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Atrial fibrillation (AF) is the most common form of clinical cardiac arrhythmia. Investigation of the pathogenic genes of AF is helpful for early screening of AF. The aim of this experiment is to screen for susceptible genes with potential pathogenic significance in both familial and non-familial AF populations, and to explore their roles in the pathogenesis of AF. Firstly, whole-exome sequencing (WES) was performed to identify the gene mutation responsible for AF on 4 patients with familial AF. Then, Sanger sequencing was used to verify the susceptibility gene mutations in the patients with non-familial AF and the healthy populations. Western blotting was used to analyze their protein expression levels. Outward potassium-ion currents were recorded using whole-cell patch clamp technique. There are 39 individuals in the family, of which 4 have suffered from AF. These four AF patients have two identical mutated genes: FAM160A2 (homozygous mutation, rs77726581 c. 1375C>T) and MUC5B (heterozygous mutation, rs199736618 c. 12272C>T). Among 52 non-familial AF patients, 5 had similar heterozygous point mutation at the same locus of FAM160A2, but heterozygous mutations of MUC5B were found in both non-familial AF and healthy populations. There was no significant difference in the protein expression level of FAM160A2 between the non-familial AF and the healthy population. The FAM160A2 gene mutation significantly reduced outward potassium ion current (compared to the wild-type, P<0.001). Thus, FAM160A2 loss-of-function mutation may be a new molecular biological mechanism for AF, which can be used for early screening for AF. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Geodesy & Geodynamics (1671-5942) is the property of Editorial Board Journal of Geodesy & Geodynamics and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Railway Science & Engineering is the property of Journal of Railway Science & Engineering Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Geomatics & Information Science of Wuhan University is the property of Geomatics & Information Science of Wuhan University and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the effects of metformin combined with gemcitabine on the proliferation，migra⁃ tion，and epithelial-mesenchymal transition（EMT）of pancreatic cancer cells. Methods The pancreatic cancer PANC-1 cells were selected and subcultured. The cell proliferation activity was measured by MTT assay when the final metformin concentrations were 0，5，10，20，40 mmol/L or the final gemcitabine concentrations were 0，0. 1，0. 2，0. 4，0. 8 μmol/L， and the follow-up experiments were carried out with the concentrations of metformin and gemcitabine that could reduce the cell proliferation activity to about 50%. Besides，PANC-1 cells were selected again and were randomly divided into three groups：the control group，metformin group，gemcitabine group，and combination group. The cells were treated with met⁃ formin or/and gemcitabine. The cell migration rate was measured by cell scratch assay. The expression levels of E-cad⁃ herin and Vimentin was detected by Western blotting. Results The proliferation activity of PANC-1 cells decreased with the increased concentrations of metformin and gemcitabine，in a concentration-dependent manner（F= 29. 14，66. 88， both P<0. 01）. After giving metformin（20 mmol/L）and gemcitabine（0. 4 μmol/L），the proliferation activity of PANC-1 cells decreased to about 50%，so the follow-up experiments were conducted with these concentrations. The cell migration rates and the expression levels of E-cadherin and Vimentin in the metformin group，gemcitabine group，and combination group were lower than those in the control group；the cell migration rate and the expression levels of E-cadherin and Vimen⁃ tin in the combination group were lower than those in the metformin and gemcitabine groups（all P<0. 05）. There was no significant difference in the cell migration rate or expression levels of E-cadherin and Vimentin between the metformin group and gemcitabine group（all P>0. 05）. Conclusion The combination therapy of metformin and gemcitabine can inhibit the proliferation，migration and EMT of pancreatic cancer cells，and metformin improves the chemosensitivity of pancreatic cancer cells to gemcitabine. [ABSTRACT FROM AUTHOR]

Copyright of Forensic Science & Technology is the property of Institute of Forensic Science, Ministry of Public Security and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Forensic Medicine / Fayixue Zazhi is the property of Journal of Forensic Medicine Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

目的探讨生长抑素(SST)对人肝癌细胞系Hep G2上皮间质转化(EMT)的影响及其可能机制。方法取对数生长期Hep G2细胞,随机分为对照组及SST低、中、高剂量组,分别给予0、100、200、400μg/m L SST处理。各组继续培养24 h,采用MTT法检测细胞增殖能力(细胞存活率),Transwell小室法检测细胞迁移能力(跨膜细胞数),Western blotting法检测细胞E-钙黏蛋白(E-cadherin)和波形蛋白(Vimentin)表达。结果对照组及SST低、中、高剂量组细胞存活率依次为100%、(78.7±6.36)%、(68.0±6.66)%和(44.0±7.23)%,跨膜细胞数依次为(53±6)、(41±2)、(28±5)和(22±3)个。SST低、中、高剂量组细胞存活率、跨膜细胞数均低于对照组(P均<0.05),且随着SST浓度升高,细胞存活率、跨膜细胞数逐渐降低(F分别为79.13、51.71,P均<0.05)。对照组及SST低、中、高剂量组E-cadherin相对表达量依次为0.20±0.04、0.28±0.04、0.46±0.06和0.75±0.07,Vimentin相对表达量依次为1.17±0.15、0.79±0.04、0.54±0.08和0.57±0.06;SST低、中、高剂量组E-cadherin相对表达量均高于对照组、Vimentin相对表达量均低于对照组(P均<0.05),且随着SST浓度升高,E-cadherin相对表达量逐渐升高(P均<0.05),而Vimentin相对表达量降低(P均<0.05)。结论 SST可抑制人肝癌细胞系Hep G2的侵袭能力,其机制可能与增加E-cadherin蛋白表达、降低Vimentin蛋白表达,继而逆转Hep G2细胞的EMT有关。 [ABSTRACT FROM AUTHOR]