Youjiang Medical College for Nationalities

Baise City, China

Youjiang Medical College for Nationalities

Baise City, China
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Li J.,Shanghai JiaoTong University | Xu Y.,CAS Shanghai Institutes for Biological Sciences | Long X.-D.,Ren Ji Hospital | Long X.-D.,Youjiang Medical College for Nationalities | And 11 more authors.
Cancer Cell | Year: 2014

Cbx4 is a polycomb group protein that is also a SUMO E3 ligase, but its potential roles in tumorigenesis remain to be explored. Here, we report that Cbx4, but not other members of the Cbx family, enhances hypoxia-induced vascular endothelial growth factor (VEGF) expression and angiogenesis in hepatocellular carcinoma (HCC) cells through enhancing HIF-1α sumoylations at K391 and K477 in its two SUMO-interacting motifs-dependent mechanisms and increasing transcriptional activity of HIF-1. The Cbx4 expression is significantly correlated with VEGF expression, angiogenesis, and the overall survival of HCC patients and also in subcutaneously and orthotopically transplanted mice HCC models. Collectively, our findings demonstrate that Cbx4 plays a critical role in tumor angiogenesis by governing HIF-1α protein. © 2014 Elsevier Inc.

Yao J.-G.,Youjiang Medical College for Nationalities | Huang X.-Y.,Youjiang Medical College for Nationalities | Long X.-D.,Youjiang Medical College for Nationalities | Long X.-D.,Shanghai JiaoTong University
International Journal of Clinical and Experimental Pathology | Year: 2014

Aflatoxin B1 (AFB1) is an important environmental carcinogen and can induce DNA damage and involve in the carcinogenesis of hepatocellular carcinoma (HCC). The deficiency of DNA repair capacity related to the polymorphisms of DNA repair genes might play a central role in the process of HCC tumorigenesis. However, the interaction of DNA repair gene polymorphisms and AFB1 in the risk of hepatocellular carcinoma has not been elucidated. In this study, we investigated whether six polymorphisms (including rs25487, rs861539, rs7003908, rs28383151, rs13181, and rs2228001) in DNA repair genes (XPC, XRCC4, XRCC1, XRCC4, XPD, XRCC7, and XRCC3) interacted with AFB1, and the gene-environmental interactive role in the risk of HCC using hospital-based case-control study (including 1486 HCC cases and 1996 controls). Genotypes of DNA repair genes were tested using TaqMan-PCR technique. Higher AFB1 exposure was observed among HCC patients versus the control group [odds ratio (OR) = 2.08 for medium AFB1 exposure level and OR = 6.52 for high AFB1 exposure level]. Increasing risk of HCC was also observed in these with the mutants of DNA repair genes (risk values were from 1.57 to 5.86). Furthermore, these risk roles would be more noticeable under the conditions of two variables, and positive interactive effects were proved in the followed multiplicative interaction analysis. These results suggested that DNA repair risk genotypes might interact with AFB1 in the risk of HCC.

Xu D.-W.,Shanghai JiaoTong University | Long X.-D.,Shanghai JiaoTong University | Long X.-D.,Youjiang Medical College for Nationalities | Xia Q.,Shanghai JiaoTong University
International Journal of Clinical and Experimental Medicine | Year: 2015

Living-donor liver transplantation (LDLT) has increasingly performed all around the world. However, LDLT donors achieve no medical benefits and are exposed to the risk of complications, and even death. The potential effects of LDLT on donor safety, donor recovery, and post-donation psychological impairment are essential to be better understood. We searched the MEDLINE database to identify articles about the quality of life (QOL) in adults after LDLT donation. Twenty-eight studies with a total of 1944 donors were included in the review. 14 of the 28 studies (50%) had a cross-sectional design, and the remaining half had a prospective design. The Physical Component Score (PCS) decreased immediately after the donation, then returned to the baseline within 6 to 12 months while the Mental Component Score (MCS) remains comparable to that of normative population throughout the procedure. Compared with the left graft (LG) donors, right graft (RG) donors were significantly older, had longer hospital stays and higher rates of postoperative complications, and a higher recipient mortality rate, while there were no difference in the PCS and MCS between the two groups. Our review clearly indicates that the LDLT donors can endure the donation procedure and return to their normal daily life without major problem in the short term. However, to improve the donor selection criteria and ensure the QOL in donors throughout donation procedure, more studies with longer follow up and larger samples are essential and predictors of poor QOL should be identified in study with sufficient response rate and ideal control groups. © 2015, E-Century Publishing Corporation. All Rights Reserved.

