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A technique is described for the detection of free fatty acids, triglycerides, wax esters and cholesterol esters on thin-layer Chromatographic plates. The fatty acids present in each fraction can be recovered from the plates after detection and quantitatively measured by gas-liquid chiomatography. This procedure has been sucessfully applied to the analysis of skin surface lipids.  相似文献   
107.
The rate of formation of plasma cholesteryl esters was determined by both in vivo and in vitro methods in 15 subjects. In vivo production of plasma cholesteryl esters was calculated from the specific activity slopes of plasma free and esterified cholesterol after an intravenous injection of [3H] mevalonic acid or [3H] cholesterol incorporated in plasma lipoproteins. In vitro production of cholesteryl esters was estimated by measuring lecithin:cholesterol acyltransferase activity in plasma. Lecithin:cholesterol acyltransferase was estimated by incubating the subjects' own plasma for 1 h at 37 degrees C. The plasma sample used for incubation was collected 2 h after the injection of radioactive precursor (when radioactivity of esterified cholesterol was very low relative to that in free cholesterol and the specific activity of free cholesterol in all of the major plasma lipoprotein classes was identical). The mean value for the production of plasma cholesteryl esters obtained by in vivo method was 126.2 +/- 41.9 mg/h, and it was not significantly different from the mean of 110.5 +/- 25.5 mg/h calculated from the results of in vitro method. The values obtained by the two methods in all 15 subjects had an excellent correlation (r = 0.93). It was found that in normotriglyceridemic subjects the values obtained by the two methods wwere essentially identical, but in hypertriglyceridemic subjects the values obtained by the in vitro method were consistently somewhat lower than the obtained by the in vivo method.  相似文献   
108.
转录因子T-bet与哮喘大鼠气道炎症及川芎嗪的干预效应   总被引:1,自引:0,他引:1  
目的:转录因子T-bet在支气管哮喘的发病中起重要作用,川芎嗪治疗哮喘有效。实验拟观察川芎嗪对哮喘大鼠气道炎症的影响和转录因子T-bet的调控作用。方法:实验于2005-11/2006-06在南京医科大学完成。①实验材料及分组:72只SPF级SD大鼠随机分为正常对照组、哮喘模型组、川芎嗪小剂量组(20mg/kg)、川芎嗪中剂量组(40mg/kg)、川芎嗪大剂量组(80mg/kg)和地塞米松组,每组12只。实验用磷酸川芎嗪注射液为丽珠集团利民制药厂生产)。②实验过程及评估:以卵蛋白腹腔注射并雾化吸入制备大鼠哮喘模型,末次雾化后24h内麻醉后处死大鼠。观察6组大鼠肺组织形态学变化;测定支气管壁厚度、支气管平滑肌厚度、嗜酸粒细胞和淋巴细胞数。采用免疫组织化学半定量法测定肺组织T-bet蛋白的表达;进行转录因子T-bet蛋白表达量与气道炎症的相关性分析。实验过程中对动物处置符合动物伦理学标准。结果:①哮喘模型组嗜酸粒细胞、淋巴细胞、支气管壁厚度和支气管平滑肌厚度,明显高于正常对照组相应指标(P均<0.01);与哮喘模型组比较,川芎嗪小、中、大剂量组和地塞米松组上述4项指标均减少(P均<0.01)。②哮喘模型组、川芎嗪小、中、大剂量组和地塞米松组的T-bet表达量低于正常对照组(P均<0.01);与哮喘模型组比较,川芎嗪小、中、大剂量组T-bet表达量增加(P均<0.01);随着川芎嗪剂量增加,T-bet表达量亦相应增加,川芎嗪小、中、大剂量组之间两两比较,差异均有统计学意义(P均<0.01)。③相关分析显示哮喘模型组T-bet蛋白表达量与嗜酸性粒细胞和淋巴细胞浸润数呈负相关(r=-0.81,-0.85,P<0.01),与支气管管壁厚度和支气管平滑肌厚度呈负相关(r=-0.77,-0.79,P<0.01)。结论:支气管哮喘大鼠存在T-bet低表达;川芎嗪可抑制气道炎症,增加转录因子T-bet蛋白的表达,纠正Th1/Th2失衡,从而治疗支气管哮喘。  相似文献   
109.
Co-cultivation of splenocytes with cis-dichlorodiamine platinum (II) treated tumor cells generate cytotoxic splenocytes, which when injected into normal mice, render them resistant to tumor challenge. Significant increases in mean survival time and 33% of tumor free survivals were observed in mice exposed to a tumor challenge on the 10th day after injection of sensitized splenocytes. Splenocytes peritoneal exudate cells obtained after in vivo immunization of mice with cis-dichlorodiamine platinum(II) treated cells retarded tumor growth in vivo when injected in different combinations in tumor bearing mice. Maximum survival time of tumor bearing mice and 20% tumor free survivals were observed when the animals were injected with a combination of immune splenocytes and normal peritoneal exudate cells. The increase in the number of macrophages of immunotherapeutically treated mice suggests that host macrophages have been activated. Splenocytes and macrophages obtained from immunotherapeutically treated mice showed an increase in cytotoxicity against tumor cells in vitro.  相似文献   
110.
Sephacryl beads containing an immobilized aminopropylcobalamin- transcobalamin-II complex serve as foci for the adherence of L1210 murine leukemia cells. Bead-cell interaction does not occur when (A) nonderivatized beads are used; (B) transcobalamin-II is omitted or presaturated with cyanocobalamin in the preparation of the bead complex; (C) intrinsic factor replaces transcobalamin-II; and (D) the complex is removed from beads by photolysis. These observations suggest that adherence results from the ability of transcobalamin-II to form a bridge between immobilized cobalamin on the bead and receptors in the plasma membrane of the cell.  相似文献   
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