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1.

001-es BibID:BIBFORM054216
Első szerző:Ajzner Éva (laboratóriumi szakorvos)
Cím:Anti-factor V auto-antibody in the plasma and platelets of a patient with repeated gastrointestinal bleeding / É. Ajzner, I. Balogh, G. Haramura, Z. Boda, K. Kalmár, G. Pfliegler, B. Dahlbäck, L. Muszbek
Dátum:2003
ISSN:1538-7933
Megjegyzések:Development of autoantibody against coagulation factor V (FV) is a rare clinical condition with hemorrhagic complications of varying severity. The aim of this study was to establish the pathomechanism of an acquired FV deficiency and characterize the FV inhibitor responsible for the clinical symptoms. A 78-year-old female was admitted to hospital with severe gastrointestinal bleeding. General clotting tests and determination of clotting factors were performed by standard methods. FV antigen and FV containing immune complexes were measured by ELISA. The FV molecule was investigated by Western blotting and by sequencing the f5 gene. The binding of patient's IgG to FV and activated FV (FVa) was demonstrated in an ELISA system and its effect on the procoagulant activity of FVa was tested in clotting tests and in a chromogenic prothrombinase assay. Localization of the epitope for the antibody was performed by blocking ELISA. FV activity was severely suppressed both in plasma and platelets. FV antigen levels were normal by ELISA using polyclonal anti-FV antibody or monoclonal antibody against the connecting region of FV, but depressed when HV1 monoclonal antibody against the C2 domain in the FV light-chain was used as capture antibody. The FV molecule was found intact. An IgG reacting with both FV and FVa was present in the patient's plasma and its binding to FV was inhibited by HV1 antibody. FV-containing immune complexes were detected in the patient's plasma and platelet lysate. The patient's IgG inhibited the procoagulant function of FVa. An anti-FV IgG was present in the patient's plasma and platelets. The autoantibody reacted with an epitope in the C2 domain of FV light chain and neutralized the procoagulant function of FVa.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of thrombosis and haemostasis. - 1 : 5 (2003), p. 943-949. -
További szerzők:Balogh István (1972-) (molekuláris biológus, genetikus) Haramura Gizella (1957-) (vezető analitikus) Boda Zoltán (1947-) (belgyógyász, haematologus, klinikai onkológus) Kalmár Kálmán Pfliegler György (1949-) (belgyógyász, hematológus, labor szakorvos) Dahlbäck, Björn Muszbek László (1942-) (haematológus, kutató orvos)
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2.

001-es BibID:BIBFORM034619
035-os BibID:PMID:10235459 WOS:000079748300036
Első szerző:Balogh István (molekuláris biológus, genetikus)
Cím:High prevalence of factor V Leiden mutation and 20210A prothrombin variant in Hungary / I. Balogh, R. Póka, G. Pfliegler, M. Dékány, Z. Boda, L. Muszbek
Dátum:1999
ISSN:0340-6245
Tárgyszavak:Orvostudományok Klinikai orvostudományok levél
egyetemen (Magyarországon) készült közlemény
Megjelenés:Thrombosis And Haemostasis 81 : 4 (1999), p. 660-661. -
További szerzők:Póka Róbert (1960-) (szülész-nőgyógyász, klinikai onkológus) Pfliegler György (1949-) (belgyógyász, hematológus, labor szakorvos) Dékány Miklós Boda Zoltán (1947-) (belgyógyász, haematologus, klinikai onkológus) Muszbek László (1942-) (haematológus, kutató orvos)
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3.

