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1.

001-es BibID:BIBFORM047427
Első szerző:Adyshev, Djanybek M.
Cím:Ezrin/radixin/moesin proteins differentially regulate endothelial hyperpermeability after thrombin / Djanybek M. Adyshev, Steven M. Dudek, Nurgul Moldobaeva, Kyung-mi Kim, Shwu-Fan Ma, Anita Kasa, Joe G. N. Garcia, Alexander D. Verin
Dátum:2013
ISSN:1040-0605
Megjegyzések:Endothelial cell (EC) barrier disruption induced by inflammatory agonists such as thrombin leads to potentially lethal physiological dysfunction such as alveolar flooding, hypoxemia and pulmonary edema. Thrombin stimulates paracellular gap and F-actin stress fiber formation, triggers actomyosin contraction and alters EC permeability through multiple mechanisms that include protein kinase C (PKC) activation. We previously have shown that the ezrin, radixin, and moesin (ERM) actin-binding proteins differentially participate in S1P-induced EC barrier enhancement. Phosphorylation of a conserved threonine residue in the C terminus of ERM proteins causes conformational changes in ERM to unmask binding sites and is considered a hallmark of ERM activation. In the present study we test the hypothesis that ERM proteins are phosphorylated on this critical threonine residue by thrombin-induced signaling events and explore the role of the ERM family in modulating thrombin-induced cytoskeletal rearrangement and EC barrier function. Thrombin promotes ERM phosphorylation at this threonine residue (Ezrin-567, Radixin-564, Moesin-558) in a PKC-dependent fashion and induces translocation of phosphorylated ERM to the EC periphery. Thrombin-induced ERM threonine phosphorylation is likely synergistically mediated by protease-activated receptors PAR1 and PAR2. Using the siRNA approach, depletion of either moesin alone, or of all three ERM proteins, significantly attenuates thrombin-induced increase in EC barrier permeability (TER), cytoskeletal rearrangements, paracellular gap formation and accumulation of di-phospho-MLC. In contrast, radixin depletion exerts opposing effects on these indices. These data suggest that ERM proteins play important differential roles in the thrombin-induced modulation of EC permeability, with moesin promoting barrier dysfunction and radixin opposing it
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
thrombin
ERM
PKC
phosphorylation
Megjelenés:American Journal of Physiology-Lung Cellular and Molecular Physiology 305 : 3 (2013), p. L240-L255. -
További szerzők:Dudek, Steven Moldobaeva, Nurgul Kim, Kyung-mi Ma, Shwu-Fan Kovács-Kása Anita (1983-) Garcia, Joe G. N. Verin, Alexander
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2.

001-es BibID:BIBFORM060756
Első szerző:Ambrus Lídia (élettanász)
Cím:Inhibition of TRPC6 by protein kinase C isoforms in cultured human podocytes / Lídia Ambrus, Attila Oláh, Tamás Oláh, György Balla, Moin A. Saleem, Petronella Orosz, Judit Zsuga, Klára Bíró, László Csernoch, Tamás Bíró, Tamás Szabó
Dátum:2015
ISSN:1582-1838
Megjegyzések:Transient receptor potential canonical-6 (TRPC6) ion channels, expressed at high levels in podocytes of the filtration barrier, are recently implicated in the pathogenesis of various forms of proteinuric kidney diseases. Indeed, inherited or acquired up-regulation of TRPC6 activities are suggested to play a role in podocytopathies. Yet, we possess limited information about the regulation of TRPC6 in human podocytes. Therefore, in this study, we aimed at defining how the protein kinase C (PKC) system, one of the key intracellular signalling pathways, regulates TRPC6 function and expression. On human differentiated podocytes, we identified the molecular expressions of both TRPC6 and several PKC isoforms. We also showed that TRPC6 channels are functional since the TRPC6 activator 1-oleoyl-2-acetyl-sn-glycerol (OAG) induced Ca2+-influx to the cells. By assessing the regulatory roles of the PKCs, we found that inhibitors of the endogenous activities of classical and novel PKC isoforms markedly augmented TRPC6 activities. In contrast, activation of the PKC system by phorbol 12-myristate 13-acetate (PMA) exerted inhibitory actions on TRPC6 and suppressed its expression. Importantly, PMA treatment markedly down-regulated the expression levels of PKCa, PKCb, and PKCg reflecting their activation. Taken together, these results indicate that the PKC system exhibits a 'tonic' inhibition on TRPC6 activity in human podocytes suggesting that pathological conditions altering the expression and/or activation patterns of podocyte-expressed PKCs may influence TRPC6 activity and hence podocyte functions. Therefore, it is proposed that targeted manipulation of certain PKC isoforms might be beneficial in certain proteinuric kidney diseases with altered TRPC6 functions.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
human podocytes
transient receptor potential canonical-6
protein kinase C isoforms
proteinuria
Megjelenés:Journal Of Cellular And Molecular Medicine. - 19 : 12 (2015), p. 2771-2779. -
További szerzők:Oláh Attila (1984-) (élettanász) Oláh Tamás (1983-) (élettanász) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Saleem, Moin A. Orosz Petronella (1986-) (klinikai orvos) Zsuga Judit (1973-) (neurológus, pszichoterapeuta, egészségügyi szakmanager) Bíró Klára (1970-) (egészségügyi menedzsment) Csernoch László (1961-) (élettanász) Bíró Tamás (1968-) (élettanász) Szabó Tamás (1968-) (gyermekgyógyász)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Gyermekgyógyászat Kutatócsoport
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3.

