1,721,205 research outputs found
Effects of caffeine on the cell cycle progression and on the production of chromosomal aberrations in human lymphocytes treated with MMC in Go and in G1
No full textTumor necrosis factor receptor-associated periodic syndrome as a model linking autophagy and inflammation in protein aggregation diseases
No full textAutophagy prevents cellular damage by eliminating insoluble aggregates of mutant misfolded proteins, which accumulate under different pathological conditions. Downregulation of autophagy enhances the inflammatory response and thus represents a possible common pathogenic event underlying a number of autoinflammatory syndromes, such as tumor necrosis factor (TNF) receptor-associated periodic syndrome (TRAPS). The pathogenesis of other monogenic or complex disorders that display symptoms of excessive inflammation also involve the autophagy pathway. Studies have shown that TRAPS-associated TNFRSF1A mutations induce cytoplasmic retention of the TNFR1 receptor, defective TNF-induced apoptosis, and production of reactive oxygen species (ROS). Furthermore, autophagy impairment may account for the pathogenic effects of TNFRSF1A mutations, thus inducing inflammation in TRAPS. In this review, we summarize the molecular interactions and functional links between autophagy with regard to nuclear factor-kappa B activation, ROS production, and apoptosis. Furthermore, we propose a complex interplay of these pathways as a model to explain the relationship between mutant protein misfolding and inflammation in genetically determined and aggregation-prone diseases. Accordingly, autophagy function should be investigated in all diseases showing an inflammatory component, and for which the molecular pathogenesis is still unclear. © 2014 Springer-Verlag Berlin Heidelberg
Caffeine potentiation of sister chromatid exchanges and chromosomal aberrations in second division cells
No full textSurveillance of birth defects: the multicommunity sets technique tested by computer simulation
No full textUsing a computer simulation for a series of births subject to various congenital malformations, the surveillance performance of the Multicommunity Sets Technique (MST) was compared to that of the Cumulative Sum Technique (CUSUM). Increases in malformation frequencies were simulated in (i) 6 out of 6 centres and (ii) only 3 out of 6 centres. MST was neither more sensitive nor more specific than CUSUM, and signalled increases with greater delay. One type of CUSUM procedure showed to accumulate more false alarms than MST in long periods of surveillance at the baseline malformation rate. The advantage of CUSUM was also shown for a single malformation with a very low baseline incidence, which according to Chen et al. (4983) should have been particularly suitable for MST surveillance. © 1986 Kluwer Academic Publishers
Flow cytometric DNA content analysis on cultured lymphocytes from workers exposed to clastogenic agents
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Caffeine post-treatment causes a shift in the chromosome aberration types induced by mitomycin C, suggesting a caffeine-sensitive mechanism of DNA repair in G2
No full textHuman lymphocytes were exposed in G1 to mitomycin C (2.5 microM for 2 h) and harvested at 3-h intervals from 48 to 84 h after stimulation. All cultures were also post-treated in G2 with caffeine (2 mM). Different types of chromosomal aberrations were scored in the first division metaphases. Caffeine increases all chromosome aberration types by promoting a premature mitosis of damaged cells. However, when the frequency of damaged cells is not affected by the caffeine post-treatment, a reduction of the frequency of the exchange-type aberrations was shown. The possibility that caffeine interferes with some mechanism of G2 repair is discussed
Kinetics of chromosomal aberrations and first mitosis division in human lymphocytes exposed to mitomycin C
No full textIn order to understand the relationship between the chromosomal damage detectable at the first mitosis after mutagen treatment and the induced mitotic delay we studied the time pattern of both mitotic indices and chromosomal aberration frequencies in human lymphocytes treated in G1 with mitomycin C (2.5 microM) and cultured in vitro in the presence of 5-bromo-2'-deoxyuridine. Mitotic delay was observed in treated cells cultured for 81 h. At this point an increase in the frequency of chromosomal aberrations is evident and a higher proportion of abnormal cells enters mitosis, the long delay being due to the extensiveness of DNA damage. The importance of cell cycle progression for the detection of the maximal amount of induced chromosomal damage is discussed
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