[The study on pathogenesis of latex allergy.].

OBJECTIVE: In order to study the pathogenesis of latex allergy and the significance in the prevention and cure of occupational diseases. METHODS: 651 cases in the out-patient department were tested with skin prick test (SPT), and the specific IgE (sIgE) to latex were detected by means of disk ELISA and Western-blot. RESULTS: It was found that the positive rate of latex SPT (37.5%) and sIgE (31.25%) were rather higher in patients in comparison with those of the normal. The positive rate of latex sIgE was much higher in the high-risk group than that of the low-risk group and the normal. The serum of the patients can react with multi-bands in the latex glove extracts. CONCLUSION: The prevalence of latex allergy is rather high, this disease is mediated by IgE. The people in high-risk should be tested by latex allergy in order to take proper occupational and daily protection.

Autophagy contributes to the enrichment and survival of colorectal cancer stem cells under oxaliplatin treatment.

Currently, chemoresistance is an important cause of treatment failure in colorectal cancer. Cancer stem cells, which are a population of multi-potent cells with the capacity to self-renew and differentiate, have been found to participate in chemoresistance. In the present study, the chemotherapeutic drug oxaliplatin induced autophagy in colorectal cancer cell lines, which in turn protected cancer cells from apoptosis. Further results showed that oxaliplatin-induced autophagy enriched the population of colorectal CSCs and participated in maintaining the stemness of colorectal CSCs, thus making the cells more resistant to chemotherapy. Taken together, the results indicate that autophagy might enhance the chemoresistance of colorectal cancer cells by protecting the stemness and chemoresistance of colorectal CSCs. Our study demonstrates that autophagy plays a pro-survival role in colorectal CSCs subjected to oxaliplatin. Therefore, targeting autophagy may be considered as a potential therapeutic strategy to address chemoresistance in the treatment of colorectal cancer.

Biphasic regulation of autophagy by miR-96 in prostate cancer cells under hypoxia.

Autophagy favors cell survival under hypoxia, and increasing evidence revealed that microRNAs regulate autophagy. We report here hypoxia increased the expression of miR-96 in prostate cancer cells, and miR-96 stimulated autophagy by suppressing MTOR. We found that inhibition of miR-96 abolished hypoxia-induced autophagy. Paradoxically, ectopic over-expression of miR-96 to a certain threshold, also abolished the hypoxia-induced autophagy. Further studies have shown that high levels of miR-96 inhibited autophagy through suppressing ATG7, a key autophagy-associated gene. Importantly, the miR-96 expression level threshold was determined, and the effects of miR-96 on autophagy on either side of the threshold were opposite. These data demonstrate hypoxia-induced autophagy is at least partially regulated by miR-96; miR-96 can promote or inhibit autophagy by principally inhibiting MTOR or ATG7 depending on the expression levels of miR-96. Our observation might reveal a novel regulatory mode of autophagy by microRNAs under hypoxia.