风疹病毒JR_(23)株感染BALB/c小鼠脑组织的病理学特征

为研究风疹病毒（ＲＶ）ＪＲ２３株感染中枢神经系统（ＣＮＳ）的特性及病理学特征,ＢＡＬＢ／ｃ 小鼠经腹腔感染ＲＶ ＪＲ２３株,并于感染后的第２１ｄ 取小鼠大脑及小脑组织,ＨＥ及免疫组织化学染色,观察小鼠脑组织ＲＶ 感染状况及病变特征。结果显示,受感染的小鼠无明显的ＣＮＳ症状,病理学特征以大脑灰质小灶性神经元变性坏死为主,病变神经元周围见增生的少突胶质细胞形成卫星现象。在神经元坏死灶中可见小胶质细胞增生,形成噬神经元现象及由小胶质细胞和少突胶质细胞构成的胶质细胞结节。神经元及神经胶质细胞内未见病毒包涵体。免疫组织化学染色显示,ＲＶ 主要分布于大脑灰质,神经元细胞、星形胶质细胞和少突胶质细胞均可受到ＪＲ２３株的感染。提示卫星现象、噬神经元现象和胶质细胞结节形成可作为ＲＶ－ＪＲ２３感染ＣＮＳ的病理学参考指标。免疫组织化学染色对确诊ＣＮＳＲＶ 的感染具有特异性     

抗人胸腺细胞单克隆抗体2G_2B_2和2G_2C_2的制备及特性鉴定

用杂交瘤技术制备２株单克隆抗体（单抗）２Ｇ２Ｂ２、２Ｇ２Ｃ２。经研究发现,它们主要与胸腺细胞、脐血及ＰＨＡ激活的外周血单个核细胞等反应;免疫组化显示其主要作用于皮质胸腺细胞;与造血系统中分化早期的瘤细胞、骨髓瘤细胞等反应阳性率较高。生物学特性鉴定结果提示,单抗均属免疫球蛋白ＩｇＧ１亚类,腹水效价达１：１２８０００,所识别抗原分子量为４５／４６ＫＤａ,无抗原调变作用。故２Ｇ２Ｂ２、２Ｇ２Ｃ２是类似ＯＫＴ１０的抗ＣＤ３８单抗,但竞争抑制结果表明三者分别作用于不同的抗原决定簇,即２Ｇ２Ｂ２、２Ｇ２Ｃ２是两个抗ＣＤ３８新单抗。     

聚膦腈在药物控释系统中的应用

聚膦腈由于其具有良好的生物相容性,可生物降解性及易于功能化的特性而成为一类独特的药物控释材料。本文就疏水性线型聚膦腈,聚膦腈水凝胶及聚膦腈高分子药物在药物控释系统中的应用作一简要综述。     

聚合酶链反应检测二甲苯集菌的24小时尿结核分枝杆菌

目的：探讨聚合酶链反应（ＰＣＲ）检测二甲苯集菌的２４小时尿结核分枝杆菌。方法：应用ＰＣＲ检测６６例疑似泌尿系结核患者二甲苯集菌的２４小时尿结核分枝杆菌,并与常规留取尿标本检测结果作比较得阳性２１例（３１．８％）,后者阳性１１例（１６．７％）,二者差异（Ｐ〈０．０５）。结论：ＰＣＲ检测尿结核分枝杆菌时,应多留取尿液送检,并经浓缩集菌后作ＰＣＲ,以提高检出阳性率。     

维持性血液透析对老年人心血管系统的影响

目的：探讨维持性血液透析对老年人心血管系统的影响;方法：对４６例老年维持性血透与５０例非老年维持性血透对患者心血管系统的影响进行了分析比较;结果：维持性血透引起血压、高血压、心律失常、心绞痛、心力衰竭等心血管并发症,老年组显著高于对照组（Ｐ〈０．０１）。因心血管并发症致死者,老年组占６０．０％;结论：维持性血液透析对老年人尤易引起心血管系统并发症,并为其主要死亡原因。故在透析中有效防治心血管并发症     

