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In CAOV3 cells, cell proliferation was increased at 48 and 72 h but cell apoptosis rate was decreased at 48 h by circ-PVT1 overexpression. Besides, circ-PVT1 negatively regulated miR-149 but not miR-183 or miR-194 in SKOV3 and CAOV3 cells. Rescue experiments showed that miR-149 knock-down increased cell proliferation but decreased apoptosis in circ-PVT1 knock-down treated SKOV3 cells, while miR-149 overexpression reduced cell proliferation but enhanced apoptosis in circ-PVT1 overexpression treated CAOV3 cells. HL 362 CONCLUSION Circ-PVT1 enhances cell proliferation but inhibits cell apoptosis through sponging miR-149 in EOC cells, which suggests that circ-PVT1 may serve as a treatment target in EOC. © 2020 Japan Society of Obstetrics and Gynecology.OBJECTIVE To present the use of an intermediate dorsal neurocutaneous flap for the reconstruction of defects on the distal foot. METHODS From September 2016 to October 2018, five patients (mean age at operation 33.8 years; range, 7-70 years; female/male = 2/3) with skin defects on one of their feet caused by road-traffic accidents, electrical injury, and syndactyly correction were retrospectively reviewed. The size of the defects ranged from 2.0 cm × 1.0 cm to 5.0 cm × 3.5 cm. All patients had undergone a reconstruction surgery using intermediate dorsal neurocutaneous flap. One patient underwent a syndactyly correction, and four patients first experienced aggressive debridement. The sizes of the flaps were between 5.0 cm × 2.0 cm and 6.0 cm × 4.0 cm. The function, appearance, and pain of the injured foot were assessed using the Chinese Manchester Foot Pain and Disability Index and visual analogue scale. RESULTS These five patients were systematically followed up for a mean of 15.8 months (range, 12-20 months) The intermediate dorsal neurocutaneous flap is an alternative and effective technique that can reliably cover minor- to medium-sized defects on the distal foot, toes, and web spaces. This surgical method leads to satisfactory functional recovery with minimal donor site morbidity, and no major vessels need to be sacrificed. This procedure offers an advisable option for orthopaedic surgeons to treat defects on the distal foot. © 2020 The Authors. Orthopaedic Surgery published by Chinese Orthopaedic Association and John Wiley & Sons Australia, Ltd.BACKGROUND Nonsyndromic hearing loss is clinically and genetically heterogeneous. In this study, we characterized the clinical features of 12 Chinese Han deaf families in which mutations in common deafness genes GJB2, SLC26A4, and MT-RNR1 were excluded. METHODS Targeted next-generation sequencing of 147 known deafness genes was performed in probands of 10 families, while whole-exome sequencing was applied in those of the rest two. RESULTS Pathogenic mutations in a total of 11 rare deafness genes, OTOF, CDH23, PCDH15, PDZD7, ADGRV1, KARS, OTOG, GRXCR2, MYO6, GRHL2, and POU3F4, were identified in all 12 probands, with 16 mutations being novel. Intrafamilial cosegregation of the mutations and the deafness phenotype were confirmed by Sanger sequencing. CONCLUSION Our results expanded the mutation spectrum and genotype-phenotype correlation of nonsyndromic hearing loss in Chinese Hans and also emphasized the importance of combining both next-generation sequencing and detailed auditory evaluation to achieve a more accurate diagnosis for nonsyndromic hearing loss. © 2020 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals, Inc.Tuberculosis (TB) is a severe infectious disease that seriously endangers human health. The immune defence mechanism of the body against TB is still unclear. The purpose of this study was to find the key molecules involved in the immune defence response during TB infection, and provide reference for the treatment of TB and further understanding of the immune defence mechanism of the body. Data from GSE83456 were downloaded from GEO data sets for analysis, and a total of 192 differentially expressed genes were screened out. Most of these genes are enriched in the interferon signalling pathway and are defence response-related. We also found that STAT1 plays an important role in the immune defence of TB infection and it is one of the key genes related to interferon signalling pathway. STAT1-related molecules including hsa-miR-448, hsa-miR-223-3p, SAMD8_hsa_circRNA 994 and TWF1_hsa_circRNA 9897 were therefore screened out. Furthermore, expression levels of hsa-miR-448 and hsa-miR-223-3p were then verified by qRT-PCR. Results showed that both hsa-miR-448 and hsa-miR-223-3p were down-regulated in plasma from patients with pulmonary TB. Taken together, our data indicate that an mRNA-miRNA-circRNA interaction chain may play an important role in the infection of MTB, and STAT1 and related molecules including hsa-miR-223-3p, has-miR-448, SAMD8_hsa_circRNA994 and TWF1_hsa_circRNA9897 were identified as potential biomarkers in the development of active TB. © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.Coral reefs are declining globally as climate change and local water quality press environmental conditions beyond the physiological tolerances of holobionts-the collective of the host and its microbial symbionts. To assess the relationship between symbiont composition and holobiont stress tolerance, community diversity metrics were quantified for dinoflagellate endosymbionts (Family Symbiodiniaceae) from eight Acropora millepora genets that thrived under or responded poorly to various stressors. These eight selected genets represent the upper and lower tails of the response distribution of 40 coral genets that were exposed to four stress treatments (and control conditions) in a 10-day experiment. Specifically, four 'best performer' coral genets were analyzed at the end of the experiment because they survived high temperature, high pCO2 , bacterial exposure, or combined stressors, whereas four 'worst performer' genets were characterized because they experienced substantial mortality under these stressors. At the end of the experiment, seven of eight coral genets mainly hosted Cladocopium symbionts, whereas the eighth genet was dominated by both Cladocopium and Durusdinium symbionts.