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Benzene, an accepted leukemogen, has been suggested to cause other hemato- and lymphopoietic cancers. Here we review the published literature for non-Hodgkin lymphoma (NHL) and occupational exposure to benzene. Six cohorts, sixteen case–control studies and two studies of other designs were identified through keyword searches of bibliographic databases. Twenty-two of twenty-four studies found no association between NHL and ever exposed to benzene compared to never; a random-effects meta-analysis gave a pooled risk estimate of 1.11 (95% confidence interval 0.94–1.30). Our finding of no effect agrees with one of two previous meta-analyses. The other meta-analysis examined if high benzene exposure increased NHL risk but a lack of consistent exposure categories within the same metric should have precluded pooling risks by exposure level. Instead, we reviewed whether dose–response relationships existed. The best available data came from six studies where exposure was estimated from historical measurements and on the whole, no trends in risks of NHL with rising cumulative, average, peak, or duration of benzene exposure were found. NHL is a heterogeneous group of malignancies and although less well-studied, benzene was not associated with any NHL subtype. In conclusion, benzene at either low or high doses does not increase the risk of NHL. 相似文献
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Extracellular suppression allows mating by pheromone-deficient sterile mutants of Saccharomyces cerevisiae 总被引:14,自引:1,他引:13
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MAT alpha haploids with mutations in the STE13 or KEX2 gene, and MATa haploids with mutations in the STE6 or STE14 gene, do not mate with wild-type cells of the opposite mating type. We found that such mutants were able to mate with partners that carry mutations (sst1 and sst2) that cause cells to be supersensitive to yeast mating pheromone action. Mating ability of MAT alpha ste13 and MAT alpha kex2 mutants could also be restored by adding normal MAT alpha cells to mating mixtures or by adding just the appropriate purified pheromone (alpha-factor). Therefore, the mating deficiencies caused by the ste13 and kex2 lesions, and by inference, the ste6 and ste14 mutations, appear to result only from secretion of an insufficient amount of pheromone or a nonfunctional pheromone. 相似文献
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Sergio M. Villordo Claudia V. Filomatori Irma Sánchez-Vargas Carol D. Blair Andrea V. Gamarnik 《PLoS pathogens》2015,11(1)
Many viral pathogens cycle between humans and insects. These viruses must have evolved strategies for rapid adaptation to different host environments. However, the mechanistic basis for the adaptation process remains poorly understood. To study the mosquito-human adaptation cycle, we examined changes in RNA structures of the dengue virus genome during host adaptation. Deep sequencing and RNA structure analysis, together with fitness evaluation, revealed a process of host specialization of RNA elements of the viral 3’UTR. Adaptation to mosquito or mammalian cells involved selection of different viral populations harvesting mutations in a single stem-loop structure. The host specialization of the identified RNA structure resulted in a significant viral fitness cost in the non-specialized host, posing a constraint during host switching. Sequence conservation analysis indicated that the identified host adaptable stem loop structure is duplicated in dengue and other mosquito-borne viruses. Interestingly, functional studies using recombinant viruses with single or double stem loops revealed that duplication of the RNA structure allows the virus to accommodate mutations beneficial in one host and deleterious in the other. Our findings reveal new concepts in adaptation of RNA viruses, in which host specialization of RNA structures results in high fitness in the adapted host, while RNA duplication confers robustness during host switching. 相似文献
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Alexander Blair 《BMJ (Clinical research ed.)》1924,2(3338):1177-1178
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In this study we present evidence to suggest that gastroduodenal mucosal defects may occur in gastric fistula dogs actively immunized with PGE2-thyroglobulin conjugate. One of four PGE2-immunized dogs developed a chronic pyloroduodenal ulcer with penetration into the pancreas and the other three had endoscopic evidence of gastric and/or duodenal erosions. In contrast, no gastroduodenal mucosal defects were seen in control dogs immunized with thyroglobulin alone. Occurrence of gastroduodenal ulcers or erosions was temporally related to formation of specific antibody to PGE2 suggesting that PGE2 antibody may be responsible for lesion formation. An increase in gastric acid secretion was not observed in PGE2-immunized dogs. Thus, it is likely that mucosal defects occur as a result of an impairment of PGE2-mediated mucosal defense mechanisms. Since gastroduodenal lesions can be visualized by endoscopy, the dog may prove to be useful in studying the role of endogenous PG in ulcer diseases. 相似文献