischemic guinea-pig heart

86%

Duda M., Czarnowska E., Kurzelewski M., Konior A., Beresewicz A.

Journal of Physiology and Pharmacology

|

2006

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tom 57

|

nr 4

Evidence indicates that ischemia/reperfusion (IR) results in endothelial dysfunction and neutrophil adhesion in the post-ischemic myocardium and that ischemic preconditioning (IPC), superoxide dismutase (SOD), and anti-endothelin-1 (ET-1) interventions prevent these effects. We tested the hypothesis that ET-1-induced superoxide (O2-) generation mediates endothelial injury and neutrophil accumulation in the IR heart, that IPC protects the endothelium and prevents the adhesion by attenuating post-ischemic ET-1, and thus O2-, generation, and that the mitochondrial ATP-dependent potassium channel (mKATP) triggers the IPC-induced protection. Langendorff-perfused guinea-pig hearts were subjected either to 30 min ischemia/35 min reperfusion (IR) or were preconditioned prior to IR with three cycles of either 5 min ischemia/5 min reperfusion or 5 min infusion/5 min wash-out of mKATP opener diazoxide (0.5 µM). Neutrophils were infused to the hearts at 15-25min of the reperfusion. Coronary flow responses to acetylcholine (ACh) and nitroprusside (SNP) served as measures of endothelium-dependent and -independent vascular function, respectively. Myocardial outflow of ET-1 and O2-, P-selectin expression, neutrophil adhesion and functional recoveries were followed during reperfusion. IR augmented ET-1 and O2- outflow, P-selectin expression, and neutrophil adhesion, and impaired ACh response. These effects were attenuated or prevented by IPC and diazoxide, and 5-hydroxydecanoate (a selective mKATP blocker) abolished the effects of IPC and diazoxide. SOD (150 U/ml) and tezosentan (5 nM, a mixed ET-1-receptor antagonist) mimicked the effects of IPC, although they had no effect on the ET-1 generation. The preventive effect of IPC, SOD and tezosentan on P-selectin expression preceded their effect on neutrophil adhesion. These data suggest that in guinea-pig heart: (i) ET-1-induced O2- generation mediates the post-ischemic endothelial dysfunction, P-selectin expression and neutrophil adhesion; (ii) IPC and diazoxide afford protection by attenuating the ET-1, and thus O2- generation; (iii) the mKATP opening triggers the IPC protection; (iv) endothelial injury promotes post-ischemic neutrophil adhesion, but not vice versa.

3

Isoprenoid depletion by statins antagonizes cytokine-induced down-regulation of endothelial nitric oxide expression and increases NO synthase activity in human umbilical vein endothelial cells

86%

Jantzen F., Konemann S., Wolff B., Barth S., Staudt A., Kroemer H. K., Dahm J. B., Felix S. B., Landsberger M.

Journal of Physiology and Pharmacology

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2007

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tom 58

|

nr 3

Endothelial dysfunction and atherosclerosis are associated with an inflammation-induced decrease in endothelial nitric oxide synthase (eNOS) expression. Based on the differences between hydrophobic and hydrophilic statins in their reduction of cardiac events, we analyzed the effects of rosuvastatin and cerivastatin on eNOS and inducible NO synthase (iNOS) expression and NOS activity in TNF-alpha-stimulated human umbilical vein endothelial cells (HUVEC). Both statins reversed down-regulation of eNOS mRNA and protein expression by inhibiting HMG-CoA reductase and isoprenoid synthesis. Cerivastatin tended to a more pronounced effect on eNOS expression compared to rosuvastatin. NOS activity - measured by conversion of [3H]-L-arginine to [3H]-L-citrulline - was enhanced under treatment with both drugs due to inhibition of HMG-CoA reductase. Statin-treatment reduced iNOS mRNA expression under normal conditions, but had no relevant effects on iNOS mRNA expression in cytokine-treated cells. Rosuvastatin and cerivastatin reverse the detrimental effects of TNF-alpha-induced down-regulation in eNOS protein expression and increase NO synthase activity by inhibiting HMG-CoA reductase and subsequent blocking of isoprenoid synthesis. These results provide evidence that statins have beneficial effects by increasing eNOS expression and activity during the atherosclerotic process.

