XW630对去卵巢大鼠骨质疏松的作用(英文)

目的:研究XW630对去卵巢大鼠骨质疏松的影响。方法:血清E_2和骨钙素(BGP)浓度用放射免疫测定法。骨组织计量学用四环素内标法。结果:去卵巢后,血清E_2水平下降61.9％,子宫减轻72.7％,动情次数减少63.6％。XW630治疗13周后,血清BGP浓度增加75.7％,动情次数略增加,但低于假手术组,血清E_2浓度及子宫重量无明显变化。与OVX组相比,XW630组骨组织计量学指标TBV/TTV,TBV/SBV和MTPD增加;Sfract(s),Sfract(d),TOS和Svf增加,OMP缩短。结论:XW630增加骨激活频率、骨小梁连接性、稳定性和张力。表明XW630促进骨形成、抑制骨吸收,对生殖系统无影响。     

针刺对小鼠实验性前列腺增生的防治作用

目的：探讨针刺治疗前列腺增生症的作用机理。方法：采用丙酸睾丸素皮下注射造成小鼠前列腺增生模型，通过针刺白环俞、会阴旁、委阳和三阴交穴，观察针刺对前列腺湿重、组织形态、血清睾丸酮、雌二醇、酸性磷酸酶含量的影响。结果：针刺对丙酸睾丸素引起的小鼠前列腺增生有显著的抑制作用，可使增生的前列腺重量明显减轻，腺上皮细胞增生明显减少，并能降低血清睾丸酮含量，抑制酸性磷酸酶活性，升高雌二醇含量。结论：针刺治疗前列腺增生症的作用机理与降低血清睾丸酮含量，升高雌二醇含量，抑制酸性磷酸酶的活性有关。     

Bidirectional Regulatory Effect of Lishen Injection(丽参注射液)on Sex Hormones in Senile Female Patients Coronary Heart Discase of kidney deficiency Type

Ｂｉｄｉｒｅｃｔｉｏｎａｌ　Ｒｅｇｕｌａｔｏｒｙ　Ｅｆｆｅｃｔ　ｏｆ　Ｌｉｓｈｅｎ　Ｉｎｊｅｃｔｉｏｎ（丽参注射液）ｏｎ　Ｓｅｘ　Ｈｏｒｍｏｎｅｓ　ｉｎ　Ｓｅｎｉｌｅ　Ｆｅｍａｌｅ　Ｐａｔｉｅｎｔｓ　ｗｉｔｈ　Ｃｏｒｏｎａｒｙ　Ｈｅａｒｔ　Ｄｉｓｅａ...     

雌二醇透皮控释贴片的初步稳定性研究

采用加速试验法测试雌二醇控释贴片的稳定性,并作室温留样观察。结果表明,加速试验前后样品的外观不变,药物含量及粘着强度稳定,薄层色谱未见分解产物;室温留样1年,各项指标均符合质量标准。推测样品室温贮存有效期可达2年。     

雌二醇诱发大鼠高血压后相关组织中Ca，Cu及Zn含量的变化

①目的探讨雌二醇诱发大鼠血压升高与某些离子的关系。②方法用原子吸收分光光度法（火焰法），检测了雌二醇诱发血压升高组及对照组大鼠血清、延髓、肾上腺、心肌和肾脏组织中Ｃａ２＋，Ｃｕ２＋和Ｚｎ２＋的含量，经ｔ检验统计处理。③结果与对照组相比，实验组大鼠血清和延髓中Ｃａ２＋的含量增加（ｔ＝２．３０３，Ｐ＜０．０５；ｔ＝２．０８５，Ｐ＜０．０５），而肾上腺和心肌中Ｃａ２＋含量减少（ｔ＝３．５１０，Ｐ＜０．０１；ｔ＝２．１０４，Ｐ＜０．０５）。血清和肾脏中Ｃｕ２＋含量增加（ｔ＝２．４５４，Ｐ＜０．０５；ｔ＝２．５６４，Ｐ＜０．０１），而延髓中Ｃｕ２＋含量减少（ｔ＝２．２５４，Ｐ＜０．０５）。延髓和肾上腺Ｚｎ２＋含量增高（ｔ＝２．５０２，Ｐ＜０．０５；ｔ＝２．１４７，Ｐ＜０．０５），而心肌和肾脏Ｚｎ２＋含量减少（ｔ＝２．０７７，Ｐ＜０．０５；ｔ＝２．４９８，Ｐ＜０．０５）。④结论Ｃａ２＋，Ｃｕ２＋和Ｚｎ２＋可能参与雌二醇诱发大鼠高血压     

