Publications by authors named "Xiaowen Wei"

6 Publications

  • Page 1 of 1

Evaluation of the AGCU Expressmarker 30 Kit composed of 31 loci for forensic application.

Forensic Sci Int 2021 Jul 19;324:110849. Epub 2021 May 19.

Department of Forensic Genetics, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China. Electronic address:

With the widespread use of STR in identification of individuals, paternity testing, as well as population genetics, many commercially robust and validated STR multiplex kits were developed. The AGCU Expressmarker 30 Kit is a new autosomal STR system that contains 29 autosomal STR loci (D3S1358, vWA, D1S1656, CSF1PO, D8S1132, D19S253, D3S3045, D8S1179, D21S11, D16S539, TPOX, D6S477, Penta D, D2S441, D5S818, TH01, FGA, D15S659, D22S1045, D19S433, D13S317, D7S820, D6S1043, D10S1435, D10S1248, D2S1338, D18S51, D12S391, and Penta E), one insertion/deletion polymorphic marker on the Y chromosome (Y indel), and the amelogenin locus. A series of validation studies were performed in this context according to the guidelines of "Validation Guidelines for Forensic DNA Analysis Methods". The sensitivity study showed that a full profile was observed with template DNA as low as 40 pg. In the stability study, all STR profiles were obtained at concentrations of humic acid up to 800 ng/μL, hematin up to 250 μM, and tannic acid up to 200 ng/μL. The mixture study demonstrated that all of the minor alleles could be called at ratios from 1:1-29:1 when the total DNA was 2 ng. In the population study, the total discrimination power for three population (Sichuan-Han, Gansu-Hui, and Guangxi-Zhuang) were above 0.9999999999999999999999999999999992, 0.999999999999999999999999999999998 and 0.999999999999999999999999999999994 as well as the cumulative probability of paternity exclusion were 0.999999999999953, 0.999999999999178, and 0.999999999999611 respectively. These results demonstrated that the AGCU Expressmarker 30 Kit is a useful tool for analyzing both forensic casework and database samples.
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http://dx.doi.org/10.1016/j.forsciint.2021.110849DOI Listing
July 2021

Adherence and Efficacy of Smoking Cessation Treatment Among Patients with COPD in China.

Int J Chron Obstruct Pulmon Dis 2021;16:1203-1214. Epub 2021 Apr 30.

Tobacco Medicine and Tobacco Cessation Centre, Center of Respiratory Medicine, China-Japan Friendship Hospital, Beijing, People's Republic of China.

Background: Smoking cessation is a key intervention for all smokers with chronic obstructive pulmonary disease (COPD). Poor treatment adherence is a challenge in clinical practice that might contribute to the lower efficacy of medication (eg, oral drug). However, it is unclear what factors will influence adherence among smokers with COPD.

Methods: This study was based on an open-label randomized controlled trial (RCT) of varenicline and bupropion for smoking cessation among patients with COPD in China. The medication was given for 12 weeks, and visits and assessments were conducted at weeks 0, 1, 2, 4, 6, 9, 12, and 24. We assessed whether the adherence to smoking cessation treatment affects the smoking cessation efficacy and evaluated predictors of adherence.

Results: A total of 136 participants were recruited from February 2019 to June 2020, and analyzed using the intention-to-treat (ITT) method. In this study, 48.5% (66/136) of the total participants had good adherence to smoking cessation, and good adherence significantly improved the efficacy of smoking cessation (OR=9.60, 95% CI 4.02-22.96, P < 0.001). After adjusting for age, gender, nationality, education, and marital status, we found older age, higher education level, having more previous quitting attempts, stronger self-efficacy and preparation in quitting smoking, recognizing hazards of smoking, longer duration of COPD, and higher St. George's Respiratory Questionnaire (SGRQ) scores were relevant to good adherence (P < 0.05).

Conclusion: To our best knowledge, this is the first study to evaluate adherence to smoking cessation treatment among patients with COPD in China. Our study found that good adherence to smoking cessation treatment significantly improved the smoking cessation efficacy, and predictors of adherence were evaluated. We call on the medical community to pay attention to the adherence to smoking cessation among patients with COPD.
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http://dx.doi.org/10.2147/COPD.S301579DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8096422PMC
April 2021

Interleukin-37 sensitize the elderly type 2 diabetic patients to insulin therapy through suppressing the gut microbiota dysbiosis.

Mol Immunol 2019 08 22;112:322-329. Epub 2019 Jun 22.

