Acute Immobilization Stress and Intraventricular Injection of CRF Suppress Naloxone-Induced LH Release in Ovariectomized Estrogen-Primed Rats

The present study was undertaken to evaluate the role and possible interaction of the endogenous opioid peptide (EOP) and corticotropin-releasing factor (CRF) in the acute stress-induced suppression of gonadotropin secretion in ovariectomized estrogen-primed rats. An intravenous (i.v.) injection of naloxone (10 or 20  mg/kg), an EOP antagonist, significantly elevated serum luteinizing hormone (LH) levels within 10  min in non-stressed animals. The naloxone-induced LH release was completely eliminated when tested 30  min after the onset of acute immobilization. In a subsequent study, it was found that suppression of the naloxone-induced LH release occurred as early as 5  min after the stress onset, and was still evident 60  min after the end of a 30-min period of immobilization. The effect of naloxone was restored 3  h after liberation of the animal from the 30-min immobilization. An intraventricular (i.c.v.) injection of CRF (1 or 5  μg) also significantly suppressed, in a dose-related manner, the effect of a subsequent i.v. injection of naloxone. However, an i.c.v. injection of α -helical CRF(9-41) (25 or 50  μg), a CRF antagonist, prior to immobilization, could not interfere with the suppressive effect of stress on naloxone-induced LH release. These results suggest that both acute immobilization stress and CRF can inhibit the LH secretory activity without mediation by EOP neurons. However, the stress-related suppression may involve non-CRF mechanism(s).     

60Co辐照血红细胞CR1分子数目的变化

目的研究不同剂量60Co γ射线辐照全血在保存期内红细胞CR1分子数目的变化.方法应用酶联法定量测定经15～35GY五个照射剂量辐照全血在保存期内红细胞CR1分子数目.结果照射后1d,15～25GY剂量组红细胞CR1分子数目相互间比较及分别与对照组比较无明显差异(P＞0.05);经30、35GY辐照红细胞CR1分子数目分别与其他剂量组和对照组比较有明显差异(P＜0.05～0.01).另外,随着保存期的延长,各剂量组和对照组红细胞CR1分子数目呈阶梯式下降,尤其在照射后3d,30和35GY剂量组红细胞CR1分子数目接近于照射后7d水平,二者相互比较无明显差异(P＞0.05).结论在一定范围内(15～25GY)60Co γ射线剂量辐照对红细胞CR1分子数目无明显影响.     

Loss of basal forebrain P75(NTR) immunoreactivity in subjects with mild cognitive impairment and Alzheimer's disease.

The long-held belief that degeneration of the cholinergic basal forebrain was central to Alzheimer's disease (AD) pathogenesis and occurred early in the disease process has been questioned recently. In this regard, changes in some cholinergic basal forebrain (CBF) markers (e.g. the high affinity trkA receptor) but not others (e.g., cortical choline acetyltransferase [ChAT] activity, the number of ChAT and vesicular acetylcholine transporter-immunoreactive neurons) suggest specific phenotypic changes, but not frank neuronal degeneration, early in the disease process. The present study examined the expression of the low affinity p75 neurotrophin receptor (p75(NTR)), an excellent marker of CBF neurons, in postmortem tissue derived from clinically well-characterized individuals who have been classified as having no cognitive impairment (NCI), mild cognitive impairment (MCI), and mild AD. Relative to NCI individuals, a significant and similar reduction in the number of nucleus basalis p75(NTR)-immunoreactive neurons was seen in individuals with MCI (38%) and mild AD (43%). The number of p75(NTR)-immunoreactive nucleus basalis neurons was significantly correlated with performance on the Mini-Mental State Exam, a Global Cognitive Test score, as well as some individual tests of working memory and attention. These data, together with previous reports, support the concept that phenotypic changes, but not frank neuronal degeneration, occur early in cognitive decline. Although there was no difference in p75(NTR) CBF cell reduction between MCI and AD, it remains to be determined whether these findings lend support to the hypothesis that MCI is a prodromal stage of AD.     

雌、孕激素受体和C-erbB-2在原发胆囊癌中的表达及意义

目的　探讨雌、孕激素受体 (ER、PgR)和C erbB 2癌基因蛋白产物在原发胆囊癌发生、发展中的作用及相互关系 ,研究它们的表达与肿瘤的病理类型、分级 ,临床分期及预后的关系 ,并为该病的临床诊治提供参考依据。方法　应用免疫组织化学法 ,检测 3 5例原发胆囊癌 ,2 0例慢性胆囊炎组织中ER、PgR和C erbB 2癌基因蛋白的表达水平。结果　在原发胆囊癌中ER、PgR和C erbB 2阳性表达率分别为 60 %、4 5 .7%和 65 .7%。ER的阳性表达与浸润及淋巴结转移密切相关 (P <0 .0 5 )。C erbB 2过度表达与胆囊癌淋巴结转移有关 (P <0 .0 5 )。ER或PgR阳性患者的累计生存率明显低于阴性者。结论　ER、PgR及C erbB 2在原发胆囊癌中的表达率显著高于其在胆囊良性病变中的表达率。ER或PgR阳性者积累生存率显著低于ER或PgR阴性者。ER可能有希望成为反映胆囊癌恶性程度和预后的一项生物学指标     