4

Arterial structure and function and its short- and long-term changes after bariatric surgery

72%

Gluszewska A., Gryglewska B., Rewiuk K., Zarzycki B., Dzieza-Grudnik A., Kwater A., Major P., Budzynski A., Gasowski J., Grodzicki T.

Journal of Physiology and Pharmacology

|

2019

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tom 70

|

nr 6

5

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Selected aspects of endothelial dysfunction and their influence on the atherosclerosis process modeled and analyzed by Petri net based approach

72%

Formanowicz D., Kozak A., Formanowicz P.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

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2011

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tom 92

|

nr 4

6

The role of cyclooxygenase [COX]-2 derived prostanoids on vasoconstrictor responses to phenylephrine is increased by exposure to low mercury concentration

72%

Pecanha F. M., Wiggers G. A., Briones A. M., Perez-Giron J. V., Miguel M., Garcia-Redondo A. B., Vassallo D. V., Alonso M. J., Salaices M.

Journal of Physiology and Pharmacology

|

2010

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tom 61

|

nr 1

29-36

We have previously demonstrated that chronic exposure to low-dose of mercury induced endothelial dysfunction and increased vasoconstrictor responses. The aim of this work was to investigate if mercury exposure alters contractile prostanoids production from cyclooxygenase-2 (COX-2) and its contribution to phenylephrine responses. For this, aortic segments from 3-month old Wistar rats daily treated with HgCl2 (1st dose 4.6 µg/kg, subsequent dose 0.07 µg/kg/day, i.m.) or vehicle for 30 days were used. Mercury treatment did not affect systolic blood pressure but increased phenylephrine-induced vasoconstriction. The non selective COX inhibitor, indomethacin (10 µmol/l) reduced the response to phenylephrine more in aortic segments from mercury-treated than control rats. The selective COX-2 inhibitor NS 398 (1 µmol/l), the thromboxane A2/prostaglandin H2 receptor (TP) antagonist SQ 29,548 (1 µmol/l), the TXA2 synthase inhibitor furegrelate (1 µmol/l), the EP1 receptor antagonist SC 19220 (1 µmol/l) and the AT1 receptor antagonist losartan (10 µmol/l) reduced phenylephrine response only in vessels from mercury-treated rats. TXA2 and PGE2 levels were greater in the incubation medium of vessels from treated than untreated rats; NS 398 decreased these levels only in the mercury group. COX-2 protein was localized in adventitial and endothelial cells. Aortic COX-2 mRNA expression and plasma angiotensin converting enzyme activity were greater in mercury-treated rats. These results suggest that treatment with low doses of mercury increases the release of COX-2-derived vasoconstrictor prostanoids and its participation in phenylephrine responses. The increased activation of the renin-angiotensin system after mercury treatment might be associated to this increased COX-2 activity.

7

Effects of prenatal hypoxia on pulmonary vascular reactivity in chickens prone to pulmonary hypertension

72%

Zoer B., Kessels L., Vereijken A., De Mey J. G. R., Bruggeman V., Decuypere E., Blanco C. E., Villamor E.

Journal of Physiology and Pharmacology

|

2009

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tom 60

|

nr 1

119-130

Among chickens, meat-producing broiler strains are highly prone to develop severe pulmonary hypertension (PH) that is accompanied by endothelial dysfunction in the conduit extrapulmonary arteries. We hypothesized that exposure to chronic prenatal mild hypoxia would accelerate PH and endothelial dysfunction in smaller intrapulpulmonary arteries from broiler chickens. Fertilized broiler and layer (White Leghorn, WL) eggs were incubated under normoxic or hypoxic conditions. Endothelium-dependent (tested with acetylcholine, ACh ) and -independent (tested with sodium nitroprusside, SNP) relaxations of the caudomedial intrapulmonary artery were studied on fetal day 19 and at 2 weeks post-hatch. The response to acute hypoxia in vitro was also studied in the 2 wk-old vessels. Relaxations induced by ACh and SNP were similar in broiler and layer chickens and were unaffected by chronic mild hypoxia during incubation. However, during in vitro acute hypoxia the broiler arteries showed a markedly enhanced contraction. Chronic prenatal hypoxia did not affect the response of intrapulmonary arteries to acute hypoxia. We conclude that early endothelial dysfunction is not present in the small pulmonary arteries of fast-growing broilers after incubation under normoxic or hypoxic conditions. The higher susceptibility of the broiler pulmonary arteries to acute hypoxia might, at least partially, explain the higher susceptibility to PH.