Effect of chronic treatment with an estrogen-progestogen combination on beta adrenergic-induced thirst.

Rats chronically administered various doses of the estrogenic agent, ethinyl estradiol, combined with the progestogen, norethynodrel, showed an estrogen-related, dose-dependent decrease in water intake in response to acute SC administration of the beta adrenergic agonist, isoproterenol (200 μg/kg of body wt). Conversely, rats receiving a constant dose of ethinyl estradiol (16 μg/kg/day) combined with norethynodrel (233 μg/kg/day) for 7 weeks drank significantly less water in response to graded doses of isoproterenol (10, 25, 50, 100 and 200 μg/kg) than controls. The slope, but not the intercept, of the regression line relating water intake to dose of isoproterenol administered was reduced significantly in the steroid-treated group. Furthermore, water intake of the treated group in response to acute administration of either epinephrine (1 mg/kg) or serotonin (1 mg/kg) was significantly less than control. These data suggest that chronic treatment with ethinyl estradiol, combined with norethynodrel, reduced beta-adrenergic responsiveness. In addition, rats treated with the same combination of ethinyl estradiol and norethynodrel showed a reduced drinking response to an osmotic thirst stimulus, i.e., IP load of 1 M NaCl solution at 1% of body wt. The fact that the response to both types of thirst stimuli was attenuated in rats receiving an estrogen combined with a progestogen suggests the possibility that treatment may have affected thirst mechanisms at the level of the central nervous system.     

Plasmacytoid blast crisis in B-cell chronic lymphocytic leukemia: effect of estradiol on growth and differentiation in vitro

Evolution of a case of chronic lymphocytic leukemia (CLL) into blast crisis was found to be characterized by three unusual features (1) the phenotype of the emerging blast cells was that of pre-plasmacytoid cells as shown by plasma cell morphology and an immunological phenotype corresponding partially with CLL- or intermediate B-cells, partially with plasma cells (terminal transferase-, common acute lymphocytic leukemia antigen-, Ia+, surface immunoglobulin heavy chains-, surface kappa light chains+, intracytoplasmic immunoglobulin A+ and G+, BA-1+, polyclonal gammaglobulin production); (2) cytogenetic analysis of spontaneous metaphases revealed that in addition to the typical CLL abnormality, trisomy 12, in all of the cells, an additional translocation between chromosomes 14 and 17 was present in 40% with a presumptive breakpoint on chromosome 14 (q12-3) never described before (commonly q32) and (3) the progression of the disease was associated with a striking increase in the expression by the transformed cells of specific binding sites for estradiol (E2) due to an actual increase in total cellular receptor proteins and not to a change in receptor affinity for E2. The functional status of the steroid receptors was confirmed by nuclear transfer of the cytoplasmic hormone-receptor complex upon temperature activation. Since the rise in E2-receptor display paralleled a large increase in the proliferative activity of the cells as well as a change in their maturation status the question was raised as to whether the E2-receptor should be considered as a physiological marker of growth rate or of cellular differentiation. Exposure of the patient's blast cells to E2 in vitro resulted in cessation of cell growth following at least one mitosis after addition of the inducer as seen from the replacement of the large blasts by small CLL-like cells without definite signs of alteration of the differentiation status. This suggests the association of E2-receptor expression with control of growth rather than cell maturation.     