001-es BibID:BIBFORM047648
Első szerző:Bácsi Attila (immunológus)
Cím:Colostrinin-Driven Neurite Outgrowth Requires p53 Activation in PC12 Cells / Attila Bacsi, G. John Stanton, Thomas K. Hughes, Marian Kruzel, Istvan Boldogh
Dátum:2005
ISSN:0272-4340
Megjegyzések:1. Colostrinin (CLN) induces maturation and differentiation of murine thymocytes,promotes proliferation of peripheral blood leukocytes, induces immunomodulatorcytokines, and ameliorates oxidative stress-mediated activation of c-Jun NH2-terminalkinases.2. Here we report that upon treatment with CLN, medullary pheochromocytoma(PC12) cells ceased to proliferate and extend neurites.3. The arrest of CLN-treated PC12 cells in the G1 phase of the cell cycle was due toan increase in the phosphorylation of p53 at serine15 (p53ser15) and expression of p21WAF1.PC12 cells treated with inhibitory oligonucleotides to p53 lacked p53ser15 and p21WAF1expression, and did not show morphological changes after CLN exposure. Transfectionwith inhibitory oligonucleotides to p21WAF1 had no effect on p53 activation; however, cellsfailed to arrest or extend neurites. An oligonucleotide inhibiting luciferase expression hadno effect on CLN-mediated p53 activation, p21WAF1 expression, growth arrest, or neuriteoutgrowth.4. We conclude that CLN induces delicate cassettes of signaling pathways common tocell proliferation and differentiation, and mediates activities that are similar to those ofhormones and neurotrophins, leading to neurite outgrowth.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
colostrinin
pheochromocytoma cell
neurite outgrowth
p53 activation
Megjelenés:Cellular And Molecular Neurobiology. - 25 : 7 (2005), p. 1123-1139. -
További szerzők:Stanton, G. John Hughes, Thomas K. Kruzel, Marian L. Boldogh István
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4.

001-es BibID:BIBFORM112824
035-os BibID:(scopus)85146088525 (cikkazonosító)101891 (wos)000923306100001
Első szerző:Bádon Emese Sarolta (orvos)
Cím:Clonal diversity in KRAS mutant colorectal adenocarcinoma under treatment : Monitoring of cfDNA using reverse hybridization and DNA sequencing platforms / Bádon Emese Sarolta, Mokánszki Attila, Mónus Anikó, András Csilla, Méhes Gábor
Dátum:2023
ISSN:0890-8508
Megjegyzések:Biological heterogeneity is a key feature of malignancies that significantly contributes to disease progression and therapy resistance. Residual/relapsed tumor foci may represent genetically divergent subclones, which remain uncovered as repeated and multiple tumor sampling is usually limited. The analysis of circulating free DNA (cfDNA) from the peripheral blood plasma (also called a liquid biopsy, LB) is a new achievement that provides an effective tool for follow-up monitoring of cancer-related genetic status. The present study highlights the phenomenon of mutational variability observed in patients with metastatic KRAS mutant colorectal cancer (mCRC) during treatment with bevacizumab in combination in a longitudinal fashion. The prospective study included 490 mCRC patients evaluated between 2020 and 2022 in our institution. Out of the 211 KRAS mutant cases (43.06%) 12 tumors were identified with multiple KRAS gene variants (5.68%). Detailed follow-up investigations were possible in 3 of these patients including the genotyping of the primary and available metastatic tumors, and the peripheral blood cfDNA. cfDNA was collected from three different time points before and between cycles of combined treatment with bevacizumab chemotherapy. KRAS gene variants were identified using reverse-hybridization strips, and next-generation sequencing (NGS), and confirmed by conventional Sanger sequencing. Interestingly, surgery and multiple treatment cycles reorganized the mutational profiles in the selected cases. The effect of the treatments resulted either in the overrepresentation of one of the pre-existing gene variants or in the appearance of new KRAS variants absent in the primary sample, according to the plasma cfDNA findings. Besides the KRAS variants demonstrated by targeted analysis, NGS mutational profiling identified some additional pathogenic variants from the cfDNA samples (including NRAS and MET alterations). In conclusion, plasma cfDNA sampling enables the monitoring of mutational heterogeneity and subclonal dynamics of the actual metastatic tumor mass in mCRC. The pattern of molecular profile potentially reflects a differential drug response determining further progression.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Molecular And Cellular Probes. - 67 (2023), p. 1-8. -
További szerzők:Mokánszki Attila (1983-) (molekuláris biológus Ph.D hallgató) Mónus Anikó András Csilla (1961-) (onkológus szakorvos) Méhes Gábor (1966-) (patológus)
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5.