8

Analysis of the correlations between oxidative stress, gelatinases and their tissue inhibitors in the human subjects with obstructive sleep apnea syndrome

72%

Hopps E., Lo Presti R., Montana M., Canino B., Calandrino V., Caimi G.

Journal of Physiology and Pharmacology

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2015

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tom 66

|

nr 6

9

Mediterranean food and health: building human evidence

72%

Visioli F., Bogani P., Grande S., Galli C.

Journal of Physiology and Pharmacology. Supplement

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2005

|

tom 56

|

nr 1

37-49

Adherence to a Mediterranean style diet affords protection from degenerative diseases such as cardiovascular disorders and cancer. Identification of the active constituents of the Mediterranean diet is crucial to the formulation of appropriate dietary guidelines. Also, research on the pharmacological properties of the "minor components" of this diet, eg vitamins and polyphenols, is very active and might lead to the formulation of functional foods and nutraceuticals. Even though in vitro data are plentiful, human studies are difficult to perform due to ethical and practical reasons. Yet, intervention trials represent the best approach to validate claims of healthful activities. This article reviews human evidence of the biological properties of olive oil and tomato constituents and illustrates a research approach by which the bioactive elements of a wild plant (Cynara cardunculus) are first studied in vitro to build biochemical evidence, then in vivo to obtain proof of their vasomodularoty activity.

10

Anti-Qa2 animal models for preeclampsia preclinical studies: a pathological elevation of blood pressure and proteinuria

72%

Hikmah E. M., Liben P., Widjiati

Folia Biologica

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2019

|

tom 67

|

nr 2

11

Mechanisms of vascular dysfunction after subarachnoid hemorrhage

72%

Kozniewska E., Michalik R., Rafalowska J., Gadamski R., Walski M., Frontczak-Baniewicz M., Piotrowski P., Czernicki Z.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

|

nr 11

145-160

The main consequence of subarachnoid hemorrhage, for those who survive bleeding, is delayed, persistent vasospasm of intracranial conduit arteries which occurs between the third and seventh day after the insult and results in symptomatic brain ischemia in about 40% of cases. This vasospasm is considered to be a major cause of disability of post-SAH patients. Despite extensive experimental and clinical research, mechanisms of vasospasm are not fully understood. Dysfunction of the endothelium resulting in enhanced production of vasoconstrictors, phenotypic changes of the receptors in endothelium and smooth muscle cells, increased sensitivity of vascular smooth muscle cells to vasoconstrictors, release of spasmogens from lysed blood clot and inflammatory response of the vascular wall have been demonstrated and discussed as pathological mechanisms participating in the development of spasm. In recent years more attention is paid to the functional and structural changes in microcirculation and a concept of microvascular spasm is evolving. Our experimental studies in rat model of SAH strongly suggest that microcirculatory dysfunction and delayed vasospasm are related to the severity of acute, transient ischemia caused by critical decrease of perfusion pressure and active vasoconstriction immediately after the bleeding.

12

Serum endocan level in diabetes mellitus of patients with cirrhosis and risk of subsequent development of spontaneous bacterial peritonitis

72%

Zuwala-Jagiello J., Pazgan-Simon M., Simon K., Kukla M., Murawska-Cialowicz E., Grzebyk E.

Journal of Physiology and Pharmacology

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2019

|

tom 70

|

nr 3

13

High concentration of uric acid failed to affect endothelial function of small mesenteric arteries, femoral arteries and aortas from aged Wistar-Kyoto rats

72%

Balis P., Berenyiova A., Radosinska J., Kvandova M., Bernatova I., Puzserova A.

Journal of Physiology and Pharmacology

|

2020

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tom 71

|

nr 3

14

Eplerenone improves vascular function and reduces platelet activation in diabetic rats

72%

Schafer A., Vogt C., Fraccarollo D., Widder J., Flierl U., Hildemann S. K., Ertl G., Bauersachs J.

