Reduced replicative capacity is a consistent characteristic of cells derived from patients with Werner syndrome. This premature senescence is phenotypically similar to replicative senescence observed in normal cell strains and includes altered cell morphology and gene expression patterns. Telomeres shorten with in vitro passaging of both WRN and normal cell strains; however, the rate of shortening has been reported to be faster in WRN cell strains, and the length of telomeres in senescent WRN cells appears to be longer than that observed in normal strains, leading to the suggestion that senescence in WRN cell strains may not be exclusively associated with telomere effects.
View Article and Find Full Text PDFBackground: Limited replicative capacity is a defining characteristic of most normal human cells and culminates in senescence, an arrested state in which cells remain viable but display an altered pattern of gene and protein expression. To survey widely the alterations in gene expression, we have developed a DNA microarray analysis system that contains genes previously reported to be involved in aging, as well as those involved in many of the major biochemical signaling pathways.
Results: Senescence-associated gene expression was assessed in three cell types: dermal fibroblasts, retinal pigment epithelial cells, and vascular endothelial cells.
Eur J Clin Microbiol Infect Dis
October 1992
The performance of the Septi-Chek AFB System (Roche) in the isolation of mycobacteria was compared to that of culture on Lowenstein-Jensen (LJ) medium and the Bactec radiometric system. The Septi-Chek AFB system detected a significantly higher number of positive specimens (62/66 versus 47/66 for Bactec and 39/56 for LJ medium) and was more often the only medium in which an isolate was recovered. The average time for detection of isolates was very similar for the Septi-Chek AFB and Bactec systems which were both significantly faster than LJ medium in the majority of isolates.
View Article and Find Full Text PDFInfection of adult male C3H/HeJ mice with a host range variant of Coxsackievirus B3 (CB3W-RD) induced resistance in these mice to an otherwise lethal dose of Coxsackievirus B1 (CB1). The protective effect induced by CB3W-RD was detectable as early as 1 day post-vaccination and was still present 10 weeks later. While untreated mice infected with CB1 died within 5 days because of massive hepatic necrosis, the liver was spared in mice immunized with CB3W-RD and then challenged with CB1.
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