肝靶向抗病毒药Lac-PLL-ACV的制备及其趋肝性研究

目的：减少抗病毒药阿昔洛韦（Acyclovir,ACV）在治疗乙型肝炎中的肝外毒副作用，获得肝靶向ACV偶联物。方法：多聚赖氨酸（Poly-L-lysine,PLL)在氰硼酸钠的催化作用下与乳糖反应生成乳糖化多聚赖氨酸，乳糖化多聚赖氨酸与咪唑化阿昔洛韦在37℃pH9.5的条件下反应合成偶联物乳糖化多聚赖氨酸－阿昔洛韦（Lactosaminated poly-L-lysine-acyclovir,Lac-PLL-ACV）。偶联物经尾静脉注射进入小鼠体内后，收集小鼠血浆及肝脏样品，用高效液相色谱法测定药物浓度，研究遇联物的体内分布和药代动力学。结果：HPLC检测证实Lac-PLL-ACV在血浆中十分稳定，不易解离出ACV。偶联物的肝最大摄取率约为60％，是ACV组的10倍以上，偶联物肝中的T1／2，AUC，CL分别为ACV的4．2倍，56．6倍和1／57，具有明显的肝靶向性。结论：乳糖化多聚赖氨酸作为肝去唾液酸糖蛋白受体（Asialoglycoprotein receptor,ASGPR)介导的一种药物载体，能使抗病毒药ACV获得较满意的肝靶向性。     

慢性乙型肝炎中可溶性白细胞介素2受体与其它血清学指标的关系

目的 :探讨血清可溶性白细胞介素 2受体 (sIL 2R)在慢性乙型病毒性肝炎 (慢乙肝 )中的发病机制及sIL 2R与肝纤维化指标、肝功能的相关关系。方法 :对 312例肝活检病人按组织病理学炎症和纤维化程度进行分级分期 ,同时检测了病人血清sIL 2R、肝功能及肝纤维化相关指标。结果 :血清sIL 2R均值较对照组明显增高 (P <0 .0 1) ,增幅随着肝脏病理炎症和纤维化程度的加重而逐渐加大 ,各组间比较差异有显著性 (P <0 .0 5或P <0 .0 1)。sIL 2R与血清白蛋白 (A)呈显著负相关 ,与血清脯氨酸肽酶 (PLD)、Ⅳ型胶原 (CⅣ )、层粘连蛋白 (LN)、透明质酸 (HA)、Ⅲ型前胶原氨基端肽 (PⅢNP)、肝功指标中的TB、DB、G、ALT、AST、AKP、γ GT呈显著正相关 (P <0 .0 5或P <0 .0 1)。结论 :慢乙肝病人血清sIL 2R水平与A呈显著负相关 ,与PLD、CⅣ、LN、HA、PⅢNP呈显著正相关 ;sIL 2R的血清水平能反映肝脏组织学病变的程度 ,可作为判断肝组织炎症和纤维化程度的参考指标。     

慢传输性便秘结肠阿片受体的病理生理改变

目的探讨慢传输性便秘(STC)的发病机制和病理生理改变。方法应用放射配体结合分析法,检测患者结肠mu、kappa阿片受体,观察其含量变化。结果STC患者结肠mu阿片受体的最大结合数(Bmax)和解离常数(KD)比正常对照组明显增加(Bmax400.950比96.304pmol,KD431.314比179.839pmol);kappa阿片受体含量检测亦有类似结果(Bmax:375.073比45.264pmol,KD485.407比141.016pmol)。结论STC患者阿片受体含量增加,内源性阿片肽活性增加。提示采用阿片受体拮抗剂可能是治疗STC的一个新途径。     

儿童慢性乙型肝炎细胞免疫功能及胸腺素疗效

目的　探讨慢性乙型肝炎(CHB)患儿细胞免疫功能及胸腺素疗效。方法　6 0例CHB患儿随机分为常规组(予常规治疗)和胸腺素组(在常规治疗基础上+胸腺素) ,并以6 0例健康儿童作为正常对照组。于治疗前、疗程结束后1mo检测T细胞亚群(CD+ 3 、CD+ 4 、CD+ 8)、血清白细胞介素2 (IL 2 )及可溶性白细胞介素2受体(sIL 2R)水平;定期复查肝功能、乙肝标志物和HBV DNA。结果　与正常对照组比较,CHB组CD+ 3 与CD+ 4 的百分率、CD+ 4 /CD+ 8及血清IL 2水平明显降低(P均<0 0 1) ,CD+ 8百分率及血清sIL 2R水平明显升高(P均<0 0 1) ;与常规组比较,胸腺素组血清ALT明显下降(P <0 0 1) ,ALT复常时间明显缩短(P <0 0 1) ,HBeAg转阴率明显上升(P <0 0 5 ) ,各免疫学指标明显恢复,差异均有统计学意义(P <0 0 1或P <0 0 5 )。结论　CHB患儿细胞免疫功能低下,胸腺素能增强细胞免疫功能,有利于病毒清除和肝功能的恢复