松龄血脉康抑制肺动脉高压的实验研究

为观察松龄血脉康胶囊对肺动脉高压大鼠肺动脉压的影响，取１００只健康Ｗｉｓｔａｒ大鼠，其中６０只背部注射野百合碱ｍｏｎｏｃｒｏｔａｌｉｎｅ，ＭＣＴ８０ｍｇ／ｋｇ复制出肺动脉高压模型。再将其分为两组，各３０只，其中一组以标准饲料喂养，另一组加用松龄血脉康胶囊１．５ｇ·ｋｇ－１·ｄ－１。其余４０只健康大鼠做为正常对照组，在实验当天、７天、１４天、２１天、２８天、３５天从各组中随机抽取５只行右心导管测肺动脉压。结果：注射ＭＣＴ后肺高压组２８天时达高峰，但加用松龄血脉康组上升幅度明显小于未用药组。结论：松龄血脉康有显著抑制大鼠肺动脉高压发展的作用     

改良哈氏棒治疗胸腰段脊柱不稳定骨折

本文报告了作者研制的改良哈氏棒治疗胸腰段脊柱不稳定骨折的临床效果。１９９１年１月～１９９４年１０月，治疗２６例，伤椎椎体前缘高度从４１．９１％，恢复至９５．５７％，椎体后缘高度从８１．０３％恢复至１００％，后凸畸形（Ｃｏｂｂ氏法）从２６°恢复至５°，有５例恢复前凸８°～１０°，神经功能恢复１．８级（Ｆｒａｎｋｅｌ分级）。作者认为回复生理前凸的纵轴上纵向撑开力，更有助于胸腰段脊柱骨折的解剖复位。     

肥胖患者胰升糖素水平变化及其对空腹血糖的影响

目的　探讨肥胖患者胰升糖素的变化特点及其对血糖的影响。方法　将 82例患者根据体重指数分为 3组 :A组 (BMI <2 4,n =2 3 )、B组 (2 4≤BMI <2 7,n =2 7)、C组 (BMI≥ 2 7,n =3 2 ) ,分别测定胰升糖素、胰岛素、空腹血糖 ,采用单因素方差分析法与Spearman等级相关性分析法进行分析。结果　 3组胰升糖素分别为 (15 6.3± 5 8.6)、(186.7± 67.5 )、(2 2 2 .2± 88.4)ng·L-1,C组与A组比较有显著性差异 (P <0 .0 1) ;3组胰岛素分别为 (15 .4± 4.7)mIU·L-1、(2 0 .6± 9.6)mIU·L-1、(2 2 .3± 10 .6)mIU·L-1,B组、C组与A组比较差异有显著意义 (P <0 .0 5、P <0 .0 1) ;B、C两组胰升糖素与空腹血糖呈正相关。结论　肥胖患者胰岛素、胰升糖素一致性增高 ,胰升糖素的增高是空腹血糖增高的重要因素。     

HCV的检测方法

从发现丙型肝炎病毒以来 ,丙肝的检测技术发展迅速 ,灵敏度和特异性都有明显的提高 ,方法学在不断改进完善。笔者就近年来丙型肝炎的实验室检测方法作简要的综述     

卡介苗激活杀伤细胞抗膀胱肿瘤作用研究

为了进一步探讨ＢＣＧ抗膀胱肿瘤的作用机理，采取１５例膀胱肿瘤患者外周血单个核细胞（ＰＢＭＣ），置于含ＢＣＧ或ＩＬ２的培养基中培养，计算扩增倍数，检测培养细胞抗自体及异体膀胱癌细胞活性。结果：卡介苗激活杀伤细胞（ＢＡＫ）与淋巴因子激活杀伤细胞（ＬＡＫ）分别于培养第７和第３天达增殖高峰，对自体瘤杀伤率分别为３６．２％和３１．４％，差异有显著性（Ｐ＜０．０５）；对异体瘤杀伤率分别为２５．２％和２８．３％，差异无显著性。结果表明：ＢＡＫ细胞抗自体瘤活性高于ＬＡＫ细胞，死ＢＣＧ对ＰＢＭＣ无激活作用，ＢＡＫ细胞抗肿瘤效应可能是ＢＣＧ抗膀胱肿瘤重要作用机理之一。     