001-es BibID:BIBFORM084884
035-os BibID:(WoS)000379164000245
Első szerző:Bereczky Zsuzsanna (orvosi laboratóriumi diagnosztika szakorvos)
Cím:Diagnostic issues in antithrombin, protein C and protein S deficiency in the hungarian population : experience of a large thrombosis laboratory / Bereczky Z., Speker M., Gindele R., Szabo Z., Oláh Z., Pfliegler G., Kerényi A., Boda Z.
Dátum:2016
ISSN:1538-7933 1538-7836
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Journal of Thrombosis and Haemostasis. - 14 : Suppl. 1 (2016), p. 98. -
További szerzők:Speker Marianna Gindele Réka (1987-) (molekuláris biológus) Szabó Zsuzsa (1990-) (kémikus) Oláh Zsolt (1974-) (belgyógyász) Pfliegler György (1949-) (belgyógyász, hematológus, labor szakorvos) Kerényi Adrienne (1970-) (laboratóriumi szakorvos) Boda Zoltán (1947-) (belgyógyász, haematologus, klinikai onkológus)
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4.

001-es BibID:BIBFORM034582
035-os BibID:PMID:2620871 WOS:A1989CB21800007
Első szerző:Boda Zoltán (belgyógyász, haematologus, klinikai onkológus)
Cím:Congenital factor XIII deficiency with multiple benign breast tumours and successful pregnancy with substitutive therapy : a case report / Z. Boda, G. Pfliegler, L. Muszbek, A. Tóth, R. Ádány, J. Hársfalvi, Z. Papp, I. Tornai, K. Rák
Dátum:1989
Megjegyzések:A 34-year-old woman with congenital factor XIII (FXIII) deficiency and multiple connective tissue tumours is reported. The subunit a of FXIII was totally absent in her plasma, platelets and histiocytes of breast fibroadenomas and considerably reduced in the monocytes (below 5%). The plasmatic level of subunit b was also reduced (25%). She had a bleeding tendency and habitual abortions. Fresh frozen plasma therapy permitted a successful pregnancy.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Congenital factor XIII deficiency
Connective tissuc tumour
Fresh frozen plasma therapy
Habitual abortion
Successful pregnancy
egyetemen (Magyarországon) készült közlemény
Megjelenés:Haemostasis. - 19 (1989), p. 348-352. -
További szerzők:Pfliegler György (1949-) (belgyógyász, hematológus, labor szakorvos) Muszbek László (1942-) (haematológus, kutató orvos) Tóth Attila (orvos) Ádány Róza (1952-) (megelőző orvostan és népegészségtan szakorvos) Hársfalvi Jolán (1949-) (klinikai biokémikus) Papp Zoltán (1942-) (szülész-nőgyógyász, genetikus) Tornai István (1954-) (belgyógyász, gasztroenterológus) Rák Kálmán (1929-2005) (belgyógyász, klinikai hematológus, véralvadás kutató)
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5.

001-es BibID:BIBFORM034512
035-os BibID:PMID:8819268
Első szerző:Boda Zoltán (belgyógyász, haematologus, klinikai onkológus)
Cím:Low molecular weight heparin as thromboprophylaxis in familial thrombophilia during the whole period of pregnancy : letters to the editor / Z. Boda, P. László, L. Rejtő, I. Tornai, G. Pfliegler, G. Blaskó, K. Rák
Dátum:1996
ISSN:0340-6245
Tárgyszavak:Orvostudományok Klinikai orvostudományok szerkesztői levél
egyetemen (Magyarországon) készült közlemény
Megjelenés:Thrombosis And Haemostasis 76 : 1 (1996), p. 128. -
További szerzők:László Pál (belgyógyász) Rejtő László (1963-) (belgyógyász, haematológus) Tornai István (1954-) (belgyógyász, gasztroenterológus) Pfliegler György (1949-) (belgyógyász, hematológus, labor szakorvos) Blaskó György (1947-) (belgyógyász, klinikai farmakológus) Rák Kálmán (1929-2005) (belgyógyász, klinikai hematológus, véralvadás kutató)
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6.

