Cation channel control of neurite morphology

The development of neuronal polarity and morphology is essential for a functioning nervous system. The present study was undertaken to explore whether blockade of specific channels alter neuronal morphology. Retinal ganglion cells were cultured in the presence of antagonists to NMDA, AMPA/kainate, L-, N-, P-, and Q-type voltage-dependent calcium channels (VDCCs). Five parameters were measured under these conditions: the number of neurites at the cell body, total neurite length, the length of the longest neurite, the number of branch points per neurite, and the diameter of the cell soma. Antagonists to NMDA and L-type VDCCs reduce the number of neurites at the cell body; antagonists to P- and Q-type VDCCs increase the number of neurites. Antagonists to the N-type VDCCs increase total neurite outgrowth, while antagonists to the NMDA and P-type channels reduce total neurite length. Antagonists to the NMDA and L-type channels increase the length of a single neurite, while decreasing the number of branch points; antagonists to the P- and Q-type VDCCs do essentially the opposite-increase the number of neurites, while decreasing the length of each. Blockade of one or more cation channels in developing retinal ganglion cells significantly perturbs neurite morphology. This study may help elucidate part of the role that cation channel signaling plays in neuritic development.     

粒细胞集落刺激因子对顺铂对卵巢癌细胞的细胞毒作用的影响

目的　了解粒细胞集落刺激因子（Ｇ－ ＣＳＦ）对顺铂对卵巢癌细胞的细胞毒作用的影响;方法　采用ＸＴＴ 比色法检测不同浓度顺铂对卵巢癌细胞株ＳＫＯＶ３、３ＡＯ 细胞生长影响;以及５０ ｍｇ／Ｌ 顺铂分别与不同浓度Ｇ－ ＣＳＦ 共同使用对ＳＫＯＶ３、３ＡＯ细胞生长的影响。结果　５０ ｍｇ／Ｌ 顺铂单独使用和与不同浓度Ｇ－ ＣＳＦ 共同使用２４ ｈ 对ＳＫＯＶ３、３ＡＯ 细胞生长的影响无显著性差异。结论　Ｇ－ ＣＳＦ 对顺铂对ＳＫＯＶ３、３ＡＯ 细胞的细胞毒作用无显著影响。     

甲基叔丁基醚的急性毒性研究

为研究国产甲基叔丁基醚（ＭＴＢＥ）的毒性,比较与国外产品的异同,选用大、小鼠及家兔,采用经口、呼吸道及皮肤等染毒途径,同时对国产及进口ＭＴＢＥ的急性毒性进行研究,结果表明：国产及进口ＭＴＢＥ的小鼠经口ＬＤ５０分别为２９４５．２和２９４４．４ｍｇ／ｋｇ,大鼠均为３４３３．６ｍｇ／ｋｇ。小鼠经呼吸道ＬＣ５０分别为７２９８８．３和９９６３０ｍｇ／ｍ３,大鼠为８５３２０和１０３４１０ｍｇ／ｍ３。急性中毒表现均为先兴奋,然后出现粘膜刺激症状,运动失调,活动减少,麻醉,最后死亡。兔经皮染毒仅见脱脂现象,无致炎、致敏或中毒作用。但对兔眼睛有较强致炎作用。结论：国产或进口ＭＴＢＥ的动物经口或经呼吸道急性毒性基本相同,均属低毒物,经皮属微毒物,但对兔眼有明显刺激和致炎作用     

慢性支气管炎与脾虚

慢性支气管炎一病,相当于祖国医学的"咳喘"病.根据前人经验和临床实践证明,痰是一个非常重要的病理产物,是造成临床诸证的根本性因素.而痰的生成,乃由湿困脾阳、脾阳不振所致,故慢性支气管炎与脾虚的关系至为密切.     

经蝶垂体腺瘤切除术中应用神经导航意义探讨

目的探讨神经导航系统在经蝶垂体腺瘤切除术中的应用的价值及意义.方法在58例经蝶垂体腺瘤切除术中应用神经导航技术.术前行三维影像重建,术中运用导航引导手术入路并监测进入鞍内的深度,随时了解肿瘤切除情况.结果57例经导航下均能精确定位,术中导航误差在2mm以内,肿瘤全切除者42例,次全切除者1 6例,术后无严重并发症.结论神经导航在经蝶窦入路垂体腺瘤切除术中起有效的辅助作用,但肿瘤切除的范围和程度仍然有赖于医生的技术与经验.     

