Description of a new species of the genus Uropsilus (Eulipotyphla: Talpidae: Uropsilinae) from the Dabie Mountains, Anhui, Eastern China.

During a terrestrial vertebrate survey of the Dabie Mountains in Anhui Province, eastern China, we collected four Asian shrew mole specimens (hereafter, shrew moles). Based on published literature and comparison with previously collected materials, the four specimens were similar to shrew moles from the mountains of Southwest China; however, no species in this group has been previously recorded from the Dabie Mountains. The genetic and morphological characteristics of the specimens were analyzed, based upon which a new species of shrew mole is described, named Uropsilus dabieshanensis sp. nov.

A genome-wide analysis reveals the MeCP2-dependent regulation of genes in BGC-823 cells.

Methyl-CpG-binding protein 2 (MeCP2) epigenetically modulates gene expression through genome-wide binding to methylated CpG dinucleotides. This study aimed to evaluate the effect of MeCP2 on the global gene expression profile of human gastric adenocarcinoma to determine the potential molecular mechanism of MeCP2. To identify the gene targets of MeCP2 in gastric cancer cells, we combined the expression microarray and chromatin immunoprecipitation approaches of MeCP2, followed by sequencing (ChIP-seq) to define the MeCP2-binding sites across the whole genome. The methylation levels of the promoters in BGC-823 cells were downloaded from the National Center for Biotechnology Information Gene Expression Omnibus database (GSM1093053). A total of 5,684 ChIP-enriched peaks were identified by comparing IP and Input, using a p-value threshold of 10-5 in ChIP-seq. The bioinformatics analysis presented a predictive model of the genome-wide MeCP2-binding pattern, in which the MeCP2 binding site is closely related to the transcription start site region in the genome. The results of motif detection showed that the MeCP2-binding regions contained not only the core CpG motif but also the extended poly (A/T) motifs. Finally, an integrative analysis of the sequence features and DNA methylation states revealed that MeCP2's function as a multifunctional transcriptional regulator may not be directly related to the methylation status of the binding site. The first MeCP2 ChIP-seq and gene expression microarray analysis in BGC-823 cells revealed that MeCP2 plays multiple roles in the regulation of gene expression depending on the microenvironment, such as sequence characteristics and the methylation levels of binding sites.

Knockdown of the FoxM1 enhances the sensitivity of gastric cancer cells to cisplatin by targeting Mcl-1.

Resistance to chemotherapy is a main obstacle for effective treatment of gastric cancer, the mechanism of which is still poorly understood. Forkhead box M1 (FoxM1) plays an important role in chemo-resistance of various tumors. This study aimed to explore whether FoxM1 mediated resistance of the gastric cancer cell line SGC7901 to the chemotherapy agent cisplatin (DDP). In the study, we detected FoxM1 and Mcl-1 expression via real time-PCR and western blot and demonstrated that FoxM1 is overexpressed in cisplatin-resistance GC cells and Mcl-1 expression is regulated by FoxM1. We examined SGC7901/DDP cell viability by MTT assay, which revealed that suppression of the FoxM1/Mcl-1 pathway impaired cell viability and thus increased sensitivity to cisplatin in gastric cancer cells. Taken together, the study implied that the FoxM1/Mcl-1 pathway may overcome cispaltin resistance of gastric cancer and provide a new therapeutic target for the treatment of gastric cancer.

miR-149 reverses cisplatin resistance of gastric cancer SGC7901/DDP cells by targeting FoxM1.

Drug resistance remains a major unresolved obstacle for gastric cancer (GC) treatment. Recently, increasing studies have showen that microRNAs (miRNAs) are involved in cancer chemotherapeutic resistance and can potentially be applied to reverse drug resistance in cancers. The relationship between miRNA-149 expression and cisplatin (DDP) resistance in GC cells is still unknown. Here, we detected miR-149 expression by using RT-PCR and found that expression of miR-149 was downregulated in SGC7901/DDP cells compared with SGC7901cells, indicating a role of miR-149 in determining cisplatin-resistance of GC cells. Then, SGC7901/DDP cells were tansfected with miR-149 mimics, MTT assay was performed to determine SGC7901/DDP cell viability, and showed that overexpression of miR-149 inhibited the cell viability after cisplatin treatment, suggesting that up-regulation of miR-149 enhanced SGC7901/DDP cell sensitivity to cisplatin. Furthermore, we confirmed that Forkhead box M1 (FoxM1) is a direct target of miR-149 in SGC7901/DDP cells by using luciferase reporter assay. Besides, we also demonstrated that miR-149 enhances SGC7901/DDP cell sensitivity to cisplatin by downregulating FoxM1 expression. In summary, our data provide new insights that miR-149 plays an important role in determining sensitivity of cisplatin-resistant GC cells by targeting FoxM1 and suggest that miR-149 could be a potential target for reversing drug resistance in GC.

Lifestyle intervention in non-alcoholic fatty liver disease in Chengyang District, Qingdao, China.

AIM: To evaluate the effect of a 6 and 12 mo lifestyle modification intervention in nonalcoholic fatty liver diseases (NAFLD) in Chengyang District of Qingdao. METHODS: Participants with NAFLD who had resided in Chengyang District for more than 5 years were enrolled in this study. After the 6 and 12 mo lifestyle modification intervention based on physical activity, nutrition and behavior therapy, parameters such as body weight, body mass index (BMI), waist circumference, serum alanine aminotransferase (ALT), aspartate aminotransferase values, serum cholesterol, triglycerides, fasting glucose, fasting insulin and visceral fat area (VFA), the liver-spleen ratio and the homeostasis model assessment of insulin resistance (HOMA-IR) were evaluated and compared between participants with and without the intervention. RESULTS: Seven hundred and twenty-four participants were assigned to the lifestyle intervention group (LS) and 363 participants were assigned to the control group (CON). After the intervention, body weights in the LS group were significantly decreased compared to those in the CON group at 6 mo (11.59% ± 4.7% vs 0.4% ± 0.2%, P = 0.001) and at 12 mo (12.73% ± 5.6% vs 0.9% ± 0.3%, P = 0.001). Compared with the CON group, BMI was more decreased in the LS group after 6 and 12 mo (P = 0.043 and P = 0.032). Waist circumference was more reduced in the LS group than in CON (P = 0.031 and P = 0.017). After the 6 and 12 mo intervention, ALT decreased significantly in the LS group (P = 0.003 and P = 0.002). After 6 and 12 mo, the metabolic syndrome rate had decreased more in the LS group compared with the CON group (P = 0.026 and P = 0.017). After 12 mo, the HOMA-IR score decreased more obviously in the LS group (P = 0.041); this result also appeared in the VFA after 12 mo in the LS group (P = 0.035). CONCLUSION: Lifestyle intervention was effective in improving NAFLD in both 6 and 12 mo interventions. This intervention offered a practical approach for treating a large number of NAFLD patients in the Chengyang District of Qingdao.