Long X.-D.,Shanghai JiaoTong University | Long X.-D.,Youjiang Medical College for Nationalities | Yao J.-G.,Youjiang Medical College for Nationalities | Zeng Z.,Wuhan University | And 8 more authors.
Hepatology | Year: 2013

X-ray repair complementing group 4 (XRCC4) is very important in maintaining overall genome stability and may play an important role in carcinogenesis. We aimed to investigate the role of polymorphisms in the coding region of this gene in hepatocellular carcinoma (HCC) caused by aflatoxin B1 (AFB1). A hospital-based case-control study, including 1,499 HCC cases and 2,045 controls without any liver diseases or tumors, was conducted in a high AFB1 exposure area (the Guangxi region) to assess the relationship between 21 polymorphisms in the coding region of XRCC4 and AFB1-related HCC risk and prognosis. Among these 21 polymorphisms, only rs28383151 modified HCC risk. These individuals with the genotypes of rs28383151 A alleles (rs28383151-GA/AA), compared with the homozygote of rs28383151 G alleles (rs28383151-GG), faced increasing risk of HCC (odds ratio [OR]: 2.17; 95% confidence interval: 1.77-2.67). Significant interactive effects between risk genotypes (OR, >1) and AFB1 exposure status were also observed in the joint-effects analysis. Furthermore, this polymorphism was correlated not only with lower XRCC4-expressing levels, but also with higher AFB1-DNA adducts levels and increasing TP53M and portal vein tumor risk. The rs28383151 polymorphism modified the recurrence-free survival and overall survival of HCC patients, especially under high AFB1 exposure conditions. Additionally, this polymorphism multiplicatively interacted with the glutathione S-transferase M1 polymorphism with respect to HCC risk (ORinteraction = 2.13). Conclusion: Genetic polymorphisms in the coding region of XRCC4 may be risk and prognostic biomarkers of AFB1-related HCC, and rs28383151 is such a potential candidate. © 2013 American Association for the Study of Liver Diseases.

Lin X.,Guangxi Medical University | Huang Z.,Youjiang Medical College for Nationalities | Chen X.,Guangxi Medical University | Rong Y.,Guangxi Medical University | And 4 more authors.
Carbohydrate Polymers | Year: 2014

A polysaccharide (PMP) was isolated from Millettia pulchra and purified by DEAE-cellulose and Sephadex G-75 chromatography. The results showed that PMP was composed of d-glucose and d-arabinose in a molar ratio of 90.79% and 9.21%, with an average molecular weight of about 14,301 Da. Furthermore, the effect of PMP on cognitive impairment induced by d-galactose in mice was evaluated. Treatment with PMP significantly reversed d-galactose-induced learning and memory impairments, as measured by behavioral tests. One of the potential mechanisms of this action was to reduce oxidative stress and suppress inflammatory responses. Furthermore, our results also showed that PMP markedly reduced the content and deposition of β-amyloid peptide, improved the dysfunction of synaptic plasticity, increased the levels of acetylcholine, but decreased cholinesterase activity. These results suggest that PMP exerts an effective protection against d-galactose-induced cognitive impairment, and PMP may be a major bioactive ingredient in M. pulchra.© 2013 Elsevier Ltd. All rights reserved.

