Endomorphin-1 and endomorphin-2 induce the expression of c-FOS immunoreactivity in the rat brain

Using FOS immunoreactivity (FOSir) as an anatomical marker of neuronal activation, we examined the effects of intracerebroventricular (i.c.v.) injections of endomorphin-1 (EM-1) and endomorphin-2 (EM-2) in the rat brain to determine the sites of action of these two mu-opioid ligands. Radiant heat tail flick latency, as a measure of behavioral effects, was prolonged by either EM-1 or EM-2 administration. Dose-dependent EM-1- and EM-2-induced FOSir were observed in various nuclei throughout the rostral-caudal axis of the rat brain. While there was some overlap, EM-1-induced FOSir was more prevalent than EM-2. The pattern of EM-induced FOSir was similar to the distribution of EM immunoreactivity (EMir). However, some sites with little or no detectable EMir exhibited FOSir, while other nuclei with marked EMir showed only sparse FOSir. EM-induced FOSir was correlated with mu-opioid receptor location in most brain areas. However, EM-induced FOSir was absent in the caudate putamen and the accumbens nucleus, both areas of high mu-opioid receptor density.     

Expression of a synapse-associated membrane protein, P84/SHPS-1, and its ligand, IAP/CD47, in mouse retina

P84 and integrin associated protein (IAP) are heterophilic binding partners that are expressed in the central nervous system in addition to a variety of other tissues. Both molecules are known to be involved in cell signaling in nonneural tissues. In the retina, both molecules are expressed prominently in plexiform layers, suggesting a possible association with synapses. Here, we examined the cellular expression and ultrastructural localization of the two molecules in the developing mouse retina. Both appeared to be expressed at one or both sides of synaptic sites, although the expression of IAP in the retina precedes that of P84. Examination of transgenic IAP-null retinae revealed a failure of P84 to become associated with synaptic sites, suggesting the interaction of P84 with IAP was necessary for P84's synaptic localization. These findings suggest that the signaling activities of P84 and IAP are localized to sites of synaptic contact in the retina. Thus this pair of synapse-associated molecules represents a bidirectional signaling system that could function to modify synaptic activity or possibly trophic interactions between central neurons.     

Application of breath-hold T2-weighted, first-pass perfusion and gadolinium-enhanced T1-weighted MR imaging for assessment of myocardial viability in a pig model

The purpose of this study was to correlate the abnormal signal area on various magnetic resonance (MR) images to the infarct area on pathologic examination and to assess the myocardial viability on the basis of MR images. T2-weighted, first-pass perfusion, and delayed gadolinium-enhanced T1-weighted images were used as "one-stop examinations" in a pig model of reperfused myocardial infarction. The results of each MR image were compared with those of 2,3, 5-triphenyltetrazolium chloride (TTC) staining. The abnormal signal areas on T2-weighted and Gd-enhanced T1-weighted images were larger than the infarct areas on TTC staining (34.7% and 32.3% vs. 28.3%; P< 0.05), whereas the nonperfused areas on perfusion images were correlated (25.6% vs, 28.3%; P = 0.139). Electron microscopic examination showed severely distorted ultrastructures in the infarct areas and mildly damaged ultrastructures in the peri-infarct areas. Perfusion images probably reflected the infarct areas, whereas T2-weighted and Gd-enhanced T1-weighted images seemed to include peri-infarct as well as infarct areas.     

平肝熄风汤对脑出血大鼠海马细胞色素C氧化酶活性和细胞凋亡影响同步研究

目的 从神经元线粒体能量代谢和细胞凋亡的角度探讨中药复方的平肝熄风汤对脑出血神经元损伤的保护作用机制。方法 采用Ⅶ型胶原酶诱导大鼠脑出血模型，以组织化学方法结合灰度值半定量测定细胞色素C氧化酶(cytochromc c oxidase，CCO)活性，采用Tunel法检测细胞凋亡结果造模12h，脑出血大鼠海马CA1区CCO活性较假手术组明显降低(P＜0.01)，凋亡细胞较假手术组明显增多(P＜0．01)随后均呈进行性加重。用平肝熄风汤治疗后町维持其CCO活性，减少细胞凋亡。结论 脑出血神经元损伤与神经元CCO活性降低及细胞凋亡有关平肝熄风汤能维持线粒体关键酶CCO活性，改善细胞有氧代谢，减少细胞凋亡，此可能为本方对脑出血继发性神经元损伤保护机制之一。     

共轭亚油酸对肥胖大鼠PPARγ基因表达及血清瘦素水平的影响

目的　研究不同剂量共轭亚油酸 (CLA)对饮食诱导肥胖大鼠PPARγ基因、瘦素、血糖、血脂的影响。方法　选用雄性Wistar大鼠 ,随机分为对照组、高脂组、高脂 +CLA组 (每 10 0g饲料含CLA分别为 0 75g、1 5 0g、3 0 0g) ,于第 12周末处死动物 ,计算脂 体比 ,测定大鼠血糖、血脂及瘦素水平 ,并应用RT PCR的方法检测大鼠白色脂肪组织过氧化物酶体增殖物激活受体γ(PPARγ)的表达水平。结果　CLA可降低肥胖大鼠血糖、甘油三酯 (TG)、总胆固醇 (TC)及瘦素水平 ,增加脂肪组织PPARγmRNA的表达水平。结论　CLA可降低肥胖大鼠血糖、血脂 ,并可通过激活PPARγ下调瘦素水平 ,有改善肥胖大鼠的瘦素抵抗作用。     