Department of Elderly Endocrinology, The First Affiliated Hospital of Zhengzhou University, 450000, Zhengzhou, Henan Province, PR China. Electronic address:

Objective: The morbidity and prevalence of type 2 diabetes mellitus (DM) are increasing in the elderly population. Interleukin 37 (IL-37) play important roles in anti-inflammatory and anti-bacteria immune responses, but its role in the development of type 2 DM in the elderly is unclear. Therefore, we investigated whether IL-37 is associated with type 2 DM in the elderly and the underlying mechanism.

Methods: Hospitalized patients (aged 65-95 years) with recently diagnosed type 2 diabetes mellitus were studied retrospectively and compared with healthy subjects without glucose metabolism abnormalities. A diabetic mouse model was established by feeding ob/ob mice (C57BL/6) a high-fat, carbohydrate-free diet. Plasma glucose and insulin levels were determined by glucose oxidase assay and radioimmunoassay, respectively. The IL-37 expression level was determined by real-time PCR, western blot and ELISA (Enzyme-linked immunoassay).

Results: Statistic analysis showed that the IL-37 level was significantly associated with type 2 DM and insulin resistance in the elderly. The patients were then divided into insulin therapy sensitive and resistant group according to their response to insulin therapy. Data showed that the IL-37 was highly expressed in the insulin therapy sensitive group. And this was related to the less severe gut microbiota dysbiosis. In the mice model, overexpressing the IL-37 could suppress the gut microbiota dysbiosis and also the diabetes development.

Conclusion: Thus our results showed that higher IL-37 was associated with increased insulin sensitive in elderly type 2 DM patients through suppressing the gut microbiota dysbiosis.
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http://dx.doi.org/10.1016/j.molimm.2019.06.008DOI Listing
August 2019

Downregulation of miR-181a alleviates renal fibrosis in diabetic nephropathy mice.

Int J Clin Exp Pathol 2018 1;11(8):4004-4011. Epub 2018 Aug 1.

Department of Geriatric Endocrinology, The First Affiliated Hospital of Zhengzhou University Zhengzhou 450003, China.

Accumulating evidence suggests that microRNAs are important regulators in the pathology of diabetes and its relevant renal injures. Little is known about the role of miR-181a in development of diabetic nephropathy. The aim of our present study was to investigate levels of miR-181a in diabetic nephropathy and explore its underlying mechanism. In the present study, Db/db and db/m mice were randomized into groups with 12 mice in each: db/m group, db/db group, and antagomiR-181a-treated db/db group. Changes in renal cortical sections were studied by histopathology. Mouse mesangial cells transfected with miR-mimic or miR-inhibitor and cell growth was measured using MTT assay. Levels of miR-181a expression were detected using qRT-PCR under different conditions. Indexes were measured using qRT-PCR and Western blot. Our results show that downregulation of miR-181a could alleviate pathological changes of diabetic nephropathy in mice. miR-181a expression was significantly upregulated in mouse mesaginal cells (P<0.05). Overexpression of miR-181a promoted extracellular matrix under high glucose by measuring related indexes such as collagen I, collagen IV, and fibronectin, which could be reversed by miR-181a inhibitors (P<0.05). Upregulation of miR-181a suppressed expression of TβRIII by binding with 3'-UTR. These findings suggest miR-181a plays as an important role in renal fibrosis of diabetic nephropathy in an animal model.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6962790PMC
August 2018

Improvement of acetic acid tolerance of Saccharomyces cerevisiae using a zinc-finger-based artificial transcription factor and identification of novel genes involved in acetic acid tolerance.

Appl Microbiol Biotechnol 2015 Mar 21;99(5):2441-9. Epub 2015 Jan 21.

School of Life Science and Biotechnology, Dalian University of Technology, Dalian, 116024, China.