Huang W.,Guangxi University | Tang Y.,Guangxi Medical University | Nong L.,Youjiang Medical College For Nationalities | Sun Y.,Guangxi University
Journal of Crohn's & colitis | Year: 2015

BACKGROUND AND AIMS: Postoperative intra-abdominal septic complications [IASCs] are the most feared risks of surgery for Crohn's disease[CD]. The risk factors for IASCs still remain controversial. The aim of this study was to assess the risk factors for IASCs in CD patients undergoing abdominal surgery.METHODS: MEDLINE, Cochrane Library, and EMBASE were searched to identify observational studies reporting the risk factors for IASCs in CD patients. A meta-analysis was conducted to investigate the impact of various risk factors on IASCs in CD. The GRADE [Grading of Recommendations Assessment, Development and Evaluation] approach was used for quality assessment of evidence on outcome levels.RESULTS: This review included 15 studies evaluating 3807 patients undergoing 4189 operations. The meta-analyses found that low albumin levels (odds ratio [OR]: 1.93; 95% confidence interval [CI]: 1.362.75), preoperative steroids use [OR: 1.99; 95% CI: 1.54-2.57], a preoperative abscess [OR: 1.94; 95% CI: 1.263.0], previous surgery history [OR: 1.50; 95% CI: 1.151.97] may be risk factors for IASCs. There were no associations between anastomosis methods [OR: 0.94; 95% CI: 0.58-1.53], biologics therapy [OR: 1.29; 95% CI: 0.792.11], and immunomodulator use [OR: 1.07; 95% CI: 0.661.73] with the risk of IASCs. Due to observational design, the quality of evidence was regarded low or moderate for these risk factors by the GRADE approach.CONCLUSIONS: This meta-analysis provides some evidence that steroids use, previous surgical history, a preoperative abscess, and low albumin levels may be associated with higher rates of IASCs in CD. Knowledge about those risk factors may influence treatment and procedure-related decisions, and possibly reduce the ss rate. Copyright © 2015 European Crohn’s and Colitis Organisation (ECCO). Published by Oxford University Press. All rights reserved. For permissions, please email:

Liu B.-Q.,Shenyang University | Gao Y.-Y.,Shenyang University | Niu X.-F.,Shenyang University | Xie J.-S.,Youjiang Medical College for Nationalities | And 3 more authors.
Biochemical and Biophysical Research Communications | Year: 2010

Resveratrol (RES), a natural plant polyphenol, is an effective inducer of cell cycle arrest and apoptosis in a variety of carcinoma cell types. In addition, RES has been reported to inhibit tumorigenesis in several animal models suggesting that it functions as a chemopreventive and anti-tumor agent in vivo. The chemopreventive and chemotherapeutic properties associated with resveratrol offer promise for the design of new chemotherapeutic agents. However, the mechanisms by which RES mediates its effects are not yet fully understood. In this study, we showed that RES caused cell cycle arrest and proliferation inhibition via induction of unfolded protein response (UPR) in human leukemia K562 cell line. Treatment of K562 cells with RES induced a number of signature UPR markers, including transcriptional induction of GRP78 and CHOP, phosphorylation of eukaryotic initiation factor 2α (eIF2α), ER stress-specific XBP-1 splicing, suggesting the induction of UPR by RES. RES inhibited proliferation of K562 in a concentration-dependent manner. Flow cytometric analyses revealed that K562 cells were arrested in G1 phase upon RES treatment. Salubrinal, an eIF2α inhibitor, or overexpression of dominant negative mutants of PERK or eIF2α, effectively restored RES-induced cell cycle arrest, underscoring the important role of PERK/eIF2α branch of UPR in RES-induced inhibition of cell proliferation. © 2009 Elsevier Inc. All rights reserved.

