CD44V6和CD15s抗原在子宫内膜癌中的表达及其与临床相关性研究

目的探讨CD44V6 、CD15s抗原表达与子宫内膜癌和侵袭转移的关系.方法应用免疫组化SABC方法对50例子宫内膜癌标本进行CD44V6和CD15s抗原检测.结果CD44V6和CD15s在子宫内膜癌中阳性表达率分别为74%和72%,两者呈正相关.CD44V6和CD15s表达与子宫内膜癌的临床分期和病理分级呈正相关,并随肿瘤细胞侵袭肌层深度的增加,阳性表达率增高.结论CD44V6 、CD15s高表达提示子宫内膜癌生物学行为不良,联合检测CD44V6 、CD15s可作为判断子宫内膜癌恶性程度、预测转移和评估预后的生物学指标.     

nm23H1和E-Cadherin在人非小细胞肺癌中的表达及临床意义

目的研究nm23H1和E-Cadherin蛋白在非小细胞肺癌(NSCLC)的表达及临床意义.方法采用S-P免疫组化法测定NSCLC中nm23H1和E-Cadherin蛋白的表达.结果有淋巴结转移的NSCLC组织中,nm23H1和E-Cadherin蛋白阳性表达率分别为29.4%(5/17)和11.8%(2/17),无淋巴结转移的则分别为82.4%(14/17)和42.9%(9/17),差异有极显著意义,P<0.01或显著意义,P<0.05.nm23H1和E-Cadherin表达与NSCLC的分期及肿瘤分化程度有关,P<0.05;基因蛋白表达在NSCLC组织中呈正相关,P<0.01.结论nm23H1和 E-Cadherin蛋白可作为判断NSCLC转移潜能及预后的重要指标.     

p16和cyclin D1在膀胱癌中的表达及预后意义

目的 :探讨膀胱癌中p16和cyclinD1蛋白的表达及意义。方法 :采用免疫组化S P法检测p16和cyclinD1蛋白在 82例膀胱移行细胞癌和 15例正常膀胱黏膜组织中的表达。结果 :p16蛋白的表达在正常膀胱黏膜中阳性率为 10 0 % ,膀胱癌为 4 0 2 % ,差异有极显著意义 ,P <0 0 0 1;膀胱癌组织cyclinD1蛋白阳性率 (6 7 1% )显著高于正常膀胱黏膜 (2 0 0 % ) ,P <0 0 0 5。随着膀胱癌分级及临床分期的增高 ,p16表达显著减少 ,而cyclinD1表达阳性率增高。cyclinD1蛋白表达阳性率在未复发组低于复发组 ,差异有极显著意义 ,P <0 0 2 5。结论 :p16的缺失表达和cyclinD1的过表达均参与了膀胱癌的发生发展过程 ,cyclinD1的过表达还与膀胱癌术后复发有关。     

胃癌中α-及β-连接素联合表达

目的 :探讨α 及β 连接素 (catenin)联合表达与胃癌侵袭转移间的关系。方法 :应用ABC染色法在同一胃癌术后标本上进行α 及β catenin抗体染色 ,计数胃癌组织中阳性细胞所占的比例。 结果 :正常胃黏膜上皮细胞全部表达α 及 β catenin。 38例胃癌组织中α 及 β catenin阳性表达率分别为2 8 9% (11/ 38)和 5 0 % (19/ 38)。存在淋巴结转移的胃癌其α 及 β catenin的阳性表达率分别为 8 7%及 2 6 1% ,均远低于无淋巴结转移者 (P <0 0 1)。α 与 β catenin共同阳性表达占 30 % ,共同阴性表达占 36 9%。α catenin(- ) / β catenin(- )表达者最易发生淋巴结转移 ,α catenin( ) / β catenin(- )表达者易发生肝转移。结论 :检测α ,β catenin联合表达可以更为精确灵敏地预测胃癌侵袭转移     

The Peripheral Benzodiazepine Receptors: A Review

Peripheral benzodiazepine receptors (PBRs) have been identified in various peripheral tissues as well as in glial cells in the brain. This review describes the tissue and subcellular distribution of the PBR in mammalian tissues and analyzes its many putative endogenous ligands. It deals with the pharmacological, structural and molecular characterization of the PBR, the proteins associated with the receptor (VDAC, ANC, PRAX-1) and their roles in cell growth and differentiation, cancer, steroid biosynthesis, and other physiological roles.     

