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1.

001-es BibID:BIBFORM016214
Első szerző:Bereczky Zsuzsanna (orvosi laboratóriumi diagnosztika szakorvos)
Cím:Protein C and protein S deficiencies : similarities and differences between two brothers playing in the same game / Bereczky Zsuzsanna, Kovács Kitti B., Muszbek László
Dátum:2010
ISSN:1434-6621
Megjegyzések:Protein C (PC) and protein S (PS) are vitamin K-dependent glycoproteins that play an important role in the regulation of blood coagulation as natural anticoagulants. PC is activated by thrombin and the resulting activated PC (APC) inactivates membrane-bound activated factor VIII and factor V. The free form of PS is an important cofactor of APC. Deficiencies in these proteins lead to an increased risk of venous thromboembolism; a few reports have also associated these deficiencies with arterial diseases. The degree of risk and the prevalence of PC and PS deficiency among patients with thrombosis and in those in the general population have been examined by several population studies with conflicting results, primarily due to methodological variability. The molecular genetic background of PC and PS deficiencies is heterogeneous. Most of the mutations cause type I deficiency (quantitative disorder). Type II deficiency (dysfunctional molecule) is diagnosed in approximately 5%-15% of cases. The diagnosis of PC and PS deficiencies is challenging; functional tests are influenced by several pre-analytical and analytical factors, and the diagnosis using molecular genetics also has special difficulties. Large gene segment deletions often remain undetected by DNA sequencing methods. The presence of the PS pseudogene makes genetic diagnosis even more complicated.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Clinical Chemistry And Laboratory Medicine. - 48 : Suppl.1 (2010), p. S53-S66. -
További szerzők:Kovács Kitti Bernadett (1985-) (neurológus) Muszbek László (1942-) (haematológus, kutató orvos)
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM072384
Első szerző:Csongrádi Alexandra (molekuláris biológus)
Cím:Optimized angiotensin-converting enzyme activity assay for the accurate diagnosis of sarcoidosis / Alexandra Csongrádi, Attila Enyedi, István Takács, Tamás Végh , Ivetta S. Mányiné, Zsófia Pólik, István Tibor Altorjay, József Balla, György Balla, István Édes, János Kappelmayer, Attila Tóth, Zoltán Papp, Miklós Fagyas
Dátum:2018
Megjegyzések:Background:Serum angiotensin-converting enzyme (ACE) activity determination can aid the early diagnosis of sarcoidosis. We aimed to optimize a fluorescent kinetic assay for ACE activity by screening the confounding effects of endogenous ACE inhibitors and interfering factors. Genotype-dependent and genotype-independent reference values of ACE activity were established, and their diagnostic accuracies were validated in a clinical study.Methods:Internally quenched fluorescent substrate, Abz-FRK(Dnp)P-OH was used for ACE-activity measurements. A total of 201 healthy individuals and 59 presumably sarcoidotic patients were enrolled into this study. ACE activity and insertion/deletion (I/D) genotype of the ACE gene were determined.Results:Here we report that serum samples should be diluted at least 35-fold to eliminate the endogenous inhibitor effect of albumin. No significant interferences were detected: up to a triglyceride concentration of 16 mM, a hemoglobin concentration of 0.71 g/L and a bilirubin concentration of 150 ?M. Genotype-dependent reference intervals were considered as 3.76?11.25 U/L, 5.22?11.59 U/L, 7.19?14.84 U/L for II, ID and DD genotypes, respectively. I/D genotype-independent reference interval was established as 4.85?13.79 U/L. An ACE activity value was considered positive for sarcoidosis when it exceeded the upper limit of the reference interval. The optimized assay with genotype-dependent reference ranges resulted in 42.5% sensitivity, 100% specificity, 100% positive predictive value and 32.4% negative predictive value in the clinical study, whereas the genotype-independent reference range proved to have inferior diagnostic efficiency.Conclusions:An optimized fluorescent kinetic assay of serum ACE activity combined with ACE I/D genotype determination is an alternative to invasive biopsy for confirming the diagnosis of sarcoidosis in a significant percentage of patients.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
ACE
angiotensin-converting enzyme
genotype
reference interval
sarcoidosis
Megjelenés:Clinical chemistry and laboratory medicine. - 56 : 7 (2018), p. 1117-1125. -
További szerzők:Enyedi Attila (1975-) (sebész) Takács István (1963-) (sebész) Végh Tamás (1975-) (aneszteziológus, intenzív terápiás szakorvos) Mányiné Siket Ivetta (1962-) (laborasszisztens) Pólik Zsófia Altorjay István (1991-) (orvos, kardiológus) Balla József (1959-) (belgyógyász, nephrológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Édes István (1952-) (kardiológus) Kappelmayer János (1960-) (laboratóriumi szakorvos) Tóth Attila (1971-) (biológus) Papp Zoltán (1965-) (kardiológus, élettanász) Fagyas Miklós (1984-) (orvos)
Pályázati támogatás:PD 116212
NKFIH
K 116940
OTKA
ÚNKP-17-4-I-DE-40
ÚNKP
GINOP-2.3.2-15-2016-00043
GINOP
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3.

