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1.

001-es BibID:BIBFORM057819
Első szerző:Csató Viktória (molekuláris biológus)
Cím:Hydrogen peroxide elicits constriction of skeletal muscle arterioles by activating the arachidonic acid pathway / Viktória Csató, Attila Pető, Ákos Koller, István Édes, Attila Tóth, Zoltán Papp
Dátum:2014
ISSN:1932-6203
Megjegyzések:Aims: The molecular mechanisms of the vasoconstrictor responses evoked by hydrogen peroxide (H2O2) have not been clearly elucidated in skeletal muscle arterioles. Methods and results: Changes in diameter of isolated, cannulated and pressurized gracilis muscle arterioles (GAs) of Wistar-Kyoto rats were determined under various test conditions. H2O2 (10-100 ?M) evoked concentration-dependent constrictions in the GAs, which were inhibited by endothelium removal, or by antagonists of phospholipase A (PLA; 100 ?M 7,7-dimethyl-(5Z,8Z)-eicosadienoic acid), protein kinase C (PKC; 10 ?M chelerythrine), phospholipase C (PLC; 10 ?M U-73122), or Src family tyrosine kinase (Src kinase; 1 ?M Src Inhibitor-1). Antagonists of thromboxane A2 (TXA2; 1 ?M SQ-29548) or the non-specific cyclooxygenase (COX) inhibitor indomethacin (10 ?M) converted constrictions to dilations. The COX-1 inhibitor (SC-560, 1 ?M) demonstrated a greater reduction in constriction and conversion to dilation than that of COX-2 (celecoxib, 3 ?M). H2O2 did not elicit significant changes in arteriolar Ca2+ levels measured with Fura-2. Conclusions: These data suggest that H2O2 activates the endothelial Src kinase/PLC/PKC/PLA pathway, ultimately leading to the synthesis and release of TXA2 by COX-1, thereby increasing the Ca2+ sensitivity of the vascular smooth muscle cells and eliciting constriction in rat skeletal muscle arterioles.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
hydrogen peroxide
phospholipase C
arachidonic acid
smooth muscle calcium
constrictions
Megjelenés:Plos One. - 9 : 8 (2014), p. 1-10. -
További szerzők:Pető Attila (1990-) (általános orvos) Koller Ákos Édes István (1952-) (kardiológus) Tóth Attila (1971-) (biológus) Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:OTKA-K108444
OTKA
OTKA-K84300
OTKA
OTKA-K109083
OTKA
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Kardiológia Kutatócsoport
SROP-4.2.2.A-11/1/KONV-2012-0017
Egyéb
SROP-4.2.2.A-11/1/KONV-2012-0024
Egyéb
Internet cím:Szerző által megadott URL
DOI
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2.

001-es BibID:BIBFORM050126
035-os BibID:Article ID: e87844
Első szerző:Fagyas Miklós (orvos)
Cím:New perspectives in the renin-angiotensin-aldosterone system (RAAS) III : endogenous inhibition of angiotensin converting enzyme (ACE) provides protection against cardiovascular diseases / Miklós Fagyas, Katalin Úri, Ivetta M. Siket, Andrea Daragó, Judit Boczán, Emese Bányai, István Édes, Zoltán Papp, Attila Tóth
Dátum:2014
ISSN:1932-6203
Megjegyzések:ACE inhibitor drugs decrease mortality by up to one-fifth in cardiovascular patients. Surprisingly, there are reports dating back to 1979 suggesting the existence of endogenous ACE inhibitors. Here we investigated the clinical significance of this potential endogenous ACE inhibition. ACE concentration and activity was measured in patient's serum samples (n=151). ACE concentration was found to be in a wide range (47-288 ng/mL). ACE activity decreased with the increasing concentration of the serum albumin (HSA): ACE activity was 56?1 U/L in the presence of 2.4?0.3 mg/mL HSA, compared to 39?1 U/L in the presence of 12?1 mg/mL HSA (values are mean?SEM). Effects of the differences in ACE concentration were suppressed in human sera: patients with ACE DD genotype exhibited a 64% higher serum ACE concentration (range, 74-288 ng/mL, median, 155.2 ng/mL, n=52) compared to patients with II genotype (range, 47-194 ng/mL, median, 94.5 ng/mL, n=28) while the difference in ACE activities was only 32% (range, 27.3-59.8 U/L, median, 43.11 U/L, and range 15.6-55.4 U/L, median, 32.74 U/L, respectively) in the presence of 12?1 mg/mL HSA. No correlations were found between serum ACE concentration (or genotype) and cardiovascular diseases, in accordance with the proposed suppressed physiological ACE activities by HSA (concentration in the sera of these patients: 48.5?0.5 mg/mL) or other endogenous inhibitors. Main implications are that (1) physiological ACE activity can be stabilized at a low level by endogenous ACE inhibitors, such as HSA; (2) angiotensin II elimination may have a significant role in angiotensin II related pathologies.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