001-es BibID:BIBFORM058970
Első szerző:Bai Péter (biokémikus)
Cím:Biology of Poly(ADP-Ribose) Polymerases : the Factotums of Cell Maintenance / Peter Bai
Dátum:2015
ISSN:1097-2765
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Molecular Cell. - 58 : 6 (2015), p. 947-958. -
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0025
TÁMOP
OTKA-K108308
OTKA
OTKA-K105872
OTKA
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6.

001-es BibID:BIBFORM028159
Első szerző:Bakó Éva (biokémikus)
Cím:Purification and partial characterization of protein phosphatases from rat thymus / Éva Bakó, Viktor Dombrádi, Ferenc Erdődi, Lawrence Zumo, Pál Kertai, Pál Gergely
Dátum:1989
ISSN:0167-4889
Megjegyzések:Protein phosphatases assayed with phosphorylase alpha are present in the soluble and particulate fractions of rat thymocytes. Phosphorylase phosphatase activity in the cytosol fraction was resolved by heparin-Sepharose chromatography into type-1 and type-2A enzymes. Similarities between thymocyte and muscle or liver protein phosphatase-1 included preferential dephosphorylation of the beta subunit of phosphorylase kinase, inhibition by inhibitor-2 and retention by heparin-Sepharose. Similarities between thymocyte and muscle or liver protein phosphatase-2A included specificity for the alpha subunit of phosphorylase kinase, insensitivity to the action of inhibitor-2, lack of retention by heparin-Sepharose and stimulation by polycationic macromolecules such as polybrene, protamine and histone H1. Protein phosphatase-1 from the cytosol fraction of thymocytes had an apparent molecular mass of 120 kDa as determined by gel filtration. The phosphatase-2A separated from the cytosol of thymocytes may correspond to phosphatase-2A0, since it was completely inactive (latent) in the absence of polycation and had activity only in the presence of polycations. The apparent molecular mass of phosphatase-2A0 from thymocytes was 240 kDa as determined by gel filtration. The catalytic subunit of thymocyte type-1 protein phosphatase was purified with heparin-Sepharose chromatography followed by gel filtration and fast protein liquid chromatography on Mono Q column. The purified type-1 catalytic subunit exhibited a specific activity of 8.2 U/mg and consisted of a single protein of 35 kDa as judged by SDS-gel electrophoresis. The catalytic subunit of type-2A phosphatase from thymocytes appearing in the heparin-Sepharose flow-through fraction was further purified on protamine-Sepharose, followed by gel filtration. The specific activity of the type-2A catalytic subunit was 2.1 U/mg and consisted of a major protein of 34.5 kDa, as revealed by SDS-gel electrophoresis.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
protein phosphatase-1
protein phosphatase-2A
polycation
heparin-Sepharose
thymocyte
rat
egyetemen (Magyarországon) készült közlemény
Megjelenés:Biochimica et Biophysica Acta (BBA). Molecular Cell Research. - 1013 : 3 (1989), p. 300-305. -
További szerzők:Kertai Pál (1927-2016) (népegészségügyi szakember) Dombrádi Viktor (1953-) (biokémikus) Erdődi Ferenc (1953-) (biokémikus) Zumo, Lawrence (1966-) Gergely Pál (1947-) (biokémikus)
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Szerző által megadott URL
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7.