001-es BibID:BIBFORM099048
Első szerző:Dzsudzsák Erika
Cím:Profiling of lactate dehydrogenase isoenzymes in COVID-19 disease / Erika Dzsudzsák, Renáta Sütő, Marianna Pócsi, Miklós Fagyas, Zoltán Szentkereszty, Béla Nagy Jr.
Dátum:2021
Megjegyzések:Introduction Serum total lactate dehydrogenase (LDH) activity was elevated and showed a positive correlation with disease severity and outcome in severe COVID-19 disease. However, it is still unknown whether the relative abundance or calculated activity of any LDH isoenzyme is predominately increased in COVID-19 subjects. Methods Twenty-two consecutive patients suffered from moderate or severe COVID-19 pneumonia were recruited into this study who showed enhanced total LDH activity. The ratio of LDH isoenzyme activities was further investigated using gel electrophoresis (Hydragel, Sebia) with densitometric evaluation. Calculated act ivity values of these isoenzymes were correlated with routine laboratory parameters, the degree of lungparenchymal affection based on chest CT and clinical outcome. Results Total LDH activity was raised in the range of 272-2141 U/L and significantly correlated with calculated LDH-3 and LDH-4 activities (r=0.765, P=0.0001; and r=0.783, P=0.0001, respectively). In contrast, the relative abundance of neither LDH isoenzyme was exclusively abnormal in COVID-19 patients. Calculated activity of LDH-3 and LDH-4 demonstrated a modest but statistically significant association with serum ferritin (r=0.437, P=0.042; r=0.505, P=0.016, respectively). When the relationship between the severity of pulmonary affection by SARS-CoV-2 infection and relative abundance of LDH isoenzymes was studied, a larger ratio of mid-zone fractions was observed in the presence of ? 50% lung parenchymal involvement. Finally, regardless of LDH isoenzyme pattern, abnormal relat ive ratio of LDH-4 and higher calculated LDH-3 and LDH-4 activity values were detected in subjects with unfavorable outcome. Conclusion No characteristic profile of LDH isoenzymes can be detected in COVID-19 pneumonia, however, elevated activities of LDH-3 and LDH-4 are associated with worse clinical outcomes.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
SARS-Cov-2
COVID-19
inflammation
LDH
electrophoresis
clinical outcome
Megjelenés:The Journal of the International Federation of Clinical Chemistry and Laboratory Medicine. - 32 : 4 (2021), p. 432-441. -
További szerzők:Sütő Renáta (1986-) (aneszteziológus) Pócsi Marianna (1989-) (klinikai laboratóriumi kutató) Fagyas Miklós (1984-) (orvos) Szentkereszty Zoltán Nagy Béla Jr. (1980-) (labordiagnosztikai szakorvos)
Pályázati támogatás:FK 135327
OTKA
FK 128809
OTKA
ÚNKP21-3-I-DE-255
Egyéb
ÚNKP-21-5-DE-458
Egyéb
BO/00069/21/5
MTA
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4.

