Alport syndrome: a genetic study of 31 families

Thirty one families with Alport syndrome including 3 families with associated syndromes were studied. The location of the COL4A5 gene, responsible for the Alport syndrome, was determined by linkage analysis with eight probes of the Xq arm and by a radiation hybrid panel. Concordant data indicated the localization of the Alport gene between DXS17 and DXS11. Four deletions and one single base mutation of the COL4A5 gene were detected. Homogeneity tests failed to show any evidence of genetic heterogeneity superimposed on clinical heterogeneity for ophthalmic signs and end-stage renal disease age.     

The trk tyrosine protein kinase mediates the mitogenic properties of nerve growth factor and neurotrophin-3.

The product of the trk proto-oncogene encodes a receptor for nerve growth factor (NGF). Here we show that NGF is a powerful mitogen that can induce resting NIH 3T3 cells to enter S phase, grow in semisolid medium, and become morphologically transformed. These mitogenic effects are absolutely dependent on expression of gp140trk receptors, but do not require the presence of the previously described low affinity NGF receptor. gp140trk also serves as a receptor for the related factor neurotrophin-3 (NT-3), but not for brain-derived neurotrophic factor. Both NGF and NT-3 induce the rapid phosphorylation of gp140trk receptors and the transient expression of c-Fos proteins. However, NT-3 appears to elicit more limited mitogenic responses than NGF. These results indicate that the product of the trk proto-oncogene is sufficient to mediate signal transduction processes induced by NGF and NT-3, at least in proliferating cells.     

The trkB tyrosine protein kinase is a receptor for brain-derived neurotrophic factor and neurotrophin-3.

trkB is a tyrosine protein kinase gene highly related to trk, a proto-oncogene that encodes a receptor for nerve growth factor (NGF) and neurotrophin-3 (NT-3). trkB expression is confined to structures of the central and peripheral nervous systems, suggesting it also encodes a receptor for neurotrophic factors. Here we show that brain-derived neurotrophic factor (BDNF) and NT-3, but not NGF, can induce rapid phosphorylation on tyrosine of gp145trkB, one of the receptors encoded by trkB. BDNF and NT-3 can induce DNA synthesis in quiescent NIH 3T3 cells that express gp145trkB. Cotransfection of plasmids encoding gp145trkB and BDNF or NT-3 leads to transformation of recipient NIH 3T3 cells. In these assays, BDNF elicits a response at least two orders of magnitude higher than NT-3. Finally, 125I-NT-3 binds to NIH 3T3 cells expressing gp145trkB; binding can be competed by NT-3 and BDNF but not by NGF. These findings indicate that gp145trkB may function as a neurotrophic receptor for BDNF and NT-3.     

The trk proto-oncogene encodes a receptor for nerve growth factor.

Two classes of receptors with distinct affinities for nerve growth factor (NGF) have been identified. The low affinity receptor (Kd approximately 10(-9) to 10(-8) M) is a cysteine-rich glycoprotein encoded by the previously characterized LNGFR gene. The structural nature of the high affinity receptor (Kd approximately 10(-11) to 10(-10) M) has yet to be established. In this study we show that the product of the human trk proto-oncogene (gp140trk) binds NGF with high affinity. Moreover, NGF could be chemically cross-linked to the endogenous gp140trk present in rat PC12 pheochromocytoma cells as well as to gp140trk ectopically expressed in mouse fibroblasts and in insect Sf9 cells. High affinity binding of NGF to gp140trk can occur in the absence of low affinity LNGFR receptors, at least in nonneural cells. Addition of NGF to PC12 cells elicits rapid phosphorylation of gp140trk on tyrosine residues and stimulates its tyrosine kinase activity. These results indicate that gp140trk is a functional NGF receptor that mediates at least some of the signal transduction processes initiated by this neurotrophic factor.     

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。     

棉株根系伤流中的细胞分裂素类物质

棉株根系伤流有明显昼夜节奏,白天多,夜晚较少。白天中又以上午9～12时的伤流量为最高。伤流中CTK量及其浓度也以白天为高。在切除地上部4天以后,从蕾期和铃期棉株已不再能收集到伤流液,但盛花期棉株在切除地上部6天以后,仍产生了相当多的伤流,其中仍含有丰富的CTK类物质。盛花期棉株根系伤流量及其中CTK水平高于铃期棉株,提示铃期棉株根系活力已开始趋向衰老。根据Sephadex LH-20柱层析及高效液相层析鉴定出棉株根系伤流中的CTK类物质有Z,ZR,和IPA。     

四川成都市郊正常成年男性血清生殖激素水平及其频数分布

本文用放射免疫测定法(RIA),测定了200～290例中国四川成都市郊30～73岁的正常成年男性血清睾酮(T)促黄体激素(LH).卵泡刺激素(FSH)及泌乳激素(PRL)的水平及其分布,进行了不同年龄水平差异显著性的观察,见到睾酮与泌乳激素水平无显著差异,促黄体激素及卵泡刺激素水平,随年龄之增加而升高,差异有显著性,并测得它们在血清中水平的分布:LH、FSH及PRL均为对数正态公布,T既非正态又非对数正态,但其频率分布较对称,接近正态分布。     

Effect of gossypol on testicular blood flow and testosterone production in rats

Rats were treated with highly purified gossypol acetic acid at doses of 15 or 30 mg/kg day-1 for 6 weeks to produce an effect on spermatogenesis as shown by reduced sperm motility and increased sperm malformation rates. The treated rats did not differ from the controls in the body weight growth curves and reproductive organ weights. When stimulated with hCG, testicular blood flow was increased in the low dose group; the testosterone concentrations in peripheral and testicular venous blood were also increased to a greater extent than those of the control group. No difference was found between the high dose and control groups in testicular blood flow or testosterone concentrations. The morphology of the Leydig cells was apparently normal, although some degenerative changes in the germinal epithelium were observed in the high dose group. Therefore, there is no evidence in our experiment to show any anti-androgenic effect following 6-week treatment of gossypol in rats, even at the dose of 30 mg/kg day-1.