ACE
HSA
endogenous ACE inhibition
angiotensin-converting enzyme
Molekuláris Medicina
Megjelenés:Plos One. - 9 : 4 (2014), p. 1-29. -
További szerzők:Úri Katalin Mányiné Siket Ivetta (1962-) (laborasszisztens) Daragó Andrea (1972-) (orvos, kardiológus) Boczán Judit (1972-) (neurológus) Bányai Emese (1984-) (orvos) Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Tóth Attila (1971-) (biológus)
Pályázati támogatás:OTKA-K84300
OTKA
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Vaszkuláris tranziens receptor potenciál (TRP) csatornák
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Kardiológia Kutatócsoport
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM050118
035-os BibID:Article ID: e87843
Első szerző:Fagyas Miklós (orvos)
Cím:New perspectives in the renin-angiotensin-aldosterone system (RAAS) I : endogenous angiotensin converting enzyme (ACE) inhibition / Miklós Fagyas, Katalin Úri, Ivetta M. Siket, Andrea Daragó, Judit Boczán, Emese Bányai, István Édes, Zoltán Papp, Attila Tóth
Dátum:2014
ISSN:1932-6203
Megjegyzések:Angiotensin-converting enzyme (ACE) inhibitors represent the fifth most often prescribed drugs. ACE inhibitors decrease 5-year mortality by approximately one-fifth in cardiovascular patients. Surprisingly, there are reports dating back to 1979 suggesting the existence of endogenous ACE inhibitors, which endogenous inhibitory effects are much less characterized than that for the clinically administered ACE inhibitors. Here we aimed to investigate this endogenous ACE inhibition in human sera. It was hypothesized that ACE activity is masked by an endogenous inhibitor, which dissociates from the ACE when its concentration decreases upon dilution. ACE activity was measured by FAPGG hydrolysis first. The specific (dilution corrected) enzyme activities significantly increased by dilution of human serum samples (23.2?0.7U/L at 4-fold dilution, 51.4?0.3U/L at 32-fold dilution, n=3, p=0.001), suggesting the presence of an endogenous inhibitor. In accordance, specific enzyme activities did not changed by dilution when purified renal ACE was used, where no endogenous inhibitor was present (655?145U/L, 605?42U/L, n=3, p=0.715, respectively). FAPGG conversion strongly correlated with angiotensin I conversion suggesting that this feature is not related to the artificial substrate. Serum samples were ultra-filtered to separate ACE (MW: 180 kDa) and the hypothesized inhibitor. Filtering through 50 kDa filters was without effect, while filtering through 100 kDa filters eliminated the inhibiting factor (ACE activity after <100 kDa filtering: 56.4?2.4U/L, n=4, control: 26.4?0.7U/L, n=4, p<0.001). Lineweaver-Burk plot indicated non-competitive inhibition of ACE by this endogenous factor. The endogenous inhibitor had higher potency on the C-terminal active site than N-terminal active site of ACE. Finally, this endogenous ACE inhibition was also present in mouse, donkey, goat, bovine sera besides men (increasing of specific ACE activity from 4-fold to 32-fold dilution: 2.8-fold, 1.7-fold, 1.5-fold, 1.8-fold, 2.6-fold, respectively). We report here the existence of an evolutionary conserved mechanism suppressing circulating ACE activity, in vivo, similarly to ACE inhibitory drugs.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
ACE
angiotensin-converting enzyme
renin-angiotensin-aldosterone system
endogenous ACE inhibition
Molekuláris Medicina
Megjelenés:Plos One. - 9 : 4 (2014), p. 1-29. -