Journal of Physiology and Pharmacology

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2010

|

tom 61

|

nr 1

45-52

Diabetes is associated with endothelial dysfunction and platelet activation, both of which contribute to increased cardiovascular risk. We investigated whether the selective mineralocorticoid receptor (MR) antagonist eplerenone improves endothelial dysfunction and reduces platelet activation in diabetic rats. Male Wistar-rats were injected with streptozotocin (50 mg/kg i.v.) to induce insulin-deficient diabetes. After 2 weeks, treatment with eplerenone (100 mg/kg/day) or vehicle was initiated for 2 weeks. Aortic superoxide production determined by lucigenin-enhanced chemiluminescence and 2-hydroxyethidium formation was significantly increased in rats with diabetes and reduced by treatment with eplerenone (chemiluminescence: control 2045±227, STZ-placebo 3977±340, p<0.05 vs. control, STZ-eplerenone 1762±307, p<0.05 vs. STZ-placebo). Endothelium-dependent vasorelaxation was significantly attenuated in diabetic rats and was normalized by eplerenone (maximum relaxation in % of precontraction: control 95±3, STZ-placebo 82±3, p<0.01 vs. control, STZ-eplerenone 99±1, p<0.01 vs. STZ-placebo). Treatment with the selective MR antagonist significantly reduced fibrinogen-binding on activated GPIIb/IIIa (immunofluorescence: control 161±7, STZ-placebo 208±16, p<0.05 vs. control, STZ-eplerenone 173±6, p<0.05 vs. STZ-placebo). Eplerenone improves endothelial function by reducing superoxide formation and increasing NO bioavailability in diabetic rats. Platelet activation was significantly reduced by eplerenone. Selective MR blockade may constitute a useful therapeutic approach for treatment of vascular dysfunction in diabetes.

15

Weight loss-dependent and -independent effects of moderate calorie restriction on endothelial cell markers in obesity

72%

Korybalska K., Luczak J., Swora-Cwynar E., Kanikowska A., Czepulis N., Kanikowska D., Skalisz H., Breborowicz A., Grzymislawski M., Witowski J.

Journal of Physiology and Pharmacology

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2017

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tom 68

|

nr 4

16

Endothelial NADH-NADPH-dependent enzymatic sources of superoxide production: relationship to endothelial dysfunction

72%

Kalinowski L., Malinski T.

Acta Biochimica Polonica

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2004

|

tom 51

|

nr 2

There is growing evidence that endothelial dysfunction, which is often defined as the decreased endothelial-derived nitric oxide (NO) bioavailability, is a crucial factor leading to vascular disease states such as hypertension, diabetes, atherosclerosis, heart failure and cigarette smoking. This is due to the fact that the lack of NO in en- dothelium-dependent vascular disorders contributes to impaired vascular relaxation, platelet aggregation, increased vascular smooth muscle proliferation, and enhanced leukocyte adhesion to the endothelium. During the last several years, it has become clear that reduction of NO bioavailability in the endothelium-impaired function disorders is associated with an increase in endothelial production of superoxide (O2 ). Because O2 - rapidly scavenges NO within the endothelium, a reduction of bioactive NO might occur despite an increased NO generation. Among many enzymatic systems that are capable of producing O2 -, NAD(P)H oxidase and uncoupled endothelial NO synthase (eNOS) apparently are the main sources of O2- in the endothelialcells. It seems that O2– generated by NAD(P)H oxidase may trigger eNOS uncoupling and contribute to the endothelial balance between NO and O2–. That is maintained at diverse levels.

17

Superoxide- and nitric oxide-derived species mediate endothelial dysfunction, endothelial glycocalyx disruption, and enhanced neutrophil adhesion in the post-ischemic guinea-pig heart

72%

Kurzelewski M., Czarnowska E., Baresewicz A.