SARS冠状病毒基因组序列分析与抗SARS药物设计

SARS冠状病毒是诱发SARS的主要病原体，文章综述了SARS冠状病毒基因组序列分析的最新进展，SARS冠状病毒编码的蛋白酶在病毒繁殖过程中具有重要功能，可以其作为靶点进行抗SARS冠状病毒药物的筛选。     

AD治疗新药物——γ-分泌酶抑制剂

家族性阿尔采末病属常染色体显性遗传 ,其中大部分与编码早老素的基因发生突变所导致的γ 分泌酶功能异常有关 ,γ 分泌酶是一包括PS二聚体、Nicastrin、PEN 2等组分的多酶复合体。γ 分泌酶剪切APP、Notch、E cadherin、ErbB 4受体酪氨酸激酶等膜蛋白。目前已发现了许多类型的γ 分泌酶抑制剂 :基于二氟酮、二氟乙醇基团的γ 分泌酶抑制剂 ;脲多肽模拟化合物 ;基于羟乙基二肽电子等配体的化合物 ;具有α 螺旋结构的小肽 ;具有 4 氯 异香豆素基本母核的非肽抑制剂 ;含有丙氨酰基团的化合物。但这些抑制剂目前大多还只是作为一种工具药来研究γ 分泌酶的结构、功能以及作用机制。其中选择性抑制Aβ生成的γ 分泌酶抑制剂很有希望成为一种高效的阿尔采末病治疗药物     

盐酸小檗碱结肠靶向给药胶囊的研制

目的 :研制盐酸小檗碱结肠靶向给药胶囊。方法 :制定质量标准 ,采用紫外分光光度法测定其含量。结果 :线性范围在 2～ 12 μg·mL-1,方法回收率为 99.2 6 % ,该胶囊的含量为标示量的 10 0 .6 3%。结论 :盐酸小檗碱结肠靶向给药胶囊制备简单 ,其质控方法准确可行。     

丙泊酚对N-甲基-D-天冬氨酸所致PC12细胞损伤的保护作用

目的　探讨静脉麻醉药丙泊酚 (PPF)脑保护作用的可能机制。方法　乳酸脱氢酶 (LDH)法及MTT比色法判断细胞损伤程度及细胞存活率 ,Fura 2 /AM荧光标记法测定细胞内Ca2 + 浓度 ( [Ca2 + ]i)的变化 ,分光光度法测定细胞一氧化氮合酶 (NOS)活性。结果　N 甲基 D 天冬氨酸 (NMDA) 3 0 0 μmol·L-1处理4h可明显导致PC1 2细胞的损伤 ,表现为LDH释放量明显增加 ,吸光度值A570nm明显降低 ,细胞存活率降低 ,同时 [Ca2 + ]i 和NOS活性则明显增加。PPF6.2 5 ,2 5 ,1 0 0 ,40 0 μmol·L-1与NMDA同时处理PC1 2细胞则使LDH释放量显著降低 ,细胞存活率增加。PPF 1 2 .5和 1 2 5 μmol·L-1可显著降低NMDA诱导的[Ca2 + ]i 水平及NOS活性的提高。结论　PPF对NMDA所致的PC1 2细胞损伤有明显的保护作用 ,其机制可能与其抑制NMDA受体的功能 ,降低 [Ca2 + ]i,减弱Ca2 + 超载 ,并降低NMDA诱导的NOS活性增加有关。提示PPF可能是通过抑制NMDA受体 Ca2 + NOS通路的功能而产生细胞保护效应     

Whole body 18FDG-PET and the response of esophageal cancer to induction therapy: results of a prospective trial.

PURPOSE: Whole-body 18F-fluorodeoxyglucose ([18F]FDG) positron emission tomography (PET) imaging before and after induction therapy was prospectively evaluated in patients with esophageal cancer to determine whether changes in PET images could measure response to therapy. PATIENTS AND METHODS: Between April 1997 and April 1999, 39 patients (34 men and five women; median age, 59 years; range, 36 to 76 years) with esophageal cancer were prospectively enrolled in a single-institution clinical trial of staging, including PET, induction therapy, restaging including PET, and esophagectomy. All patients undergoing esophagectomy after induction therapy (n = 17) were followed either to recurrence, to death, or through a disease-free interval of at least 24 months. RESULTS: PET after standard staging studies and before therapy imaged undetected sites of metastatic disease in six patients (15%). Restaging (including PET) after induction therapy did not identify any patients with disease progression or any patients with loco-regionally unresectable disease at exploration. The median decrease in the standardized uptake value (SUV) during induction therapy was 59%. After R0 esophagectomy, the 2-year disease-free and overall survival was 38% and 63%, respectively, among patients who had a less than 60% decrease in SUV, and 67% and 89%, respectively, among patients who had a greater than 60% decrease in SUV (P =.055 and P =.088, respectively). CONCLUSION: Compared with conventional imaging, PET detects additional sites of metastatic disease at initial evaluation. After induction therapy, PET did not add to the estimation of loco-regional resectability and did not detect new distant metastases. However, changes in [18F]FDG PET may predict disease-free and overall survival after induction therapy and resection in patients with esophageal cancer. Further evaluation in larger trials is warranted.