CCL

Összesen 10 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM058137
Első szerző:Bagi Zsolt (orvos)
Cím:Type 2 diabetic mice have increased arteriolar tone and blood pressure : enhanced release of COX-2-derived constrictor prostaglandins / Zsolt Bagi, Nora Erdei, Attila Toth, Wei Li, Thomas H. Hintze, Akos Koller, Gabor Kaley
Dátum:2005
ISSN:1079-5642
Megjegyzések:OBJECTIVE: Type 2 diabetes mellitus (T2-DM) is frequently associated with vascular dysfunction and elevated blood pressure, yet the underlying mechanisms are not completely understood. We hypothesized that in T2-DM, the regulation of peripheral vascular resistance is altered because of changes in local vasomotor mechanisms. METHODS AND RESULTS: In mice with T2-DM (C57BL/KsJ-(db-)/db-), systolic and mean arterial pressures measured by the tail cuff method were significantly elevated compared with those of control (db+/db-) animals (db/db, 146+/-5 and 106+/-2 mm Hg versus control, 133+/-4 and 98+/-4 mm Hg, respectively; P<0.05). Total peripheral resistance, calculated from cardiac output values (measured by echocardiography) and mean arterial pressure were significantly elevated in db/db mice (db/db, 25+/-6 versus control, 15+/-1 mm Hg[middot]mL(-1)[middot]min(-1)). In isolated, pressurized gracilis muscle arterioles (diameter approximately 80 microm) from db/db mice, stepwise increases in intraluminal pressure (from 20 to 120 mm Hg) elicited a greater reduction in diameter than in control vessels at each pressure step (at 80 mm Hg, db/db, 66+/-4% versus control, 79+/-3%). The passive diameters of arterioles (obtained in Ca2+-free solution) and the calculated myogenic index were not significantly different in the 2 groups. The presence of the prostaglandin H2/thromboxane A2 receptor antagonist SQ29548 did not affect arteriolar diameters of control mice but reduced the enhanced arteriolar tone of db/db mice back to control levels (at 80 mm Hg, 80+/-4%). The inhibitor of cyclooxygenase-1 (COX-1), SC-560, did not affect the basal tone of arterioles, whereas NS-398, an inhibitor of COX-2, caused a significant shift in the arteriolar pressure-diameter curve of vessels from db/db mice (at 80 mm Hg, 76+/-3%) but not in those of control mice. Also, in aortas of db/db mice, expression of COX-2 was enhanced compared with controls. CONCLUSIONS: Collectively, these findings suggest that in mice with T2-DM, the basal tone of skeletal muscle arterioles is increased because of an enhanced COX-2-dependent production of constrictor prostaglandins. These alterations in microvascular prostaglandin synthesis may contribute to the increase in peripheral resistance and blood pressure in T2-DM.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Arteriosclerosis Thrombosis and Vascular Biology. - 25 : 8 (2005), p. 1610-1616. -
További szerzők:Erdei Nóra (1979-) (orvos) Tóth Attila (1971-) (biológus) Li, Wei (1987-) (kutató) Hintze, Thomas H. Koller Ákos Kaley Gábor
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

2.

001-es BibID:BIBFORM078386
035-os BibID:(WoS)000468782700014 (Scopus)85066509621
Első szerző:Balogh Enikő (molekuláris biológus)
Cím:Hypoxia Triggers Osteochondrogenic Differentiation of Vascular Smooth Muscle Cells in an HIF-1 (Hypoxia-Inducible Factor 1)-Dependent and Reactive Oxygen Species-Dependent Manner / Balogh Enikő, Tóth Andrea, Méhes Gábor, Trencsényi György, Paragh György, Jeney Viktória
Dátum:2019
ISSN:1079-5642
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Arteriosclerosis Thrombosis And Vascular Biology. - 39 : 6 (2019), p. 1088-1099. -
További szerzők:Tóth Andrea (1992-) (molekuláris biológus) Méhes Gábor (1966-) (patológus) Trencsényi György (1978-) (biológus, biokémikus, molekuláris biológus) Paragh György (1953-) (belgyógyász) Jeney Viktória (1971-) (vegyész, kémia tanár)
Pályázati támogatás:K116024
NKFIH
GINOP-2.3.2-15-2016-00005
GINOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