Journal of Physiology and Pharmacology

|

2005

|

tom 56

|

nr 2

The study was aimed at testing the hypothesis that a toxic product of the reaction between superoxide (O2-) and nitric oxide (NO) mediates, not only endothelial dysfunction, but also endothelium-glycocalyx disruption, and increased neutrophil (PMN) accumulation in the heart subjected to ischemia/reperfusion (IR) injury. Accordingly, we studied if scavengers of either O2- or NO, or a compound that was reported to attenuate cardiac production of peroxynitrite, would prevent endothelial injury and subsequent PNM adhesion in IR heart. Langendorff-perfused guinea-pig hearts were subjected to 30 min ischemia/35 min reperfusion, and infusion of PMN between 15 and 25 min of the reperfusion. Coronary flow responses to acetylcholine (ACh) and sodium nitroprusside (SNP) were used as measures of endothelium-dependent and -independent vascular function, respectively. PMN adhesion and endothelium glycocalyx ultrastructure were assessed in histological preparations. IR impaired the ACh, but not SNP, response by approximately 60%, caused endothelium-glycocalyx disruption, and approximately nine-fold increase in PMN adhesion. These alterations were prevented by superoxide dismutase (150 U/ml), NO synthase inhibitor, L-NAME (10 µM), NO scavenger, oxyhemoglobin (25 µM), and NO donor, SNAP (1 µM), and were not affected by catalase (600 u/ml). The glycocalyx-protective effect of these interventions preceded their effect on PMN adhesion. The data imply that PMN adhesion in IR guinea-pig heart is a process secondary to functional and/or structural changes in coronary endothelium, and that a toxic product of the reaction between superoxide and NO mediates these endothelial changes.

18

Postprandial response of ghrelin and PYY and indices of low-grade chronic inflammation in lean young women with polycystic ovary syndrome

72%

Zwirska-Korczala K., Sodowski K., Konturek S. J., Kuka D., Kukla M., Brzozowski T., Cnota W., Wozniak-Grygiel E., Jaworek J., Buldak R., Rybus-Kalinowska B., Fryczkowski M.

Journal of Physiology and Pharmacology. Supplement

|

2008

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tom 59

|

nr 2

The aim of the study were to aswer the question 1.) Whether circulating pro-inflammatory markers of endothelial dysfunction and due to chronic low-grade inflammation of obesity, are altered in untreated lean, young relatively healthy polycystic ovary syndrome (PCOS) patients in comparison with healthy controls; 2.) Whether postprandial plasma concentration pattern of ghrelin and PYY can be predictable as risk factors for atherosclerosis and depend of obesity. Forty young women with PCOS were divided in two groups: 19 lean and 21 obese. The control group included 20 lean, healthy volunteers. Plasma total and active ghrelin, total PYY and PYY3-36, serum adiponectin and insulin were measured using RIA technique, serum sCD40L, visfatin, sP-, sE-selectins, resistin by EIA. Composition of test meal was: 527 kcal total and consisted of 24.1% fat, 54.4% carbohydrate and 21.5% protein. Total and active ghrelin and total PYY were significantly lower in obese PCOS women, whereas active ghrelin was also significantly lower in lean PCOS women compared to controls. Postprandial plasma total ghrelin levels decrease were blunted in lean and obese compared to controls (12.8 % and 18.2% vs 28.2 %). Postprandial plasma active ghrelin decreased in lean and obese PCOS groups (49.9 % and 44.1 %) and controls (63.8 %). PCOS subjects exhibited smaller rises in postprandial levels of total PYY. Postprandial plasma PYY3-36 levels increased in obese PCOS women (30.9 %) and controls (41%), whereas lean PCOS women exhibited blunted increase (11.5%). sCD40L levels increased, whereas adiponectin decreased in PCOS groups independently, whereas rise in visfatin, sE- and sP-selectin and the fall in adiponectin was associated with obesity. sP- and sE -selectins correlated positively with obesity. In summary, our study provides the first evidence that lean untreated young PCOS women contribute to the so called "pancreatic islet adaptation to insulin resistance" because of ghrelin and PYY profiles. We confirmed existing of low-grade chronic inflammation in early stage of visceral obesity in lean PCOS patients. The lost endogenous "islet adaptation to insulin resistance" may lead to endothelial dysfunction and promote acceleration of atherosclerosis.

19

Impairment of microcirculation in juvenile idiopathic arthritis - studies by nailfold videocapillaroscopy and correlation with serum levels of sICAM and VEGF

58%

Gorska A., Kowal-Bielecka O., Urban M., Chlabicz S., Sienkiewicz J., Gorski S.

