酶组化显示睾丸LDH－X方法的再探讨

对小鼠睾丸冰冻切片ＬＤＨ－Ｘ的显示方法作了进一步探讨。实验表明，以Ｌ－２－羟基－３－甲基戊酸（ＨＭＶ）为特异性底物，能相当有效地显示睾丸ＬＤＨ－Ｘ的分布，且该底物的配制方法简便易行。在显示ＬＤＨ－Ｘ的孵育液中采用萘酚蓝（ＮＢ）作中间递电子体较吩嗪甲基硫酸酯更具优越性。     

Chronic opioid treatment of neuroblastoma X dorsal root ganglion neuron hybrid F11 cells results in elevated GM1 ganglioside and cyclic adenosine monophosphate levels and onset of naloxone-evoked decreases in membrane K+ currents

Prolongation of the action potential duration of dorsal root ganglion (DRG) neurons by low (nM) concentrations of opioids occurs through activation of excitatory opioid receptors that are positively coupled via G_s regulatory protein to adenylate cyclase. Previous results suggested GM1 ganglioside to have an essential role in regulating this excitatory response, but not the inhibitory (APD-shortening) response to higher (μM) opioid concentrations. Furthermore, it was proposed that synthesis of GM1 is upregulated by prolonged activation of excitatory opioid receptor functions. To explore this possibility we have utilized cultures of hybrid F11 cells to carry out closely correlated electrophysiological and biochemical analyses of the effects of chronic opioid treatment on a homogeneous population of clonal cells which express many functions characteristic of DRG neurons. We show that chronic opioid exposure of F11 cells does, in fact, result in elevated levels of GM1 as well as cyclic adenosine monophosphate (AMP), concomitant with the onset of opioid excitatory supersensitivity as manifested by naloxone-evoked decreases in voltage-dependent membrane K⁺ currents. Such elevation of GM1 would be expected to enhance the efficacy of excitatory opioid receptor activation of the G_s/adenylate cyclase/cyclic AMP system, thereby providing a positive feedback mechanism that may account for the remarkable supersensitivity of chronic opioid-treated neurons to the excitatory effects of opioid agonists as well as antagonists. These in vitro findings may provide novel insights into the mechanisms underlying naloxone-precipitated withdrawal syndromes and opioid-induced hyperalgesia after chronic opiatf addiction in vivo. © 1995 Wiley-Liss, Inc.     

雌性大鼠、小鼠生殖系统与人子宫内膜甾体激素分泌细胞的研究

对雌性大鼠、小鼠的生殖系统,人的子宫内膜与蜕膜进行了3-β-羟基甾体脱氢酶(3-β-HSDH)和脂类的组织化学研究。结果表明:在大鼠和小鼠的卵巢内,颗粒黄体细胞和膜黄体细胞3-β-HSDH呈强阳性反应,卵泡膜内层细胞与间质细胞呈中等程度阳性反应;大鼠与小鼠子宫内膜的表面上皮与腺上皮呈阳性反应;人早孕期蜕膜中的子宫腺上皮细胞与大蜕膜细胞呈阳性反应:在大鼠与小鼠的输卵中偶尔见到阳性反应物质;在人的子宫内膜中,没有见到阳性反应。本研究证明,雌性大鼠和小鼠除卵巢有分泌甾体素的功能外,子宫也有分泌甾体激素的功能。人早孕期蜕膜组织中的子宫腺与大蜕膜细胞都能分泌甾体激素。     

An efficient procedure for the regioselective synthesis of 10-methoxy-11-hydroxyaporphine from (R,S)-10,11-dihydroxyaporphine

A regioselective preparation of 10-methoxy-11-hydroxyaporphine (“Apocodeine,1b”) from (R,S)-10, 11-dihydroxyaporphine(apomorphine,1a) is described. The isopropylidene ketal ring of 10,11-(isopropylidenyldioxy) aporphine (2) obtained by the isopropylidenation of apomorphine, was regioselectively opened by the ten equivalent of trimethylaluminum to give 10-hydroxy-11-t-butyloxyaporphine (3). The free 10-hydroxyl position of 3 was methylated with methyl p-toluenesulfonate/NaH, and afforded 10-methoxy-11-t-butyloxyaporphine (4) in high yield. Selective debutylation gave the desired 10-methoxy-11-hydroxyaporphine (“apocodeine”,1b) in good yield.     