További szerzők:Úri Katalin Mányiné Siket Ivetta (1962-) (laborasszisztens) Daragó Andrea (1972-) (orvos, kardiológus) Boczán Judit (1972-) (neurológus) Bányai Emese (1984-) (orvos) Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Tóth Attila (1971-) (biológus)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Vaszkuláris tranziens receptor potenciál (TRP) csatornák
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Kardiológia Kutatócsoport
K84300
OTKA
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

001-es BibID:BIBFORM050119
035-os BibID:Article ID: e87844
Első szerző:Fagyas Miklós (orvos)
Cím:New perspectives in the renin-angiotensin-aldosterone system (RAAS) II : albumin suppresses angiotensin converting enzyme (ACE) activity in human / Miklós Fagyas, Katalin Úri, Ivetta M. Siket, Gábor Á. Fülöp, Viktória Csató, Andrea Daragó, Judit Boczán, Emese Bányai, István Elek Szentkirályi, Tamás Miklós Maros, Tamás Szerafin, István Édes, Zoltán Papp, Attila Tóth
Dátum:2014
ISSN:1932-6203
Megjegyzések:About 8% of the adult population is taking angiotensin-converting enzyme (ACE) inhibitors to treat cardiovascular disease including hypertension, myocardial infarction and heart failure. These drugs decrease mortality by up to one-fifth in these patients. We and others have reported previously that endogenous inhibitory substances suppress serum ACE activity, in vivo, similarly to the ACE inhibitor drugs. Here we have made an effort to identify this endogenous ACE inhibitor substance. ACE was crosslinked with interacting proteins in human sera. The crosslinked products were immunoprecipitated and subjected to Western blot. One of the crosslinked products was recognized by both anti-ACE and anti-HSA (human serum albumin) antibodies. Direct ACE-HSA interaction was confirmed by binding assays using purified ACE and HSA. HSA inhibited human purified (circulating) and human recombinant ACE with potencies (IC50) of 5.7?0.7 and 9.5?1.1 mg/mL, respectively. Effects of HSA on the tissue bound native ACE were tested on human saphenous vein samples. Angiotensin I evoked vasoconstriction was inhibited by HSA in this vascular tissue (maximal force with HSA: 6.14?1.34 mN, without HSA: 13.54?2.63 mN), while HSA was without effects on angiotensin II mediated constrictions (maximal force with HSA: 18.73?2.17 mN, without HSA: 19.22?3.50 mN).The main finding of this study is that HSA was identified as a potent physiological inhibitor of the ACE. The enzymatic activity of ACE appears to be almost completely suppressed by HSA when it is present in its physiological concentration. These data suggest that angiotensin I conversion is limited by low physiological ACE activities, in vivo.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
ACE
Renin-angiotensin-aldosterone system
human serum albumin
endogenous ACE inhibition
Molekuláris Medicina
Megjelenés:Plos One. - 9 : 4 (2014), p. 1-28. -
További szerzők:Úri Katalin Mányiné Siket Ivetta (1962-) (laborasszisztens) Fülöp Gábor Áron (1988-) (általános orvos) Csató Viktória (1986-) (molekuláris biológus) Daragó Andrea (1972-) (orvos, kardiológus) Boczán Judit (1972-) (neurológus) Bányai Emese (1984-) (orvos) Szentkirályi István (1970-) (szívsebész) Maros Tamás Miklós (1969-) (szívsebész) Szerafin Tamás (1960-) (szívsebész, mellkassebész) Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Tóth Attila (1971-) (biológus)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Kardiológia Kutatócsoport
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Vaszkuláris tranziens receptor potenciál (TRP) csatornák
K84300
OTKA
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM074180
035-os BibID:(cikkazonosító)e0197890 (WOS)000434786600008 (Scopus)85048322440
Első szerző:Fejes Zsolt (molekuláris biológus)
Cím:Endothelial cell activation is attenuated by everolimus via transcriptional and post-transcriptional regulatory mechanisms after drug-eluting coronary stenting / Fejes Z., Czimmerer Z., Szük T., Póliska S., Horváth A., Balogh E., Jeney V., Váradi J., Fenyvesi F., Balla G., Édes I., Balla J., Kappelmayer J., Nagy B. Jr.
