CCL

Összesen 5 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM009347
Első szerző:Baskurt, Oguz K.
Cím:Parameterization of red blood cell elongation index : shear stress curves obtained by ektacytometry / Baskurt O. K., Hardeman M. R., Uyuklu M., Ulker P., Cengiz M., Németh N., Shin S., Alexy T., Meiselman H. J.
Dátum:2009
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Scandinavian Journal of Clinical and Laboratory Investigation. - 69 : 7 (2009), p. 777-788. -
További szerzők:Hardeman, Max R. Uyuklu, Mehmet Ulker, Pinar Cengiz, Melike Németh Norbert (1975-) (kutatóorvos) Shin, Sehyun Alexy Tamás Meiselman, Herbert J.
Internet cím:elektronikus változat
DOI
Borító:

2.

001-es BibID:BIBFORM062100
Első szerző:Németh Norbert (kutatóorvos)
Cím:Interpretation of osmotic gradient ektacytometry (osmoscan) data : a comparative study for methodological standards / Norbert Nemeth, Ferenc Kiss, Kornel Miszti-Blasius
Dátum:2015
ISSN:0036-5513
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Scandinavian Journal Of Clinical & Laboratory Investigation. - 75 : 3 (2015), p. 213-222. -
További szerzők:Kiss Ferenc (1982-) (kutatóorvos) Miszti-Blasius Kornél (1977-) (laboratóriumi szakorvos)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

001-es BibID:BIBFORM086144
Első szerző:Posta Niké
Cím:Hemoglobin oxidation generates globin-derived peptides in atherosclerotic lesions and intraventricular hemorrhage of the brain, provoking endothelial dysfunction / Niké Posta, Éva Csősz, Melinda Oros, Dávid Pethő, László Potor, Gergő Kalló, Zoltán Hendrik, Katalin Éva Sikura, Gábor Méhes, Csaba Tóth, József Posta, György Balla, József Balla
Dátum:2020
ISSN:0023-6837
Megjegyzések:The lysis of red blood cells was shown to occur in human ruptured atherosclerotic lesions and intraventricular hemorrhage (IVH) of the brain. Liberated cell-free hemoglobin was found to undergo oxidation in both pathologies. We hypothesize that hemoglobin-derived peptides are generated during hemoglobin oxidation both in complicated atherosclerotic lesions and IVH of the brain, triggering endothelial cell dysfunction. Oxidized hemoglobin and its products were followed with spectrophotometry, LC?MS/MS analysis and detection of the cross-linking of globin chains in complicated atherosclerotic lesions of the human carotid artery and the hemorrhaged cerebrospinal liquid of preterm infants. The vascular pathophysiologic role of oxidized hemoglobin and the resultant peptides was assessed by measuring endothelial integrity, the activation of endothelial cells and the induction of proinflammatory genes. Peptide fragments of hemoglobin (VNVDEVGGEALGRLLVVYPWTQR, LLVVYPWTQR, MFLSFPTTK, VGAHAGEYGAELERMFLSFPTTK, and FLASVSTVLTSKYR) were identified in ruptured atherosclerotic lesions and in IVH of the human brain. Fragments resulting from the oxidation of hemoglobin were accompanied by the accumulation of ferryl hemoglobin. Similar to complicated atherosclerotic lesions of the human carotid artery, a high level of oxidized and cross-linked hemoglobin was observed in the cerebrospinal fluid after IVH. Haptoglobin inhibited hemoglobin fragmentation provoked by peroxide. The resultant peptides failed to bind haptoglobin or albumin. Peptides derived from hemoglobin oxidation and ferryl hemoglobin induced intercellular gap formation, decreased junctional resistance in the endothelium, and enhanced monocyte adhesion to endothelial cells. Enhanced expression of TNF and the activation of NLRP3 and CASP1 followed by the increased generation of IL-1? and nuclear translocation of the NF-?? transcription factor occurred in response to hemoglobin-derived peptides, and ferryl hemoglobin in endothelium was upregulated in both pathologies. We conclude that the oxidation of hemoglobin in complicated atherosclerotic lesions and intraventricular hemorrhage of the brain generates peptide fragments and ferryl hemoglobin with the potential to trigger endothelial cell dysfunction.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Laboratory Investigation. - 100 : 7 (2020), p. 986-1002. -
További szerzők:Csősz Éva (1977-) (biokémikus, molekuláris biológus) Oros Melinda (1975-) (molekuláris biológus) Pethő Dávid Potor László Kalló Gergő (1989-) (molekuláris biológus) Hendrik Zoltán (1986-) (orvos) Sikura Katalin Éva (1985-) (biológus) Méhes Gábor (1966-) (patológus) Tóth Csaba (1968-) (sebész, érsebész) Posta József (1948-) (vegyész, analitikus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:OTKA-K-132828
OTKA
EFOP-3.6.3-VEKOP-16- 2017-00009
EFOP
GINOP-2.3.2-15-2016-00043
GINOP
EFOP-3.6.2-16- 2017-00006
GINOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

