吡喹酮杂质的研究

用LC-MS和HPLC法以对照品对照,确定吡喹酮合成过程中产生的主要杂质是(1,11b)-位不饱和的吡喹酮,利用催化氢化法可把含该杂质过量的吡喹酮粗品转化为合格品.     

中药复方抗癌实验研究进展

抗癌中药复方是中医临床预防、治疗肿瘤的主要途径，明确中医药复方的抗癌机理，则是指导临床用药，发现更有效的抗癌新药的关键。回顾近10年抗癌复方的实验研究，从建立动物模型、提取有效成分、探讨抑瘤作用、调节免疫功能等方面进行总结。     

松果菊润喉片的免疫药理学研究

目的 观察松果菊润喉片对小鼠免疫功能及其化痰的影响。方法 进行免疫及化痰实验。结果 松果菊润喉片能增强小鼠腹腔巨噬细胞碳粒廓清速度,促进抗体(溶血素)水平的产生,促进二硝基氯苯所引发的迟发性变态性反应的足趾肿胀;对气管黏膜排泄酚红有明显促进作用。结论 松果菊润喉片有促进排痰、提高机体免疫功能的作用。     

Effects of thimerosal on NGF signal transduction and cell death in neuroblastoma cells.

Signaling through neurotrophic receptors is necessary for differentiation and survival of the developing nervous system. The present study examined the effects of the organic mercury compound thimerosal on nerve growth factor signal transduction and cell death in a human neuroblastoma cell line (SH-SY5Y cells). Following exposure to 100 ng/ml NGF and increasing concentrations of thimerosal (1 nM-10 microM), we measured the activation of TrkA, MAPK, and PKC-delta. In controls, the activation of TrkA MAPK and PKC-delta peaked after 5 min of exposure to NGF and then decreased but was still detectable at 60 min. Concurrent exposure to increasing concentrations of thimerosal and NGF for 5 min resulted in a concentration-dependent decrease in TrkA and MAPK phosphorylation, which was evident at 50 nM for TrkA and 100 nM for MAPK. Cell viability was assessed by the LDH assay. Following 24-h exposure to increasing concentrations of thimerosal, the EC50 for cell death in the presence or absence of NGF was 596 nM and 38.7 nM, respectively. Following 48-h exposure to increasing concentrations of thimerosal, the EC50 for cell death in the presence and absence of NGF was 105 nM and 4.35 nM, respectively. This suggests that NGF provides protection against thimerosal cytotoxicity. To determine if apoptotic versus necrotic cell death was occurring, oligonucleosomal fragmented DNA was quantified by ELISA. Control levels of fragmented DNA were similar in both the presence and absence of NGF. With and without NGF, thimerosal caused elevated levels of fragmented DNA appearing at 0.01 microM (apoptosis) to decrease at concentrations >1 microM (necrosis). These data demonstrate that thimerosal could alter NGF-induced signaling in neurotrophin-treated cells at concentrations lower than those responsible for cell death.     

冶炼厂烟尘PM_(2.5)复合污染探讨

目的　通过本研究确定 ,现有除尘设备是否还存在PM2 5复合污染。方法　通过化学、电子显微镜及电子能谱、GC MS等仪器对上述样品多种污染成分及粒径进行定性、定量测定。结果　上述复合污染成分 :水 2 2 % ,有机物 34 75 % ,无机物 4 3 75 %。无机物以Cu、C、Pb、Al为主 ,它们的粒径≤ 1 1μm ,有机污染物14 0多种 ,以酚类及PAHs为主 ,无机物中除铅、砷等重金属 ,还有砷酸、磷酸。结论　在现有除尘设备条件下的冶炼厂烟尘污染为多种重金属、酸性氧化物及几十种有机污染物 (酚类及PAHs)的复合污染 ,它们的粒径分布大多≤ 1 1μm。     

锂的神经元保护作用及对铅神经毒性的拮抗效应

目的　探讨铅的神经毒性、锂的神经元保护作用以及锂对铅神经毒性的拮抗效应 ,研究不同浓度氯化锂和醋酸铅对原代培养皮层神经元生长及存活的影响。方法　建立新生大鼠皮层神经元原代培养技术 ,通过加入不同浓度氯化锂、醋酸铅及同时加入 5mmol L的氯化锂和不同浓度醋酸铅 ,显微镜下观察神经细胞的生长和存活情况 ,目镜测量神经元突起长度 ,噻唑蓝 (MTT)还原法检测细胞生长活力。结果　各浓度氯化锂均可促进神经元突起生长 (P <0 0 5 ) ,1 2 5mmol L以上浓度的氯化锂可使神经元生长活力降低 (P <0 0 5 ) ;醋酸铅 (≥ 10 - 7mol L)能抑制神经元生长 ,其神经元突起长度明显短于对照组 (P <0 0 1) ,各浓度的醋酸铅均可使神经元生长活力降低 (P <0 0 1) ;5mmol L浓度的锂对染铅神经元有明显的保护作用和促生长作用 ,表现为铅浓度为 10 - 6 mol L与 10 - 5mmol L组的神经元突起长度较单纯染铅组长 (P <0 0 1) ,使铅浓度为10 - 8～ 10 - 5mol L的神经元生长活力提高 (P <0 0 1)。结论　锂有神经元保护作用 ,而铅对神经元表现出毒性效应 ;锂对染铅神经元有一定的保护作用     

