腺病毒介导的HSV—tk基因治疗大鼠脑胶质瘤实验研究

目的：带有ＨＳＶ－ｔｋ基因的重组腺病毒（ＡｄＨＣＭＶ－ｔｋ）结合核苷类似物（ＮＡ）治疗大鼠Ｃ６脑胶质瘤。方法：用Ｘ－ｇａｌ染色测定ＡｄＨＣＭＶ－ｌａｃＺ转染大鼠Ｃ６胶质瘤细胞的效率。用ＡｄＨＣＭＶ－ｔｋ／ＡＣＶ、ＧＣＶ离体及活体治疗大鼠Ｃ６胶质瘤。结果：ＡｄＨＣＭＶ－ｌａｃＺ感染Ｃ６细胞效率达１００％，ＡｄＨＣＭＶ－ｔｋ感染Ｃ６细胞，在病毒感染复数为１０００时，ＧＣＶ和ＡＣＶ半致死剂量分别为３μｇ／ｍｌ和２０μｇ／ｍｌ，Ａｄ－ＨＣＭＶ－ｔｋ／ＡＣＶ治疗大鼠Ｃ６胶质瘤模型，大鼠生存期超过９０天，而对照组分别为１７．０±１．６天（生理盐水组）、１４．５±１．３天（ＡｄＨＣＭＶ－ｌａｃＺ组），Ｐ＜０．００１。结论：重组腺病毒对靶细胞感染效率可达１００％，ＡｄＨＣＭＶ－ｔｋ用ＧＣＶ的杀伤Ｃ６胶质瘤细胞比ＡＣＶ强，而ＨＳＶ－ｔｋ／ＡＣＶ用腺病毒介导治疗大鼠脑肿瘤疗效显著。     

溴氰菊酯对白纹伊蚊（Aedesalbopictus）C6／36细胞株的细胞遗传学效应

本研究选择１０μｇ／ｍｌ、２０μｇ／ｍｌ、４０μｇ／ｍｌ浓度的溴氰菊酯处理白纹伊蚊Ｃ６／３６细胞，以ＭＭＣ作为阳性对照物，观察溴氰菊酯处理２４ｈ后对Ｃ６／３６细胞染色体畸变率和姐妹染色单体互换（ＳＣＥ）频率的影响。结果显示，三个浓度的溴氰菊酯对Ｃ６／３６细胞染色体畸变率均没有显著影响（Ｐ＜０．０５）；溴氰菊酯浓度在４０μｇ／ｍｌ时可诱导Ｃ６／３６细胞ＳＣＥ频率轻度增高（Ｐ＞０．０５），而溴氰菊酯浓度在１０μｇ／ｍｌ、２０μｇ／ｍｌ时，对Ｃ６／３６细胞ＳＣＥ频率没有诱导作用。表明溴氰菊酯对Ｃ６／３６细胞的遗传学效应较弱     

A HIGH FREQUENCY OF INHERITED DEFICIENCY OF COMPLEMENT COMPONENT C4 IN DARWIN ABORIGINES

Abstract A high frequency of serum complement component C4A deficiency may explain the higher prevalence and greater severity of systemic lupus erythematosus reported in Australian Aborigines. Inherited deficiencies of serum complement components C4A, C4B, and C2 were examined in two Australian Aboriginal populations from Darwin and Alice Springs and compared with the prevalence of complement deficiencies in white Australian blood donors. The frequency of C4A deficiency alleles was 29% in Darwin Aborigines compared with 12% in Alice Springs and 17% in Canberra blood donors. Partial C4B deficiency was also higher in Darwin Aborigines than in the other populations. Inherited deficiency of serum complement component C2 was not observed.     

肝细胞癌SCT表现和相关基因表达的初步研究

目的　探讨肝细胞癌细胞中nm2 3 H1基因和C erbB 2基因的表达和其与SCT表现的关系。方法　对 3 6例经手术病理证实且行螺旋CT动、静脉双期增强扫描的肝细胞癌病例 ,观察其SCT表现特征 ,如包膜、子灶、门静脉癌栓、肝门淋巴结转移、肿瘤的大小和强化特征。用免疫组织化学的方法检测癌组织中nm2 3 H1基因和C erbB 2基因的表达情况。结果　肝细胞癌细胞中 ,nm2 3 H1阳性 2 1例 ,阳性率为 5 8.3 % ,转移高危组 (子灶、门脉癌栓、肝门淋巴结转移 )nm2 3 H1基因的表达低于转移低危组 (P <0 .0 5 ) ;C erbB 2基因阳性 2 2例 ,阳性率为 71.1% ,C erbB 2基因的表达在中等大小肝癌组表达高于小肝癌组和大肝癌组 (P <0 .0 5 )。结论　肝细胞癌的SCT表现与nm2 3 H1和C erbB 2基因的表达有一定关系     

