Therapeutic effect and the mechanism of the action of human urinary trypsin inhibitor (MTI) on experimental acute pancreatitis were studied. MTI significantly increased survival rate of animals with experimental acute pancreatitis induced by the infusion of trypsin or phospholipase A2 into pancreas or by a closed duodenal loop. The efficacy of MTI on these types of pancreatitis were higher than those of aprotinin. Pancreatic enzymes were released from pancreatic slice by trypsin or phospholipase A2, and this release was inhibited by MTI. Further, these pancreatic enzymes caused a secondary release of enzymes from other pancreatic slice, suggesting that these enzymes injured pancreatic tissue and that a chain reaction of pancreatic enzyme activation may play an important role in the pathogenesis of acute pancreatitis. MTI suppressed the secondary enzyme-induced pancreatic injury more strongly than aprotinin. These results suggest that MTI may suppress pathogenesis and development of pancreatitis by inhibiting the chain reaction of pancreatic enzyme activation.

We have investigated the in vivo antitumor mechanism of natural human tumor necrosis factor (n‐TNF) isolated from a culture of human leukemic B cell line (BALL‐1), especially its action as an immunomodulator, and found that the in vivo antitumor effect of n‐TNF on Meth A sarcoma implanted in BALB/c mice pretreated with monoclonal antibody against T cell‐specific surface antigen (Thy‐1) was significantly diminished. Furthermore, when BALB/c mice were treated with T cell subset‐specific monoclonal antibodies, anti‐L3T4 or anti‐Lyt‐2.2, the antitumor effect of n‐TNF on Meth A sarcoma was significantly reduced. Therefore, it was suggested that the in vivo antitumor mechanism of n‐TNF might involve a T cell‐mediated immunological route.

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Summary Urokinase (UK) preparations, obtained at random on the commercial market from ten manufacturers, were investigated for their degree of purification by measurement of their coagulant activity, lysozyme activity, kinin‐ and brady‐kinin‐like activity, endotoxin content and hepatitis B surface antigen (HBs antigen). The results indicated that the UK preparations could be divided into two groups: ‘clean’ UK which contained no detectable biologically active substances, and ‘dirty’ UK which contained abundant biological active substances. When ‘dirty’ UK containing high procoagulant activity was injected into rabbits, the coagulation system was activated. Separation of the pro‐coagulant activity from the UK components may be difficult on an industrial scale by gel filtration. Since ‘clean’ UK contains no detectable biologically active substances, its specific activity was the highest among the UK preparations.