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001-es BibID:	BIBFORM029089
Első szerző:	Ádány Róza (megelőző orvostan és népegészségtan szakorvos)
Cím:	Factor XIII of blood coagulation as a nuclear crosslinking enzyme / Ádány R., Bárdos H., Antal M., Módis L., Sárváry A., Szűcs S., Balogh I.
Dátum:	2001
Megjegyzések:	Intracellular localization and distribution of Factor XIII subunit A (FXIIIA) was investigated in association with monocyte-macrophage differentiation in a long term culture of human monocytes by light- and electron microscopical as well as biochemical and immunobiochemical techniques. To allow the detection of FXIIIA in cells with well-preserved ultrustructure, immunosera against glutaraldehyde-derivatized recombinant FXIIIA were developed in rabbits, then characterized and used in this study. In the early phase of macrophage differentiation intranuclear accumulation of FXIIIA was detected as a transient phenomenon in cells of the 2nd day culture by optical sectioning with 0,7 microm steps in laser scanning confocal microscopy and immunoblotting technique. FXIIIA could be detected by immunoelectron microscopic postembedding staining over electrodense DNA-containing areas. Fluoresceinated monodansylcadaverine incorporation assay was used to demonstrate that FXIIIA is not only present in the nuclei, but also expresses its transglutaminase activity. Our finding of the nuclear accumulation of FXIIIA in differentiating human macrophages is also unique in that a blood clotting factor has, for the first time, been localized in nuclei and has been shown to be an intracellular crosslinking enzyme. The possible role of nuclear FXIIIA in association with cellular processes involving chromatin structure remodeling, such as cell death, cell differentiation or cellular proliferation requires further in-depth investigation.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Thrombosis and Haemostasis. - 85 : 5 (2001), p. 845-851. -
További szerzők:	Bárdos Helga (1969-) (megelőző orvostan és népegészségtan szakorvos) Antal Miklós (1951-) (orvos, anatómus) Módis László (1939-) (anatómus, kötőszövetbiológus) Sárváry Attila (1971-) (népegészségtan szakorvos) Szűcs Sándor (1958-) (biokémikus, vegyész) Balogh Imre
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM006761
Első szerző:	Inbal, Amir
Cím:	Impaired wound healing in factor XIII deficient mice / Inbal, A., Lubetsky, A., Krapp, T., Castel, D., Shaish, A., Dickneitte, G., Modis, L., Muszbek, L., Inbal, A.
Dátum:	2005
ISSN:	0340-6245
Megjegyzések:	Factor XIII that stabilizes fibrin clots in the final stages of blood coagulation also participates in wound healing, as can be inferred from a delay in wound repair in some patients with inherited FXIII deficiency. In this study we evaluated the effect of FXIII on wound healing in FXIII-deficient mice. Three groups of mice (n = 10) were employed: control group, FXIII-deficient group and FXIII-deficient group treated with FXIII concentrate. Excisional wounds were left unsutured and undressed, and mice were followed for eleven days. FXIII-deficient mice exhibited impaired wound healing as has been demonstrated by 15%, 27% and 27% decrease in percentage of wound closure on day 4, 8 and 11, respectively. On day 11 complete healing was observed in control (100% closure), 73.23% in FXIII-deficient and 90.06% in FXIII deficient/FXIII-treated groups (p = 0.007 by ANOVA and p = 0.001 by t-test between control and FXIII-deficient groups). Scoring system representing maturation rate of the wounds showed that the scores for the control, FXIII-deficient and FXIII deficient/FXIII treated groups were 94.9 +/- 4.7, 61.5 +/- 14.5 and 94.5 +/- 6.4, respectively (p < 0.001 by ANOVA). Histological analysis of the lesions performed at day 11 disclosed delayed reepithelization and necrotized fissure in FXIII-deficient mice and normal healing in FXIII-deficient/FXIII-treated mice. The findings of this study confirm that in FXIII-deficient mice wound healing is delayed and the cellular and tissue defects can be corrected by treatment with FXIII, providing evidence for the essential role of FXIII in wound repair and remodeling.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Analysis of Variance Animals Exons Factor XIII/genetics/physiology Gene Deletion Inflammation/metabolism Male Mice Mice, Inbred CBA Time Factors Wound Healing
Megjelenés:	Thrombosis and Haemostasis. - 94 : 2 (2005), p. 432-437. -
További szerzők:	Lubetsky, Aharon Krapp, Tanya Castel, David Shaish, Aviv Dickneitte, Gerhardt Módis László (1939-) (anatómus, kötőszövetbiológus) Muszbek László (1942-) (haematológus, kutató orvos) Inbal, Aida
Internet cím:	DOI
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