Dátum:2018
ISSN:1932-6203
Megjegyzések:We previously found higher level of endothelial cell (EC) activation in patients who suffered from in-stent restenosis after bare-metal stenting compared to subjects who underwent drug-eluting stenting (DES) showing no complications. Here we investigated the potential transcriptional and post-transcriptional regulatory mechanisms by which everolimus attenuated EC activation after DES. We studied the effect of everolimus on E-selectin (SELE) and VCAM1 mRNA levels when human coronary artery (HCAECs) and human umbilical vein ECs were challenged with recombinant TNF-? (100 ng/mL) for 1-24 hours in the presence or absence of everolimus using 0.5 ?M concentration locally maintained by DES. EC activation was evaluated via the levels of IL-1? and IL-6 mRNAs with miR-155 expression by RT-qPCR as well as the nuclear translocation of nuclear factor kappa beta (NF-?B) detected by fluorescence microscopy. To investigate the transcriptional regulation of E-selectin and VCAM-1, TNF-?-induced enhancer RNA (eRNA) expression at p65-bound enhancers in the neighboring genomic regions of SELE and VCAM1 genes, including SELE_-11Kb and VCAM1_-10Kb, were measured in HCAECs. Mature and precursor levels of E-selectin and VCAM-1 repressor miR-181b were quantified to analyze the post-transcriptional regulation of these genes in HCAECs. Circulating miR-181b was analyzed in plasma samples of stented subjects by stem-loop RT-qPCR. TNF-? highly elevated E-selectin and VCAM-1 expression at transcriptional level in ECs. Levels of mature, pre- and pri-miR-181b were repressed in ECs by TNF-?, while everolimus acted as a negative regulator of EC activation via inhibited translocation of NF-?B p65 subunit into cell nuclei, lowered eRNA expression at SELE and VCAM1 genes-associated enhancers and modulated expression of their post-transcriptional repressor miR-181b. Significant negative correlation was observed between plasma miR-181b and soluble E-selectin and VCAM-1 in patients. In conclusion, everolimus attenuates EC activation via reduced NF-?B p65 translocation causing decreased E-selectin and VCAM-1 expression at transcriptional and post-transcriptional level after DES.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
coronary stenting
endothelial cell
enhancer RNA
everolimus
inflammation
microRNA
Megjelenés:Plos One. - 13 : 6 (2018), p. 1-20. -
További szerzők:Czimmerer Zsolt (1981-) (molekuláris biológus) Szűk Tibor (1967-) (kardiológus) Póliska Szilárd (1978-) (biológus) Horváth Attila (1988-) (programtervező informatikus) Balogh Enikő (1987-) (molekuláris biológus) Jeney Viktória (1971-) (vegyész, kémia tanár) Váradi Judit (1973-) (gyógyszerész, gyógyszertechnológus) Fenyvesi Ferenc (1977-) (gyógyszerész, gyógyszertechnológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Édes István (1952-) (kardiológus) Balla József (1959-) (belgyógyász, nephrológus) Kappelmayer János (1960-) (laboratóriumi szakorvos) Nagy Béla Jr. (1980-) (labordiagnosztikai szakorvos)
Pályázati támogatás:GINOP-2.3.2-15-2016-00043
GINOP
Internet cím:DOI
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6.

