二补助育汤对胚胎着床障碍小鼠子宫血管生成相关因子表达的影响

目的：探讨二补助育汤对胚胎着床障碍模型小鼠子宫内膜形态及血管生成素-1（Ang-1）mRNA、血管内皮生长因子（VEGF）mRNA的表达和定位的影响。方法：24只ICR雌性小鼠随机分为空白组、模型组、戊酸雌二醇组、二补助育汤组，每组6只，用米非司酮建立胚胎着床障碍动物模型，各组给予相应药物灌胃，妊娠第5天处死小鼠后，检测各组妊娠率、平均着床位点数、子宫内膜Ang-1和VEGF mRNA表达量及其蛋白定位。结果：模型组小鼠平均胚胎着床位点数、Ang-1 mRNA、VEGF mRNA表达量明显低于空白组（均P<0.05）；与模型组比较，二补助育汤组平均胚胎着床位点数、Ang-1 mRNA、VEGF mRNA表达量显著提高（均P<0.05）。结论：二补助育汤可提高子宫内膜Ang-1和VEGF蛋白表达量，促进子宫内膜血管生成，从而提高子宫内膜容受性。     

Effects of acute and chronic desipramine treatment on somatostatin receptors in brain

The effects of acute (5 mg/kg, IP twice daily for 2 days) and chronic (5 mg/kg IP twice daily for 21 days) administration of desipramine (DMI) on [¹²⁵I]-Tyr¹¹-somatostatin binding sites in brain were examined. There was no change in [¹²⁵I]Tyr¹¹-somatostatin binding in membranes prepared from the frontal cortex, striatum, and hippocampus of rats acutely or chronically treated with DMI as compared to non treated animals. [¹²⁵I]Tyr¹¹-Somatostatin binding was increased in membranes prepared from the rat nucleus accumbens only after chronic DMI administration. Scatchard analysis of the binding data from the nucleus accumbens showed that [¹²⁵I]Tyr¹¹-somatostatin labels a single population of somatostatin binding sites with an affinity constant, K_d, of 1.8±0.60 nM and a B_max of 330±90 fmol/mg protein. Chronic treatment with DMI increased the B_max (500±140 fmol/mg protein) but had no effect on the K_d. This finding shows a regional effect of DMI on [¹²⁵I]Tyr¹¹-somatostatin binding sites in rat brain and suggests that somatostatin may play a role in the pathophysiology of depression.     

Ontogenetic Development of 5-HT1D Receptors in Human Brain: An Autoradiographic Study

The pattern of pre- and postnatal appearance of 5-HT_1D receptors throughout the different areas of the human brain was studied by quantitative in vitro autoradiography, using [¹²⁵I]GTI (serotonin O -carboxymethyl-glycyl-[¹²⁵I]tyrosinamide) as a ligand. The anatomical distribution of 5-HT_1D receptors in neonatal, infant and children's brain was in good agreement with that observed in the adult, the basal ganglia and substantia nigra being the most intensely labelled areas. The development of these receptors throughout the human brain was mainly postnatal: low densities of [¹²⁵I]GTI binding sites were observed at the fetal/neonatal stage in most regions analyzed, in contrast with the high levels of labelling found in infant and children's brains. Indeed, in a number of regions, including the globus pallidus, substantia nigra and visual cortex, a peak of overexpression of 5-HT_1D receptors was observed in the first decade of life. Such overexpression could support a regulatory role for 5-HT_1D receptors in advanced periods of the CNS developmental process. Our results also indicate that the administration of drugs acting on 5-HT_1D receptors during the early postnatal period of life could result in modifications of their properties, as these receptors are already functional in this period.     

DNA damage by the glycation products of glyceraldehyde 3-phosphate and lysine

Summary In order to evaluate whether base modifications, apurinic/apyrimidinic site formation, strand breaks, or a combination of these lesions results from the interaction of glycation products with DNA, plasmid DNA was first reacted with these products, and then subjected to digestion with endonuclease III and endonuclease IV of Escherichia coli. Analysis of the differential effects of digestions with these enzymes by electrophoresis on agarose gels demonstrated that reactive glycation products produce both base modification and apurinic/apyrimidinic sites in DNA, in addition to the strand breaks observed after incubation with glycation products alone. These types of DNA damage may occur in specific diabetic cells where elevated levels of glycating sugars are associated with pathologic dysfunction. [Diabetologia (1994) 37: 145–149] Received: 28 May 1993 and in revised form: 30 August 1993     

吗啡及纳洛酮对淋巴细胞体外增殖的作用(英文)

目的:研究吗啡对不同淋巴细胞增殖的作用及纳洛酮的影响.方法:观察吗啡对未成熟的、静止的及活化的脾脏淋巴细胞体外增殖影响及纳洛酮的阻断作用.结果:吗啡(1×10~(-10)—1×10~(-6)mol L~(-1))能增加Con A诱导的T-细胞的增殖,1 μmol L~(-1)还能促进LPS诱导的B-细胞的增殖,同时这些增强作用都能被纳洛酮50μmol L~(-1)阻断,纳洛酮单独亦能促进活化T-细胞的增殖.而吗啡1×10~(-10)—1×10~(-5)mol L~(-1)对静止的脾脏淋巴细胞及Con A活化的胸腺淋巴细胞的增殖都无影响.但是吗啡1mmol L~(-1)能广泛抑制静止的、LPS活化的脾脏细胞及Con A活化的胸腺,脾脏淋巴细胞增殖,且都不能被纳洛酮阻断.结论:吗啡对活化T-和B-细胞的促进作用是由细胞表面的阿片受体介导的,此阿片受体随着淋巴细胞的成熟和活化而变化,而吗啡1 mmol L~(-1)对淋巴细胞增殖的抑制作用却不是由经典的阿片受体介导的.     

糖皮质激素受体高、低亲和力位点在急性淋巴细胞性白血病治疗中的意义

研究了１０例正常人和２９例急性淋巴细胞性白血病（急淋）患者外周血糖皮质激素受体高、低亲和力结合位，或（ＧＣＲＨ、ＧＣＲＬ），利用Ｒｕ３８４８６对ＧＣＲＬ进行封闭，对部分患者ＧＣＲＨ、ＧＣＲＬ在激素联合化疗前后水平的变化进行了动态观察。结果表明，正常对照组ＧＣＲＨ、ＧＣＲＬ分别为４６０８±１８８９位点／细胞和１３５２３８±８８５０９位点／细胞，两者相关良好。急淋患者ＧＣＲＨ、ＧＣＲＬ分别为６０５２±３８８８位点／细胞和１２６４０５±１０２１３３位点／细胞，经过糖皮质激素药物联合化疗后，其水平分别为３６１６±１９６２位点／细胞和１４３５９７±１１２２８９位点／细胞，ＧＣＲＨ下降明显（Ｐ＜０．０１），下降率为４０．３％；而ＧＣＲＬ化疗前后差异不显著（Ｐ＞０．０５）。提示ＧＣＲＬ在介导糖皮质激素联合化疗疗效的维持中起重要的作用。