作业场所空气中氢化三联苯的紫外分光光度法测定

目的　测定作业场所空气中氢化三联苯。方法　空气中氢化三联苯用 4 0 %乙醇水溶液吸收采集 ,紫外分光光度法定量测定。结果　方法的检测限为 0 87mg m3,当标准溶液浓度为 0～ 2 0mg L时 ,相对标准偏差为 4 6 %～ 2 3% ,线性范围为 0～ 4 0mg m3。采样效率为 97 3% ,样品在采样管中稳定时间为 7天。结论　通过现场试验 ,该方法简易、快速、准确可靠 ,各项试验指标均符合劳动卫生监测要求 ,适用于作业场所空气中氢化三联苯的测定     

硒对碘过量小鼠肝脏I型脱碘酶活性的影响

目的　研究碘过量摄入对小鼠肝脏I型脱碘酶 (IDI)活性的影响及硒的干预作用。方法　将 4 0只Balb c小鼠按体重随机分为 5组 :正常对照组、碘过量I组 (3mg L)、碘过量I+Se(1mg L)组、碘过量II组 (5mg L)以及碘过量II+Se(1mg L)组 ,分别喂饲碘过量水或碘过量 +硒水以及正常鼠饲料。 3个月后 ,取血、尿及脏器测定相关指标。结果　碘过量组小鼠出现了弥漫胶质性甲状腺肿 ;与正常对照组相比 ,两个碘过量的血清TT4水平显著升高 ,而碘过量II组血清TT3水平显著降低 ;碘可显著降低肝硒水平及I型脱碘酶活性 ,补硒可明显增加碘过量小鼠的肝硒储备 ,抑制碘过量I组脱碘酶活性的降低。结论　碘过量摄入降低小鼠肝硒水平及肝脏I型脱碘酶活性 ,可能是引起血清TT4升高、出现甲状腺肿的原因 ,补硒具有一定的干预作用。     

微流芯片检测流感病毒多重逆转录聚合酶链反应产物的实验研究

[目的 ]　建立应用微流芯片检测甲 1型、甲 3型、乙型流感病毒多重逆转录聚合酶链反应 (mRT -PCR)产物的方法 ,在mRT -PCR扩增核酸的基础上自动化灵敏的定量检测扩增产物 ,快速检测甲亚型、乙型流感病毒 ,帮助临床快速诊断和鉴别诊断其他呼吸道病毒感染 ,以及明确流感病毒在人群中感染、流行情况。　 [方法 ]　采用经MDCK细胞分离培养的甲 1型、甲 3型、乙型流感病毒毒株病毒液 ,使用 3组特异引物经mRT -PCR扩增核酸 ,扩增产物分别采用毛细管电泳技术经Caliper10 0 0微流芯片分析仪自动化检测和经 2 %琼脂糖凝胶电泳法检测。　[结果 ]　设计三组引物对相应甲 1型、甲 3型、乙型流感病毒靶基因的mRT -PCR扩增产物片段分别为 43 0bp、2 10bp、3 91bp ,本实验mRT -PCR扩增产物经 2 %琼脂糖凝胶电泳 ,与Marker比照 ,DNA条带基本在此位点附近 ;产物采用毛细管电泳法经Caliper10 0 0微流芯片分析仪后 ,分别于 413bp、2 0 3bp、3 79bp处出现陡峭的峰 ,如图所示。　[结论 ]　应用微流芯片采用毛细管电泳法可对流感病毒mRT -PCR产物进行定位及相对定量 ,有助于快速诊断流感病毒感染 ,有助于对流感的监测。     

补锌对急性冷应激大鼠解偶联蛋白水平的影响

目的　研究补锌对大鼠耐寒力的影响及其可能机制。方法　雄性SD大鼠 6 0只 ,随机分为 4组 ,1、3组正常进水进食 ,2、4组给予正常饲料 ,饮高锌水 [补锌 1mg (kg·d) ],5d后 ,3,4组大鼠于 - 15℃的冷室中暴露 2h ,测各组直肠温度后与 1,2组一同宰杀 ,测定血浆和组织中的锌含量 ;用3 H标记的鸟嘌呤核苷酸 (3 H GTP)与线粒体上解偶联蛋白 (UCP)相结合 ,用液体闪烁仪测定其放射性活性 ,经ScatchardPlot测定出两者结合的解离常数 (Kd)和最大结合量 (Bmax)。结果　未补锌组和补锌组直肠温度下降的幅度分别为 - 2 95± 0 6 1和 - 1 16± 0 39℃ (P <0 0 5 ) ;冷暴露可以增加组织的锌水平 ;补锌组、冷暴露组与对照组相比Bmax增加 ,Kd值无明显差别。结论　适量补锌可以通过增加棕色脂肪组织线粒体中UCP含量提高机体的耐寒力。     

乌鲁木齐市老年人群ApoE基因与脑梗死、心肌梗死关联性研究

目的研究乌鲁木齐市老年人群载脂蛋白E(ApoE)基因与脑梗死(CI)和心肌梗死(MI)之间的相关性.方法应用聚合酶链式反应扩增技术及限制性片段长度多态性技术对56例脑梗死患者、60例心肌梗死患者及104例对照者的ApoE基因进行分型,分别计算各组ApoE等位基因、基因型的频率.结果脑梗死组和心肌梗死组ε3/ε4、ε4/ε4基因型频率明显高于对照组(P＜0.05),ε2/ε2基因型频率明显低于对照组(P＜0.05);脑梗死组的ApoEε4等位基因频率明显高于对照组(P＜0.05);ApoE基因多态与心肌梗死间未发现关联.结论 ApoEε4等位基因可能是脑梗死潜在的危险因子,ε2等位基因对脑梗死的发生可能具有一定保护作用.