ascites/protease

Ascitic fluid and ascites tumor cells from Swiss mice bearing Ehrlich ascites tumor were assayed for components of the kallikrein-kinin system at various times during tumor growth. Changes in component levels were correlated with those in the plasma. Ascitic fluid contained an acetone-activated

1. Previous studies have documented activation of protease enzymes, such as the plasma kallikrein-kinin system, in hepatic cirrhosis. Increased plasma kinin generation could contribute to pathological systemic vasodilatation in cirrhosis, and reduced systemic vascular resistance has been suggested

To improve the ability to predict the occurrence of coagulation disorders in ascites retransfusion and, in addition, to better define the nature of the coagulation disorder, several proteases and antiproteases were analyzed in ascites and plasma before ascites retransfusion in 17 patients.

Urinary trypsin inhibitor (UTI; Mr 40 kDa) is a Kunitz-type protease inhibitor that efficiently inhibits cell-associated trypsin and plasmin activities. The aim of this study is to examine the expression pattern of UTI in the human ovarian carcinoma ascites fluid by Western blotting, zymography,

Ehrlich ascites cells have been shown to possess a protease with beta-naphthylamidase activity located on the surface of these cells. This enzyme is protected from the inhibitory action of protein inhibitors of trypsin (EC 3.4.21.4) in free solution, but is inhibited by high concentrations of active

Serine proteases, such as alpha-chymotrypsin or elastase, caused an aggregation of rat ascites tumour cell lines, AH-130, AH-109A and YS, in a protein free medium which preserved the cell viability. This aggregation, which was monitored spectrophotometrically, was dependent upon the protease

Ehrlich ascites cells in mice have been shown to have a cell-surface trypsin-like neutral protease (TLNP) with proteolytic and beta-naphthylamidase activity. This activity is inhibited by low-mol.-wt inhibitors of trypsin but not by 11 high-mol.-wt inhibitors of trypsin in free solution. We believe

Ehrlich ascites tumour (EAT) cells possess a trypsin-like neutral protease on the cell surface. The antimetastatic triazene drug potassium p-(3,3-dimethyl-1-triazeno) benzoate (DM-COOK) inhibits this neutral protease, and also trypsin. Incubation of EAT cells with human erythrocytes (ratio of 1 to

Yellowtail ascites virus (YAV) is an aquabirnavirus that causes ascites in yellowtail, a fish often used in sushi. Segment A of the YAV genome codes for a polyprotein (pVP2-VP4-VP3), where processing by its own VP4 protease yields the capsid protein precursor pVP2, the ribonucleoprotein-forming VP3,

Fibrinolysis induced by the infusion of plasminogen activators into the circulation has been shown to cause coagulation disorders in ascites retransfusion. Dexamethasone is known to inhibit the synthesis of plasminogen activators by peritoneal macrophages. We therefore assessed its potential in

The concentrations of several proteases and antiproteases known to be present in ascites were tested in plasma and ascitic fluid with regard to their ability to separate ascites according to malignant or nonmalignant disease. Seventeen patients with proven malignant ascites and 37 with ascites due

In patients with ovarian tumors, a novel protease inhibitor which is very stable in acid (AS-PI, acid stable protease inhibitor) was identified in the ascites and tumor fluid as well as in the urine and plasma. The highest AS-PI activity was observed in the tumor fluid of ovarian carcinomas (10.7

The effects of protease inhibitors(PI), t-AMCHA, gabexate, aprotinin and heparin on the growth of mouse MM2 ascites tumor (MAT) and on several components of fibrinolysis were studied. The drugs were administered intraperitoneally one time daily for 12 days, one day after the tumor transplant. The

A Ca2+-activated neutral protease is described which, when tested against various native proteins, appears to be specific for vimentin, the 58,000-Mr subunit protein of intermediate-sized (7--11 nm) filaments in Ehrlich-ascites-tumour cells. The protein subunits of other classes of

Ehrlich ascites tumours (EAT) were grown in mice by injecting 1 × 10(6) cells intraperitoneally. In mice which received one or more injections of 30 mg soybean trypsin inhibitor (TI) i.p. during tumour growth, the number of recoverable tumour cells was significantly reduced by up to 92%. Also, the