Encephalomyocarditis (EMC) virus-induced sialodacryoadenitis in mice

The mode of occurrence of the D variant of encephalomyocarditis (EMC-D) virus-induced acute sialodacryoadenitis was investigated using three strains of mice differing in their sensitivity to EMC-D virus-induced diabetes (C57BL/6: resistant; BALB/c: moderately sensitive; DBA/2: highly sensitive). Mice were intranasally inoculated with high (10(5) PFU/mouse) or low dose (10(2) PFU/mouse) of EMC-D virus. Although there were individual differences, the blood virus titer generally reached the peak earlier in the high-dose group than in the low-dose group. Signals of viral RNA and histopathological changes were seen in parotid glands and intraorbital and extraorbital lachrymal glands. In these glands, signals of viral RNA and histopathological changes were detected only in acinar cells and initial lesions were characterized by pyknosis of acinar cells. Coagulative necrosis with interstitial inflammatory cell infiltration developed later in parotid glands of BALB/c mice of the high-dose group and in intraorbital and extraorbital lachrymal glands of all groups except for C57BL/6 mice of the low-dose group. Such changes were not observed in epithelial cells of the ductal system. The present results indicate that EMC-D virus shows clear tissue and cell tropism within the salivary and lachrymal glands, probably due to the distribution of receptors for EMC virus.     

Transcription from the gene encoding the herpesvirus entry receptor nectin-1 (HveC) in nervous tissue of adult mouse

Hepatitis C virus core protein, in addition to being a component of the viral capsid, has a number of regulatory functions. Here we showed two bodies of evidence indicating that a fraction of the core protein species is a substrate of the ubiquitin (Ub)-proteasome pathway of targeted proteolysis. First, the core protein processing the C-terminal hydrophobic region is metabolically unstable, and incubation with a proteasome inhibitor led to a significant accumulation of the protein. Second, an in vivo ubiquitylation assay indicates conjugation of multi-Ub chain to the unstable core protein. In contrast, a stable form of core protein, p21, is also able to be ubiquitylated, but it links to a single or only a few Ub moiety. Therefore, processing event(s) at the C-terminal hydrophobic domain of HCV core protein may affect the ubiquitylation pathway, particularly the efficiency of the multi-Ub chain assembly, resulting in stable, matured core proteins.     

Epidemiologic survey and genetic analysis of endemic hepatitis C virus infection in a Japanese town with a high prevalence of hepatitis B virus carriers

Mass screening for hepatitis C virus antibody was carried out in 875 inhabitants (313 men and 562 women) of a town in Japan with a high rate of hepatitis B virus infection. The overall rate of positivity for anti-HCV was 8.8% (6.4% in men and 10,1% in women). The rate of positivity for hepatitis B virus surface antigen was 11.2%. Five subjects (0.6%) were positive for both markers. HCV-RNA was detected in 65 (88.4%) of 77 individuals who were positive for anti-HCV and in 1 (1.5%) of 60 individuals negative for anti-HCV. The genotype of the HCV genome was determined by PCR analysis using type-specific primers in 60 individuals. HCV type 1b was detected in 51 subjects (85%), type 2a in 3 subjects (5%), and type 2b in 6 subjects (10%). None of the individuals was infected with more than one genotype. The nucleotide sequences of the partial nonstructural 5 region of HCV type 1b genotype obtained from 6 individuals showed at least 92.0% homology in the nucleotide sequence, and 94.8% homology in the amino acid sequence. Homology among these clones was greater than their homology with previously described type 1 b sequences. The findings suggest that there was a specific local origin of HCV infection, although it was not possible to identify any single source of HCV infection. The results also indicate the presence of asymptomatic HCV carriers. © 1995 Wiley-Liss, Inc.     

Molecular Evidence for the Existence of Two Distinct Subgroups in Cucumber Mosaic Cucumovirus

Infectious full-length cDNA clones from the genomic RNAs of a subgroup II cucumber mosaic cucumovirus strain (Trk7) were obtained. Sequence analysis of the whole genome revealed strong homology (99%) to the genome of Q-CMV, the only subgroup II strain whose entire genomic nucleotide sequence had been available in the database, and an overall 75% homology to those of subgroup I strains. We provide sequence comparisons of different parts of 1a, 2a and 2b proteins of Cucumovirus species, and propose phylogenetic trees based on these protein sequences.     

survivin的siRNA靶向干扰膀胱癌的实验研究

目的实验研究靶向转染survivin的小分子干扰RNA（small interfering RNA，siRNA）对膀胱癌生物学行为的影响。方法设计1对survivin编码基因序列特异的siRNA，用脂质体转染T24膀胱癌细胞株。采用流式细胞术检测转染效率和细胞凋亡；荧光实时定量PCR检测干扰前后survivin的mRNA表达；用survivin的siRNA片段插入空载体后建立重组载体pRNAT-U6、1／Neo-survivin。结果脂质体转染T24细胞后的转染效率为92．3％；survivin编码基因序列特异的siRNA能有效下调survivin基因的表达，呈时间和剂量依赖性，最大效应浓度为100nmol／L，此时survivin表达水平下调了75．91％，并显著地抑制了细胞生长，抑制率达55．29％，差异有统计学意义（P〈0．01）；细胞凋亡率亦增至45．70％，与对照相比差异有统计学意义（P〈0．01）。用限制性内切酶将空载体线性化，T4DNA连接酶将siRNA片段插入空载体中，对该重组表达载体进行鉴定，获得RNA干扰质粒载体pRNAT-U6．1／Neo-survivin。结论siRNA．survivin能显著下调膀胱癌细胞survivin基因表达水平，促进细胞凋亡，抑制肿瘤细胞增殖，可能成为膀胱癌基因治疗的新工具。成功构建的靶向survivin基因表达的RNA干扰质粒载体为进一步应用RNA干扰技术进行survivin基因功能研究奠定了基础。     

Electron-autoradiographic study of RNA synthesis in epithelial cells of the renal tubules of albino rats poisoned with mercuric chloride

Department of Biology, Grodno Medical Institute. Department of Pathological Anatomy, A. V. Vishnevskii Institute of Surgery, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR D. S. Sarkisow.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 107, No. 3, pp. 357–360, March, 1989.     

Bacterial mortality in culture and in septic wounds

Department of Pathological Anatomy, A. V. Vishnevskii Institute of Surgery, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR D. S. Sarkisov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 106, No. 10, pp. 464–467, October, 1988.