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排序方式: 共有495条查询结果,搜索用时 15 毫秒
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CG Teo 《Oral diseases》2002,8(S2):88-90
Oral hairy leukoplakia (OHL) and Kaposi's sarcoma (KS) are commonly encountered in the HIV-infected patient. A unique feature of OHL is non-cytolytic high level of replication of Epstein–Barr virus (EBV) in the glossal epithelium. The expression of viral-encoded anti-apoptotic proteins concomitant to replicative proteins probably underlies this phenomenon. The question of whether OHL arises from activation of EBV latent in the tongue, or from superinfection by endogenous EBV shed via non-glossal sites or by exogenous EBV remains unresolved. Human herpesvirus 8 (HHV8) is now seen as necessary but not sufficient cause of KS. Expression of HHV8-encoded oncogenic proteins in endothelial cells probably explains the aberrant proliferation of these cells in KS lesions. Studies into why KS is so commonly observed at the palate in HIV-infected patients may provide important clues to its pathogenesis. 相似文献
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Retroviruses are associated with a variety of diseases, including immunological and neurological disorders, and various forms of cancer. In humans, the Human T-cell Leukaemia/Lymphotropic virus type 1 (HTLV-1), which belongs to the Oncovirus family, is the aetiological agent of two diverse diseases: Adult T-cell leukaemia/lymphoma (ATLL) (Poiesz et al. 1980; Hinuma et al. 1981; Yoshida et al. 1982), as well as the neurological disorder tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HAM) (Gessain et al. 1985; Rodgers-Johnson et al. 1985; Osame et al. 1986). HTLV-1 is the only human retrovirus known to be the aetiological agent of cancer. A genetically related virus, HTLV-2, has been identified and isolated (Kalyanaraman et al. 1982). However, there has been no demonstration of a definitive aetiological role for HTLV-2 in human disease to date. Simian T-cell lymphotropic viruses types 1 and 2 (STLV-1 and -2) and bovine leukaemia virus (BLV) have also been classified in same group, Oncoviridae, based upon their similarities in genetic sequence and structure to HTLV-1 and -2 (Burny et al. 1988; Dekaban et al. 1995; Slattery et al. 1999). This article will focus on HTLV-1, reviewing its discovery, molecular biology, and its role in disease pathogenesis. 相似文献
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M J Harrod J M Friedman G Currarino R M Pauli L O Langer 《American journal of medical genetics》1984,18(2):311-320
Two unrelated infants seen for evaluation of short stature at 14 and 27 months, respectively, had clinical and radiographic findings consistent with the diagnosis of spondyloepiphyseal dysplasia congenita (SED congenita). No other anomalies were noted. Both sets of parents were normal, both family histories were unremarkable, and neither couple was consanguineous. Both families were counseled that SED congenita is an autosomal dominant disorder and that sporadic cases probably result from new mutations; a low recurrence risk was given. Both families subsequently produced a second affected child. Our experiences suggest that genocopies of autosomal dominant SED congenita exist that are clinically and radiographically indistinguishable, at least within the first 3 years. Autosomal recessive inheritance seems most likely, although alternative explanations are possible. Genetic heterogeneity should be considered when providing genetic counseling for sporadic SED congenita in young children. 相似文献
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Harrod KS Jaramillo RJ Rosenberger CL Wang SZ Berger JA McDonald JD Reed MD 《American journal of respiratory cell and molecular biology》2003,28(4):451-463
