肝移植患者术后早期精神症状的观察

目的探讨肝脏移植术后早期精神系统并发症发生的原因和防治经验。方法回顾性分析 12 5例原位肝脏移植患者的临床资料 ,以术后 2周作为观察时点 ,分析肝脏移植术后早期精神系统并发症发生的原因 ,总结防治经验。结果有症状组和无症状组在性别、年龄、肝功能以及血环孢素A浓度方面无明显差异 ;但有症状组的无肝期时间 (93 74± 2 8 98)min和手术时间 (4 14 6 5±6 1 92 )min却长于无症状组 (P <0 0 5 ) ;另外 ,术前有无肝性脑病、术后感染以及静脉使用免疫抑制剂和术后精神症状的发生明显相关。结论肝脏移植术后早期精神系统并发症发生的原因是多方面的 ,通过积极的对症支持治疗 ,预后良好。     

豚鼠爆震性聋耳蜗结构与功能的动态变化

目的 探讨爆震性聋与耳蜗损伤之间的关系。方法 通过畸变产物耳声发射及扫描电镜进行研究。结果 豚鼠爆震后即刻出现听阈的提高，与爆震前相比，DPOAEs幅值于1kHz处开始出现非常显著的减低（P〈0．05），在8kHz处两者的差值更大（P〈0．05），DPOAEs幅值随频率升高而逐渐下降，以高频段更为严重。爆震后20天DPOAEs幅值在0．5、0．7、1kHz处基本恢复至爆震前水平，在1．5—8kHz处较爆震后即刻明显提高，但仍低于爆震前水平（各频率均P〈0.05）。爆震后40天DPOAEs幅值与爆震后20天无明显改变（各频率均P〉0．05）。扫描电镜下见豚鼠爆震后即刻出现IHC纤毛排列紊乱，第一排OHC形态基本正常，第二排OHC部分纤毛扭曲或倒伏，尚可看到鸟翼状结构，第三排OHC倒伏、分散，部分折断；20天组IHC纤毛排列仍然紊乱，第一排OHC纤毛基本正常，第二、第三排OHC纤毛排列极度扭曲，以第三排更为严重，少数OHC溶解变性，空位由支持细胞取代；40天组与20天组无明显差别。结论 爆震性聋出现耳蜗HC结构改变及功能减退，提示耳蜗损伤与爆震性聋紧密相关。     

Polymorphic distribution of Y-chromosome haplotype and mitochondrial DNA in the Bouyei people in China

In the evolution of humans, many kinds of mutations in the human genome have been accumulated, providing credible genetic evidence for the study of human origins and migrations. The "out-of-Africa" hypothesis of modern human evolution and the genetic origin of the Japanese has come about by studying mitochondrial DNA.l,2 Recently, researchers have recognized the power of Y-chromosome markers in resolving migratory patterns of modern humans as more and more Y-chromosome single nucleotide polymorphism markers have been found. The markers on the nonrecombinant part of the Y-chromosome allows for the reconstruction of intact haplotypes which are probably the best genetic tools to study human migrations. We can analyze the paternal history of some people in different areas by Y-chromosome haplotypes.     

富血小板血浆与骨再生

急性臂丛神经炎是一种少见病,但人们往往认识不足,在早期,易被误诊为神经根型颈椎病或胸廓出口综合征。为了提高对本病的认识,降低误诊和漏诊率,本文就急性臂丛神经炎的诊断、鉴别诊断与治疗进行综述。1诊断名词与病因急性臂丛神经炎,病因尚未明了,但却有典型的临床特征。最初由Parsonage等[1]和Turner等[2]报道为肩胛带综合征和麻痹性臂丛神经炎,后被称之为:Parsonage-Turner综合征。其他诊断名词有:急性臂丛神经炎,神经源性肌萎缩,术后原发性臂丛神经炎等[3,4]。     

沉默树突状细胞恒定链以增强其抗肿瘤作用的体外实验研究

目的初步观察用小分子干扰RNA(siRNA)沉默树突状细胞(DCs)恒定链(Ii)后,DCs疫苗的体外抗肿瘤效果。方法从小鼠骨髓分离骨髓前体细胞,细胞经100 ng/ml GM-CSF和100 ng/ml IL-4诱导培养6 d后,转染针对DCs Ii链特异的Ii-siRNA,转染后加用50 ng/ml TNF-α继续诱导细胞成熟48 h,然后分别用Western blot检测沉默效果及CCK-8试剂盒检测DCs刺激同种异体淋巴细胞增殖的能力;此外,DCs共转染Ii-siRNA和小鼠胃癌前体细胞MFC的总RNA后,与同种异体淋巴细胞共培养,通过ELISA检测培养上清IFN-γ/和IL-4的水平,并收集致敏淋巴细胞进行体外杀伤实验。结果Ii-siRNA明显抑制DCs Ii的表达。沉默Ii链能够增强DCs的淋巴细胞增殖能力,并促使淋巴细胞向Th1的方向漂移[IFN-γ:(5107±351)pg/ml,IL-4:(65±13)pg/ml,P＜0．05]。淋巴细胞经共转染Ii-siRNA和MFC RNA的DCs激活后,明显而特异地杀伤靶肿瘤细胞(杀伤百分率: 66．94%±2．75%,P＜0．05)。结论通过siRNA沉默DCs的Ii链可能是一种行之有效的增强抗肿瘤免疫的方法。     