001-es BibID:BIBFORM078411
035-os BibID:(PMID)30734834 (WoS)000472512500009 (Scopus)85061242629
Első szerző:Baksa Brigitta (fogorvos)
Cím:Characterization of functional subgroups among genetically identified cholinergic neurons in the pedunculopontine nucleus / Baksa B., Kovács A., Bayasgalan T., Szentesi P., Kőszeghy Á., Szücs P., Pál B.
Dátum:2019
ISSN:1420-682X
Megjegyzések:The pedunculopontine nucleus (PPN) is a part of the reticular activating system which is composed of cholinergic, glutamatergic and GABAergic neurons. Early electrophysiological studies characterized and grouped PPN neurons based on certain functional properties (i.e. the presence or absence of the A-current, spike latency, and low threshold spikes). Although other electrophysiological characteristics of these neurons were also described (as high threshold membrane potential oscillations, great differences in spontaneous firing rate and the presence or absence of the M-current), systematic assessment of these properties and correlation of them with morphological markers are still missing. In this work, we conducted electrophysiological experiments on brain slices of genetically identified cholinergic neurons in the PPN. Electrophysiological properties were compared with rostrocaudal location of the neuronal soma and selected morphometric features obtained with post hoc reconstruction. We found that functional subgroups had different proportions in the rostral and caudal subregions of the nucleus. Neurons with A-current can be divided to early-firing and late-firing neurons, where the latter type was found exclusively in the caudal subregion. Similar to this, different parameters of high threshold membrane potential oscillations also showed characteristic rostrocaudal distribution. Furthermore, based on our data we propose that high threshold oscillations rather emerge from neuronal somata and not from the proximal dendrites. In summary, we demonstrated the existence and spatial distribution of functional subgroups of genetically identified PPN cholinergic neurons, which are in accordance with differences found in projection and in vivo functional findings of the subregions. Being aware of functional differences of PPN subregions will help the design and analysis of experiments using genetically encoded opto- and chemogenetic markers for in vivo experiments.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
pedunculopontine nucleus
cholinergic neuron
spike delay
A-current
rostrocaudal gradient
high threshold oscillation
Megjelenés:Cellular And Molecular Life Sciences. - 76 : 14 (2019), p. 2799-2815. -
További szerzők:Kovács Adrienn (1989-) (molekuláris biológus) Bayasgalan, Tsogbadrakh (1983-) (Általános orvos) Szentesi Péter (1967-) (élettanász) Kőszeghy Áron (1983-) (Ph.D hallgató, élettanász) Szűcs Péter (1974-) (kutatóorvos) Pál Balázs (1975-) (élettanász)
Pályázati támogatás:KTIA_13_NAP-A-I/10
Egyéb
2017-1.2.1-NKP-2017-00002
Egyéb
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8.

001-es BibID:BIBFORM014138
Első szerző:Bálint Bálint László (kutató orvos)
Cím:Arginine Methylation Provides Epigenetic Transcription Memory for Retinoid-Induced Differentiation in Myeloid Cells / Balint L. Balint, Attila Szanto, Andras Madi, Uta-Maria Bauer, Petra Gabor, Szilvia Benko, Laszlo G. Puskas, Peter J. A. Davies, Laszlo Nagy
Dátum:2005
ISSN:0270-7306
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Molecular And Cellular Biology. - 25 : 13 (2005), p. 5648-5663. -
További szerzők:Szántó Attila (1976-) (orvos, biokémikus) Mádi András (1967-) (biológus) Bauer, Uta-Maria Gábor Petra Benkő Szilvia (1973-) (molekuláris biológus) Puskás László G. Davies, Peter J. A. Nagy László (1966-) (molekuláris sejtbiológus, biokémikus)
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9.

001-es BibID:BIBFORM073493
Első szerző:Balogh László (kardiológus)
Cím:Effect of factor XIII levels and polymorphisms on the risk of myocardial infarction in young patients / Balogh László, Katona Éva, Mezei Zoltán A., Kállai Judit, Gindele Réka, Édes István, Muszbek László, Papp Zoltán, Bereczky Zsuzsanna
Dátum:2018
ISSN:0300-8177
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Molecular And Cellular Biochemistry. - 448 : 1-2 (2018), p. 199-209. -
További szerzők:Katona Éva (1961-) (klinikai biokémikus) Mezei Zoltán András (1980-) (orvos) Kállai Judit (1983-) (molekuláris biológus) Gindele Réka (1987-) (molekuláris biológus) Édes István (1952-) (kardiológus) Muszbek László (1942-) (haematológus, kutató orvos) Papp Zoltán (1965-) (kardiológus, élettanász) Bereczky Zsuzsanna (1974-) (orvosi laboratóriumi diagnosztika szakorvos)
Pályázati támogatás:EFOP-3.6.2-16-2017-00006
EFOP
K 113097
OTKA
K 109783
OTKA
K 116228
OTKA
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10.