001-es BibID:BIBFORM034625
Első szerző:Bonnefoy, Arnaud
Cím:The subendothelium of the HMEC-1 cell line supports thrombus formation in the absence of von Willebrand factor and collagen types I, III and VI / Bonnefoy A., Harsfalvi J., Pfliegler G., Fauvel-Lafeve F., Legrand C.
Dátum:2001
ISSN:0340-6245
Megjegyzések:The macromolecular composition of the extracellular matrix (ECM) produced by the human microvascular endothelial cell line (HMEC-1) was determined by ELISA and its thrombogenicity was studied in blood perfusion assays. Results were compared with those obtained with the ECM produced by human umbilical vein endothelial cells (HUVEC). The HMEC-1's ECM contains collagen type IV, fibronectin, laminin and thrombospondin, but no detectable levels of collagen types I, III and VI, or von Willebrand factor (vWF), whereas all these components were found in the ECM synthesized by HUVEC. HMEC-1's ECM was perfused with low-molecular-weight heparin-anticoagulated blood at two wall shear rates (650/s and 2,600/s), representative of moderate and high arterial wall shear rates, in parallel plate flow chambers for 5 min. This resulted in the formation of large platelet aggregates, compared to essentially a monolayer of adherent platelets on HUVEC's ECM. Interestingly, large thrombi were formed at 2,600/s when HMEC-1's ECM was perfused with the blood of a patient with severe type III von Willebrand disease lacking both plasma and platelet vWF, indicating that vWF was not absolutely required for thrombus formation on this matrix. Thrombin generated on the HMEC-1's ECM contributed importantly to the large platelet thrombi formed, shown by performing blood perfusion experiments in the presence of thrombin inhibitors. Our results indicate that 1) platelet adhesion and aggregate formation on a subendothelium may occur at a high shear rate (2600/s) without the participation of collagen types I, III and VI, and vWF; and 2) the HMEC-1 cell line may prove useful for in vitro studies of the thrombogenic properties of microvascular subendothelium which in most cases does not contain fibrillar collagens and vWF.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Thrombus formation
von Willebrand factor
collagen
HMEC-1
shear rate
extra cellular matrix (ECM)
Megjelenés:Thrombosis And Haemostasis. - 85 : 3 (2001), p. 552-559. -
További szerzők:Hársfalvi Jolán (1949-) (klinikai biokémikus) Pfliegler György (1949-) (belgyógyász, hematológus, labor szakorvos) Fauvel-Lafeve, Francoise Legrand, Chantal
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7.

001-es BibID:BIBFORM034509
035-os BibID:PMID:7545323 WOS:A1995QM81900034
Első szerző:Crawford, Neville
Cím:Targeting platelets containing electro-encapsulated iloprost to balloon injured aorta in rats / N. Crawford, A. Chajara, G. Pfliegler, B. El. Gamal, L. Brewer, L. Capron
Dátum:1995
ISSN:0340-6245
Megjegyzések:Drugs can be electro-encapsulated within platelets and targeted to damaged blood vessels by exploiting the platelet's natural haemostatic properties to adhere to collagen and other vessel wall constituents revealed by injury. A rat aorta balloon angioplasty model has been used to study the effect on platelet deposition of giving iloprost loaded platelets i.v. during the balloon injury. After labelling the circulating platelets with 111-Indium before balloon injury, time course studies showed maximum platelet deposition on the injured aorta occurred at about 1 h post-injury and the deposition remained stable over the next 2-3 h. When iloprost-loaded platelets were given i.v. during injury and the circulating platelet pool labelled with 111-Indium 30 min later, platelet deposition, measured at 2 h postinjury, was substantially and significantly reduced compared with control platelet treatment. Some anti-proliferative effects of iloprost-loaded platelets given i.v. during injury have also been observed. Whereas the incorporation of [3H]-thymidine into aorta intima-media DNA at 3 days post injury was 62-fold higher in balloon injured rats than in control sham operated rats, thymidine incorporation into intima/media of rats which had received iloprost loaded platelets during injury was reduced as compared with rats subjected only to the injury procedure. The reduction was only of near significance, however, but at 14 days after injury the total DNA content of the aorta intima/media of rats given iloprost loaded platelets during injury was significantly reduced. Although iloprost loaded platelets can clearly inhibit excessive platelet deposition, other encapsulated agents may have greater anti-proliferative effects.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Thrombosis And Haemostasis. - 73 : 3 (1995), p. 535-542. -
További szerzők:Chajara, A. Pfliegler György (1949-) (belgyógyász, hematológus, labor szakorvos) El-Gamal, Basiouny Brewer, L. Capron, L.
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8.