001-es BibID:BIBFORM033821
035-os BibID:(WoS)000300876300003 (Scopus)84857734407
Első szerző:Tsakiris, Ioannis (orvos)
Cím:Carboxypeptidase-M is regulated by lipids and CSFs in macrophages and dendritic cells and expressed selectively in tissue granulomas and foam cells / Tsakiris I., Torocsik D., Gyongyosi A., Dozsa A., Szatmari I., Szanto A., Soos G., Nemes Z., Igali L., Marton I., Takats Z., Nagy L., Dezso B.
Dátum:2012
ISSN:0023-6837
Megjegyzések:Granulomatous inflammations, characterized by the presence of activated macrophages (MAs) forming epithelioid cell (EPC) clusters, are usually easy to recognize. However, in ambiguous cases the use of a MA marker that expresses selectively in EPCs may be needed. Here, we report that carboxypeptidase-M (CPM), a MA-differentiation marker, is preferentially induced in EPCs of all granuloma types studied, but not in resting MAs. As CPM is not expressed constitutively in MAs, this allows utilization of CPM-immunohistochemistry in diagnostics of minute granuloma detection when dense non-granulomatous MAs are also present. Despite this rule, hardly any detectable CPM was found in advanced/active tubercle caseous disease, albeit in early tuberculosis granuloma, MAs still expressed CPM. Indeed, in vitro both the CPM-protein and -mRNA became downregulated when MAs were infected with live mycobacteria. In vitro, MA-CPM transcript is neither induced remarkably by interferon-γ, known to cause classical MA activation, nor by IL-4, an alternative MA activator. Instead, CPM is selectively expressed in lipid-laden MAs, including the foam cells of atherosclerotic plaques, xanthomatous lesions and lipid pneumonias. By using serum, rich in lipids, and low-density lipoprotein (LDL) or VLDL, CPM upregulation could be reproduced in vitro in monocyte-derived MAs both at transcriptional and protein levels, and the increase is repressed under lipid-depleted conditions. The microarray analyses support the notion that CPM induction correlates with a robust progressive increase in CPM gene expression during monocyte to MA maturation and dendritic cell (DC) differentiation mediated by granulocyte-MA-colony-stimulating factor+IL-4. M-CSF alone also induced CPM. These results collectively indicate that CPM upregulation in MAs is preferentially associated with increased lipid uptake, and exposure to CSF, features of EPCs, also. Therefore, CPM-immunohistochemistry is useful for granuloma and foam MA detections in tissue sections. Furthermore, the present data offer CPM for the first time to be a novel marker and cellular player in lipid uptake and/or metabolism of MAs by promoting foam cell formation.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
open access article
Megjelenés:Laboratory Investigation. - 92 : 3 (2012), p. 345-361. -
További szerzők:Töröcsik Dániel (1979-) (bőrgyógyász) Gyöngyösi Adrienn (1982-) (biológus) Dózsa Anikó (1978-) (Ph.D hallgató, orvos) Szatmári István (1971-) (biológus) Szántó Attila (1976-) (orvos, biokémikus) Soós Györgyike (1959-) (pathológus) Nemes Zoltán (1942-) (patológus) Igali László Márton Ildikó (1954-) (fogszakorvos) Takáts Zoltán Nagy László (1966-) (molekuláris sejtbiológus, biokémikus) Dezső Balázs (1951-) (pathológus)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

5.

001-es BibID:bibEBI12844
Első szerző:Vályi-Nagy István
Cím:Undifferentiated keratinocytes control growth, morphology, and antigen expression of normal melanocytes through cell-cell contact / Vályi-Nagy, I. T. , Hirka, G., Jensen, P. J., Shih, I. M., Juhász, I., Herlyn, M.
Dátum:1993
ISSN:0023-6837 1530-0307
Megjegyzések:BACKGROUND: Melanocytes in the normal human epidermis are generally dendritic and neither proliferate nor express melanoma-associated antigens. In culture, on the other hand, melanocytes are bi- to tripolar, proliferate with 2 to 4 day doubling times, and express melanoma-associated antigens. This observation prompted us to investigate the regulatory role of keratinocytes for growth, morphology, and antigen expression of melanocytes. EXPERIMENTAL DESIGN: Melanocytes and keratinocytes were cultured under three different co-culture conditions: (a) separated by a semiporous membrane, (b) in monolayer cultures allowing direct contact between cells, and (c) in three-dimensional epidermal reconstructs. RESULTS: Melanocytes separated from keratinocytes by semiporous membranes remained di- and tripolar and could not proliferate in medium optimal for keratinocytes. When cell-cell contact was established between melanocytes and undifferentiated, but not differentiated, keratinocytes, melanocytes proliferated at a rate similar to keratinocytes and they developed multiple dendrites. In co-cultures allowing the multi-layered growth of keratinocytes, melanocytes were nonproliferative when juxtaposed to undifferentiated keratinocytes in the basal layer, but proliferated when surrounded by differentiated keratinocytes in the intermediate and upper layers. Expression of melanoma-associated antigens on melanocytes decreased to similar levels as in normal skin when melanocytes were in direct contact with undifferentiated, but not differentiated, keratinocytes. CONCLUSIONS: Undifferentiated, but not differentiated, keratinocytes control growth, morphology, and antigen expression of melanocytes through direct cell-cell contact. These results suggest that the phenotypic characteristics of nevus and melanoma cells in the dermis, i.e., proliferation and expression of tumor-associated antigens, may be due to their loss of contact with undifferentiation keratinocytes.
Tárgyszavak:idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Laboratory Investigation. - 69 : 2 (1993), p. 152-159. -
További szerzők:Hirka G. Jensen, P. J. Shih, Ie-Ming Juhász István (1956-) (bőrgyógyász, bőrsebész, kozmetológus, klinikai onkológus) Herlyn, Meenhard
Borító:
Rekordok letöltése1