中国宁夏盖蛛属一新种：（蜘蛛目：皿蛛科）

本文记述蜘蛛目皿蛛科皿蛛亚科盖蛛属一新种——六盘盖蛛,新种Neriene liupanensis。标本采自宁夏六盘山自然保护区。     

高胆固醇血症家兔红细胞在交、直流电场中的电泳行为

本文对高胆固醇血症家兔红细胞在交、直流电场中的电泳行为进行了多指标测定,结果显示,高脂组与正常组相比红细胞聚集能力增强,变形能力及膜流动性下降,表明高脂血症可能较易导致血栓形成。中药有效成分8501有对抗高脂引起的红细胞上述改变的作用,提示8501可能对血栓和动脉粥样硬化斑块形成有防治作用。     

银额果蝇的B染色体研究:1.昆明群体的Bs数目和频率

本研究发现银额果蝇昆明群体有丝分裂中期核型中存在B染色体,出现频率为69.1%。目前,在已研究过的来自各个地区的银额果蝇中,昆明群体的B染色体频率最高。B染色体数目为1-6条。该群体内单雌系间的B染色体数目不同,个体间和细胞间的B染色体数目也不同。在核型中,B染色体最小,形态稳定,点状,C-带和G-带呈阳性。     

毛腿鼠耳蝠(Myotis fimbriarus)血液的研究

本文对毛腿鼠耳蝠血液的有形成分和百分比等项正常数值进行了测定,并对各类血细胞的主要形态作了描述。 所测的各项数值与前人报道的数据比较,其红细胞数目和血红素含量都高于同属的其他种,也较其他哺乳动物为高。毛腿鼠耳蝠与该属有些种类的淋巴细胞数目占全部白细胞的百分数最高,也明显高于其他哺乳动物。     

刺激大鼠迷走神经向中端对其不同脑区5-HT含量的影响

采用荧光分光光度法,测定脑内5-HT的含量,观察电刺激两侧颈迷走神经向中端对大鼠海马、下丘脑和中-桥脑内5-HT含量的影响,结果如下:(1)刺激迷走神经向中端后,三脑区的5-HT含量均显著增加(P<0.05-0.005);(2)侧脑室内注射新斯的明(10μg/10μl)或烟碱(10μg/10μl)后,刺激迷走神经向中端使三脑区5-HT含量增多的效应显著提高(p<0.01-0.001);(3)侧脑室内注射六烃季胺(250μg/10μl)后,刺激迷走神经向中端使三脑区5-HT含量增多的效应显著下降(p<0.05-0.005);(4)侧脑室内注射阿托品(10μg/10μl)或纳洛酮(10μg/10μl)后,不影响刺激迷走神经向中端引起的三脑区5-HT含量增多的效应(p>0.05)。由此看来,迷走传入冲动很可能先使脑内Ach释放增多,然后,Ach作用于N-胆碱受体而导致海马、下丘脑和中-桥脑内5-HT含量增加。以上结果表明,在脑内,迷走传入纤维和5-HT能神经元之间可能存在着机能联系。     

Reduced cyclosporin accumulation in multidrug-resistant cells

Cyclosporin accumulation was reduced by 50% or more in multidrug- resistant CHRC5 CHO cells with high levels of P-glycoprotein expression compared to drug sensitive AuxB1 CHO cells. This difference could be overcome by verapamil which is known to interact with P-glycoprotein and reverse multidrug resistance. The difference in cyclosporin accumulation between sensitive and resistant cells decreased with increasing cyclosporin concentrations suggesting that cyclosporine itself regulated its own accumulation through interaction with P-glycoprotein. Indeed, cyclosporin also reversed differences in vinblastine accumulation between resistant and sensitive cell lines. Since P-glycoprotein is highly expressed in the kidney which is also a target for cyclosporin toxicity, the effects of verapamil on cyclosporin accumulation were studied in two renal cell lines, rat mesangial cells and LLCPK1, cells. Verapamil increased cyclosporin accumulation by approximately 70%. These results suggest that cellular cyclosporine accumulation is regulated at least in part by its interaction with P-glycoprotein.     

