褶纹冠蚌珍珠囊发育的研究

以褶纹冠蚌(Cristaria plicata Leach)为实验对象,应用光学显微技术和扫描电子显微技术研究珍珠囊的发育,结果表明在水温16℃左右时约需30d形成具有单层上皮细胞的珍珠囊,6个月后稳定分泌珍珠质。构成珍珠囊的上皮细胞从高柱状逐渐变成扁平状或立方形,细胞的碳酸酐酶污性也日益增强。大部分移植细胞小片的结缔组织与母蚌的结缔组织共同成层排列在珍珠囊腔外围。游走细胞在珍珠囊的早期发育阶段十分活跃。本文还阐明了珍珠囊液是存在于上皮细胞与珍珠表面之间的一薄层流体状物质。碳酸钙结晶的核化(nucleation)和初期生长都发生在珍珠囊液中。     

我国汉族人群的乙二醛酶Ⅰ遗传多态性

用琼脂糖平板凝胶电泳技术分析了我国六个城市的汉族共1238人的红细胞乙二醛酶I的遗传多态性。每个汉族人群的受检人数和GLO1*1基因频率分别为:郑州200人(0.1023),哈尔滨195人(0.1103),呼和浩特210人(0.1259),贵阳204人(0.1373),兰州210人(0.1476),西安199人(0.1508)。中国不同地区汉族人群之间的GLOI基因频率分布存在显著性差异,但这种差异明显小于中国不同少数民族之间的差异。     

血红细胞超氧化物歧化酶(SOD)制备工艺的研究初报

本文报告了本实验室设计的由血红细胞自溶液60℃热变性, 乙醇——氯仿法除血红蛋白,旋转蒸发法减压浓缩抽去氯仿、乙醇,硫酸铵分级盐析法沉降SOD,Sepbadex G-75层析提纯SOD等步骤构成的一条成本低、设计合理、简便实用的分离纯化SOD的工艺路线。     

Selenium status of patients with Balkan endemic nephropathy

The selenium (Se) contents in common cereals in endemic and nonendemic areas in Serbia are very low. Plasma Se levels of both patients and healthy subjects, were also low, reflecting low Se intakes. Patients with Balkan endemic nephropathy (BEN) had significantly lower (p<0.05) plasma Se levels than healthy individuals, both from regions close to endemic areas, and from Belgrade. Mean plasma Se of BEN patients was slightly but insignificantly higher in samples taken immediately after dialysis than in those taken before, suggesting that very little of the Se present in plasma is dialyzable. Plasma SeGSH-Px activities before and after hemodialysis in both BEN and Nonendemic chronic renal failure (NCRF) patients were not significantly different, but BEN patients had lower enzyme activities than those with NCRF and healthy controls. In BEN patients, a significant correlation between plasma Se and SeGSH-Px activity was found. NCFR patients were with diagnoses: TBC of kidneys, chronic glomerulonephritis, chronic pyelonephritis, and polycystic kidneys.     

On the mechanism of sulfite activation of chloroplast thylakoid ATPase and the relation of ADP tightly bound at a catalytic site to the binding change mechanism

Washed chloroplast thylakoid membranes upon exposure to [3H]ADP retain a tightly bound [3H]ADP on a catalytic site of the ATP synthase. The presence of sufficient endogenous or added Mg2+ results in an enzyme with essentially no ATPase activity. Sulfite activates the ATPase, and many molecules of ATP per synthase can be hydrolyzed before most of the bound [3H]ADP is released, a result interpreted as indicating that the ADP is not bound at a site participating in catalysis by the sulfite-activated enzyme [Larson, E. M., Umbach, A., & Jagendorf, A. T. (1989) Biochim. Biophys. Acta 973, 75-85]. We present evidence that this is not the case. The Mg2(+)- and ADP-inhibited enzyme when exposed to MgATP and 20-100 mM sulfite shows a lag of about 1 min at 22 degrees C and of about 15 s at 37 degrees C before reaching the same steady-state rate as attained with light-activated ATPase that has not been inhibited by Mg2+ and ADP. The lag is not eliminated if the enzyme is exposed to sulfite prior to MgATP addition, indicating that ATPase turnover is necessary for the activation. The release of most of the bound [3H]ADP parallels the onset of ATPase activity, although some [3H]ADP is not released even with prolonged catalytic turnover and may be on poorly active or inactive enzyme or at noncatalytic sites. The results are consistent with most of the tightly bound [3H]ADP being at a catalytic site and being replaced as this Mg2(+)- and ADP-inhibited site regains equivalent participation with other catalytic sites on the activated enzyme.(ABSTRACT TRUNCATED AT 250 WORDS)     

db—cAMP对转化细胞钙调素基因表达与细胞骨架的影响

We have demonstrated that the distribution of microtubules (MT), microfilaments (MF) and fibronectin (FN) were diminished, while the gene expression of the calmodulin and c-fos enhanced in the transformed C3 H10 T1/2 cells. After treatment with 1 mM db-cAMP for 1 hr. and 2 hrs., there was an early and rapidly reduced in gene expression of calmodulin and c-fos respectively. After db-cAMP treatment for 4-5 days, the number of Capping cells of ConA binding decreased significantly and the cell surface microvilli decreased also. The growth of treated cells was inhibited markedly. By using 4F1 cDNA probe, which is preferentially expressed in G1 phase, we have found that the db-cAMP treated cells were accumulated at G1 phase. Of particular interest is the fact that the distribution of microtubules, microfilaments and fibronectin were recovered after treatment with 1 mM db-cAMP for 6 days. It is suggested that the inhibition of proliferation, alteration of phenotype and recovery of cytoskeleton in transformed cells after treatment with db-cAMP are related to the inhibition of gene expression of calmodulin.     

隆线溞[Daphnia(Ctenodaphnia)carinata]卵鞍的超微结构

在不利的环境条件下,枝角类中有一部分种类可以形成卵鞍(ephippium),内含休眠卵。本文应用扫描电镜和透射电镜对隆线溞的卵鞍进行了超微结构的研究。研究表明:卵鞍外面大部分略呈浅的蜂窝状,内面则排布着多数卵石状小突起。卵鞍分为内外两层,两层的超微结构截然不同;各层又可分为三小层。     

Identification of a frameshift mutation responsible for the silent phenotype of human serum cholinesterase, Gly 117 (GGT----GGAG).

A frameshift mutation that causes a silent phenotype for human serum cholinesterase was identified in the DNA of seven individuals of two unrelated families. The mutation, identified using the polymerase chain reaction, causes a shift in the reading frame from Gly 117, where GGT (Gly)----GGAG (Gly+ 1 base) to a new stop codon created at position 129. This alteration is upstream of the active site (Ser 198), and, if any protein were made, it would represent only 22% of the mature enzyme found in normal serum. Results of analysis of the enzymatic activities in serum agreed with the genotypes inferred from the nucleotide sequence. Rocket immunoelectrophoresis using alpha-naphthyl acetate to detect enzymatic activity showed an absence of cross-reactive material, as expected. One additional individual with a silent phenotype did not show the same frameshift mutation. This was not unexpected, since there must be considerable molecular heterogeneity involved in causes for the silent cholinesterase phenotype. This is the first report of a molecular mechanism underlying the silent phenotype for serum cholinesterase. The analytical approach used was similar to the one we recently employed to identify the mutation that causes the atypical cholinesterase variant.