001-es BibID:BIBFORM068933
Első szerző:Hudák Renáta
Cím:Laboratory characterization of leukemic cell procoagulants / Renáta Hudák, Ildikó Beke Debreceni, Ivett Deák, Gabriella Gál Szabó, Zsuzsanna Hevessy, Péter Antal-Szalmás, Bjarne Osterud, János Kappelmayer
Dátum:2017
ISSN:1434-6621
Megjegyzések:Background: In acute myeloid leukemias, there is anincreased chance to develop thrombotic disorders. Wehypothesized that in addition to leukemic promyelocytes,monocytic leukemia cells may also have a higher procoagulantactivity.Methods: Fibrin formation was assessed by a one-stageclotting assay using a magnetic coagulometer. The thrombingeneration test (TGT) of magnetically isolated normalhuman monocytes, intact leukemic cells and their isolatedmicroparticles was performed by a fluorimetric assay.Phosphatidylserine (PS) expression of leukemic cells andmicroparticle number determinations were carried out byflow cytometry.Results: All cell lines displayed a significant procoagulantpotential compared to isolated normal human monocytes.In the TGT test, the mean of lagtime and the time to peakparameters were significantly shorter in leukemic cells(3.9?4.7 and 9.9?10.3 min) compared to monocytes (14.9and 26.5 min). The mean of peak thrombin in variousmonocytic leukemia cell lines was 112.1?132.9 nM vs.75.1 nM in monocytes; however, no significant differencewas observed in the ETP parameter. Factor VII-deficientplasma abolished all procoagulant activity, whereas factorXII-deficient plasma did not affect the speed of fibrinformation and thrombin generation but modulated theamount of thrombin. Factor XI-deficient plasma affectedthe time to peak values in one leukemic cell line and alsoattenuated peak thrombin. Leukemia cell-derived microparticlesfrom all three cell lines exerted a procoagulanteffect by significantly shortening the lagtime in TGT; therewas a nonsignificant difference in case of ETP parameter.Conclusions: All investigated monocytic leukemia celllines exhibited significant thrombin generation. This phenomenonwas achieved by the procoagulants on the surfaceof leukemic cells as well as by their microparticles.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
monocytic leukemia
tissue factor
Megjelenés:Clinical Chemistry and Laboratory Medicine 55 : 8 (2017), p. 1215-1223. -
További szerzők:Bekéné Debreceni Ildikó (1970-) (biológus) Deák Ivett Gál Szabó Gabriella Hevessy Zsuzsanna (1966-) (laboratóriumi szakorvos) Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Osterud, Bjarne Kappelmayer János (1960-) (laboratóriumi szakorvos)
Pályázati támogatás:TÁMOP-4.2.4.A/2-11-1-2012-0001
TÁMOP
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5.

001-es BibID:BIBFORM047531
Első szerző:Kárai Bettina (orvos)
Cím:Flow cytometry in the diagnosis of myelodysplastic syndromes / Bettina Kárai, Eszter Szánthó, János Kappelmayer, Zsuzsa Hevessy
Dátum:2012
Megjegyzések:Myelodysplastic syndromes are clonal hematopoietic stem cell disorders. Their exact etiology is unknown. Myelodysplasticsyndromes cause progressive bone marrow failure resulting in pancytopenia and refractory, transfusion-dependent anemia.One can observe typical morphological alterations in the erythroid, myeloid and/or megakaryocytic cell lineage. Blast countsmay also be increased. The pathologic cells are genetically unstable, and a myelodysplastic syndrome might transform into acutemyeloid leukemia. The overall survival of these diseases range between few months to around ten years. Correct diagnosis andaccurate prognostic classification is essential. In the past decades several scoring systems were established beginning with theFrench-American-British classification to the most recent Revised International Prognostic Scoring System. In all of theseclassifications bone marrow morphology is still the most important factor, though nowadays the genetic aberrations and flowcytometry findings are also included. The diagnosis and prognostic classification of myelodysplastic syndromes remain a greatchallenge for hematologists.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The Electronic Journal Of The International Federation Of Clinical Chemistry And Laboratory Medicine. - 23 : 4 (2012), p. 109-116. -
További szerzők:Szánthó Eszter (laboratóriumi szakorvos jelölt) Kappelmayer János (1960-) (laboratóriumi szakorvos) Hevessy Zsuzsanna (1966-) (laboratóriumi szakorvos)
Pályázati támogatás:TAMOP-4.2.2.B-11/1/KONV
TÁMOP
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6.