001-es BibID:BIBFORM072903
035-os BibID:(cikkazonosító)e0194166 (WOS)000428603100051 (Scopus)85044720189
Első szerző:Kovács György (belgyógyász, gasztroenterológus)
Cím:Significance of serological markers in the disease course of ulcerative colitis in a prospective clinical cohort of patients / Gyorgy Kovacs, Nora Sipeki, Boglarka Suga, Tamas Tornai, Kai Fechner, Gary L. Norman, Zakera Shums, Peter Antal-Szalmas, Maria Papp
Dátum:2018
ISSN:1932-6203
Megjegyzések:Background & aimsTo determine the prognostic potential of classic and novel serologic antibodies regarding unfavorable disease course in a prospective ulcerative colitis (UC) patient cohort, since few and conflicting data are available in the literature regarding this matter.Methods187 consecutive patients were studied prospectively (median follow-up: 135 months) from a single referral IBD center in Hungary. Sera were tested for different IgA/IgG type autoantibodies (anti-neutrophil cytoplasmic [ANCA], anti-DNA-bound-lactoferrin [anti-LFS], anti-goblet cell [anti-GAB] and anti-pancreatic [PAB: anti-CUZD1 and anti-GP2)]) by indirect immunofluorescence technique and for anti-microbial (anti-Saccharomyces cerevisiae [ASCA] IgG/IgA and anti-OMP Plus? IgA) antibodies by enzyme-linked immunosorbent assays.ResultsA total of 73.6%, 62.4% and 11.2% of UC patients were positive for IgA/IgG type of atypical perinuclear-ANCA, anti-LFS and anti-GAB, respectively. Occurrences of PABs were 9.6%, while ASCA IgA/IgG and anti-OMP IgA were 17.6% and 19.8%, respectively. Antibody status was stable over time. IgA type PABs were more prevalent in patients with primary sclerosing cholangitis (37.5% vs. 4.7% for anti-CUZD1 and 12.5% vs. 0% for anti-GP2, p<0.001 for both). IgA type ASCA and anti-CUZD1 antibodies were associated with higher risk of requirement for long-term immunosuppressant therapy in Kaplan-Meier analysis (pLogRank <0.01 for both). However, in multivariate Cox-regression analysis only ASCA IgA (HR: 2.74, 95%CI: 1.46?5.14, p<0.01) remained independent predictor. UC-related hospitalization due to disease activity was only associated with multiple antibody positivity (for 3 or more; HR 2.03 [95% CI: 1.16?3.56]; p = 0.013). None of the individual antibodies or their combination was associated with the risk of development of extensive disease or colectomy.ConclusionEven with low prevalence rates, present study gives further evidence to the role of certain antibodies as markers for distinct phenotype and disease outcome in UC. Considering the result of the multivariate analysis the novel antibodies investigated do not seem to be associated with poor clinical outcome in UC, only a classic antibody, IgA subtype ASCA remained an independent predictor of long-term immunosuppressive therapy.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Plos One. - 13 : 3 (2018), p. 1-18. -
További szerzők:Sipeki Nóra (1987-) (általános orvos) Suga Boglárka Tornai Tamás István (1984-) (belgyógyász) Fechner, Kai Norman, Gary L. Shums, Zakera Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Papp Mária (1975-) (belgyógyász, gasztroenterológus)
Pályázati támogatás:OTKA-115818
OTKA
RH/885/2013
Egyéb
BO/00426/11
Egyéb
IOIBD Research Grant (2012-2015)
Egyéb
Internet cím:Szerző által megadott URL
DOI
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7.