001-es BibID:BIBFORM034615
035-os BibID:PMID:1280865
Első szerző:El-Gamal, Basiouny
Cím:Effect of platelet encapsulated Iloprost on platelet aggregation and adhesion to collagen and injured blood vessels in vitro / B. A. B. El-Gamal, G. Pfliegler, N. Crawford
Dátum:1992
ISSN:0340-6245
Megjegyzések:A novel approach to site-directed delivery of drugs in vivo using blood platelets as carrier vehicles is being investigated. In this context some initial studies are reported on the effect of platelet encapsulated anti-platelet drugs on platelet aggregation and adhesion to fibrillar collagen and injured arteries in vitro. The stable prostacyclin analogue Iloprost has been encapsulated within human and pig platelets by high voltage electroporation (Hughes and Crawford 1989 and 1990). After resealing the platelets, the packaged drug has a negligible effect upon platelet adhesion to a surface of fibrillar collagen or to damaged aorta (stripped to the tunica media to simulate deep injury). The rate of platelet recruitment to the collagen shows no dose dependency with respect to intracellular Iloprost concentrations. After high Iloprost loading, as few as 2% drug loaded platelets in a mixture with control (sham encapsulated) platelets, inhibit agonist-induced platelet aggregation > 50%. The prior deposition of a "lawn" of Iloprost-loaded platelets onto fibrillar collagen or damaged aorta has a substantial inhibitory effect (50-70%) upon the secondary recruitment of normal platelets compared with recruitment to a "lawn" of normal platelets. This inhibition of secondary recruitment occurs even in the presence of a platelet activator. If reduction of platelet recruitment to a vessel wall lesion results in a decrease in the local concentration of platelet granule-derived smooth muscle cell chemotactic and proliferative factors, this site-directed drug delivery may well have application for the prevention of restenosis following balloon angioplasty procedures.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Thrombosis And Haemostasis. - 68 : 5 (1992), p. 606-614. -
További szerzők:Pfliegler György (1949-) (belgyógyász, hematológus, labor szakorvos) Crawford, Neville
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9.

001-es BibID:BIBFORM014375
Első szerző:Fodor Mariann (szemész)
Cím:Transient visual loss triggered by scuba diving in a patient with a petrous epidermoid and combined thrombotic risk factors / Fodor Mariann, Facskó Andrea, Berényi Ervin, Sziklai István, Berta András, Pfliegler György
Dátum:2007
Megjegyzések:A 25-year-old woman who developed transient neurological abnormalities after scuba diving is reported. The subsequent day she experienced transient left-side monocular blindness. Arterial ocular occlusion in apparently healthy young women is unusual, and a search for the cause of this devastating vascular event is mandatory. Occlusion of the left branch retinal artery, total occlusion of the left internal carotid artery, and a petrous apex epidermoid were found, together with a shortened prothrombin time (INR: 0.73), a slightly elevated serum cholesterol level (6.1 mmol/l) and combined thrombophilia (elevated FVIIIC plus type 2 sticky platelet syndrome). This case underlines the complex mechanism of thromboembolic diseases, and the importance of the acquired trigger (in the present case scuba diving) in addition to the long-term anatomical and biochemical risk factors.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Transient monocular blindness
Internal carotid artery occlusion
Petrous epidermoid
Platelet hyperaggregability
Elevated FVIIIC
Scuba diving
Megjelenés:Pathophysiology of Haemostasis and Thrombosis. - 36 : 6 (2007), p. 311-314. -
További szerzők:Facskó Andrea (1953-) (szemész) Berényi Ervin (1964-) (radiológus) Sziklai István (1954-) (fül-orr-gégész) Berta András (1955-) (szemész, gyermekszemész) Pfliegler György (1949-) (belgyógyász, hematológus, labor szakorvos)
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10.

