选择性κ阿片激动剂K-Ⅱ与U-50488的药理作用比较

K-Ⅱ系k阿片激动剂U-50488的同类物。通过部分离体和整体实验比较了K-Ⅱ与U-50488的药理作用。实验发现,K-Ⅱ抑制电刺激兔输精管收缩的IC₅₀值为0.42 nmol/L,U-50488为26.5 nmol/L;K-Ⅱ抑制小鼠运动功能(横筛法)的ED₅₀值为1.7 mg/g,U-50488为15.3 mg/kg;K-Ⅱ的小鼠LD₅₀值为152.5 mg/kg,U-50488为118.4 mg/g;K-Ⅱ明显降低小鼠自发活动的作用比U-50488强5倍。结果表明,K-Ⅱ是一个药理作用较U-50488强的k受体激动剂。     

Toxicity of 5-methoxymethyl-2'-deoxyuridine in hamsters and evaluation of its mutagenicity by sister chromatid exchanges and hypoxanthine guanine phosphoribosyl transferase assays

Toxic effects of 5-methoxymethyl-2'-deoxyuridine (MMdUrd), a drug with antiviral activity against herpes simplex virus, were investigated in Chinese golden hamsters. Pathological, hematological, and clinical chemistry parameters were studied. Systemic toxicity was not observed in hamsters after intraperitoneal (ip) administration of MMdUrd in single doses up to 3000 mg/kg and in repeated dosages of 600 mg/kg daily for 15 days. No gross or microscopic lesions related to MMdUrd treatment were observed in the tissues examined from the animals of subchronic toxicity study. Administration of a single dose of 6000 mg/kg of MMdUrd ip caused cloudy swelling, increased mitotic figures, varied nuclear sizes, and scattered coagulation necrosis of hepatocytes on the second day after drug administration. These hepatic lesions were not observed in animals sacrificed on the fourth and sixth days postadministration of MMdUrd. Microscopic examination of marrow smears from control and MMdUrd-treated animals revealed no differences in morphological features of hematopoiesis, nor were significant differences observed between treated and control animals for hematological parameters. Increased concentrations of alanine amino transferase were observed on the first and second day in animals, given a single dose of 6000 mg/kg of MMdUrd. Increases in sister chromatid exchanges and the number of azaguanine-resistant mutants were observed after exposure to a high concentration of MMdUrd (1024 micrograms/ml).     

用气相色谱研究抗氧化剂对膜脂肪酸的保护作用

本文应用气相色谱技术直接测定三种生物膜(人红细胞膜,人血小板膜和鼠肝线粒体膜)多不饱和脂肪酸的含量变化,检测脂质过氧化程度。实验证实几种多羟酚类化合物(儿茶精,阿魏酸钠和没食子酸及其衍生物)不同程度地抑制(OH)诱导的脂质过氧化反应,并呈量效和构效关系。这类抗氧化剂对保护生物膜的结构与功能是有益的。     

关于全科医生若干问题的答复

本对医学院校学生就全科医生有关问题给于相应的答复，其中还包括自１９９７年以来由美国全科医学会举办的学生代表大会上所提出的一些问题，例如：什么是全科医生？全科医生的行业范围是什么？全科医生的工作，生活及收入情况如何等等问题。（Ａｍ．Ｆａｍ．Ｐｈｙｓｉｃｉａｎ１９９０．６０：１６７－１７４）。     

骨纤维结构不良的诊断和治疗进展

目的:对长期以来关于骨纤维结构不良大量相关研究及文献进行回顾,综述骨纤维结构不良的诊断和治疗的最新进展。资料来源:通过计算机互联网检索OVID数据库1966-01/2006-10关于骨纤维结构不良的文献,检索词:Osteofibrous dysplasia,限定语言种类为English。同时检索1994-01/2006-10中国全文期刊数据库有关骨纤维结构不良的文献,检索词为:骨纤维结构不良,限定语言种类为中文。资料选择:选择与骨纤维结构不良相关的观察对比研究、经验总结、个案报道、最新研究进展等文献,力求资料全面,排除重复研究。资料提炼:共收集相关国内外文献41篇,排除重复性研究11篇,采用30篇,包括关于骨纤维结构不良定义、发病机制、病理、诊断及治疗等。资料综合:①骨纤维结构不良是一种起源于纤维组织的良性骨肿瘤。发病率低、误诊率高。目前具体发病机制不明,现认为与常染色体显性遗传有关。②骨纤维结构不良好发于胫骨,症状为局部肿块。特征性影像学表现为胫骨中段前侧皮质膨胀性密度减低。确诊方法为病理检查。重点与骨纤维异常增殖症、造釉细胞瘤相鉴别,现有大量研究证明该病与造釉细胞瘤有联系。③治疗上过去认为10岁以前应保守治疗,10岁后选择手术治疗,目前倾向于早期骨膜外切除手术治疗。结论:骨纤维结构不良发病率低,对该病认识较少,误诊率较高,重点需与骨纤维异常增殖症、造釉细胞瘤相鉴别,应提高对该病的认识与重视程度,对可疑者行病理检查,确诊者行骨膜外切除,切除范围较大的病例行重建手术。