p38丝裂原活化蛋白激酶在糖尿病大鼠神经病理性痛中的作用

目的探讨p38丝裂原活化蛋白激酶（p38MAPK）在链脲菌素诱导的糖尿病大鼠神经病理性痛中的作用。方法雌性Wistar大鼠31只，3月龄，体重180～220g，随机分为3组：对照组（C组，n=10）、糖尿病神经病理性痛组（D组，n=11）和p38MAPK抑制剂组（Ⅰ组，n=10）。D组、Ⅰ组单次腹腔注射链脲菌素65mg／kg制备糖尿病模型。糖尿病模型制备成功后，Ⅰ组尾静脉注射p38MAPK抑制剂SB203580 0．5mg／kg，1次／周，连续4周；C组和D组尾静脉注射等体积的生理盐水。给药4周后，测定机械缩足反应阈值（MWT）、左侧坐骨神经传导速率（NCV）、背根神经节（DRG）和脊髓的磷酸化p38MAPK水平。结果与C组比较，D组、Ⅰ组MWT下降，NCV减慢，伴有脱髓鞘现象，DRG和脊髓的磷酸化p38MAPK水平升高；与D组比较，Ⅰ组MWT升高，NCV增快，脱髓鞘程度减轻，DRG和脊髓的磷酸化p38MAPK水平下降。结论p38MAPK信号转导通路参与了糖尿病大鼠神经病理性痛的形成。     

部分背根切断对备用背根节NT-3表达的影响

目的　探讨部分去背根后备用背根节 (L6 )各类细胞NT 3及其mRNA的含量变化。　方法　对成年雄性猫行单侧部分背根切断术 (切除一侧L1 ～L5,L7～S2 DRG ,保留L6 为备用根 )。取正常组一侧和术后 3d及 7d组手术侧的L6 DRG制作 2 0 μm厚冰冻切片 ,分别用NT 3抗体及NT 3cRNA探针行免疫组织化学及原位杂交染色。观察NT 3及其mRNA在DRG各类细胞的分布 ,测定NT 3及其mRNA在神经元和卫星细胞的光密度值 ,所得数据用q检验进行统计分析。　结果　部分去背根后 ,各时相备用背根节大神经元内NT 3的光密度值较正常者进行性减少 ,(P <0 0 5 ) ,而NT 3mRNA的光密度值术后 3d减少 ,7d回升至近正常者水平。比较之 ,小神经元和卫星细胞NT 3及其mRNA的光密度值进行性增多 (P <0 0 5 )。　结论　部分背根切断对备用背根节各类细胞NT 3表达的影响不同 ,其功能意义可能与NT 3参与脊髓Ⅱ板层可塑性有关     

甲氨喋呤对胶原诱导性关节炎大鼠滑膜骨桥蛋白和整合素αVβ3表达的影响

目的 探讨甲氨喋呤对胶原诱导性关节炎(collagen-induced arthritis,CIA)大鼠滑膜骨桥蛋白(osteopontin,OPN)及其受体整合素αvβ3表达的影响及其作用机制.方法 建立CIA大鼠模型,分为模型组和甲氨喋呤(MTX)组,后者用MTX进行干预治疗;采用免疫组织化学染色技术检测滑膜组织OPN和整合素αvβ3的表达,ELISA方法检测血清TNF-α水平.结果 ① CIA模型组和MTX组大鼠的滑膜OPN、整合素αvβ3表达均明显高于正常大鼠对照组(均为P<0.01);与模型组比较,MTX组OPN和整合素αVβ3的表达减少(均为P<0.01). ②正常对照组和MTX组大鼠血清TNF-α水平显著性低于模型组大鼠(均为P<0.01).结论 滑膜OPN和整合素αvβ3异常表达在CIA发病中具有重要意义.MTX通过下调滑膜OPN和整合素αvβ3的表达,降低血清TNF-α水平从而达到治疗CIA的作用.     

Assessment of the epidemic potential of a new strain of rotavirus associated with the novel G9 serotype which caused an outbreak in the United States for the first time in the 1995-1996 season

Rotavirus causes severe morbidity in developed countries and frequent deaths (> or = 500,000 per year) in less-developed countries. Historically, four serotypes--G1, G2, G3, and G4-have predominated; they are distinguished by one of two surface neutralization antigens (VP7). However, in 1983 and 1984 we described a new rotavirus serotype, designated G9, in five children hospitalized for diarrhea in Philadelphia, Pa. G9 rotavirus was not identified again in the Western Hemisphere until it caused ca. 50% of the rotavirus disease detected in Philadelphia in the 1995-1996 season. This outbreak allowed us to question whether a rotavirus strain completely new to a well-studied community would target either very young infants or older children, cause especially severe disease, or completely displace previously extant serotypes. We observed a significant excess of G9 infections in younger infants (especially in those < 6 months old) that might be attributed to the lack of G9-specific antibodies in mothers. Of further note, six of the seven oldest patients with rotavirus diarrhea were infected with the G9 strains (not significant). However, the age distribution of children with rotavirus did not differ over a 5-year study period regardless of the infecting serotype. Patients with diarrhea associated with G9 strains did not have disease more severe than that caused by the G1, G2, or G3 serotype. G9 strains did not displace the other serotypes but were virtually completely replaced by G1 or G2 serotypes in the three subsequent rotavirus seasons. We conclude that the abrupt appearance of this novel rotavirus serotype did not present a special threat to public health in the community.