丁香郁金配伍的药理研究

丁香郁金配伍属中药配伍禁忌“十九畏”之一，本文就二者单独使用和配伍后的抗炎、镇痛、止泻、抗溃疡等指标进行了动物药效学试验。二药配伍后镇痛、抗炎及止泻作用有下降趋势；抗溃疡作用不受影响；对试验动物胸腺指数和脾脏指数无明显影响。实验结果，二者配伍似属“相恶”。     

产科诊断剂量超声波对培养细胞影响的实验研究

采用模拟在人体中使用的实测超声剂量，对体外培养的Ｌ－９２９株细胞进行辐照，通过细胞回复能力试验，观察回复前后的细胞增殖与抑制。对体外培养的人胚肺纤维细胞经１次及５次辐照，观察了ＤＮＡ及细胞核面积的影响。并通过电镜观察了细胞超微结构的变化。上述实验结果，均提示经辐照后细胞有增殖趋向     

The effect of fluconazole and ketoconazole on the metabolism of sulphamethoxazole

1 Cytochrome P450-mediated bioactivation of sulphamethoxazole to a hydroxylamine has been implicated in the hypersensitivity reactions associated with co-trimoxazole administration. Inhibiting the formation of the hydroxylamine may be one method of preventing the high frequency of toxicity which is observed in HIV-infected patients. Therefore, in this study, we have investigated the ability of fluconazole and ketoconazole, known cytochrome P450 inhibitors, to inhibit the formation of sulphamethoxazole hydroxylamine.
2 Ten healthy male volunteers were given co-trimoxazole (800  mg sulphamethoxazole and 160  mg trimethoprim) alone or 1  h after either fluconazole (150  mg) or ketoconazole (200  mg) in a randomized fashion with a washout period of at least 1 week between each phase. Urine was collected for 24  h, and sulphamethoxazole and its metabolites were quantified by electrospray LC-MS.
3 Ketoconazole had no effect on the urinary recovery of sulphamethoxazole or any of its metabolites. In contrast, fluconazole significantly ( P <0.001) inhibited the formation of sulphamethoxazole hydroxylamine by 50.0±15.1%. Fluconazole also inhibited the oxidation of sulphamethoxazole to the 5-methylhydroxy and 5-methylhydroxy acetate metabolites by 69.9±15.8% and 64.0±12.0%, respectively, but had no effect on the amount of sulphamethoxazole, N₄-acetyl sulphamethoxazole, or sulphamethoxazole N₁-glucuronide excreted in urine.
4 The potential clinical benefit of using fluconazole to prevent hypersensitivity to co-trimoxazole in patients with AIDS needs to be assessed in a prospective study using both metabolite formation and the clinical occurrence of adverse reactions as end-points.     

THE INTERACTION BETWEEN ENALAPRILAT AND SELECTED α-ADRENOCEPTOR ANTAGONISTS IN ISOLATED RAT TAIL ARTERIES

1. Isolated perfused rat tail artery preparations were used to investigate the effects of the angiotensin converting enzyme inhibitor enalaprilat on the actions of a series of α-adrenoceptor antagonists. The agonist used was phenylephrine. 2. Enalaprilat (1 μmol/L) potentiated the competitive α₁-adrenoceptor antagonist actions of phentolamine (10–100 nmol/L) and yohimbine (0.3–3.0 μmol/L) as well as the non-competitive antagonist action of phenoxybenzamine (50–100 pmol/L). 3. The competitive α₁-adrenoceptor antagonist action of prazosin (1–10 nmol/L) was not affected by enalaprilat. 4. For the competitive α₁-adrenoceptor antagonists, including prazosin, there appeared to be an inverse relationship between antagonist potency and the extent of potentiation by enalaprilat. 5. The results support the hypothesis and angiotensin II modulates vascular smooth muscle α₁-adrenoceptor function.     

Competition for sucrose-pellets in triads of male wistar rats: effects of acute and subchronic chloridazepoxide

Within triads of male Wistar rats, some animals almost completely abstain from competition for palatable sucrose pellets (so-called poor-performing rats), whereas other rats consistently win the competition (so-called high-performing rats). Subchronic (5 mg/kg; 5 consecutive days), but not acute (0.1–20 mg/kg), treatment with chlordiazepoxide temporarily helped poor-performing rats to behave more competitively. This finding, considered together with parallel studies (using high-performing rats), suggested that chloridazepoxide's beneficial effect was only demonstrable when the poor-performing rats had become tolerant to the drug's initial sedative effect.     

钕激光照射对大鼠肿瘤生长的抑制作用

目的:研究钕激光照射对大鼠肿瘤生长的抑制作用.方法:采用钕激光在实验组荷瘤大鼠的肿瘤区及其肿瘤区周围进行照射,并观察抑制肿瘤的效果.结果:实验组大鼠肿瘤体的生长速度明显慢于对照组大鼠肿瘤体的生长速度.结论:用钕激光照射对抑制癌肿瘤的生长速度有明显的作用.     

Proliferation of DU145 prostate cancer cells is inhibited by suppressing insulin-like growth factor binding protein-2

BACKGROUND: Insulin-like growth factor binding protein-2 (IGFBP-2) is expressed by all human prostate cancer cell lines and dramatically increases in the serum of prostate cancer patients. However, the role of IGFBP-2 in prostatic tumorigenesis is not known. The aim of the present study was to investigate the effects of IGFBP-2 on the proliferation of DU145 human prostate cancer cells in culture. METHODS: Using cell proliferation assays, we examined the effects of exogenously administered and endogenously modulated levels of IGFBP-2 on the proliferation of DU145 cells. RESULT: Cell growth was stimulated by exogenously administered IGFBP-2, but significantly retarded (P < 0.05) by its neutralizing antibody. Overexpression of IGFBP-2 by transfection also stimulated cell growth, which was significantly (P < 0.05) inhibited in transfectants expressing antisense mRNA to IGFBP-2. Furthermore, the proliferation of IGFBP-2 overexpressing cells was significantly dampened by exogenously administered IGFBP-2 antibody. CONCLUSIONS: IGFBP-2 is an autocrine growth factor for DU145 human prostate cancer cells and cell proliferation can be significantly retarded by neutralizing or inhibiting its synthesis. These findings provide a strong rationale for targeting IGFBP-2 in the testing of novel strategies to treat prostate cancer.     

牡蛎功能短肽的制备及ACE抑制活性

以新鲜无壳牡蛎为原料,采用酶水解的方法制备牡蛎短肽,经SephadexG 15分离,并用HPLC测定其相对分子质量分布,通过HPLC法定量马尿酸测定各组分的ACE(血管紧张素转化酶)抑制活性。结果表明,牡蛎水解液中相对分子质量较大和较小部分的ACE抑制活性偏低,只有相对分子质量在一定范围内的短肽,对ACE具有较好的抑制作用,质量浓度为0.4mg/mL的牡蛎功能短肽的ACE抑制率为51.4%.     

JX-1对雄性小鼠生殖细胞致突变作用的研究

本文采用小鼠精子试验和小鼠睾丸DNA合成抑制试验,检测了JX-1对雄性生殖细胞的致突变作用。实验结果表明JX-1对小鼠精子总数、精子活动率及精子畸形率均无统计学意义的增加,与小鼠睾丸DNA合成抑制试验阴性反应一致。作者认为JX-1对雄性生殖细胞为一种非诱变剂。