001-es BibID:BIBFORM039753
Első szerző:Katona Éva (klinikai biokémikus)
Cím:Measurement of factor XIII activity in plasma / Katona Éva, Pénzes Krisztina, Molnár Éva, Muszbek László
Dátum:2012
ISSN:1434-6621
Megjegyzések:Abstract Coagulation factor XIII (FXIII) is converted by thrombin and Ca2+ into an active transglutaminase (FXIIIa) in the final phase of coagulation cascade. Its main function is the mechanical stabilization of fibrin clot and its protection from fibrinolysis by cross-linking of fibrin chains and α2-plasmin inhibitor to fibrin. In non-substituted patients FXIII deficiency is a severe hemorrhagic diathesis, not infrequently with fatal consequences. The main reason for using FXIII assays is the diagnosis of FXIII deficiency. The aim of this review is to provide a comprehensive critical evaluation of the methods reported for the determination of FXIII activity in the plasma. Such methods are based on two principles: 1) measurement of labeled amines incorporated by FXIIIa into a glutamine residue of a substrate protein, 2) monitoring ammonia released from a peptide bound glutamine residue by FXIIIa using NAD(P)H dependent glutamate dehydrogenase indicator reaction. The incorporation assays are sensitive, but cumbersome and time-consuming, they are difficult to standardize and cannot be automated. The ammonia release assays are less sensitive, but quick, well standardized, and can be automated; this type of assay is recommended for the screening of FXIII deficiency. The traditional clot solubility assay should not be used for this purpose.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekuláris Medicina
Megjelenés:Clinical Chemistry and Laboratory Medicine. - 50 : 7 (2012), p. 1191-1202. -
További szerzők:Pénzes-Daku Krisztina (1978-) (biológus) Molnár Éva (1977-) (analitikus) Muszbek László (1942-) (haematológus, kutató orvos)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
A véralvadás XIII-as faktorának (FXIII) struktúrája, funkciója, előfordulása egyéb testnedvekben és kapcsolata trombotikus megbetegedésekkel
OTKA-NKTH CNK 80776
OTKA
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
ETT
Egyéb
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7.

001-es BibID:BIBFORM056708
Első szerző:Kovács Bettina (orvos)
Cím:Progressive chromogenic anti-factor Xa assay and its use in the classification of antithrombin deficiencies / Bettina Kovács, Zsuzsanna Bereczky, Anna Selmeczi, Réka Gindele, Zsolt Oláh, Adrienne Kerényi, Zoltán Boda, László Muszbek
Dátum:2014
ISSN:1434-6621
Megjegyzések:Background: Antithrombin (AT) is a slow-acting progressiveinhibitor of activated clotting factors, particularlythrombin and activated factor X (FXa). However, the presenceof heparin or heparan sulfate accelerates its effectby several magnitudes. AT deficiency, a severe thrombophilia,is classified as type I (quantitative) and type II(qualitative) deficiency. In the latter case mutations mayinfluence the reactive site, the heparin binding-site (HBS)and exert pleiotropic effect. Heterozygous type II-HBSdeficiency is a less severe thrombophilia than other heterozygoussubtypes. However, as opposed to other subtypes,it also exists in homozygous form which representsa very high risk of venous thromboembolism.Methods: A modified anti-FXa chromogenic AT assay wasdeveloped which determines both the progressive (p) andthe heparin cofactor (hc) activities, in parallel. The methodwas evaluated and reference intervals were established.The usefulness of the assay in detecting type II-HBS ATdeficiency was tested on 78 AT deficient patients including51 type II-HBS heterozygotes and 18 homozygotes.Results: Both p-anti-FXa and hc-anti-FXa assays showedexcellent reproducibility and were not influenced by highconcentrations of triglyceride, bilirubin and hemoglobin.Reference intervals for p-anti-FXa and hc-anti-FXa ATactivities were 84%-117% and 81%-117%, respectively.Type II-HBS deficient patients demonstrated low (heterozygotes)or very low (homozygotes) hc-anti-FXa activitywith normal or slightly decreased p-anti-FXa activity. Thep/hc ratio clearly distinguished wild type controls, typeII-HBS heterozygotes and homozygotes.Conclusions: Concomitant determination of p-anti-FXaand hc-anti-FXa activities provides a reliable, clinicallyimportant diagnosis of type II-HBS AT deficiency and distinguishesbetween homozygotes and heterozygotes.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
anti-factor Xa assay
antithrombin
antithrombin deficiency
heparin binding-site
thrombophilia
Megjelenés:Clinical Chemistry and Laboratory Medicine. - 52 : 12 (2014), p. 1797-1806. -
További szerzők:Bereczky Zsuzsanna (1974-) (orvosi laboratóriumi diagnosztika szakorvos) Selmeczi Anna (1982-) (orvos) Gindele Réka (1987-) (molekuláris biológus) Oláh Zsolt (1974-) (belgyógyász) Kerényi Adrienne (1970-) (laboratóriumi szakorvos) Boda Zoltán (1947-) (belgyógyász, haematologus, klinikai onkológus) Muszbek László (1942-) (haematológus, kutató orvos)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Trombózis Kutató Központ Kutatócsoport
PD-101120
OTKA
K-109543
OTKA
MTA-DE
MTA
Vascularis Biológia, Thrombosis-Haemostasis Kutatócsoport
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8.