001-es BibID:BIBFORM038137
Első szerző:Balogh István (molekuláris biológus, genetikus)
Cím:Analysis of Gas6 in human platelets and plasma / Istvan Balogh, Sassan Hafizi, Jonas Stenhoff, Karin Hansson, Björn Dahlback
Dátum:2005
ISSN:1079-5642
Megjegyzések:OBJECTIVE: Gas6 is a member of the vitamin K-dependent protein family. Gas6-deficient mice were found to be resistant to thrombosis because of defective platelet function. Mouse Gas6 was demonstrated to be present in platelets and found to be involved in platelet aggregation. The aim of this study was to investigate the presence of Gas6 in human platelets and plasma and determine its role in platelet function. METHODS AND RESULTS: The presence of Gas6 in human platelets and plasma was analyzed using sensitive immunologic methods. Mass spectrometry and ELISA were used to identify and quantify Gas6 in plasma. Gas6 was demonstrated to be present in human plasma, at a concentration determined to be 13 to 23 ng/mL (0.16 to 0.28 nM). Furthermore, plasma Gas6 levels were found to be lower in patients administered with warfarin. However, Gas6 was undetectable in human platelets. CONCLUSIONS: This is the first report to identify and quantify Gas6 in human plasma. However, Gas6 protein was not detected in human platelets, suggesting that any potential platelet-specific function could be because of Gas6 from the circulation. These findings open up new directions regarding the role of Gas6 in normal and pathophysiological situations such as inflammation, autoimmune disease, thrombosis and arteriosclerosis.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Arteriosclerosis Thrombosis And Vascular Biology. - 25 : 6 (2005), p. 1280-1286. -
További szerzők:Hafizi, Sassan Stenhoff, Jonas Hansson, Karin Dahlbäck, Björn
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

001-es BibID:BIBFORM040766
Első szerző:Bereczki Dániel (neurológus)
Cím:Should soluble CD40 ligand be measured from serum or plasma samples? / Dániel Bereczki, Emőke Nagy, András Pál, Mária T. Magyar, József Balla
Dátum:2003
ISSN:1079-5642
Tárgyszavak:Orvostudományok Klinikai orvostudományok szerkesztői levél
Megjelenés:Arteriosclerosis Thrombosis And Vascular Biology 23 : 6 (2003), p. 1129-1130. -
További szerzők:Nagy Emőke (neonatológus, gyermekgyógyász) Pál András Magyar Mária Tünde (1970-) (neurológus) Balla József (1959-) (belgyógyász, nephrológus)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

5.

001-es BibID:BIBFORM073825
Első szerző:Bermudez, Beatriz
Cím:Leukocyte Overexpression of Intracellular NAMPT Attenuates Atherosclerosis by Regulating PPARγ-Dependent Monocyte Differentiation and Function / Beatriz Bermudez, Tuva Borresdatter Dahl, Indira Medina, Mathijs Groeneweg, Sverre Holm, Sergio Montserrat-de la Paz, Mat Rousch, Jeroen Otten, Veronica Herias, Lourdes M. Varela, Trine Ranheim, Arne Yndestad, Almudena Ortega-Gomez, Rocio Abia, Laszlo Nagy, Pal Aukrust, Francisco J. G. Muriana, Bente Halvorsen, Erik Anna Leonardus Biessen
Dátum:2017
ISSN:1079-5642
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Arteriosclerosis Thrombosis And Vascular Biology 37 : 6 (2017), p. 1157-1167. -
További szerzők:Dahl, Tuva Borresdatter Medina, Indira Groeneweg, Mathijs Holm, Sverre Montserrat-de la Paz, Sergio Rousch, Mat Otten, Jeroen Herias, Veronica Varela, Lourdes M. Ranheim, Trine Yndestad, Arne Ortega-Gomez, Almudena Abia, Rocio Nagy László (1966-) (molekuláris sejtbiológus, biokémikus) Aukrust, Pal Muriana, Francisco J. G. Halvorsen, Bente Biessen, Erik Anna Leonardus
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

6.