Active production of anti-human T-lymphotropic virus type I (HTLV-I) IgM antibody in HTLV-I-associated myelopathy

We investigated the presence of anti-human T-lymphotropic virus type I (HTLV-I) IgM in sera and cerebrospinal fluid from patients with HTLV-I-associated myelopathy (HAM) by Western blot analysis. Analyses of 36 serum samples revealed that most patients (31/36; 86.1%) had anti-HTLV-I IgM, whereas only four of 23 (17.4%) HTLV-I carriers had it. In studies of cerebrospinal fluid, anti-HTLV-I IgM was detected in 24 of 36 (66.7%) HAM patients, whereas none was detected in nine HTLV-I carriers. The differences were statistically significant (p less than 0.01). These results suggest that persistent active replication of HTLV-I occurs in the central nervous system as well as in the peripheral blood of HAM patients, and may contribute to the development of HAM.     

Multidrug transport in human glioblastoma cells is inhibited by transforming growth factors type beta 1, beta 2, and beta 1.2

The transforming growth factors type beta 1, beta 2, and beta 1.2 suppress multidrug transport in human pat-1 glioblastoma cells and even in cells that strongly over-express mdr genes and are resistant to inhibition of multidrug transport by chemosensitizers. Thus, inhibition of multidrug transport by cytokines might be a new approach to increase cellular accumulation of chemotherapeutic agents in multidrug resistant glial tumor cells. Interestingly, a member of the more distantly related decapentaplegic subgroup of transforming growth factors, the bone morphogenetic protein BMP 2, did not inhibit multidrug transport.     

ABO血型与肝炎病毒感染关系的探讨

目的：探讨ABO血型与肝炎病毒感染的关系，方法：应用疾病关联分析方法对HBsAg和,抗－HCV阳性献血者与同期健康献血者的ABO血型资料进行比较分析。结果：ABO血型与HBsAg和抗－HCV阳性率之间无显著性相关关系（P＞0．05），结论：乙型肝炎和丙型肝炎病毒感染与ABO血型无显著性相关。     

窒息鼠脑组织型纤溶酶原激活物活性变化与脑水肿的关系

目的：探讨窒息对鼠脑分泌组织型纤溶酶原激活物（TPA）的影响与脑水肿的关系。方法：通过“延迟剖宫产术”致胎鼠宫内窘迫，实验分空白对照组，窒息15min组，窒息30min组，窒息15min复氧30min组，窒息30min复氧30min五个实验组，每组各取8例测试脑组织TAP的活性及含水量，结果：窒息后鼠脑TPA活性与含水量均升高（P＜0．01），结论：窒息可致TAP活性增高，同时发生脑水肿，高活性的TPA可能是脑缺氧缺血致不可逆神经元损伤的一个重要媒介。     

Herpes simplex virus latency in the nervous system – a new model

Permissive herpes simplex virus (HSV) infection in tissue culture results in host cell destruction. Latent HSV infection in vivo occurs in neurons of peripheral sensory ganglia (PSG) and it therefore can not take place in neurons in which the virus has completed a lytic replication cycle similar to that present in vitro. Our hypothesis, based on experimental data and observations in humans, suggests that establishment of latent infection and reactivation of HSV-1 does not involve neuronal cell loss. Latency is established in neurons in which the virus does not replicate and is determined, in part, by the tissue levels of a herpes transactivating protein (Vmw65) that is a component of the viral tegument. We also suggest that reactivation of latent infection does not involve destruction of neurons and is due to replication of virus at the peripheral mucocutaneous tissues to where virus or viral DNA have been transported from the nervous tissue. Alternatively, reactivation is initiated in the PSG using a replication cycle which does not involve irreversible damage to neurons. This model explains the lack of damage to neurons which continue to serve as permanent reservoirs of latent virus for the entire life of the host.