新疆乌鲁木齐县农村住宅卫生设施状况的调查与评价

本文报告了乌鲁木齐县两种不同类型住宅的卫生设施状况，重点对上下水设施，厕所及周围卫生状况进行了调查。结果表明：小二楼住宅有给排水设施及卫生间；砖土木结构平房内只有上水（自来水），但无下水道及卫生间。因均饮用城市自来水，故两类住宅人群肠道传染病发病率无显著性差异（Ｐ＞０．０５）。对Ｂ村六年几种肠道传染病发病率的动态分析表明，改水是预防和降低肠道传染病发病的有效措施。调查结果还表明，住宅设施完善与否，     

原发性甲状旁腺功能亢进的骨骼X线分析(附36例报告)

本文分析了36例原发性甲状旁腺功能亢进的骨骼X线改变,认为主要的骨病征象可概括为指骨的骨膜下骨吸收、颅骨的磨玻璃样及颗粒状改变、骨皮质下的囊肿样改变和棕色瘤,骨的突起或肌腱韧带附着处的骨吸收,以及软骨下骨吸收。骨皮质下囊变的征象对鉴别诊断很有帮助。作者认为骨质疏松和反复泌尿系结石可提示甲状旁腺功能亢进的早期表现,应及时检查血钙磷以确诊。     

Coplanar PCBs in fish and mussels from marine and estuarine waters of New York State.

Thirty samples of striped bass from marine and estuarine waters of New York State, six samples of mussels from Long Island Sound, and one composite sample of freshwater mussels from Troy were analyzed by a recently developed method which combines sulfuric acid cleanup, carbon chromatography, and high-resolution gas chromatography for the determination of non-ortho- and mono-ortho-substituted polychlorinated biphenyls (PCBs), which are biologically active congeners of PCBs and approximate isostereomers of 2,3,7,8-tetrachlorodibenzo-P-dioxin of (2,3,7,8-TCDD). Non-ortho coplanar PCBs ranged from 0.2 to 37.1 ppb in fish. The highest concentrations of 37.1 ng/g of 3,3',4,4'-tetrachlorobiphenyl (77) and 7.5 ng/g of 3,3',4,4',5-pentachlorobiphenyl (126) were detected in a fish caught near Troy/Albany, New York. Mono-ortho-substituted PCBs ranged from 0.4 to 790 ppb in fish, with the major components identified as 2,3',4,4',5-penta-(118) and 2,3,3',4,4'-pentachlorobiphenyls (105). When concentrations were converted to 2,3,7,8-TCDD picogram equivalents, 99% of the equivalents were derived from three congeners (77, 105, and 126), 3,3',4,4',5-pentachlorobiphenyl (126) accounting for approximately 80% of the activity. At Troy pg/g TCDD equivalents derived from PCB were approximately 3000, whereas the actual 2,3,7,8-TCDD concentration was only 20 pg/g; hence, accurate coplanar PCB measurement is important.     

Inhibition of GABA-gated chloride channel function by arachidonic acid

The effects of arachidonic acid and its metabolites on gamma-aminobutyric acid (GABAA) receptor function were determined in rat cerebral cortical synaptoneurosomes. Incubation of synaptoneurosomes with phospholipase A2 decreased muscimol-induced 36Cl- uptake. Arachidonic acid, the major unsaturated fatty acid released by phospholipase A2, also inhibited muscimol-induced 36Cl uptake. Similar inhibition was obtained with other unsaturated fatty acids (docosahexaenoic, oleic) but not with saturated fatty acids (stearic, palmitic). The effect of arachidonic acid on muscimol responses was inhibited by bovine serum albumin (BSA), and BSA enhanced muscimol responses directly, indicating the generation of endogenous arachidonic acid in the synaptoneurosome preparation. The generation of endogenous arachidonic acid was also indicated by the ability of 2 inhibitors of arachidonic acid metabolism, indomethacin and nordihydroguaiaretic acid (NDGA), to inhibit muscimol-induced 36Cl uptake. We conclude that arachidonic acid probably has both direct and indirect actions on muscimol responses since both enzyme inhibitors inhibited muscimol responses but did not prevent the effect of exogenously added arachidonic acid. In additional experiments, arachidonic acid metabolites generated by cyclooxygenase, prostaglandins D2, E2 and F2 alpha, each decreased muscimol responses; prostaglandins F2 alpha was the most potent inhibitor. Since the unsaturated fatty acids and their metabolites are most susceptible to peroxidation, a generating system of superoxide radicals was tested on muscimol responses. A combination of xanthine and xanthine oxidase inhibited muscimol-induced 36Cl uptake in a concentration-dependent manner. We propose that the inhibition of GABAA neurotransmission by arachidonic acid and its metabolites can lead to increased neuronal excitability. This mechanism may play an important role in the development of neuronal damage following seizures or cerebral ischemia.