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Apoptosis: molecular regulation of cell death 总被引:1,自引:0,他引:1
AJ Hale CA Smith LC Sutherland VE Stoneman VL Longthorne AC Culhane GT Williams 《Canadian Metallurgical Quarterly》1996,236(1):1-26
This article focuses on the few disorders that produce chronic cholestasis in infants and children. Cholestasis is defined, and a framework for thinking about pathophysiology is provided. Medical management is discussed in the context of the consequences and complications of chronic cholestasis. The limited differential for chronic cholestasis is discussed, and approaches to diagnosis and management of specific disorders are provided. 相似文献
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AC Macías Rodríguez DJ Feria Lorenzo FJ Mena Navarro 《Canadian Metallurgical Quarterly》1998,21(236):51-58
To inform nursing professionals about their role in the prevention of traffic accidents, a grave health-related problem, is the purpose of this article. To begin with, factors which can deteriorate one's capacity to drive vehicles, and over which nursing professionals can intervene, will be presented. These factors include alcohol, other drugs, medicines, individual morbidity, the factor of aging and the use of security devices. A special reference will be made about widely used medicines. Finally the role that a nurse can fulfill will be explained. This role can be directed to various sections of the general public, be of varying natures, be exercised with greater or lesser ease, and lastly can have more or less effect upon those to whom it is destined. 相似文献
996.
SE Browne AC Bowling U MacGarvey MJ Baik SC Berger MM Muqit ED Bird MF Beal 《Canadian Metallurgical Quarterly》1997,41(5):646-653
The etiology of the selective neuronal death that occurs in Huntington's disease (HD) is unknown. Several lines of evidence implicate the involvement of energetic defects and oxidative damage in the disease process, including a recent study that demonstrated an interaction between huntingtin protein and the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Using spectrophotometric assays in postmortem brain tissue, we found evidence of impaired oxidative phosphorylation enzyme activities restricted to the basal ganglia in HD brain, while enzyme activities were unaltered in three regions relatively spared by HD pathology (frontal cortex, parietal cortex, and cerebellum). Citrate synthase-corrected complex II-III activity was markedly reduced in both HD caudate (-29%) and putamen (-67%), and complex IV activity was reduced in HD putamen (-62%). Complex I and GAPDH activities were unaltered in all regions examined. We also measured levels of the oxidative damage product 8-hydroxydeoxyguanosine (OH8dG) in nuclear DNA, and superoxide dismutase (SOD) activity. OH8dG levels were significantly increased in HD caudate. Cytosolic SOD activity was slightly reduced in HD parietal cortex and cerebellum, whereas particulate SOD activity was unaltered in these regions. These results further support a role for metabolic dysfunction and oxidative damage in the pathogenesis of HD. 相似文献
997.
I Huez L Créancier S Audigier MC Gensac AC Prats H Prats 《Canadian Metallurgical Quarterly》1998,18(11):6178-6190
The mRNA of vascular endothelial growth factor (VEGF), the major angiogenic growth factor, contains an unusually long (1,038 nucleotides) and structured 5' untranslated region (UTR). According to the classical translation initiation model of ribosome scanning, such a 5' UTR is expected to be a strong translation inhibitor. In vitro and bicistronic strategies were used to show that the VEGF mRNA translation was cap independent and occurred by an internal ribosome entry process. For the first time, we demonstrate that two independent internal ribosome entry sites (IRESs) are present in this 5' UTR. IRES A is located within the 300 nucleotides upstream from the AUG start codon. RNA secondary structure prediction and site-directed mutagenesis allowed the identification of a 49-nucleotide structural domain (D4) essential to IRES A activity. UV cross-linking experiments revealed that IRES A activity was correlated with binding of a 100-kDa protein to the D4 domain. IRES B is located in the first half of the 5' UTR. An element between nucleotides 379 and 483 is required for its activity. Immunoprecipitation experiments demonstrated that a main IRES B-bound protein was the polypyrimidine tract binding protein (PTB), a well-known regulator of picornavirus IRESs. However, we showed that binding of the PTB on IRES B does not seem to be correlated with its activity. Evidence is provided of an original cumulative effect of two IRESs, probably controlled by different factors, to promote an efficient initiation of translation at the same AUG codon. 相似文献
998.
AC Lekven U Tepass M Keshmeshian V Hartenstein 《Canadian Metallurgical Quarterly》1998,125(14):2747-2758
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We observed 36 HIV-infected patients to evaluate whether the presence of tandem 2-long terminal repeat circular unintegrated HIV-1 DNA (2-LTR) in peripheral blood mononuclear cells (PBMC) at baseline was associated with acceleration of HIV disease. Detection of 2-LTR at baseline correlated with high plasma HIV-1 RNA levels (p < .01), recovery of culturable HIV-1 from plasma (p = .02), and progression to AIDS during follow-up (p = .01). More patients with 2-LTR (68%) than without 2-LTR (31%) had a decline in CD4 levels of >50 cells/mm3 over the first 18 months of follow-up (p = .04), and the average annual CD4 decline was 35% in patients with 2-LTR compared with 16% in those without 2-LTR (p = 0.06). Detection of 2-LTR in PBMC at baseline was an independent predictor of high plasma HIV-1 RNA levels and subsequent CD4 cell decline in this cohort of patients with predominantly nonsyncytium-inducing (NSI) isolates at baseline. The presence of 2-LTR in PBMC appears to be reflective of ongoing HIV-1 replication, as measured by plasma HIV-1 RNA levels, and identifies persons at risk for immunologic and clinical decline. 相似文献