001-es BibID:BIBFORM016217
Első szerző:Muszbek László (haematológus, kutató orvos)
Cím:Antithrombin deficiency and its laboratory diagnosis / Muszbek László, Bereczky Zsuzsanna, Kovács Bettina, Komáromi István
Dátum:2010
ISSN:1434-6621
Megjegyzések:Antithrombin (AT) belongs to the serpin family and is a key regulator of the coagulation system. AT inhibits active clotting factors, particularly thrombin and factor Xa; its absence is incompatible with life. This review gives an overview of the protein and gene structure of AT, and attempts to explain how glucosaminoglycans, such as heparin and heparan sulfate accelerate the inhibitory reaction that is accompanied by drastic conformational change. Hypotheses on the regulation of blood coagulation by AT in physiological conditions are discussed. Epidemiology of inherited thrombophilia caused by AT deficiency and its molecular genetic background with genotype-phenotype correlations are summarized. The importance of the classification of AT deficiencies and the phenotypic differences of various subtypes are emphasized. The causes of acquired AT deficiency are also included in the review. Particular attention is devoted to the laboratory diagnosis of AT deficiency. The assay principles of functional first line laboratory tests and tests required for classification are discussed critically, and test results expected in various AT deficiency subtypes are summarized. The reader is provided with a clinically oriented algorithm for the correct diagnosis and classification of AT deficiency, which could be useful in the practice of routine diagnosis of thrombophilia.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Clinical Chemistry And Laboratory Medicine. - 48 : Suppl.1 (2010), p. S67-S78. -
További szerzők:Bereczky Zsuzsanna (1974-) (orvosi laboratóriumi diagnosztika szakorvos) Kovács Bettina (1975-) (orvos) Komáromi István (1957-) (vegyész, molekuláris biológus, biokémikus)
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DOI
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9.

001-es BibID:BIBFORM012807
Első szerző:Shemirani, Amir-Houshang (kutató orvos, laboratórium szakorvos)
Cím:Rapid detection of the factor XIII Val34Leu (163 G-->T) polymorphism by real-time PCR using fluorescence resonance energy transfer detection and melting curve analysis / Shemirani A. H., Muszbek L.
Dátum:2004
ISSN:1434-6621
Megjegyzések:The Val34Leu polymorphism in the A subunit of blood coagulation factor XIII (FXIII-A) is located in the acti- vation peptide, just three amino acids upstream of the thrombin cleavage site. The Val?Leu replacement accelerates the rate of the proteolytic activation of FXIII and it seems to provide protection against myo- cardial infarction. Methods available for the assess- ment of the FXIII-A Val34Leu polymorphismare rather time-consuming, laborious and not easily applicable for large-scale studies. In this study a new method based on real-time PCR with fluorescence resonance energy transfer (FRET) detection and melting curve analysis was developed. The rapid, simple method was adapted to the widely used real-time PCR instru- ment, LightCycler (Roche Diagnostics). The results showed 100% coincidence with those obtained by the traditional PCR-restriction fragment length polymor- phism (RFLP) assay and fluorescent DNA sequencing. Using this method, an allele frequency of 24.2% was obtained (ns113), which well agrees with the allele frequency obtained by PCR-RFLP on a different group of the same ethnic Hungarian population (25.9%).
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
factor XIII
fluorescence resonance energy transfer
gene polymorphism
real-time PCR
Megjelenés:Clinical Chemistry And Laboratory Medicine. - 42 : 8 (2004), p. 877-879. -
További szerzők:Muszbek László (1942-) (haematológus, kutató orvos)
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10.