The endometrial nuclear estradiol receptor of the pregnant cow has a molecular weight of 53,000 in 6 M guanidine-HCl.

Cell nuclei isolated from the endometrium of the 3 months pregnant cow were dialysed against 6 M guanidine-HCl + 0.1 M 2-mercaptoethanol. The resulting material (after eliminating the bulk of DNA by centrifugation) was filtered on a Sepharose 6/b column equilibrated in the above denaturing solvent. The molecular weight of the denatured "nuclear" estradiol receptor, estimated by a method described previously (T. Erdos and J. Fries (1974) Biochem. Biophys. Res. Commun. 58, 932-939), was about 53,000. This value is similar to that of the cytoplasmic receptor (55,000) but dissimilar to that of the cytoplasmic receptor transformed by the action of the Receptor Transforming Factor (35,000) estimated under the same experimental conditions, suggesting that the latter form of the receptor is not the biological precursor of the "nuclear" receptor. However, according to indirect estimates, probably not more than 10% of the "nuclear" receptor has been renatured in these experiments. Therefore the alternative that the results obtained are not representative for the "nuclear" receptor, cannot be excluded.     

Myometrial cells in primary culture: Characterization and hormonal profile

A method for primary culture of ovine myometrial cells is described. After dissection, myometrium of ewe uteri was digested in trypsin and collagenase. The cells were preplated for l h at 37°C. The non-attached cells were grown in appropriate medium supplemented with 2% fetal calf serum. They had a doubling time of 3 days, reached confluency at 10 days and did not exhibit contact inhibition. Cultures were maintained up to 22 days. Characterization of the cells was achieved by electron microscopy, analysis of myosin in cell extracts and assessment of hormone sensitivity. The cells were found to contain myofilaments,Characteristic of smooth muscle. A high content of myosin (6–13%) was demonstrated on SDS-polyacrylamide gel electrophoresis: this was confirmed by ATPase activity assay. Cells responded to estradiol stimulation by increased protein synthesis, and bound [³H]estradiolin a specific and saturable way.These results suggest that myometrial cells grown in primary culture should provide a useful model for studying the hormonal control of contractile protein synthesis.     

Modulation of hypoglycemia-induced increases in plasma epinephrine by estrogen in the female rat

Clinical studies have demonstrated that estrogen replacement therapy suppresses stress-induced increases in plasma catecholamines. The present study determined whether normal circulating levels of estrogen can modulate hypoglycemia-induced increases in plasma epinephrine (EPI). In anesthetized female rats, insulin-induced hypoglycemia (0.25 U/kg) increased plasma EPI concentration to a significantly greater extent in 14-day ovariectomized (OVEX) rats compared to that in sham-operated controls. In 17beta-estradiol (E2)-replaced OVEX rats, the hypoglycemia-induced rise in plasma EPI was reduced significantly when compared to that in vehicle-replaced OVEX rats. OVEX and E2 replacement had no effect on tyrosine hydroxylase or phenylethanolamine N-methyltransferase mRNA levels in the adrenal medulla. In isolated adrenal medullary chromaffin cells, agonist-induced increases in intracellular Ca2+ were unaffected by 48-hr exposure to 10 nM E2. In contrast, acute (3-min) exposure to micromolar concentrations of E2 dose-dependently and reversibly inhibited agonist-induced Ca2+ transients. In addition, in OVEX rats, a constant infusion of E2 significantly reduced the insulin-induced increase in plasma EPI concentration compared to that in vehicle-infused controls. These data demonstrate that physiologic levels of circulating E2 can modulate hypoglycemia-induced increases in plasma EPI. This effect seems independent of steroid influence on adrenal medullary secretion or biosynthesis. In contrast, acute exposure to high levels of E2 can also suppress hypoglycemia-induced increases in plasma epinephrine, due at least in part to inhibition of stimulus-secretion coupling.