001-es BibID:BIBFORM013687
Első szerző:Papp Mária (belgyógyász, gasztroenterológus)
Cím:Presence of Anti-Microbial Antibodies in Liver Cirrhosis : a Tell-Tale Sign of Compromised Immunity? / Papp Maria, Norman Gary L., Vitalis Zsuzsanna, Tornai Istvan, Altorjay Istvan, Földi Ildikó, Udvardy Miklos, Shums Zakera, Dinya Tamas, Orosz Peter, Lombay Bela, Par Gabriella, Par Alajos, Veres Gabor, Csak Timea, Osztovits Janos, Szalay Ferenc, Lakatos Peter Laszlo
Dátum:2010
ISSN:0163-2116
Megjegyzések:Bacterial translocation plays important role in the complications of liver cirrhosis. Antibody formation against various microbial antigens is common in Crohn's disease and considered to be caused by sustained exposure to gut microflora constituents. We hypothesized that anti-microbial antibodies are present in patients with liver cirrhosis and may be associated with the development of bacterial infections. Methodology/Principal Findings: Sera of 676 patients with various chronic liver diseases (autoimmune diseases:266, viral hepatitis C:124, and liver cirrhosis of different etiology:286) and 100 controls were assayed for antibodies to Saccharomyces cerevisiae(ASCA) and to antigens derived from two intestinal bacterial isolates (one gram positive, one gram negative, neither is Escherichia coli). In patients with liver cirrhosis, we also prospectively recorded the development of severe episodes of bacterial infection. ASCA and anti-OMP PlusTM antibodies were present in 38.5% and 62.6% of patients with cirrhosis and in 16% and 20% of controls, respectively (p,0.001). Occurrence of these antibodies was more frequent in cases of advanced cirrhosis (according to Child-Pugh and MELD score; p,0.001) or in the presence of ascites (p,0.001). During the median follow-up of 425 days, 81 patients (28.3%) presented with severe bacterial infections. Anti-microbial antibody titers (p = 0.003), as well as multiple seroreactivity (p = 0.036), was associated with infectious events. In logistic regression analysis, the presence of ascites (OR:1.62, 95%CI:1.16?2.25), co-morbidities (OR:2.22, 95%CI:1.27?3.86), and ASCA positivity (OR:1.59, 95%CI:1.07?2.36) were independent risk factors for severe infections. A shorter time period until the first infection was associated with the presence of ASCA (p = 0.03) and multiple seropositivity (p = 0.037) by Kaplan-Meier analysis, and with Child-Pugh stage (p = 0.018, OR:1.85) and co-morbidities (p,0.001, OR:2.02) by Cox-regression analysis. Conclusions/Significance: The present study suggests that systemic reactivity to microbial components reflects compromised mucosal immunity in patients with liver cirrhosis, further supporting the possible role of bacterial translocation in the formation of anti-microbial antibodies.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Haptoglobin polymorphism
Crohn's disease
Disease behavior
Th1/Th2 orientation
Primary sclerosing cholangitis
egyetemen (Magyarországon) készült közlemény
Megjelenés:PloS One. - 5 : 9 (2010), p. e12957-1-e12957-9. -
További szerzők:Norman, Gary L. Vitális Zsuzsanna (1963-) (belgyógyász, gasztroenterológus) Tornai István (1954-) (belgyógyász, gasztroenterológus) Altorjay István (1954-) (belgyógyász, gasztroenterológus, onkológus) Földi Ildikó (1981-) (orvos) Udvardy Miklós (1947-) (belgyógyász, haematológus) Shums, Zakera Dinya Tamás (1974-) (sebész szakorvos, onkológus szakorvos) Orosz Péter (Miskolc) Lombay Béla Jr. Pár Gabriella Pár Alajos Veres Gábor (1969-2020) (csecsemő- és gyermekgyógyász, gasztroenterológus) Csak Timea Osztovits János Szalay Ferenc (belgyógyász) Lakatos Péter (Semmelweis Egyetem)
Internet cím:DOI
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Borító:

8.