海南文昌汉族人群中两种葡萄糖-6-磷酸脱氢酶基因突变的研究

目的:分析海南文昌人群中葡萄糖-6-磷酸脱氢酶基因1376G→T、95A→G突变。方法:应用硝基四氮唑蓝定量法进行G6PD缺乏症的筛查,用等位基因特异PCR检测1376G→T、95A→G突变。结果:在358位海南文昌汉族人中,发现G6PD缺乏症患者20例,其中9例患者有1376G→T突变,3例患者有95A→G突变。结论:1376G→T、95A→G突变是文昌人群中常见的突变。     

REGULATING FUNCTION OF COENZYMIZATION AND DECOENZYMIZATION OF THE LACTATE DEHYDROGENASE ISOZYMES IN THE MOUSE TISSUES DURING HYPOXIA

Objective. To study the characteristics of changes of LDH enzyme patterns of mice under slight hypoxia.Methods. Mice treated with artificial hypoxia, various tissues were made for the test of LDH enzymatic activity by the specific staining technique. LDH (1 -5) relative percentage enzymatic activity (RPEA) were measured with CS-910 dual-wavelength thin layer chromatography scanner.Results. The RPEA of LDH isozymes of various tissues after slight hypoxia shifted to the isozymes LDH1 and LDH2, whose principal subunits are H subunits, and the RPEA of LDH,(H4), LDH2(H3M) increased, while RPEA of LDH5(M4) in various tissues decreased prominently except the cardiac muscle, and that of LDH4(HM3) decreased as well. After polyacrylamide gel electrophoresis (PAGE) of the hypoxia treated cardiac muscle specimen was made, activity subbands originated regularly in the isozyme patterns of LDH, with the regularity of LDH1 (0 subband), LDH2 (0-1 subbands), LDH3 (0-2 subbands), LDH4 (1-3 subbands), LDH5 (2-4 subbands).     

β受体阻滞在心血管疾病中的临床应用研究进展

依据国内外的临床研究和循证医学分析,对β受体阻滞剂在心血管疾病方面的合理应用以及适应证,给药方法进行循证性举证,提示β受体阻滞剂可明显改善心血管疾病的临床预后,除非有禁忌证及不能酎受者,β受体阻滞剂应作为心血管疾病的常规治疗病物广泛应用于心血管疾病。     

CD11b在肺纤维化患者的表达及红霉素对其影响

目的探讨CD11b在肺纤维化患者外周血中性粒细胞上的表达及红霉素对它的影响.方法肺纤维化患者(A组,n=13)13例经红霉素治疗3个月,收集治疗前后及健康对照组(B组,n=13)13例的外周血中性粒细胞涂片,用桥联酶免疫法测定CD11b表达阳性的中性粒细胞百分率.结果A组治疗前后,患者外周血中性粒细胞CD11b的表达阳性率均显著高于健康对照组(P＜0.01);A组治疗前,患者外周血中性粒细胞CD11b的表达阳性率显著高于治疗后(P＜0.01).结论肺纤维化患者外周血中性粒细胞CD11b的表达阳性率显著高于健康对照组;红霉素能抑制肺纤维化患者外用血中性粒细胞CD11b的表达.     

Regulation of neuronal differentiation in neuron-enriched primary cultures from embryonic rat cerebra by platelet activating factor and the structurally related glycerol ether lipid, dodecylglycerol.

Primary cultures enriched in neurons dissociated from embryonic rat cerebra were used to demonstrate that platelet activating factor and the structurally related ether glycerolipid, dodecylglycerol, are readily taken up in small amounts by neurons and that they stimulate the differentiation of neurons. The stimulation of neuronal differentiation was observed as a precocious development of axon-like extensions which correlated with a concentration-dependent increase in neuronal-specific enzyme activities. This stimulation of morphological and neurochemical factors by either platelet activating factor or dodecylglycerol was almost completely abolished by triazolam, a known inhibitor of platelet activating factor function. Neither platelet activating factor nor dodecylglycerol at the concentrations used to achieve stimulation of neuronal differentiation compromised the plasma membrane, as indicated by the lack of leakage of cytoplasmic lactic acid dehydrogenase.