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001-es BibID:BIBFORM045829
035-os BibID:PMID:1485715
Első szerző:Fülöp Tamás Jr
Cím:Transmembrane signaling changes with aging / T. Fülöp Jr, Gy. Barabás, Z. Varga, J. Csongor, M. Hauck, S. Szücs, I. Seres, A. Mohacsi, D. Kékessy, J. P. Despont, L. Robert, A. Penyige
Dátum:1992
ISSN:0077-8923
Megjegyzések:Altered immune response and transmembrane signaling with aging has previously been demonstrated. The aim of the present study was to characterize PMNLs and lymphocyte G proteins and to determine whether their relative amounts are altered with aging. First we studied the effects of FMLP on PMNLs IP3 formation. It was found that in any group of elderly the PMNLs IP3 formation was significantly decreased compared to that of young subjects. In FMLP receptor binding affinity no measurable difference exists in either low- or high-affinity FMLP receptors. The autoradiogram of 32P-ADP-ribosylated proteins by CT in lymphocytes of young individuals showed a major polypeptide of 40 kDa, and two much less prevalent components of 52 and 45 kDa. In contrast, in lymphocytes of elderly subjects the major polypeptide was 45 kDa, and the two others were very weakly labeled. In PMNLs, CT labeled the 45-kDa band quite strongly, mainly in the elderly, and the 52- and 40-kDa bands were very weakly labeled, mainly in young subjects. When PT was used, no age-related pattern changes could be demonstrated, while differences could be observed between the two types of cells.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
AGE-RELATED DECLINE
PHOSPHATIDYLINOSITOL BREAKDOWN
LYMPHOCYTES-T
G-PROTEIN
Megjelenés:Annals of The New York Academy of Sciences. - 673 (1992), p. 165-171. -
További szerzők:Barabás György (1933-) (sejtbiológus, molekuláris genetikus) Varga Z. Csongor József Hauck Mátyás (biokémikus) Szűcs Sándor (1958-) (biokémikus, vegyész) Seres Ildikó (1954-) (biokémikus) Mohácsi A. (orvos) Kékessy D. Despont, J. P. Robert, Ladislas Penyige András (1954-) (molekuláris genetikus)
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2.

001-es BibID:BIBFORM046864
Első szerző:Fülöp Tamás (népegészségügyi szakember, egészségfejlesztő)
Cím:Age-dependent changes in transmembrane signalling : identification of G proteins in human lymphocytes and polymorphonuclear leukocytes / Fulop Tamás, Barabas György, Varga Zsuzsa, József Csongor, Csabina Sándor, Szucs Sándor, Seres Ildikó, Szikszay Edit, Jeney Zsolt, Penyige András
Dátum:1993
ISSN:0898-6568
Megjegyzések:In human neutrophils (PMNLs) we found that in the elderly IP3 formation was significantly decreased compared to that of young subjects. For FMLP receptor binding affinity and number no measurable differences occurred upon ageing, studying both the low or the high affinity receptors. The amount of ADP-ribosylated G proteins, catalysed by pertussis toxin (PT) or cholera toxin (CT), was significantly increased in PMNLs of the elderly. In lymphocytes, the PT-catalysed ADP ribosylation of G proteins was also increased with ageing, while the CT-catalysed ribosylation was decreased. The autoradiogram of [32P]ADP-ribosylated proteins by CT in lymphocytes of young individuals showed a major polypeptide of 40,000 M(r). In contrast, in lymphocytes of the elderly, the major polypeptide was 45,000 M(r). In PMNLs, CT labelled quite strongly the 45,000 M(r) band, mainly in the elderly. When PT was used, no age-related pattern changes could be demonstrated, while differences could be observed between the two types of cells. The use of antiserum P680 (G alpha common) showed no age-related pattern changes, while the intensity of the labelled proteins varies with age and cell type. The antiserum U46 (Go alpha) could identify in lymphocytes of young subjects two polypeptides 68,000 and 41,000 M(r). The prominent polypeptide in lymphocytes of the elderly was the 70,000 M(r) and no other polypeptides could be recognized. In PMNLs of young subjects the U46 and serum identified a range of species. In PMNLs of the elderly all these bands were weakly labelled. The present data indicate changes in the pattern and the quantity of G proteins in lymphocytes and PMNLs of elderly subjects.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cellular Signalling. - 5 : 5 (1993), p. 593-603. -
További szerzők:Barabás György (1933-) (sejtbiológus, molekuláris genetikus) Varga Zsuzsa (1951-) (biokémikus, nephrológus) József Csongor Csabina Sándor Szűcs Sándor (1958-) (biokémikus, vegyész) Seres Ildikó (1954-) (biokémikus) Szikszay Edit Jeney Zsolt Penyige András (1954-) (molekuláris genetikus)
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3.