001-es BibID:BIBFORM118032
035-os BibID:(scopus)85182577070 (wos)001141169800001
Első szerző:Szabó Attila Ádám (orvos)
Cím:Get reliable laboratory findings : how to recognize the deceptive effects of angiotensin-converting enzyme inhibitor therapy in the laboratory diagnostics of sarcoidosis? / Szabó Attila Ádám, Enyedi Enikő Edit, Altorjay István Tibor, Hajnal Péter, Pintér Tamás Bence, Mányiné Ivetta Siket, Váradi Csongor, Bányai Emese, Tóth Attila, Papp Zoltán, Fagyas Miklós
Dátum:2024
ISSN:1434-6621
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Clinical Chemistry And Laboratory Medicine. - [Epub ahead of print] (2024). -
További szerzők:Enyedi Enikő Edit (1995-) (orvosi laboratóriumi analitikus) Altorjay István (1991-) (orvos, kardiológus) Hajnal Péter (1994-) (orvos) Pintér Tamás Bence (1998-) (molekuláris biológus) Mányiné Siket Ivetta (1962-) (laborasszisztens) Váradi Csongor (1984-) (sebész, mellkassebész szakorvos) Bányai Emese (1984-) (orvos) Tóth Attila (1971-) (biológus) Papp Zoltán (1965-) (kardiológus, élettanász) Fagyas Miklós (1984-) (orvos)
Pályázati támogatás:Richter Gedeon Talentum Alapítvány
Egyéb
ÚNKP-23-3-II-DE-253
Egyéb
ÚNKP-23-3-II-DE-289
Egyéb
ÚNKP-23-5-DE-482
Egyéb
BO/00069/21/5
MTA
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11.

001-es BibID:BIBFORM083115
Első szerző:Szánthó Eszter (laboratóriumi szakorvos jelölt)
Cím:Evaluation of sample quality as preanalytical error in flow cytometry analysis in childhood acute lymphoblastic leukemia / Szánthó Eszter, Kárai Bettina, Ivády Gergely, Baráth Sándor, Száraz-Széles Marianna, Kappelmayer János, Hevessy Zsuzsanna
Dátum:2019
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of the International Federation of Clinical Chemistry and Laboratory Medicine. - 30 : 4 (2019), p. 385-395. -
További szerzők:Kárai Bettina (1984-) (orvos) Ivády Gergely (1979-) (laboratóriumi szakorvos) Baráth Sándor (1977-) (biológus) Széles Mariann Kappelmayer János (1960-) (absztraktok) Hevessy Zsuzsanna (1966-) (laboratóriumi szakorvos)
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12.

001-es BibID:BIBFORM083114
Első szerző:Szilágyi Bernadett
Cím:Role of sepsis modulated circulating microRNAs / Szilágyi Bernadett, Fejes Zsolt, Pócsi Marianna, Kappelmayer János, Nagy Béla Jr.
Dátum:2019
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Journal of the International Federation of Clinical Chemistry and Laboratory Medicine. - 30 : 2 (2019), p. 128-145. -
További szerzők:Fejes Zsolt (1988-) (molekuláris biológus) Pócsi Marianna (1989-) (klinikai laboratóriumi kutató) Kappelmayer János (1960-) (laboratóriumi szakorvos) Nagy Béla Jr. (1980-) (labordiagnosztikai szakorvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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