001-es BibID:BIBFORM051862
Első szerző:Szánthó Eszter (laboratóriumi szakorvos jelölt)
Cím:Serum Thymidine Kinase Activity : analytical Performance, Age-Related Reference Ranges and Validation in Chronic Lymphocytic Leukemia / Eszter Szánthó, Harjit Pal Bhattoa, Mária Csobán, Péter Antal-Szalmás, Anikó Újfalusi, János Kappelmayer, Zsuzsanna Hevessy
Dátum:2014
ISSN:1932-6203
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Plos One. - 9 : 3 (2014), p. e91647. -
További szerzők:Bhattoa Harjit Pal (1973-) (laboratóriumi szakorvos) Csobán Mária Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Ujfalusi Anikó (1968-) (gyermekorvos, laboratóriumi szakorvos) Kappelmayer János (1960-) (absztraktok) Hevessy Zsuzsanna (1966-) (laboratóriumi szakorvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

9.

001-es BibID:BIBFORM050127
035-os BibID:Article ID: e87845
Első szerző:Úri Katalin
Cím:New perspectives in the renin-angiotensin-aldosterone system (RAAS) IV : circulating ACE2 as a biomarker of systolic dysfunction in human hypertension and heart failure / Katalin Úri, Miklós Fagyas, Ivetta Mányiné Siket, Attila Kertész, Zoltán Csanádi, Gábor Sándorfi, Marcell Clemens, Roland Fedor, Zoltán Papp, István Édes, Attila Tóth, Erzsébet Lizanecz
Dátum:2014
ISSN:1932-6203
Megjegyzések:Background. Growing evidence exists for soluble Angiotensin Converting Enzyme-2 (sACE2) as a biomarker in definitive heart failure (HF), but there is little information about changes in sACE2 activity in hypertension with imminent heart failure and in reverse remodeling. Methods, Findings. Patients with systolic HF (NYHAII-IV, enrolled for cardiac resynchronisation therapy, CRT, n=100) were compared to hypertensive patients (n=239) and to a healthy cohort (n=45) with preserved ejection fraction (EF>50%) in a single center prospective clinical study. The status of the heart failure patients were checked before and after CRT. Biochemical (ACE and sACE2 activity, ACE concentration) and echocardiographic parameters (EF, left ventricular end-diastolic (EDD) and end-systolic diameter (ESD) and dP/dt) were measured. sACE2 activity negatively correlated with EF and positively with ESD and EDD in all patient's populations, while it was independent in the healthy cohort. sACE2 activity was already increased in the hypertensive group, where signs for imminent heart failure (slightly decreased EF and barely increased NT-proBNP levels) were detected. sACE2 activities further increased in patients with definitive heart failure (EF<50%), while sACE2 activities decreased with the improvement of the heart failure after CRT (reverse remodeling). Serum angiotensin converting enzyme (ACE) concentrations were lower in the diseased populations, but did not show a strong correlation with the echocardiographic parameters.Conclusions. Soluble ACE2 activity appears to be biomarker in heart failure, and in hypertension, where heart failure may be imminent. Our data suggest that sACE2 is involved in the pathomechanism of hypertension and HF.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
ACE2
angiotensin-converting enzyme 2
heart failure
hypertension
Megjelenés:Plos One. - 9 : 4 (2014), p. 1-32. -
További szerzők:Fagyas Miklós (1984-) (orvos) Mányiné Siket Ivetta (1962-) (laborasszisztens) Kertész Attila Béla (1973-) (kardiológus) Csanádi Zoltán (1960-) (kardiológus) Sándorfi Gábor (1976-) (belgyógyász, kardiológus) Clemens Marcell (1979-) (kardiológus) Fedor Roland (1975-) (sebész) Papp Zoltán (1965-) (kardiológus, élettanász) Édes István (1952-) (kardiológus) Tóth Attila (1971-) (biológus) Lizanecz Erzsébet (1978-) (orvos)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Kardiológia Kutatócsoport
Internet cím:DOI
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