Acetic acid is present in cellulosic hydrolysate as a potent inhibitor, and the superior acetic acid tolerance of Saccharomyces cerevisiae ensures good cell viability and efficient ethanol production when cellulosic raw materials are used as substrates. In this study, a mutant strain of S. cerevisiae ATCC4126 (Sc4126-M01) with improved acetic acid tolerance was obtained through screening strains transformed with an artificial zinc finger protein transcription factor (ZFP-TF) library. Further analysis indicated that improved acetic acid tolerance was associated with improved catalase (CAT) activity. The ZFP coding sequence associated with the improved phenotype was identified, and real-time RT-PCR analysis revealed that three of the possible genes involved in the enhanced acetic acid tolerance regulated by this ZFP-TF, namely YFL040W, QDR3, and IKS1, showed decreased transcription levels in Sc4126-M01 in the presence of acetic acid, compared to those in the control strain. Sc4126-M01 mutants having QDR3 and IKS1 deletion (ΔQDR3 and ΔIKS1) exhibited higher acetic acid tolerance than the wild-type strain under acetic acid treatment. Glucose consumption rate and ethanol productivity in the presence of 5 g/L acetic acid were improved in the ΔQDR3 mutant compared to the wild-type strain. Our studies demonstrated that the synthetic ZFP-TF library can be used to improve acetic acid tolerance of S. cerevisiae and that the employment of an artificial transcription factor can facilitate the exploration of novel functional genes involved in stress tolerance of S. cerevisiae.
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http://dx.doi.org/10.1007/s00253-014-6343-xDOI Listing
March 2015

Influence of CYP2C9 and VKORC1 genotypes on the risk of hemorrhagic complications in warfarin-treated patients: a systematic review and meta-analysis.

Int J Cardiol 2013 Oct 7;168(4):4234-43. Epub 2013 Aug 7.

Institute of Geriatric Cardiology, General Hospital of Chinese People's Liberation Army, Beijing 100853, China.

Background: The main challenge for warfarin anticoagulation is the risk for hemorrhagic complications. Although certain pharmacogenetic factors may explain the individual variabilities about the therapeutic warfarin dose requirement, the genetic factors to warfarin hemorrhagic complications due to over-anticoagulation are largely unknown. To interpret the potential role of warfarin-related genotypes on over-anticoagulation and hemorrhagic complications, we conducted a meta-analysis based on 22 published studies.

Methods: A comprehensive search was applied to the reports on over-anticoagulation and hemorrhagic complications published prior to December 31, 2012 in PubMed and EMBASE. References were identified by strict inclusion and exclusion criteria, with additional information obtained by consulting with the authors of primary studies. The roles of genotypes in CYP2C9 and VKORC1 on over-anticoagulation (INR > 4) and hemorrhagic complications were analyzed by Revman 5.0.2 software.

Results: A total of 6272 patients in 22 reports were included in the meta-analysis, including studies of 18 from Caucasians (3 from both Caucasian and African-American), 3 from Asians, and 1 from Brazilians. Compared to CYP2C9 wild genotype (CYP2C9*1), both CYP2C9*2 (rs 1799853, c. 430 C > T, p. Arg144Cys) and *3 (rs 1057910, c. 1075 A >C, p. Ile359Leu) confer significantly higher risk for warfarin over-anticoagulation and hemorrhagic complications. After stratification by CYP2C9 allele status, significantly higher risk for hemorrhagic complications was found only in carriers of at least 1 copy of CYP2C9*3 [For total hemorrhages: *1/*3 HR: 2.05 (1.36-3.10), p < 0.001; *3/*3 HR: 4.87 (1.38-17.14), p = 0.01; For major hemorrhages: *1/*3 HR: 2.43 (1.17-5.06), p = 0.02; *3/*3 HR: 4.81 (0.95-24.22), p = 0.06]. Furthermore, similar susceptibility of total hemorrhage by CYP2C9 genotypes was observed in Caucasians and Asians. After stratification by the occurrence time, both CYP2C9*2 and *3 are risk factors for over-anticoagulation within 30 days of warfarin treatment [*2 HR: 1.64 (1.11-2.43), p = 0.01; *3 HR: 2.48 (1.56-3.96), p < 0.001], and only CYP2C9*3 showed higher risk for over-anticoagulation after 30 days [HR: 1.86 (1.08-3.20), P = 0.03]. For VKORC1 c. -1639G > A (rs 9923231) genotypes, GA and AA contributed significantly higher risk for over-anticoagulation within 30 days [HR: 2.14 (1.75-2.62), p < 0.001], but not for over-anticoagulation after 30 days [HR:0.78 (0.46-1.33), p = 0.36]. No significant association was found between VKORC1 genotypes and hemorrhagic complications.

Conclusions: Both CYP2C9 and VKORC1 genotypes are associated with an increased risk for warfarin over-anticoagulation, with VKORC1 c. -1639G > A more sensitive early in the course of anticoagulation. CYP2C9*3 is the main genetic risk factor for warfarin hemorrhagic complications.
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http://dx.doi.org/10.1016/j.ijcard.2013.07.151DOI Listing
October 2013
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