Antibodies to peptide determinants in transforming growth factor beta and their applications

Polyclonal antibodies have been raised to a series of synthetic peptides which correspond to essentially all regions of the transforming growth factor beta 1 (TGF-beta 1) molecule. All antisera were evaluated for their abilities to react with TGF-beta 1 and TGF-beta 2 in either the native or reduced form in enzyme-linked immunosorbent assays, Western blots, and immunoprecipitation assays. While all antisera demonstrated some ability to recognize TGF-beta 1 in these systems, there was limited cross-reactivity with TGF-beta 2, suggesting that substantial sequence or conformational differences exist between the two growth factors. On Western blots 5-10 ng of purified human platelet TGF-beta 1 could be detected when probed with affinity-purified peptide antisera generated against peptides corresponding to residues 48-77, 50-75, and 78-109 of the 112 amino acid TGF-beta 1 monomer. Antisera raised against peptides 50-75 and 78-109 were most effective in immunoprecipitating reduced and native 125I-TGF-beta 1, respectively. The antisera also were tested for their effectiveness in blocking the binding of 125I-TGF-beta 1 to its receptor. Anti-peptide 78-109 and anti-peptide 50-75 blocked 80% and 40% of the binding, respectively, while antibodies against amino-terminal peptides were without effect. These data suggest that the carboxyl-terminal region of TGF-beta 1 may play a significant role in the binding of the native ligand to its receptor.     

Altered plasma membrane ultrastructure in multidrug-resistant cells

Multidrug resistance is mediated by P-glycoprotein, an integral plasma membrane component which is thought to function as a drug export pump. This model can explain drug resistance, but fails to account for the broader pleiotropy of the multidrug resistance phenotype. We report here a freeze-fracture study revealing increases in the densities of protoplasmic face intramembrane particles in multidrug-resistant Chinese hamster ovary (CHO) and human leukemic cells. The intramembrane particle density in a CHO cell revertant which had lost the characteristics of the multidrug resistance phenotype was indistinguishable from that of the drug-sensitive parental cell line. This demonstration of a global multidrug resistance-linked change in plasma membrane architecture may have significant implications for understanding the variety of concurrent membrane-related changes which are not easily explained by the current model for multidrug resistance.     

A surface component on GH3 pituitary cells that recognizes transforming growth factor-beta, activin, and inhibin

We have examined the ability of various forms of activin and inhibin, which are structurally related to transforming growth factor-beta (TGF-beta), to interact with various types of cell surface TGF-beta binding sites. Activin AB, inhibin A, and inhibin B were unable to compete with 125I-TGF-beta 1 for binding to the TGF-beta receptor types I, II, or III that coexist in human skin fibroblasts, rat liver epithelial cells, and mink lung epithelial cells. In contrast, activins and inhibins effectively competed for TGF-beta 1 binding to GH3 rat pituitary tumor cells. Binding of TGF-beta 1 to GH3 cells was mediated by about 2700 sites/cell with a Kd = 90 pM. Affinity labeling of these GH3 binding sites by cross-linking to 125I-TGF-beta 1 yielded 70-74-kDa labeled complexes distinct from previously identified TGF-beta binding components. Labeling of these 70-74-kDa components with 125I-TGF-beta 1 was inhibited by TGF-beta 1, TGF-beta 2, activin AB, and inhibin B at concentrations in the high picomolar to low nanomolar range, but it was not significantly affected by other polypeptide hormones and growth factors tested. The 70-74-kDa labeled GH3 components represent a novel type of cell surface TGF-beta binding protein that is unique in its ability to recognize various other members of the TGF-beta family of bioactive polypeptides.     

Effects of ethinyl estradiol on intestinal membrane structure and function in the rabbit

Structural and functional properties of the small intestinal microvillus membrane were evaluated in the rabbit after administration of ethinyl estradiol, a synthetic estrogen with a demonstrated propensity to alter hepatic membrane lipid fluidity, and promote cholestasis. In the jejunum, no estrogen-induced changes in microvillus membrane total lipid, cholesterol or phospholipid content were observed. However, the ileal microvillus membrane in estradiol-treated animals demonstrates significant reductions vs. controls (per mg protein) in total lipid (0.55 milligrams vs. 0.89 milligrams) [corrected] and phospholipid (206.7 micrograms vs. 304.91 micrograms) (p less than 0.001) content, as well as modifications in specific phospholipid species. The increase in the ileal microvillus membrane cholesterol: phospholipid molar ratio (0.65 vs. 0.51, p less than 0.05) was associated with a significant decrease in membrane lipid fluidity reflected by an increase in fluorescence anisotropy measurements utilizing diphenyl hexatriene as the fluorophore (r at 25 degrees C = 0.306 vs. 0.282, p less than 0.05). Thermotropic lipid phase transitions, assessed by Arrhenius plots of both fluorescence data and ileal microvillus membrane p-nitrophenylphosphatase activity demonstrate that phase changes occur between and 24 and 28 degrees C in both treated and untreated groups. Within the temperature range studied (40-10 degrees C) no differences from control were observed in microvillus membrane alkaline phosphatase activity following estrogen treatment. These data therefore indicate that ethinyl estradiol-induced effects on microvillus membrane lipid composition and physical properties occur predominantly in the ileum and appear to be related, in part, to specific alterations in the availability of phospholipid following estrogen treatment.