001-es BibID:BIBFORM132222
Első szerző:Pikó Péter (biológus)
Cím:Effect of smoking and its exposure on the HDL subfraction profile / Pikó Péter, Al Ashkar Habib, Helu Nihad Kharrat, Kovács Nóra, Pál László, Szücs Sándor, Seres Ildikó, Paragh György, Ádány Róza
Dátum:2025
ISSN:0021-9150
Megjegyzések:Background and Aims: Smoking is a preventable risk factor for cardiovascular disease (CVD) and other non-communicable diseases. Studies have shown that smoking reduces high-density lipoprotein cholesterol (HDL-C) and increases triacylglycerol (TG) levels, thereby increasing the risk of developing atherosclerosis. The aim of the present study was to investigate the effects of smoking and smoking exposure on lipidomic profiles (total cholesterol (TC), HDL-C, TG, LDL, apoA-I, and apoB-100), focusing on HDL subfractions, in 137 nonsmokers and 177 smokers from the Hungarian population. Methods: The HDL was separated using the Lipoprint HDL? system, which identifies ten subfractions (HDL-1? 10) and three subclasses: large (HDL-L), intermediate (HDL-I), and small (HDL-S). Four outcome variables were used to assess smoking exposure: current smoking status, number of cigarettes per day (CPD), duration of smoking (DoS), and heaviness of smoking index (HSI). Multivariate linear regression and receiver operating characteristic (ROC) curve analysis were used, and p-values adjusted by the Benjamini-Hochberg method <0.05 were considered significant. Results: Smoking and its exposures significantly reduced HDL-C and apoA-I levels, while increasing the TG levels and the TG/HDL-C and apoA-I/apoB-100 ratios. Significant reductions in concentrations were observed between smoking and HDL-2 to HDL-8, and between CPD and HDL-3 to HDL-9 and all subclasses. Similarly, significant reductions were observed between DoS and HDL-4 to HDL-7 andHDL-I, and between HSI and HDL-3 to HDL-10 and HDL-I to HDL-S. Despite the quantitative changes, smoking did not significantly modify the distribution of the subfractions and subclasses. Conclusions: Our results confirm that smoking adversely alters the lipid profile and significantly reduces the levels of almost all HDL subfractions , especially HDL 5,-6 and-7 and HDL-I, thereby accelerating the development of atherosclerosis.
Tárgyszavak:Orvostudományok Egészségtudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Atherosclerosis. - 407 : Suppl. (2025), p. 56-57. -
További szerzők:Al Ashkar, Habib (1998-) (népegészségügyi szakember) Helu, Nihad Kharrat (1992-) (PhD hallgató) Kovács Nóra (1989-) (népegészségügyi szakember) Pál László (1987-) (népegészségügyi szakember, egészségfejlesztő) Szűcs Sándor (1958-) (biokémikus, vegyész) Seres Ildikó (1954-) (biokémikus) Paragh György (1953-) (belgyógyász) Ádány Róza (1952-) (megelőző orvostan és népegészségtan szakorvos)
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