Although epidemiologic data strongly suggest a role for inhaled environmental pollutants in modulating the susceptibility to respiratory infection in humans, the underlying cellular and molecular mechanisms have not been well studied in experimental systems. The current study assessed the impact of inhaled diesel engine emissions (DEE) on the host response in vivo to a common pediatric respiratory pathogen, respiratory syncytial virus (RSV). Using a relatively resistant mouse model of RSV infection, prior exposure to either 30 microg/m3 particulate matter (PM) or 1,000 microg/m3 PM of inhaled DEE (6 h/d for seven consecutive days) increased lung inflammation to RSV infection as compared with air-exposed RSV-infected C57Bl/6 mice. Inflammatory cells in bronchoalveolar lavage fluid were increased in a dose-dependent manner with regard to the level of DEE exposure, concomitant with increased levels of inflammatory mediators. Lung histology analysis indicated pronounced peribronchial and peribronchiolar inflammation concordant with the level of DEE exposure during infection. Mucous cell metaplasia was markedly increased in the airway epithelium of DEE-exposed mice following RSV infection. Interestingly, both airway and alveolar host defense and immunomodulatory proteins were attenuated during RSV infection by prior DEE exposure. DEE-induced changes in inflammatory and lung epithelial responses to infection were associated with increased RSV gene expression in the lungs following DEE exposure. These findings are consistent with the concept that DEE exposure modulates the lung host defense to respiratory viral infections and may alter the susceptibility to respiratory infections leading to increased lung disease. 相似文献
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Arif JM; Gairola CG; Glauert HP; Kelloff GJ; Lubet RA; Gupta RC 《Carcinogenesis》1998,19(8):1515-1517
The present study investigated the effects of dietary oltipraz on cigarette
smoke-related lipophilic DNA adduct formation. Female Sprague- Dawley rats
were exposed daily to sidestream cigarette smoke in a whole- body exposure
chamber 6 h/day for 4 consecutive weeks. One group of rats was maintained
on control diet while another group received the same diet supplemented
with either a low (167 p.p.m.) or high (500 p.p.m.) dose of oltipraz,
starting 1 week prior to initiation of smoke exposure until the end of the
experiment. Analysis of lipophilic DNA adducts by the nuclease P1-mediated
32P-post-labeling showed up to five smoke-related adducts. Adduct no. 5
predominated in both the lung and the heart while adduct nos 3 and 2
predominated in the trachea and bladder, respectively. Quantitative
analysis revealed that the total adduct level was the highest in lungs
(270+/-68 adducts/10(10) nucleotides), followed by trachea (196+/-48
adducts/10(10) nucleotides), heart (141+/-22 adducts/10(10) nucleotides)
and bladder (85+/-16 adducts/10(10) nucleotides). High dose oltipraz
treatment reduced the adduct levels in lungs and bladder by >60%, while
the reduction in lungs in the low-dose group was approximately 35%. In
trachea, the effect of low and high dietary oltipraz on smoke DNA adduction
was equivocal, while smoke-related DNA adducts in the heart were minimally
inhibited by high-dose oltipraz. In a repeat experiment that employed a
3-fold lower dose of cigarette smoke, oltipraz (500 p.p.m.) was found to
inhibit the formation of DNA adducts in rat lungs and trachea by 80 and
65%, respectively. These data clearly demonstrate a high efficacy of
oltipraz in inhibiting the formation of cigarette smoke-induced DNA adducts
in the target tissues.
相似文献
10.
Mutation of the p53 tumor suppressor gene in spontaneously occurring osteosarcomas of the dog 总被引:8,自引:0,他引:8
Inactivation of the p53 tumor suppressor gene has been implicated in the
pathogenesis of numerous human cancers, including osteosarcomas.
Appendicular osteosarcomas of the dog appear to be a good model for their
human equivalent with regard to biologic behavior, epidemiology and
histopathology. We individually screened exons 5-8 of the p53 gene for
mutations in 15 canine appendicular osteosarcomas using 'Cold' SSCP to
compare the role of this gene in human and canine osteosarcoma
tumorigenesis. Seven of the tumors (47%) exhibited point mutations, with
one tumor possessing two mutations within different exons. Of these, seven
were missense mutations and the eighth was a 'silent' mutation potentially
affecting the exon 6-7 splicing region. Five of the missense mutations were
located in highly conserved regions IV and V, while another corresponded
with the highly conserved codon 220 mutational hotspot located outside the
conserved domains. The locations and types of mutations were nearly
identical to those reported in human cancer. These findings provide strong
evidence of the involvement of p53 mutations in the development of canine
appendicular osteosarcomas. Canine osteosarcomas appear to be a promising
model for their human equivalent on a clinical, pathologic, and molecular
level.
相似文献