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1.
001-es BibID:
BIBFORM006762
Első szerző:
Inbal, Aida
Cím:
Platelets but not monocytes contribute to the plasma levels of factor XIII subunit A in patients undergoing autologous peripheral blood stem cell transplantation / Inbal, A., Muszbek, L., Lubetsky, A., Katona, E., Levi, I., Karpati, L., Nagler, A.
Dátum:
2004
ISSN:
0957-5235
Megjegyzések:
Factor XIII subunit A (FXIII A) is synthesized by megakaryocytes, and monocytes/macrophages. In addition, the liver has been reported as an extrahaematopoietic source of FXIII A. At present, the extent of contribution of either haematopoietic or extrahaematopoietic sources to the plasma FXIII A level is unknown. We studied the effect of bone marrow aplasia due to high-dose chemotherapy followed by autologous peripheral blood stem cell transplantation (ASCT) on plasma FXIII A activity and concentration in 20 patients with haematological or solid tumour malignancies. A multiple linear regression model was used to assess the effect of gender, age, malignancy and treatment types, platelet and monocyte counts, abnormal liver function tests, prothrombin time, and number of platelet transfusions on FXIII activity measured in plasma before and following ASCT. Significant correlation between platelet counts and FXIII A activity in plasma was observed (r = 0.51, P = 0.0001), which remained after the adjustment for the aforementioned parameters (multiple R = 0.52, P = 0.0001). In contrast, no significant correlation between FXIII A levels and monocyte counts was observed (r = 0.19), and this lack of correlation persisted after the adjustment. These results suggest that in the ASCT model, following myeloablation, platelets but not monocytes are the haematopoietic cells that contribute significantly to plasma FXIII A levels. In addition, extra-haematopoietic sources of FXIII synthesis may also contribute to FXIII levels in plasma.
Tárgyszavak:
Orvostudományok
Elméleti orvostudományok
idegen nyelvű folyóiratközlemény külföldi lapban
Blood Platelets
Factor XIII
Hematologic Neoplasms
Humans
Leukocyte Count
Monocytes
Peripheral Blood Stem Cell Transplantation
Platelet Count
Regression Analysis
Time Factors
Transplantation, Autologous
Megjelenés:
Blood Coagulation and Fibrinolysis. - 15 : 3 (2004), p. 249-253. -
További szerzők:
Muszbek László (1942-) (haematológus, kutató orvos)
Lubetsky, Aharon
Katona Éva (1961-) (klinikai biokémikus)
Levi, Itai
Kárpáti Levente (1968-) (okleveles vegyész)
Nagler, Arnon
Borító:
Saját polcon:
2.
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
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DOI
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