Mechanism of the tumor necrosis factor alpha-mediated induction of endothelial tissue factor.

This study examines the regulation of the human tissue factor (TF) promotor in vitro and in vivo. Transient transfections were performed in bovine aortic endothelial cells to investigate the role of two fundamentally different AP-1 sites and a closely located NF-kappa B site in the human TF promoter. The NF-kappa B site is functionally active, since overexpression of NF-kappa B(p65) resulted in induction of TF mRNA and activity.

Tissue factor expression in an animal model of hydronephrosis.

Background: Hydronephrosis is associated with interstitial fibrosis and occlusion of renal capillaries by fibrin. However, the mechanisms leading to fibrin formation is unknown.

Methods And Results: Twenty days after unilateral ligation of the ureter, interstitial fibrosis occurred in the ligated kidney.

Expression of receptors for advanced glycation end products in peripheral occlusive vascular disease.

The cellular interactions of advanced glycation end products (AGEs), which have been hypothesized to contribute to the development of vascular lesions, occur, at least in part, through their binding to a novel integral membrane protein, the receptor for AGEs (RAGE). Studies of human vascular segments show that endothelial RAGE expression at the antigen and mRNA level was variable and usually at low levels in samples from healthy individuals. In contrast, patients with a range of peripheral occlusive vascular diseases, with or without underlying diabetes, demonstrated prominent enhancement of endothelial RAGE expression.

Antiparasitic treatment of patients with P. falciparum malaria reduces the ability of patient serum to induce tissue factor by decreasing NF-kappa B activation.

Serum from patients with P. falciparum malaria at day 1 (pretherapy) induces tissue factor (TF) in cultured endothelial cells. TF induction depends on de novo transcription as shown in Nuclear Run On assays.

Elevated thrombomodulin plasma levels as a result of endothelial involvement in plasmodium falciparum malaria.

We used thrombomodulin (TM) to assess the participation of the vascular endothelium in human Plasmodium falciparum (P.F.) malaria.

[Separation of urologic tumors cells from Cell Saver blood using a membrane filter. A new method in autotransfusion?].

Tumor cells of three urological longterm cell lines have been labelled with 35[S]-Methionin and added to red cell concentrates. Red cell concentrates rich in tumor cells were passed through a cell saver and two special membranfilters under standard conditions. The 35[S]-Methionin labelled tumor cells were detected by liquid scintillation counting.

Activation of the host response in human Plasmodium falciparum malaria: relation of parasitemia to tumor necrosis factor/cachectin, thrombin-antithrombin III, and protein C levels.

Purpose: Hemostatic alterations and elevated tumor necrosis factor/cachectin (TNF alpha) serum levels may contribute to the pathogenesis of organ complications in human Plasmodium falciparum malaria. Therefore, we examined whether altered protein C (PC) and thrombin-antithrombin III (TAT) plasma levels correlated with TNF alpha serum concentrations, parasitemia, and the clinical course of human P. falciparum malaria.