血管新生在多发性骨髓瘤中的临床意义

目的　研究多发性骨髓瘤患者骨髓中血管新生的情况及临床意义。方法　应用免疫组化及原位杂交染色技术 ,对 4 2例多发性骨髓瘤患者治疗前后及 10例正常对照骨髓中微血管密度 (MVD)及血管内皮细胞生长因子(VEGF)表达进行检测。结果　多发性骨髓瘤患者治疗前骨髓中VEGF的阳性率为 5 2 .4 % (2 2 / 4 2 ) ,VEGF阳性组MVD显著高于阴性组 (P <0 .0 1) ;多发性骨髓瘤患者骨髓中MVD及VEGF表达均显著高于正常对照组 (P <0 .0 1) ;多发性骨髓瘤Ⅲ期患者骨髓中MVD显著高于Ⅰ、Ⅱ期患者 (P <0 .0 5 )。多发性骨髓瘤患者治疗前后MVD无显著变化 (P >0 .0 5 )。结论　血管新生及其正性调节因子VEGF在多发性骨髓瘤发生、发展中起着重要的作用。     

Glial fibrillary acidic protein synthesized in vitro using messenger RNA from Jimpy mouse spinal cord

Glial fibrillary acidic (GFA) protein was synthesized in vitro in a rabbit reticulocyte lysate system programmed with messenger RNA (mRNA) extracted from Jimpy mouse spinal cord. It was identical in molecular weight and charge to that synthesized from normal mouse mRNA and GFA protein extracted from normal mouse cord. These data suggest that the Jimpy mutation does not affect the primary phenotypic expression of GFA protein.     

Conversion of a radiolabelled ecdysone precursor, 2,22,25-trideoxyecdysone, by embryonic and larval tissues of Locusta migratoria

A high specific activity tritiated ecdysone precursor, 2,22,25-trideoxyecdysone, was used to probe the capacity of various embryonic and larval tissues to perform the last 3 hydroxylation steps in ecdysone biosynthesis. Embryos at early stages of development, prior to the differentiation of their endocrine glands and embryonic heads, thoraces and abdomens of later stages, were found to have the capacity to hydroxylate the precursor to ecdysone. Larval epidermis and fat body are also able to transform 2,22,25-trideoxyecdysone into ecdysone; Malpighian tubules and midgut hydroxylate the precursor at C-2 but are apparently unable to hydroxylate both at C-22 and C-25. Larval prothoracic glands convert the precursor to ecdysone at a very efficient rate, which is 1-2 magnitudes higher than that of the other tissues investigated; several data argue for the existence of a privileged sequence of hydroxylations, C-25, C-22, C-2, in the larval prothoracic glands.     

Genetic contributions to the risk assessment of microcystin in the environment

Of the known toxins produced by cyanobacteria, microcystins and nodularins are the most significant threat to human and animal health. Knock-out studies have confirmed that microcystins are produced nonribosomally by a multienzyme complex consisting of peptide synthetases, polyketide synthases, and tailoring enzymes. Gene clusters for microcystin biosynthesis have been identified and sequenced in the distantly related cyanobacterial genera Microcystis, Planktothrix, and Anabaena. Homologous genes have been detected in a nodularin-producing Nodularia strain. Subsequently, microcystin biosynthesis (mcy) genes have been used to establish molecular techniques for the detection of toxigenic cyanobacteria in laboratory and field studies. mcy genes of unknown origin can be assigned to the producing species. Techniques are currently being developed for the quantification of mcy genes in field populations. These initial genetic investigations pave the way for a molecular monitoring of microcystin- and nodularin-producing cyanobacteria and for studying the dynamics of toxic cyanobacteria in lakes. Furthermore, microcystin-deficient mutants have significantly increased our knowledge about the impact of the toxins on Microcystis-Daphnia interactions. The experience gained on microcystin biosynthesis genes will be valuable for a risk assessment of microcystin in the environment and for future water management and lake-restoration strategies.     

Diversion of prostaglandin endoperoxide metabolism by selective inhibition of thromboxane A2 biosynthesis in lung, spleen or platelets.

Infusion of arachidonic acid through the guinea pig lung or the cat spleen causes a release of thromboxane A2 and prostaglandins, as measured by bioassay. After incubation of human platelets with arachidonate similar metabolites are formed, as demonstrated chromatographically. Infusion of imidazole (50-75 microgram/ml) through the lung or spleen specifically inhibits thromboxane A2 production and diverts the pathway to the prostaglandins, mainly prostaglandin F2alpha. In human platelets imidazole causes a dose-dependent inhibition of thromboxane A2 formation (ID50 5.5 X 10(-4) M). This inhibition is accompanied by a dose-dependent increase in prostaglandin F2alpha. Since thromboxane A2 induces platelet aggregation and is a potent vasoconstrictor, diversion of pathways to prostaglandins with opposite or less potent action might be of relevance in the treatment of cardiovascular diseases.