lncRNA DGCR5 inhibits the proliferation of colorectal cancer cells by downregulating miR-21.

Long non-coding RNA (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) serves roles as a tumor suppressor or oncogene in different types of cancer. The current study aimed to explore the role of DGCR5 in colorectal cancer (CRC). It was revealed that the expression of DGCR5 was downregulated, while microRNA (miR)-21 was upregulated in CRC. The expression level of DGCR5 in tumor tissue decreased, while expression levels of miR-21 increased, with advancing stages of the disease. The expression levels of DGCR5 and miR-21 were inversely associated in tumor tissues. In CRC cells in vitro, miR-21 overexpression failed to significantly affect DGCR5, while DGCR5 overexpression resulted in reduced expression levels of miR-21. DGCR5 overexpression showed no significant effects on cancer cell migration and invasion, but suppressed cancer cell proliferation in vitro. miR-21 overexpression increased cancer cell proliferation and attenuated the effects of DGCR5 overexpression. Therefore, lncRNA DGCR5 may inhibit the proliferation of CRC cells by downregulating miR-21.

Efficiency of anisodamine for organophosphorus-poisoned patients when atropinization cannot be achieved with high doses of atropine.

Poisoning by organophosphorus insecticides is a major global public health problem. Although atropine has been widely used to treat organophosphate (OP) poisoning, sometimes atropinization cannot be achieved, even with high doses of atropine. Hence, we aimed to assess the effect of anisodamine for organophosphorus poisoned patients for whom atropinization could not be achieved through high doses of atropine. In this study, sixty-four OP-poisoning patients, all of whom accepted routine treatments but who did not attain atropinization after high doses of atropine for 12 h, were enrolled. The result showed that the time to atropinization was 24.3±4.3 h in the anisodamine group, significantly shorter than in the atropine group (29.2±7.0 h, p<0.05); the hospital stay in the anisodamine group was 5.3±2.5 days, significantly shorter than the 6.9±2.3 days needed by the atropine group (p<0.05). We draw a conclusion that anisodamine can shorten the process of atropinization and hospital stay in organophosphorus poisoned patients for whom atropinization cannot be achieved with high doses of atropine.