Abstract Recent studies have found that lncRNA-MEG3(MEG3) plays an important role in the development of EMs (Endometriosis), but the specific mechanism needs to be further explored. This study aimed to investigate the effect of MEG3 on the proliferation, invasion of EMs cells. The authors used RT-qPCR to detect the expression of MEG3 and miR-21-5p in EMs tissues and hESCs cells, MTT and Transwell to detect cell proliferation and invasion, western blotting assay to detect the expression of DNMT3B and Twist, MSP to detect the methylation of Twist. The present study's detection results showed that MEG3 was lowly expressed in EMs tissues and hESCs cells, and overexpression of MEG3 could down-regulate miR-21-5p and inhibit endometrial cell proliferation and invasion. In addition, overexpression of MEG3 upregulated the expression of DNMT3B and promoted the methylation of TWIST. In conclusion, the present findings suggest that MEG3 is downregulated in EMs tissues, and overexpression of MEG3 can promote the activity of DNA methyltransferase DNMT3B by downregulating miR-21-5p, thereby promoting the methylation of Twist, downregulating Twist level to inhibits hESCs cells proliferation and invasion.

ABSTRACT Screening promising L. thermophiles with high productivity, high efficiency and strong adaptability are very important in lactic acid industry. For this purpose, 80MeV/u carbon ions were applied to irradiate L. thermophiles. After high-throughput screening, a mutant, named SRZ50, was obtained. Different carbon sources or nitrogen sources were provided to investigate carbon or nitrogen source utilization between mutant SRZ50 and wild type, and different fermentation periods were also chose to study fermentation characteristic between mutant SRZ50 and wild type. The results showed that mutant SRZ50 exhibited the enhanced L-(+)-lactic acid production from wild type. When glucose or fructose was the sole carbon source, the L(+)-lactic acid production by mutant SRZ50 was both the highest, respectively, 23.16 ± 0.72 g/L or 23.24 ± 0.66 g/L, which had a significant increase from that of wild type (P<0.01), following obvious increase in biomass (P<0.05). When yeast powder was the sole nitrogen source, it can promote mutant SRZ50 to accumulate the highest L-(+)-lactic acid accumulation, which also had a significant increase from that of wild type (P<0.01). Under different fermentation periods, it was obtained that mutant SRZ50 all exhibited significant increase in L-(+)-lactic acid accumulation from wild type. In conclusion, a mutant strain with improved production profiles for L-(+)-lactic acid, was obtained, indicating that heavy ions can be an efficient tool to improve metabolic product accumulations in microbes.

Endosulfan is an organochlorine insecticide, widely used in insect control. Unfortunately, it is also an acute neurotoxic compound to both insects and mammals, including humans, and has been responsible for many severe poisonings and several fatal cases. Endosulfan also imitates or enhances the effect of the female hormone estrogen, having the capability of causing reproductive and developmental damage in both, animals and humans, and its exposure has been linked to liver tissue injury. This persistent lipophilic compound is one of the most abundant organochlorine pesticides in the environment, capable of undergoing long range transport to remote locations such as the Arctic. It is practically water-insoluble, but readily adheres to clay particles and persists in soil and water for several years. Its indiscriminate and injudicious use in the control of insects on a wide range of agricultural products and in the extermination of house-hold pests, has considerably increased the hazard risk for human health. Also, this compound has a high fatality rate in humans when ingested accidentally, from food or water contaminated, or in suicidal cases. The aim of this article is to review and summarize chemical, biochemical, environmental, and toxicological data of endosulfan and draw attention to its toxicological potential risk to human health.