阻断RAAS不同部位对自发性高血压大鼠的心肌胶原酶mRNA表达的影响

目的　观察阻断肾素 -血管紧张素 -醛固酮系统 (RAAS)不同部位对自发性高血压大鼠 (SHR)心肌中胶原酶表达的影响。方法　对 15只 2 6周龄SHR分别采用苯那普利、Losartan和安体舒通治疗 12周 ,用点杂交方法检测治疗前后大鼠心肌胶原酶mRNA的变化。另取 2 6周龄的SHR(SHR 2 6)和未预任何治疗的 3 8周龄SHR(SHR 3 8)各 5只作为对照。结果　SHR 2 6和SHR 3 8组胶原酶mRNA量与SHR 2 6组大鼠比较差别无统计学意义 (P >0 .0 5 )。 3个治疗组中 ,苯那普利SHR组的胶原酶mRNA较未治疗组明显增加 (P <0 .0 5 ) ,其余两治疗组则无明显变化 (P >0 .0 5 )。结论　在阻断RAAS的 3种药物中 ,仅苯那普利增加胶原酶mRNA的表达。     

Paraganglioma of the Cauda Equina Region – Report of two Cases and Review of the Literature

Summary  A paraganglioma of cauda equina region is extremely rare and except for secreting tumour, the pre-operative diagnosis of paraganglioma is very difficult. Two cases of non-functional paragangliomas of the cauda equina region are reported, one was attached to the filum terminale and the other to a rootlet looking very much like a vascular neurinoma. Both were successfully removed by surgery. An extensive review of the literature permits one to find 77 other cases. The clinical, radiological, pathological (ultrastructural and immunohistochemical) features and surgical findings of all theses cases are discussed. Surgery remains the treatment of choice. No effect of radiotherapy on recurrence prevention has ever been demonstrated.     

Detection of anterior horn lesions by MRI in central European tick-borne encephalomyelitis

We report a case of central European tick-borne encephalitis with cervical myelitis presenting clinically as a lower motor neuron syndrome of the upper limbs with proximal asymmetrical pareses and atrophies. There were no sensory deficits nor signs of lesions of the spinal pathways or signs of encephalitis or meningitis. The affected motor fibers of the upper limbs were electrically inexcitable, but sensory findings were normal. Electromyography of the paralyzed muscles revealed pathological denervation activity without voluntary activation. The initial magnetic resonance imaging (MRI) showed a large hyperdense lesion in the anterior part of the cervical cord from C3 to T1. Despite the fact that MRI changes disappeared completely within 6 weeks the patient showed only little improvement in the paralyzed muscles after 6 months. To our knowledge, these MRI changes in patients with tick-borne encephalitis, consistent with an isolated anterior horn lesion, have never been reported previously. The course may have been aggravated by an initial antibiotic treatment with cephalosporins. Received: 4 May 1999 Received in revised form: 22 July 1999 Accepted: 26 July 1999     

Autoimmune maintenance and neuroprotection of the central nervous system

The genesis of immune privilege high in the evolutionary tree suggests that immune privilege is necessary, if not advantageous for the progressive development of the CNS. Upon reaching a certain degree of complexity, it seems as if the CNS was obliged to restrain the immune system from penetrating the blood-brain barrier. CNS autoimmunity against myelin proteins is known to be a contributory factor in the pathophysiology of multiple sclerosis and in the animal model of experimental autoimmune encephalomyelitis (EAE) (Wekerle, 1993). Such autoimmunity has therefore been regarded as detrimental and hence obviously undesirable. However, recent findings in our laboratory suggest that T-cell autoimmunity to CNS self-antigens (Moalem et al., 1999), if expressed at the right time and the right place, can do much good in the CNS. We shall review the experiments briefly, and then discuss their implications for our understanding of immune privilege and CNS maintenance after injury.     

Dendritic cells in experimental allergic encephalomyelitis and multiple sclerosis

The mechanisms by which autoimmune diseases are triggered and by which the activation of autoreactive T cells is initiated and maintained are not yet fully understood. As the most potent antigen presenting cells (APC), and also being responsible for antigen transport as well as primary sensitisation of T cells, dendritic cells (DC) are capable of breaking the state of self-ignorance and inducing aggressive autoreactive T cells. In the development of autoimmune diseases, different types of DC exhibit distinct properties for inducing Th1/Th2 cell responses. Appropriate cytokines can convert immunogenic DC to tolerogenic DC. Utilizing the possibility to promote the tolerogenic effects of DC, a new therapeutic tool might soon become available to treat multiple sclerosis and other autoimmune diseases.