Tang R.-G.,The Affiliated Hospital of Youjiang Medical College for Nationalities | Huang Y.-Z.,The Affiliated Hospital of Youjiang Medical College for Nationalities | Yao L.-M.,Youjiang Medical College for Nationalities | Xiao J.,Youjiang Medical College for Nationalities | And 2 more authors.
Gene | Year: 2013

Epidemiological evidence has shown two polymorphisms (namely RS#1800468G > A and RS#1800471G > C) of transforming growth factor-beta 1 (TGF-β1) gene may be involved in the cancer development. However, their role in the carcinogenic process of esophageal squamous cell carcinoma (ESCC) has been less well elaborated. We conducted a hospital-based case-control study including 391 ESCC cases and 508 controls without any evidence of tumors to evaluate the association between these two polymorphisms and ESCC risk and prognosis for Zhuangese population by means of polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and amplification refractory mutation system (ARMS)-PCR techniques. We found that individuals with the genotypes with RS#1800471 C allele (namely RS#1800471-GC or -CC) had an increased risk of ESCC than those without above genotypes (namely RS#1800471-GG, adjusted odds ratio 3.26 and 5.65, respectively). Further stratification analysis showed that this polymorphism was correlated with tumor histological grades and TNM (tumor, node, and metastasis) stage, and modified the serum levels of TGF-β1. Additionally, RS#1800471 polymorphism affected ESCC prognosis (hazard ratio, 3.40), especially under high serum levels of TGF-β1 conditions. However, RS#1800468 polymorphism was not significantly related to ESCC risk. These findings indicated that TGF-β1 RS#1800471G > C polymorphism may be a genetic modifier for developing ESCC in Zhuangese population. © 2012 Elsevier B.V.

Guo J.Y.,Youjiang Medical College for Nationalities
Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery | Year: 2012

To investigate single nucleotide polymorphisms(SNPs) and haplotypes of interleukin-18(IL-18) gene associated with the susceptibility to colorectal cancer(CRC). Two SNPs of IL-18 gene promoter -137G/C and -607C/A in 170 patients with CRC and 160 healthy controls matched by age and sex in a Chinese population were analyzed using polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP) strategy. Frequency of haplotypes and linkage disequilibrium of IL-18 gene in different groups were analyzed by SHEsis programs. The distributions of IL-18 gene -607C/A polymorphism did not differ between CRC patients and healthy controls, but IL-18 gene -137G/C polymorphism was significantly different(P<0.05). The relative risk of C allele for CRC was 1.814 times of the G allele (OR=1.814,95% CI:1.246-2.642). Consistent with the results of the genotyping analyses, IL-18 -137G/C and -607C/A polymorphisms showed strong linkage disequilibrium(|D'|=0.945), frequency of the -137C/-607A haplotype in patients with CRC was significantly higher than that in healthy controls(P<0.05). The -137C/-607A haplotype was associated with a significantly increased risk of CRC(OR=1.637, 95% CI:1.100-2.437). IL-18 gene -137G/C polymorphism and -137C/-607A haplotype are associated with CRC. -137C allele may be an important genetic susceptibility gene for CRC.

Wei X.,Youjiang Medical College for Nationalities
Zhong yao cai = Zhongyaocai = Journal of Chinese medicinal materials | Year: 2013

To investigate the effects of solanum lyratum Thunberg alkaloid (STA) on induction of apoptosis and the expression of NF-kappaB signaling pathway related genes in A549 cells. A549 cells was treated with STA in vitro. The proliferation inhibitory effect was evaluated by MTT assay. Induction of cell apoptotic rate was determined by flow cytometry method (FCM) after Annexin V-FITC/PI double staining. The expression of NF-kappaB/p65 in nuclei, Survivin, IkappaBalpha and p-1kaapaBalpha in cytosol were detected by western blot. STA exhibited strong proliferation inhibitory effect in a dose-and -time-dependent manner against A549 cells. After treated with STA for 24 h, the apoptotic rate was increased significantly. The expression of IkappaBalpha protein was increased markedly,while those of NF-kappaB/p65, Survivin and p-IkappaBalpha proteins were decreased markedly. STA can induce apoptosis of lung adenocarcinoma A549 cells, its mechanisms may be related to inhibition of NF-kappaB signaling pathway.

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