Biomedical subjects

L Kircheis

Publications and source records attributed to L Kircheis.

3 recordsLinked to original sources

PubMed2000

Collagen patch coated with fibrin glue components. Treatment of suture hole bleedings in vascular reconstruction.

BACKGROUND: Bleeding from suture holes during vascular reconstruction, particularly when polytetrafluoroethylene (PTFE) prostheses are used, is still a problem which can lead to intraoperative delay and increased blood loss. The aim of this prospective, randomised, open, controlled multicentre study was to evaluate whether the use of a new local haemostyptic would reduce intraoperative blood loss and the time to haemostasis. METHODS: Thirty patients received a new haemostyptic (TachoComb H, Nycomed Pharma AG), whereas another 30 patients were treated with compresses. The vascular reconstructions were either anastomoses or patch angioplasties and were performed using PTFE vascular prostheses. RESULTS: The mean time to haemostasis of suture hole bleeding in the haemostyptic group (326.0 sec) was significantly shorter compared to the control group (514.3 sec) (p=0.006). The median intraoperative blood loss was 24.5 g in the treatment group and 57.3 g in the control group (p=0.045). CONCLUSIONS: It was shown that collagen patches coated with components of fibrin glue significantly reduce the time to haemostasis as well as blood loss at the operation site in patients undergoing vascular reconstruction with PTFE grafts.

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PubMedDate not supplied

Early embryonic cells activate the alternative complement system.

Murine embryonic stem cells, embryonic carcinoma cells and pre-implantation embryos were found to be extremely sensitive to cytolysis by normal human serum as compared to matured cells. The cytolytic activity to embryonic cells was not removed by pre-absorption of serum with spleen lymphocytes. Conditions which block both complement activation pathways or, selectively, the alternative pathway completely abrogated the activity of human serum against embryonic cells whereas the activity was retained under conditions which block the classical complement pathway, indicating that embryonic cells activate the alternative complement system (ACS). The cytotoxic effect to murine embryonic cells was reproduced using syngeneic murine serum. Concerning the mechanism of ACS-activation, the expression of regulators of complement activation and of membrane bound sialic acid was analysed. Embryonic cells express mRNA for Crry similarly to other cells but additionally express Cr2-transcripts not found in most adult cells. Embryonic cells have strikingly low levels of membrane-bound sialic acid compared to adult cells.

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PubMedDate not supplied

Selective lysis of early embryonic cells by the alternative pathway of complement--a possible mechanism for programmed cell death in embryogenesis.

Early embryonic cells and early mouse embryos were shown to activate the alternative pathway of complement, and to be highly sensitive to complement-mediated cytolysis (Kircheis et al, In Vivo 9: 85-98, 1995). Under further development embryonic cells become resistant. The induction of resistance to the alternative pathway of complement correlates with: a) altered splicing of Cr2-transcript and b) changes in the acidic glycolipids under differentiation. Early embryonic cells have low amounts of sialic acid-containing glycolipids or express mainly GM3. The induction of differentiation changes the glycolipid pattern leading to an increase in membrane-bound sialic acid. The importance of membrane-bound sialic acid in the restriction of complement activation is demonstrated by increased sensitivity to complement after pre-treatment of cells with neuraminidase. The results indicate that there is target-specific lysis of early embryonic cells by the alternative pathway of complement. Early embryonic cells activate the alternative pathway of complement by expressing activators and low levels of membrane-bound sialic acid. Induction of differentiation changes the glycolipid pattern, leading to an increase in membrane-bound sialic acid sufficient to restrict complement-activation on the cell surface.

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