Induction of proliferative lesions of ventral prostate, seminal vesicle, and other accessory sex glands in rats by N-methyl-N-nitrosourea: effect of castration, pretreatment with cyproterone acetate and testosterone propionate and rat strain.

Wistar (Cpb:WU), F344 or Sprague-Dawley rats were sequentially treated with cyproterone acetate (CA) for 21 days, testosterone propionate (TP) for 3 days, followed by a single i.v. injection of N-methyl-N-nitrosourea (MNU). One group of Wistar rats was castrated 4 weeks after MNU injection, and another group 58 weeks after MNU, when the first prostatic carcinoma was detected. Control groups received only CA + TP, CA, MNU, or they remained untreated. Early or late castration inhibited the development of atypical hyperplasia of the ventral prostate in Wistar rats. This lesion was induced by the CA + TP + MNU treatment in F344 rats, but not Sprague-Dawley rats; in Wistar rats, it was induced by CA + TP treatment, irrespective of whether MNU was given. Hypertrophic-hyperplastic lesions of the seminal vesicle were induced by MNU, irrespective of pretreatment, and their development was prevented by early castration and inhibited by late orchiectomy. Dorsolateral prostate carcinomas and preneoplasia occurred only in low incidence in Wistar and Sprague-Dawley rats. These lesions were absent in F344 rats that had received treatment with CA + TP + MNU. No dorsolateral prostate (pre)neoplasia was found in Wistar rats subjected to early orchiectomy, but rats castrated at 58 weeks had an incidence similar to that for the intact group treated with CA + TP + MNU. This finding supports the contention that androgens are required for the development of MNU-induced prostatic cancer in rats but that advanced carcinomas are androgen insensitive. Differences in incidence and localization of prostatic proliferative lesions between F344 and Wistar rats and between dorsolateral and ventral prostate could not be explained by differences in epithelial cell proliferative responses to CA + TP treatment at the time of MNU injection, since they were similar in ventral and dorsolateral prostate and were more prominent in F344 rats than in Wistar rats. DNA damage as estimated by MNU-induced unscheduled DNA synthesis also did not differ between dorsolateral and ventral prostate.     

4－氨基吡啶诱发组胺释放及某些药物的拮抗作用

４－氨基吡啶（４－ＡＰ）有组胺释放作用。小鼠ｉｐ４－ＡＰ５ｍｇ·ｋｇ－１后，肺中组胺含量明显减低，血中组胺含量显著增高。钙拮抗剂硝苯啶、ＴＭＢ－８及钾通道开放剂米诺地尔均能明显抑制４－ＡＰ诱发的小鼠ＰＭＣ释放组胺。结果提示，ＭＣ可能存在钾通道，４－ＡＰ诱发ＭＣ释放组胺可能与它阻滞钾通道，从而使钙通道开放，增加Ｃａ２＋内流有关。     

Long-term experience with implanted intrathecal drug administration systems for failed back syndrome and chronic mechanical low back pain

Background  

Continuous intrathecal drug delivery has been shown in open studies to improve pain and quality of life in those with intractable back pain who have had spinal surgery. There is limited data on long term effects and and even less for patients with mechanical back pain without prior spinal surgery.     

电化学方法研究环丙沙星及其镁、锰络合物与脱氧核糖核酸的相互作用

用电化学的方法,研究环丙沙星(CPFX)及其镁、锰络合物与脱氧核糖核酸(DNA)的相互作用及其极谱伏安行为。结果在0.1mol·L^-1NH₃-NH₄Cl(pH9.2)溶液中,环丙沙星可与DNA作用,产生一新的极谱峰 Ep=-1.72V(vsAg/AgCl),在有Mg²⁺或Mn²⁺存在时则生成三元络合物,产生一电位更负的新峰,峰电位Ep=-1.78V,提示Mg²⁺或Mn²⁺离子参与药物与DNA的作用。对它们的还原峰性质研究表明,电极还原反应是完全不可逆的,电流具有吸附性。本文还探讨了电极还原机理,认为参与电极还原的是三元络合物中的环丙沙星分子,进一步推测CPFX-Mg是嵌入DNA的双螺旋结构中。