001-es BibID:BIBFORM043579
Első szerző:Cauwenberghs, Nancy
Cím:Antithrombotic effect of platelet glycoprotein Ib-blocking monoclonal antibody Fab fragments in nonhuman primates / Cauwenberghs N., Meiring M., Vauterin S., van Wyk V., Lamprecht S., Roodt J. P., Novák L., Harsfalvi J., Deckmyn H., Kotzé H. F.
Dátum:2000
Megjegyzések:Platelet adhesion in arterial blood flow is mainly supported by the platelet receptor glycoprotein (GP) Ib, which interacts with von Willebrand factor (vWF) that is bound to collagen at the site of vessel wall injury. Antibody 6B4 is a monoclonal antibody (MoAb) raised against purified human GPIb. MoAb 6B4 inhibits both ristocetin- and botrocetin-induced, vWF-dependent human platelet agglutination. MoAb 6B4 furthermore blocks shear-induced adhesion of human platelets to collagen I. We studied the antithrombotic effect of this inhibitory murine MoAb 6B4 in a baboon model of arterial thrombosis. When injected into baboons, intact IgG and its F(ab')(2) fragments caused almost immediate thrombocytopenia, whereas injection of the Fab fragments alone did not. Fab fragments were subsequently used to investigate their in vivo effect on platelet deposition onto a thrombogenic device, consisting of collagen-rich, glutaraldehyde-fixed bovine pericardium (0.6 cm(2)), at a wall shear rate ranging from 700 to 1000 s(-1). Baboons were either pretreated with Fabs to study the effect of inhibition on platelet adhesion or treated 6 minutes after placement of the thrombogenic device to investigate the effect on interplatelet cohesion. Pretreatment of the animals with bolus doses ranging from 80 to 640 microgram/kg Fab fragments significantly reduced (111)In-labeled platelet deposition onto the collagen surface by approximately 43% to 65%. Only the highest dose caused a significant prolongation (doubling) of the bleeding time. Ex vivo ristocetin-induced platelet agglutination was equally reduced. Treatment with a bolus of 110 microgram/kg Fab fragments after a thrombus was allowed to form for 6 minutes had no effect on further platelet deposition. We therefore conclude that Fab fragments or derivatives of inhibitory anti-GPIb antibodies may be useful compounds to prevent thrombosis.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
platelet adhesion
platelet aggregation
thrombosis
glycoprotein Ib
monoclonal antibodies
Megjelenés:Arteriosclerosis, Thrombosis, and Vascular Biology. - 20 : 5 (2000), p. 1347-1353. -
További szerzők:Meiring, Muriel Vauterin, Stephan van Wyk, Veronika Lamprecht, Seb Roodt, Jan P. Novák Levente (1967-) (biológus) Hársfalvi Jolán (1949-) (klinikai biokémikus) Deckmyn, Hans Kotzé, Harry F.
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

7.

001-es BibID:BIBFORM010055
Első szerző:Chari, Ramya
Cím:Protein kinase C[delta] differentially regulates platelet functional responses / Chari R., Getz T., Nagy B., Jr., Bhavaraju K., Mao Y., Bynagari Y. S., Murugappan S., Nakayama K., Kunapuli S. P.
Dátum:2009
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Arteriosclerosis, Thrombosis, and Vascular Biology. - 29 : 5 (2009), p. 699-705. -
További szerzők:Getz, Todd Nagy Béla Jr. (1980-) (labordiagnosztikai szakorvos) Bhavaraju, Kamala Mao, Yingying Bynagari, Yamini Saraswathy Murugappan, Swaminathan Nakayama, Keiko Kunapuli, Satya P.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
Borító:

8.