化合物Ib对阿霉素肾病大鼠干预效果的实验研究

目的了解血管紧张素受体拮抗剂化合物Ib对大鼠阿霉素肾病综合征病理及相关临床指标的干预作用及可能机制。方法采用阿霉素肾病(AN)模型,将70只大鼠分为阿霉素肾病组、化合物Ib(5 mg/kg,10 mg/kg,20 mg/kg)组和坎地沙坦酯治疗组,检测大鼠给予药物治疗后24 h尿蛋白排泄量、血清总蛋白、白蛋白及总胆固醇等血生化指标变化,并设正常对照组。结果化合物Ib(5 mg/kg,10 mg/kg,20 mg/kg)可明显降低造模大鼠24 h尿蛋白含量,增加血总蛋白及白蛋白含量,降低总胆固醇含量。结论化合物Ib对阿霉素肾病大鼠的肾脏具有保护效应,减轻肾损伤,降低蛋白尿。     

乐胃饮干预功能性消化不良大鼠SP和VIP的研究

[目的]通过实验研究,揭示乐胃饮治疗功能性消化不良的作用机制。[方法]Wistar大鼠随机分为正常对照组、自然恢复组、吗叮啉组、参苓白术丸组、乐胃饮低剂量组、乐胃饮中剂量组、乐胃饮高剂量组等7组,每组6只。分别给予各组按2ml/100g按组分别灌服蒸馏水、吗叮啉、参苓白术丸液、乐胃饮低中高剂量液,每天1次,自造模结束后一天起连续给药14天。观察胃黏膜形态,检测胃肠激素SP和VIP。[结果]乐胃饮能有效增加实验鼠胃窦组织中SP和降低VIP含量。[结论]乐胃饮能提高胃肠道神经兴奋性,调节胃肠道平滑肌的收缩,这可能是乐胃饮治疗FD的主要作用机制。     

Stretch of mammalian nerve in vitro: effect on compound action potentials

Stretch of nerve has been reported to decrease the amplitude of the compound action potential (CAP) with a complete block appearing in approximately 30 minutes. But for the most part, those experiments were carried out in vivo, and it is generally accepted that the failure of responses was due to a closure of vessels supplying the nerve with a resulting ischemia and anoxia. These studies were undertaken to determine if stretch of nerve has effects that are independent of interference with its vascular supply. In the studies, lengths of rat sciatic and dog peroneal nerves were removed and placed in a chamber supplied with oxygen in which their CAPs were continuously elicited and recorded. This in vitro preparation obviated interference with the nerve's metabolism on stretching. We have previously shown that the form change termed 'beading,' appearing within 10 seconds and reversing as quickly on relaxation, can be elicited with tensions of only several grams. We wished to determine if stretch adequate to produce beading could alter CAPs with the same rapidity. Tensions below 2 g had little effect. On applying tensions of 10-100 g, levels well above those needed to bead the fibers, both increases and decreases of CAP amplitude were seen. The changes occurred within 10 seconds of stretch application, the time at which beading arises with stretch. Although the decreases of CAP amplitudes could be accounted for by beading, the degree of CAP change did not correspond to the amount of tension applied. We hypothesize that the constrictions in the beaded fibers increase axial resistivity and diminish local currents so as to block conduction. The lack of an increasing degree of decreased CAP amplitude with increases in tension is ascribed to the inhibition of elongation offered by the collagen fibrils present in nerve. Collagenase applied to nerves allowed a further increase in length, producing a 'hyperbeading,' showing much longer lengths of beading constrictions on stretch. This would further increase axial resistance and is taken to account for the greater decreases of CAP amplitudes seen following collagenase treatment. To account for those cases where increases of CAP amplitude were seen on stretch, we hypothesize that stretch can also cause an increase in the excitability of the nodes. The outcome of stretch in any given nerve would be the resultant of two opposing actions; beading of the internodes causes a decrease of local currents leading to block of CAPs, while an increased excitability of the nodes acts to augment the responses.     

密封控温技术制备β-环糊精包合物及影响工艺的因素

目的以苯甲酸为模型药物采用新的密封控温技术制备包合物,考察制备工艺中的各种影响因素。方法将主、客分子密封于容器内,通过控制加热温度、时间等因素使主、客分子形成包合物。结果加热温度、时间及载体的晶型等因素对包合过程都会产生影响。结论对苯甲酸-β-环糊精系统采用密封控温技术制备包合物的条件为控温90℃密封加热3 h为最佳;无定形性β-环糊精系统的包合率高于结晶性β-环糊精。