001-es BibID:BIBFORM063574
035-os BibID:(WoS)000374979000010 (Scopus)84959145645
Első szerző:Gindele Réka (molekuláris biológus)
Cím:Founder effect is responsible for the p.Leu131Phe heparin-binding-site antithrombin mutation common in Hungary : phenotype analysis in a large cohort / R. Gindele, Z. Olah, P. Ilonczai, M. Speker, A. Udvari, A. Selmeczi, G. Pfliegler, E. Marjan, B. Kovacs, Z. Boda, L. Muszbek, Z. Bereczky
Dátum:2016
ISSN:1538-7933
Megjegyzések:Background: Antithrombin (AT) is a key regulatorof the coagulation. In type II deficiency, the heparinbinding-site defect (type II HBS) is considered to be relativelylow thrombosis risk. Objectives: Our aims were tosearch for SERPINC1 mutation(s) and to describe the clinicaland laboratory phenotype of a large number of ATBudapest3 (ATBp3, p.Leu131Phe) carriers and confirm thepresence of a founder effect. Patients/Methods: AT-deficientpatients were recruited and carriers of ATBp3,n = 102 (63 families) were selected. To investigate the foundereffect, eight intragenic single nucleotide polymorphisms,a 50-length dimorphism, and five microsatellitemarkers were detected. Clinical and laboratory data of thepatients were collected and analyzed. Results: In AT deficiency,16 different causative mutations were found, andthe great majority of patients were of type II HBS subtype.Most of them (n = 102/118, 86.5%) carried the ATBp3mutation. The ATBp3 mutant allele was associated withone single haplotype, while different haplotypes weredetected in the case of normal allele. The anti?factor Xa?based AT activity assay that we used could detect allATBp3 patients with high sensitivity in our cohort. ATBp3homozygosity (n = 26) was associated with thrombosis at ayoung age and conferred a high thrombotic risk. Half ofthe heterozygotes (n = 41/76, 53.9%) also had venous and/or arterial thrombosis, and pregnancy complications werealso recorded. Conclusion: In Hungary, the founder mutation,ATBp3, is the most common AT deficiency. Ourstudy is the first in which the clinical characterization ofATBp3 mutation was executed in a large population.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
antithrombin III deficiency
antithrombin III
thrombophilia
founder effect
venous thromboembolism
Megjelenés:Journal Of Thrombosis And Haemostasis. - 14 : 4 (2016), p. 704-715. -
További szerzők:Oláh Zoltán Ilonczai Péter (1977-) (orvos, belgyógyász, haematológus szakorvos) Speker Marianna Udvari Á. Selmeczi Anna (1982-) (orvos) Pfliegler György (1949-) (belgyógyász, hematológus, labor szakorvos) Marján Erzsébet Kovács Bettina (1975-) (orvos) Boda Zoltán (1947-) (belgyógyász, haematologus, klinikai onkológus) Muszbek László (1942-) (haematológus, kutató orvos) Bereczky Zsuzsanna (1974-) (orvosi laboratóriumi diagnosztika szakorvos)
Pályázati támogatás:PD101120
OTKA
K116228
OTKA
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Trombózis Kutató Központ Kutatócsoport
11003
MTA
TKI227
MTA
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11.

