To determine the incidence and clinical relevance of active human herpesvirus 6 (HHV-6) infection, 92 consecutive unselected recipients of autologous or allogeneic stem cell grafts were investigated in a prospective longitudinal study. Active infection was assessed by the presence of viral deoxyribonucleic acid (DNA) in 846 peripheral blood mononuclear cell specimens and 115 plasma specimens, by means of a specially developed polymerase chain reaction designed to avoid detection of latent genome. The incidence of HHV-6 infection observed was 42.5%, irrespective of the type or source of graft, and infection was significantly associated with partial (P=.002) or total myelosuppression (P=.01) and fever (P<. 000001). Infusion of bone marrow as the source of graft, reactivation occurring before platelet or neutrophil engraftment, and presence of HHV-6 DNA in plasma were identified as risk factors for symptomatic HHV-6 infection (P<.002).

Taken together, the results suggest that PM2.5 exposure destroys BTB integrity through excessive ROS-mediated autophagy. Our finding could contribute to a better understanding of PM2.5-induced male reproductive toxicity.

Di-(2-ethylhexyl) phthalate (DEHP) is an environmental endocrine disruptor widely used in China that is harmful to the male reproductive system. Many studies have shown that DEHP causes testicular toxicity through oxidative stress, but the specific mechanism is unknown. Because the Notch pathway is a key mechanism for regulating cell growth and proliferation, we investigated whether Notch is involved in DEHP-induced testicular toxicity and whether vitamins E and C could rescue testicular impairment in Sprague-Dawley (SD) rats. Compared with the control group, we found that DEHP exposure induced testicular toxicity through oxidative stress injury, and it decreased the testosterone level (P < .01) and upregulated nuclear factor-erythroid 2 related factor (Nrf2) expression (P < .01). Therefore, because oxidative stress might be the initiating factor of DEHP-induced testicular toxicity, treatment with the antioxidant vitamins E and C activated the Notch1 signaling pathway in the testis and in Leydig cells. Treatment with vitamins E and C normalized the oxidative stress state after DEHP exposure and restored testicular development to be similar to the control group. In summary, antioxidant vitamins E and C may be used to treat DEHP-induced testicular toxicity.

No abstract