Folia Histochemica et Cytobiologica

|

2008

|

tom 46

|

nr 4

443-447

20

Superoxide is a potential culprit of caspase-3 dependent endothelial cell death induced by lysophosphatidylcholine

58%

Park S., Kim J. A., Choi S., Suh S. A.

Journal of Physiology and Pharmacology

|

2010

|

tom 61

|

nr 4

375-381

Oxidative stress in the vascular wall has intimately been implicated in the apoptosis of human umbilical vein endothelial cells (HUVECs) by lysophosphatidylcholine (LPC). However, the major type of reactive oxygen species (ROS) in this apoptotic signaling pathway remains to be clarified. In this study, we report that superoxide mediate LPC-induced caspase-3 dependent apoptosis in cultured HUVECs. The stimulation of HUVECs with LPC evoked apoptosis and ROS generation, and inhibited nitric oxide (NO) production in a dose-dependent manner. The classical caspase-3 dependent apoptosis was determined after 16 hours treatment by Western blotting using an antibody against cleaved caspase-3. The caspase-3 activation induced by LPC was prominently inhibited by antioxidants or NO donors and enhanced by NO inhibitors. Especially, LPC-induced caspase-3 activation was inhibited by superoxide dismutase (SOD) and enhanced by ammonium tetrathiomolybdate, SOD inhibitor. Additionally, xanthine/xanthine oxidase mixture increased the caspase-3 activation but catalase failed to reduce this superoxide-induced caspase-3 activation. These findings indicate that the superoxide generation caused by LPC activates the caspase-3 which results in HUVECs death. This study reveals some evidences linking superoxide with caspase-3 activation and provides a new dimension to superoxide-mediated caspase-3 activation in developing the endothelial dysfunction and atherosclerosis.

Ograniczanie wyników

Decreased immunoreactivity of von Willebrand factor may reflect persistent nature of the endothelial dysfunction in non-ischemic heart failure

Ischemic preconditioning prevents endothelial dysfunction, P-selectin expression, and neutrophil adhesion by preventing endothelin and O2-generation in the post-ischemic guinea-pig heart

Isoprenoid depletion by statins antagonizes cytokine-induced down-regulation of endothelial nitric oxide expression and increases NO synthase activity in human umbilical vein endothelial cells

Arterial structure and function and its short- and long-term changes after bariatric surgery

Selected aspects of endothelial dysfunction and their influence on the atherosclerosis process modeled and analyzed by Petri net based approach

The role of cyclooxygenase [COX]-2 derived prostanoids on vasoconstrictor responses to phenylephrine is increased by exposure to low mercury concentration

Effects of prenatal hypoxia on pulmonary vascular reactivity in chickens prone to pulmonary hypertension

Analysis of the correlations between oxidative stress, gelatinases and their tissue inhibitors in the human subjects with obstructive sleep apnea syndrome

Mediterranean food and health: building human evidence

Anti-Qa2 animal models for preeclampsia preclinical studies: a pathological elevation of blood pressure and proteinuria

Mechanisms of vascular dysfunction after subarachnoid hemorrhage

Serum endocan level in diabetes mellitus of patients with cirrhosis and risk of subsequent development of spontaneous bacterial peritonitis

High concentration of uric acid failed to affect endothelial function of small mesenteric arteries, femoral arteries and aortas from aged Wistar-Kyoto rats

Eplerenone improves vascular function and reduces platelet activation in diabetic rats

Weight loss-dependent and -independent effects of moderate calorie restriction on endothelial cell markers in obesity

Endothelial NADH-NADPH-dependent enzymatic sources of superoxide production: relationship to endothelial dysfunction

Superoxide- and nitric oxide-derived species mediate endothelial dysfunction, endothelial glycocalyx disruption, and enhanced neutrophil adhesion in the post-ischemic guinea-pig heart

Postprandial response of ghrelin and PYY and indices of low-grade chronic inflammation in lean young women with polycystic ovary syndrome

Impairment of microcirculation in juvenile idiopathic arthritis - studies by nailfold videocapillaroscopy and correlation with serum levels of sICAM and VEGF

Superoxide is a potential culprit of caspase-3 dependent endothelial cell death induced by lysophosphatidylcholine