001-es BibID:BIBFORM034508
Első szerző:Pfliegler György (belgyógyász, hematológus, labor szakorvos)
Cím:Inhibition of platelet recruitment to arterial lesions by predeposition of platelets containing encapsulated iloprost / George Pfliegler, Basiouny El-Gamal, Juan José Badimon, Lina Badimon, Neville Crawford
Dátum:1994
ISSN:0340-6245
Megjegyzések:Drugs can be encapsulated within blood platelets by reversible electroporation and can be haemostatically targeted to vessel wall injury sites. Initial studies with iloprost-loaded pig platelets and pig aorta tunica media in perfusion circuits are presented. After autologous reconstitution into blood, no significant difference was observed in the deposition of 111Indium labelled sham-loaded and untreated platelets onto the tunica media during perfusion under low and high shear conditions. In paired experiments (n = 10 pairs), the deposition of iloprost-loaded platelets was significantly lower (mean 61%) after 5 min perfusion than the deposition from blood containing sham-loaded (control) platelets. A similar significant reduction (mean 54%) was seen after 10 min perfusion. Pre-perfusion of iloprost-loaded platelets for 10 min under low shear conditions (212/s), followed by 5 min perfusion of 111Indium labelled normal platelets, significantly reduced the secondary platelet deposition (p < 0.01) when compared with the deposition seen when control untreated platelets were preperfused. Significant differences (p < 0.001) in secondary deposition were also observed when primary and secondary platelet perfusions were made under high shear (1690/s). Histology of the tunica media segments post perfusion, supported the inhibitory effect of predeposited iloprost-loaded platelets on secondary platelet recruitment. By exploiting their natural haemostatic propensity, drug-loaded platelets can be targeted to vessel wall injury sites. Appropriate drugs could be packaged that may passivate the carrier platelets at the lesion inhibiting thrombus formation or they may act as a depot for sustained drug release.(
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Thrombosis And Haemostasis. - 72 : 4 (1994), p. 604-610. -
További szerzők:El-Gamal, Basiouny Badimon, Juan José Badimon, Lina Crawford, Neville
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12.

001-es BibID:BIBFORM034617
035-os BibID:PMID:8477909
Első szerző:Tornai István (belgyógyász, gasztroenterológus)
Cím:Endothelium releases more von Willebrand factor and tissue-type plasminogen activator upon venous occlusion in patients with liver cirrhosis than in normals / I. Tornai, J. Hársfalvi, Z. Boda, M. Udvardy, G. Pfliegler, K. Rak
Dátum:1993
Megjegyzések:Venous occlusion was used in 8 patients with liver cirrhosis and in 10 normals to investigate the pathomechanism of long-term elevation of plasma von Willebrand factor antigen (vWFAg) in liver cirrhosis. The following parameters were determined at baseline, and immediately, 60 min and 24 h after 10 min venous occlusion: vWFAg, ristocetin cofactor (RiCoF), in vitro platelet retention (Adeplat T), and tissue-type plasminogen activator (t-PA). Every baseline value in the liver cirrhosis group was significantly higher than in the controls. In both groups the 10-min values were significantly higher than their corresponding baseline results. Hence, comparing the two groups, in liver cirrhosis a significantly higher release of vWFAg and t-PA could be observed. These findings suggest on the one hand that the increased release contributes substantially to the sustained elevation of plasma vWF level in liver cirrhosis. On the other hand, the results indicate that not only the vascular surface of the diseased liver but most probably the total endothelium plays an important role in this phenomenon.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Haemostasis. - 23 : 1 (1993), p. 58-64. -
További szerzők:Hársfalvi Jolán (1949-) (klinikai biokémikus) Boda Zoltán (1947-) (belgyógyász, haematologus, klinikai onkológus) Udvardy Miklós (1947-) (belgyógyász, haematológus) Pfliegler György (1949-) (belgyógyász, hematológus, labor szakorvos) Rák Kálmán (1929-2005) (belgyógyász, klinikai hematológus, véralvadás kutató)
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