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Glycoproteins present in human follicular fluid that inhibit the zona- binding capacity of spermatozoa 总被引:1,自引:0,他引:1
Previous studies have suggested that human follicular fluid contains
factors that reduce the zona-binding capacity of spermatozoa. The present
study provides further evidence of the existence of such factors. Using the
hemizona binding assay (HZA), we have shown that the inhibitory effect of
human follicular fluid on the zona-binding capacity of spermatozoa is
concentration-dependent, an inhibitory effect being detected when the
concentration of human follicular fluid was > or = 10%. A 1%
concentration of human follicular fluid did not possess this inhibitory
activity. Heating human follicular fluid at 56 degrees C for 30 min did not
affect its inhibitory properties; treatment with proteinase-K abolished
such inhibition. Human follicular fluid was fractionated sequentially by
concanavalin-A affinity chromatography, Mono Q ion-exchange chromatography
and Superose-12 gel filtration. The zona binding inhibitory activity
resided in the fraction which bound to the lectin and Mono Q column and
contained molecules with native molecular weights of 32 and 192 kDa. Sodium
dodecyl sulphate-polyacrylamide gel electrophoresis analysis suggested that
the 192 kDa glycoprotein was a tetramer, while the 32 kDa glycoprotein
remained as a single molecular species under denaturing conditions. We
conclude that two glycoproteins were responsible for the zona binding
inhibitory activity of human follicular fluid. The physiological role of
these factors remains unclear.
相似文献
4.
MW Lieberman R Barrios G Kala SV Kala ED Lykissa CN Ou 《Environmental health perspectives》1999,107(9):A444-A445
Respond on comments on Lieberman's article: Cyclosiloxanes Produce Fatal Liver and Lung Damage in Mice. Environ Health Perspect 107:161-165 相似文献
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Kangaroo Care with a ventilated preterm infant 总被引:4,自引:0,他引:4
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Modulation of in vitro eosinophil progenitors by hydrocortisone: role of accessory cells and interleukins 总被引:1,自引:0,他引:1
The growth of human eosinophil progenitors (CFU-Eo) and the modulation of growth by hydrocortisone were studied as functions of the presence of lymphocytes and monocytes in marrow cells under study; and the source of colony-stimulating factors, specifically, media conditioned by macrophage-like cell line, GCT; phytohemagglutinin-stimulated mononuclear cells (PHA-LCM); or the T cell line, MO. CFU-Eo growth was greatest in marrow containing accessory cells as compared to marrow depleted of accessory cells; and in marrow treated with phytohemagglutinin-stimulated leukocyte conditioned media (PHA-LCM) or MO (T cell line)-conditioned medium (MO-CM) as compared with GCT cell- conditioned medium (GCT-CM). Hydrocortisone reproducibly inhibited eosinophil progenitor growth in unfractionated marrow stimulated by GCT- CM. This effect was abrogated by admixing irradiated mononuclear cells or T lymphocytes with the target marrow or by adding interleukin 1 or interleukin 2 (IL-1, IL-2). Inhibition by hydrocortisone did not occur when monocyte and T lymphocyte depleted marrow was studied. Unlike GCT- CM, MO-CM and PHA-LCM stimulated equal proportions of eosinophil progenitors in nondepleted and accessory cell-depleted marrow and demonstrated less hydrocortisone inhibition. However, both GCT-CM and PHA-LCM produced in the presence of hydrocortisone stimulated significantly fewer CFU-Eos in both unfractionated and accessory cell- depleted marrow target populations. These results indicate that the growth of CFU-Eo and inhibition of growth by hydrocortisone is a direct function of a monocyte-T cell interaction and probably is mediated through effects on the production/release of eosinophil colony stimulating factor (Eo-CSF). 相似文献
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Interactions between vascular endothelial cells and blood platelets have been investigated using a model microcirculation consisting of microcarrier beads colonized with human umbilical vein endothelial cells (HUVECs) and perfused with washed platelet suspensions. To simulate the effects of endothelial desquamation and exposure of subendothelium, fibrillar collagen in suspension was coinjected with the platelets. In this model, neither the passage of platelets alone nor collagen alone stimulated prostacyclin (PGI2) production by the HUVECs. Platelets activated by coinjection with collagen released thromboxane A2 (TXA2), and this was associated with the simultaneous production of PGI2 by the HUVECs. By means of double-isotope experiments with [3H]arachidonic acid (AA) incorporated into platelets and [14C]-AA into HUVECs, it was shown that all the PGI2 generated was derived from platelet AA and/or endoperoxides. This interpretation was strengthened by the finding that PGI2 production was not prevented by treatment of HUVECs with indomethacin followed by perfusion with collagen-stimulated platelets. AA metabolites in double-isotope label experiments were further characterized by reverse-phase chromatography, and it was shown that both cyclooxygenase and lipoxygenase products of the HUVECs were derived from platelet membrane lipid. Thrombin regularly produced transient PGI2 release, but showed rapid tachyphylaxis. Platelet-derived compounds including ADP, ATP, and platelet-activating factor (PAF) did not produce PGI2 release by HUVECs in this system. Thus, the transfer of AA and metabolites from collagen- stimulated platelets is likely to be the mechanism for PGI2 production in the context of minor degrees of endothelial desquamation. 相似文献
9.
目的研究呼吸纯氧对健康人听感觉门控P50的影响。方法右利手、健康男性大学生志愿者28名,根据随机数字表分为对照组(n=12)和实验组(n=16)。佩戴面罩,对照组呼吸空气,实验组呼吸医用纯氧60 min。应用条件-测试刺激,记录吸氧前(pre0)、吸氧20 min(Oxy20)、吸氧50 min(Oxy50)、吸氧后30 min(post30)的脑电图,计算听觉P50潜伏期和P50感觉门控电位(S1与S2振幅之差)。结果 S1刺激在4个时间点各组P50潜伏期相对稳定(P0.7);吸氧50 min时,实验组比对照组P50潜伏期缩短(P0.05)。S2刺激在4个时间点各组P50潜伏期相对稳定(P0.30),两组间比较无显著性差异(P0.05)。对照组P50门控电位比较稳定(P=0.70),而实验组随吸氧时间逐渐延长,电位越来越高,停止吸氧后,电位迅速回落,Oxy20和post30(P=0.04)、Oxy50和post30(P=0.02)相比均有显著性差异。组间比较,4个时间点均无显著性差异(P0.05)。结论健康人吸60 min纯氧,可能缩短对刺激的反应时间,有增强听觉门控电位的趋势。 相似文献
10.
Emmanuel T Idowu Henry CN Ajaegbu Ahmed I Omotayo Oluwagbemiga O Aina Olubunmi A Otubanjo 《African health sciences》2015,15(4):1262-1270