001-es BibID:BIBFORM074228
Első szerző:Fülöp Tibor (kardiológus)
Cím:Adaptation of Vasomotor Function of Human Coronary Arterioles to the Simultaneous Presence of Obesity and Hypertension / Tibor Fulop, Eva Jebelovszki, Nora Erdei, Tamas Szerafin, Tamas Forster, Istvan Edes, Akos Koller, Zsolt Bagi
Dátum:2007
ISSN:1079-5642
Megjegyzések:Objectives: We hypothesized that simultaneous presence of obesity and hypertension activates adaptive vascular mechanisms affecting dilations of human coronary arterioles.Methods and Results: Agonist-induced dilations were assessed in isolated pressurized coronary arterioles from patients(n 38) who underwent cardiac surgery. Among normotensives we found that dilations to bradykinin (BK) and the NO-donor, sodium-nitroprusside (SNP) were reduced in obese subjects (BK, 10 7 mol/L, lean:90 4%, obese:64 7%; SNP, 10 6 mol/L, lean:89 7%, obese:76 5%). However, among hypertensives, both BK- and SNP-induced dilations were significantly enhanced in obese patients, when compared with lean individuals (BK, lean:71 7%, obese:85 3%; SNP, lean:60 6%, obese:83 2%). Correspondingly, in hypertensive patients, but not in those of normotensives, a positive correlation was found between body mass index (BMI) and BK-induced (P 0.036, r 0.46), and also SNP-evoked (P 0.031, r 0.44) coronary dilations. Moreover, in additional 55 hypertensive patients flow-mediated (FMD) and nitroglycerin (NTG)-induced dilations of the brachial artery were assessed. In obese hypertensive individuals, FMD- and NTG-induced dilations were greater (FMD:6.2 0.7%, NTG:17.2 0.9%), than in leanhypertensive patients (FMD:3.7 0.6%, NTG:13.6 1.1%). Correspondingly, FMD- and NTG-induced dilations were positively correlated with BMI (P 0.020, r 0.31 and P 0.033, r 0.29, respectively).Conclusions:These findings are the first to suggest that obesity may lead to activation of adaptive vascular mechanisms to enhance the dilator function of coronary and peripheral arterial vessels in hypertensive patients. (Arterioscler Thromb Vasc Biol. 2007;27:2348-2354.)
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
obesity
hypertension
coronary microcirculation
flow-mediated dilation
nitrate
Megjelenés:Arteriosclerosis Thrombosis And Vascular Biology. - 27 : 11 (2007), p. 2348-2354. -
További szerzők:Jebelovszki Éva Erdei Nóra (1979-) (orvos) Szerafin Tamás (1960-) (szívsebész, mellkassebész) Forster Tamás Édes István (1952-) (kardiológus) Koller Ákos Bagi Zsolt (1974-) (orvos)
Pályázati támogatás:F-048837
OTKA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

9.

001-es BibID:BIBFORM012889
Első szerző:Nagy Emőke (neonatológus, gyermekgyógyász)
Cím:Red cells, hemoglobin, heme, iron, and atherogenesis / Emőke Nagy, John W. Eaton, Viktória Jeney, Miguel P. Soares, Zsuzsa Varga, Zoltán Galajda, József Szentmiklósi, Gábor Méhes, Tamás Csonka, Ann Smith, Gregory M. Vercellotti, György Balla, József Balla
Dátum:2010
Megjegyzések:We investigated whether red cell infiltration of atheromatous lesions promotes the later stages of atherosclerosis. METHODS AND RESULTS: We find that oxidation of ferro (FeII) hemoglobin in ruptured advanced lesions occurs generating ferri (FeIII) hemoglobin and via more extensive oxidation ferrylhemoglobin (FeIII/FeIV=O). The protein oxidation marker dityrosine accumulates in complicated lesions, accompanied by the formation of cross-linked hemoglobin, a hallmark of ferrylhemoglobin. Exposure of normal red cells to lipids derived from atheromatous lesions causes hemolysis and oxidation of liberated hemoglobin. In the interactions between hemoglobin and atheroma lipids, hemoglobin and heme promote further lipid oxidation and subsequently endothelial reactions such as upregulation of heme oxygenase-1 and cytotoxicity to endothelium. Oxidative scission of heme leads to release of iron and a feed-forward process of iron-driven plaque lipid oxidation. The inhibition of heme release from globin by haptoglobin and sequestration of heme by hemopexin suppress hemoglobin-mediated oxidation of lipids of atheromatous lesions and attenuate endothelial cytotoxicity. CONCLUSIONS: The interior of advanced atheromatous lesions is a prooxidant environment in which erythrocytes lyse, hemoglobin is oxidized to ferri- and ferrylhemoglobin, and released heme and iron promote further oxidation of lipids. These events amplify the endothelial cell cytotoxicity of plaque components.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Red cells, hemoglobin
egyetemen (Magyarországon) készült közlemény
Megjelenés:Arteriosclerosis, Thrombosis, and Vascular Biology 30 : 7 (2010), p. 1347-1353. -
További szerzők:Eaton, John W. Jeney Viktória (1971-) (vegyész, kémia tanár) Soares, Miguel P. Varga Zsuzsa (1951-) (biokémikus, nephrológus) Galajda Zoltán (1962-) (szívsebész, érsebész) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Méhes Gábor (1966-) (patológus) Csonka Tamás (1984-) (pathológus) Smith, Ann Vercellotti, Gregory M. Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:OTKA-K75883
OTKA
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
elektronikus változat
DOI
Borító:

10.

001-es BibID:BIBFORM076938
035-os BibID:(WoS)000460459200017 (Scopus)85062410676
Első szerző:Sikura Katalin Éva (biológus)
Cím:Potential Role of H-Ferritin in Mitigating Valvular Mineralization / Katalin Éva Sikura, László Potor, Tamás Szerafin, Abolfazl Zarjou, Anupam Agarwal, Paolo Arosio, Maura Poli, Zoltán Hendrik, Gábor Méhes, Melinda Oros, Niké Posta, Lívia Beke, Ibolya Fürtös, György Balla, József Balla
Dátum:2019
ISSN:1079-5642
Megjegyzések:Objective- Calcific aortic valve disease is a prominent finding in elderly and in patients with chronic kidney disease. We investigated the potential role of iron metabolism in the pathogenesis of calcific aortic valve disease. Approach and Results- Cultured valvular interstitial cells of stenotic aortic valve with calcification from patients undergoing valve replacement exhibited significant susceptibility to mineralization/osteoblastic transdifferentiation in response to phosphate. This process was abrogated by iron via induction of H-ferritin as reflected by lowering ALP and osteocalcin secretion and preventing extracellular calcium deposition. Cellular phosphate uptake and accumulation of lysosomal phosphate were decreased. Accordingly, expression of phosphate transporters Pit1 and Pit2 were repressed. Translocation of ferritin into lysosomes occurred with high phosphate-binding capacity. Importantly, ferritin reduced nuclear accumulation of RUNX2 (Runt-related transcription factor 2), and as a reciprocal effect, it enhanced nuclear localization of transcription factor Sox9 (SRY [sex-determining region Y]-box 9). Pyrophosphate generation was also increased via upregulation of ENPP2 (ectonucleotide pyrophosphatase/phosphodiesterase-2). 3H-1, 2-dithiole-3-thione mimicked these beneficial effects in valvular interstitial cell via induction of H-ferritin. Ferroxidase activity of H-ferritin was essential for this function, as ceruloplasmin exhibited similar inhibitory functions. Histological analysis of stenotic aortic valve revealed high expression of H-ferritin without iron accumulation and its relative dominance over ALP in noncalcified regions. Increased expression of H-ferritin accompanied by elevation of TNF-α (tumor necrosis factor-α) and IL-1β (interleukin-1β) levels, inducers of H-ferritin, corroborates the essential role of ferritin/ferroxidase via attenuating inflammation in calcific aortic valve disease. Conclusions- Our results indicate that H-ferritin is a stratagem in mitigating valvular mineralization/osteoblastic differentiation. Utilization of 3H-1, 2-dithiole-3-thione to induce ferritin expression may prove a novel therapeutic potential in valvular mineralization.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
arteriosclerosis
chronic kidney disease
phosphate
stenosis
vascular calcification
Megjelenés:Arteriosclerosis Thrombosis and Vascular Biology. - 39 : 3 (2019), p. 413-431. -
További szerzők:Potor László Szerafin Tamás (1960-) (szívsebész, mellkassebész) Zarjou, Abolfazl (1979-) (kutató orvos) Agarwal, Anupam Arosio, Paolo Poli, Maura Hendrik Zoltán (1986-) (orvos) Méhes Gábor (1966-) (patológus) Oros Melinda (1975-) (molekuláris biológus) Posta Niké Beke Lívia Fürtös Ibolya Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1 
Corvina könyvtári katalógus v8.2.27 © 2023 Monguz kft. Minden jog fenntartva.