ABSTRACT
Objective To study the construction and function of platelet (PL) and the protection of PL by blood anesthesia during the eardiopulmonary bypass (CPB). Methods Bovine serum albumin (BSA) was immobi-lized on the surface of polyethylene terephthalate(PET) which was used as artificial vascular materials,to obtain the samples of PET-BSA. (1) The quantity of PL adhesion of PET and PET-BSA samples were investigated by lactate de-hydrogenase(LDH) test. (2) The quantity of PL activation was investigated by a-granule membrane protein-140 (GMPI40) test. (3)PL adhesion test was conducted on the surface of the samples and the morphology of the adhered PL was examined by scanning electron microscopy (SEM). (4)30 patients undergoing cardiac surgery under CPB were randomly divided into aprotinin group and control group,quantities of FDP, PK, PLG and thromboxance B2 (TXB2) in the blood were measured in various time, PLs were observed by electron microscopy, and postoperative blood loss from chest and medium were recorded during first 24 hours. Results Compared with the control group,the quantity of PL adhesion on the PET-BSA samples significantly decreased and the quantity of PL activation of the PET-BSA group was only 20% of the control group. The results of SEM showed PL on PET-BSA surface was few,whereas on the PET sur-face overlaped and had pseudopodium. The decomposition of PLG is fewer in blood anaesthesia group,indicated the fi-brinolytie system was inhibited and construction of PL was protected. Conclusion During CPB,plasma proteins com-pete against each other to adhere on the tube of CPB,then PL interact to the adhered proteins,and PL combine with conformation changed fibrin at its C extreme of γ chain. At the same time,PL is activated and its GPⅡb/Ⅲa point is ex-posed. The function of blood anesthesia of aprotinin is to inhibit the activation of PIg; and PK,protect the GPⅡb of PL from being destroyed, and protect the coagulation funeion of PL of postoperation.
ABSTRACT
Objective To investigate the relationship between tumor suppressor gene DPC4 and the development and prognosis of pancreatic carcinoma. Methods Relevant literatures of recent years were reviewed. Results DPC4 was located on chromosome 18. Its product was Smad 4 protein. Smad 4 protein was the central component of the transforming growth factor-beta signaling pathway, and all the biological effect was the results of interaction of Smad 4 and different Smads. The gene was deleted or inactive in about 50% of pancreatic carcinomas. The deletion of DPC4 had a great relation to the development and prognosis of pancreatic carcinoma. Conclusion The alteration of tumor suppressor gene DPC4 is connected with the development and prognosis of pancreatic carcinoma. However, this research should be further studied.