001-es BibID:BIBFORM020219
035-os BibID:WOS:000287469400023
Első szerző:Bányász Tamás (élettanász)
Cím:Sequential dissection of multiple ionic currents in single cardiac myocytes under action potential-clamp / Banyasz T., Horvath B., Jian Z., Izu L. T., Chen-Izu Y.
Dátum:2011
ISSN:0022-2828
Megjegyzések:The cardiac action potential (AP) is shaped by myriad ionic currents. In this study, we develop an innovative AP-clamp Sequential Dissection technique to enable the recording of multiple ionic currents in the single cell under AP-clamp. This new technique presents a significant step beyond the traditional way of recording only one current in any one cell. The ability to measure many currents in a single cell has revealed two hitherto unknown characteristics of the ionic currents in cardiac cells: coordination of currents within a cell and large variation of currents between cells. Hence, the AP-clamp Sequential Dissection method provides a unique and powerful tool for studying individual cell electrophysiology.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Molecular and Cellular Cardiology 50 : 3 (2011), p. 578-581. -
További szerzők:Horváth Balázs (1981-) (élettanász) Jian, Zhong Izu, Leighton T. Chen-Izu, Ye
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11.

001-es BibID:BIBFORM047845
Első szerző:Barta Judit (kardiológus)
Cím:Protection of Calpain-1 induced cTnI degradation by PKA phosphorylation in vitro / J. Barta, A. Tóth, Z. Hertelendi, I. Édes I., K. Jaquet, A. Reidlich, Z. Papp
Dátum:2002
ISSN:0022-2828
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
Megjelenés:Journal of Molecular and Cellular Cardiology. - 34 (2002), p. A7. -
További szerzők:Tóth Attila (orvos) Hertelendi Zita (1978-) (orvos) Édes István (1952-) (kardiológus) Jaquet, Kornelia Reidlich Alexander Papp Zoltán (1965-) (kardiológus, élettanász)
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12.

001-es BibID:BIBFORM015742
Első szerző:Barta Judit (kardiológus)
Cím:Calpain-1-sensitive myofibrillar proteins of the human myocardium / Barta Judit, Tóth Attila, Édes István, Vaszily Miklós, Papp Gy. Julius, Varró András, Papp Zoltán
Dátum:2005
Megjegyzések:Calpain-1 is a ubiquitous intracellular Ca2+-activated protease, which has been implicated in the pathogenesis of reversible myocardial depression (i.e. myocardial stunning) that follows ischemia and reperfusion via myofibrillar protein degradation. However, the target proteins of this degradative process in the human myocardium have not yet been identified. In order to compare the levels of Calpain-1 susceptibility within a set of human myofibrillar proteins (titin, alpha-fodrin, desmin, troponin T (cTnT), troponin I (cTnI) and alpha-actinin), crude left ventricular tissue homogenates were incubated for 0.5, 15, 30, 60 or 120 min in the presence of Calpain-1 (1 U or 5 U). Differences in the kinetics and extents of protein degradation were subsequently evaluated by using silver-stained SDS-polyacrylamide gels and Western immunoblot analyses. These assays revealed myofibrillar proteins with high (titin and alpha-fodrin), moderate (desmin and cTnT), or low (cTnI and alpha-actinin) relative Calpain-1 susceptibilities. The level of phosphorylation of cTnI did not explain its relatively low Calpain-1 susceptibility. Moreover, the molecular mass distributions of the truncated alpha-fodrin, desmin and cTnI fragments resulting from Ca2+-dependent autoproteolysis exhibited marked similarities with those of their Calpain-1-clipped products. These in vitro results shed light on a number of structural (titin, alpha-fodrin, desmin and alpha-actinin) and regulatory (cTnT and cTnI) proteins within the contractile apparatus as potential targets of Calpain-1. Their degradation may contribute to the development of postischemic stunning in the human myocardium.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
calpain
desmin
stunning
titin
troponin I
troponin T
Megjelenés:Molecular and Cellular Biochemistry. - 278 : 1-2 (2005), p. 1-8. -
További szerzők:Tóth Attila (1971-) (biológus) Édes István (1952-) (kardiológus) Vaszily Miklós (1949-) (szívsebész) Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Papp Zoltán (1965-) (kardiológus, élettanász)
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