PMA和IM诱导的新生儿脐带血淋巴细胞增殖反应

为比较新生儿脐带血和成人外周血淋巴细胞对抗CD     

Preparation and characterization of monoclonal antibody against recombinant human tissue factor pathway inhibitor

OBJECTIVE: To prepare and identify monoclonal antibody (McAb) against recombinant human tissue factor pathway inhibitor (rhTFPI) and to use it for measurement of TFPI by ELISA, and to evaluate the effects of the McAb on dilute prothrombin time (PT) and activated partial thromboplastin time (APTT). METHODS: After intrasplenic immunization of Balb/c mouse with TFPI, hybridoma technique was used to raise monoclonal antibody against rhTFPI. The McAb was well-characterized and labelled with horseradish peroxidase (HRP) by using assay of TFPI in ELISA. Furthermore, the McAb was added to normal and factor IX deficient plasma for observation of dilute PT and APTT. RESULTS: Two hybridomas (4F4, 4F8) secreting McAb against TFPI were established. The Ig class and subclass of the McAb purified from 4F8 was IgG1. Immunoblotting results indicated that the McAb4F8 only recognized a single band of TFPI with molecular weight of 34.8 KD. The results of Sandwich enzyme-linked immunosorbent assay (ELISA) by using the HRP labelled McAb4F8 showed that the mean of TFPI in normal human plasma is 103.2 +/- 11.5 micrograms/L. The McAb 4F8 was also proved to shorten markedly dilute prothrombin time of factor IX deficient plasma and normal plasma. CONCLUSIONS: We established two hybridomas cell lines (4F4, 4F8) and obtained the McAb4F8 against TFPI and reported the levels of TFPI in healthy adult human plasma by Sandwich ELISA with HRP labelled McAb4F8 in Chinese.     

Experimental study on liver microcirculation disturbance following transplantation and the protective effect of prostaglandin E1 in the rat

Objective To determine the effect of PGE1 on liver microcirculation disturbance following orthotopic liver transplantation in rats.Methods Forty male adult Wistar rats were divided randomly into 3 groups. Eight transplantations were established in both the experimental and control group, while in the sham group, the liver was dissected like in the experimental group, but no resection was performed. In the experimental group, PGE1 (0.5 μg/kg*min-1) was injected intravenously into the donor before the operation, and added (1 mg/L)to the flush and preservation fluid, while PGE1 was replaced by normal saline in the control group. Confocal laser scan microscopy, biochemical test, and optical and electronic microscopy were used.Results In the control group the reperfusion state was poor,leukocyte infiltration appeared in the center of lobule,and transaminase rose after transplantation. In the experimental group distinctive improvement was seen as compared with the control group (P<0.05). Histological findings showed progressive degeneration and necrosis following transplantation in the control group, while in the experimental group the histological changes were improved to some degree by the use of PGE1.Conclusions In liver transplantation, ischemic reperfusion damage may lead to hepatic microcirculation disturbance, which is the major cause of graft failure. Infusing PGE1 into the donor intravenously before ischemia and adding PGE1 to the cold storage fluid could improve hepatic microcirculation, and thus reducing ischemic reperfusion damage in liver transplantation.In liver transplantation, ischemic reperfusion damage may lead to hepatic microcirculation disturbance, which is the major cause of graft failure. Infusing PGE1 into the donor intravenously before ischemia and adding PGE1 to the cold storage fluid could improve hepatic microcirculation, and thus reducing ischemic reperfusion damage in liver transplantation.     

GTPγS及GDPβS对SHRSP内脏阻力血管平滑肌钙通道的影响

目的 研究Ｇ蛋白激动剂ＧＴＰγＳ和抑制剂ＧＤＰβＳ对卒中易感型自发性高血压大鼠（ＳＨＲＳＰ）及常压大鼠肠系膜动脉Ａ４－Ａ５分支阻力血管平滑肌钙通道的影响。方法 应用膜片箝全细胞钡电流方式。结果 （１）ＧＴＰγＳ使ＳＨＲＳＰ和Ｗｉｓｔａｒ两种大鼠阻力血和平滑肌全细胞峰值钡电流明显增加,且ＳＨＲＳＰ大鼠显著大于Ｗｉｓｔａｒ大鼠。ＧＤＰβＳ则可报制两种大鼠的全细胞峰值钡电流,对于ＳＨＲＳＰ大鼠的帽程度显     

Integration of linkage analyses and disease association studies

The REGD procedure of the S.A.G.E. [1994] system was used to determine the mode of inheritance of the rare disease given in Problem 1. The likelihood ratio test statistic indicated that we should reject the hypotheses of dominant and recessive inheritance at the 0.01 level, so codominant inheritance was assumed. The estimated penetrance values computed from the β estimates given by the S.A.G.E. output were 1.0, 0.7, and 0.0 for the AA, AB, and BB genotypes respectively. A sample of three markers from each chromosome was used to determine which chromosome(s) gave evidence of having loci linked to the disease locus. The lod minus 0.83 support interval, which has been shown to provide the best approximation to 95% coverage among interval estimates [Nemesure et al., in press], was obtained for each of these markers. The criterion for rejecting the hypothesis of close linkage using the support interval methodology required that the left side of the lod minus 0.83 support interval about the maximum likelihood estimate, $ {\rm \hat \theta } $, includes only values greater than θ = 0.10. This criterion suggested that chromosomes 2, 3, and 6 did not contain the disease genes. Classical lod-score linkage analysis using the usual criteria of 3.0 for linkage and -2.0 for exclusion did not result in any regions being identified. On dropping the required lod score to 1.0, chromosomes 1, 3, and 6 gave results in favor of linkage with lod scores of 1.94 (θ = 0.19), 1.20 (θ = 0.24), and 1.30 (θ = 0.23), respectively. Association studies comparing unrelated cases to unrelated controls were done for all markers on all chromosomes. Two associations were observed which were significant at the 0.05 level after adjusting for the large number of multiple comparisons being made. The strongest association observed was between allele 7 of marker 23 on chromosome 5 and the disease (χ = 52.20, or = 4.7) and the second strongest was between allele 8 of marker 31 on chromosome 1 (χ = 20.10, OR = 3.4). ©1995 Wiley-Liss, Inc.     

Hypothetic association between greater sympathetic activity and prostate cancer

Among men, prostate cancer is the most common cancer diagnosed, and the second leading cause of death from cancer in the industrialized countries. In spite of substantial progress in research, diagnosis and treatment, the causes of prostate cancer remain largely unknown. In this paper, we propose the hypothesis that prostate cancer represents another entity in the constellation of disease incited by the greater sympathetic activity that develops with age. However, the specific mechanisms of changes of increased prostatic cell proliferation and carcinogenesis caused by the autonomic nervous system have not yet been clarified. In regard to this matter, future studies should outline a more complete mechanism.