{"title":"Diagnostic value of IMP3 in pancreatic cancer: a meta-analysis [Retraction].","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>[This retracts the article on p. 10603 in vol. 8, PMID: 26379850.].</p>","PeriodicalId":13892,"journal":{"name":"International journal of clinical and experimental medicine","volume":"9 6","pages":"12417"},"PeriodicalIF":0.1,"publicationDate":"2016-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5557167/pdf/ijcem0009-12417.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36197901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Lentivirus-mediated <i>TPD52L2</i> depletion inhibits the proliferation of liver cancer cells in vitro [Retraction].","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>[This retracts the article on p. 2334 in vol. 8, PMID: 25932170.].</p>","PeriodicalId":13892,"journal":{"name":"International journal of clinical and experimental medicine","volume":"9 6","pages":"12416"},"PeriodicalIF":0.1,"publicationDate":"2016-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5260932/pdf/ijcem0009-12416.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36197897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Parathyroid hormone plus alendronate in osteoporosis: a meta-analysis of randomized controlled trials [Retraction].","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>[This retracts the article on p. 3338 in vol. 8, PMID: 26064224.].</p>","PeriodicalId":13892,"journal":{"name":"International journal of clinical and experimental medicine","volume":"9 1","pages":"467"},"PeriodicalIF":0.1,"publicationDate":"2016-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5557165/pdf/ijcem0009-0467.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36197903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of early external X-ray radiation on arterial restenosis post percutaneous transluminal angioplasty [Retraction].","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>[This retracts the article on p. 14944 in vol. 8, PMID: 26628976.].</p>","PeriodicalId":13892,"journal":{"name":"International journal of clinical and experimental medicine","volume":"9 1","pages":"466"},"PeriodicalIF":0.1,"publicationDate":"2016-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5557166/pdf/ijcem0009-0466.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36197899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tae-Dong Kim, Sangphil Oh, Stan A Lightfoot, Sook Shin, Jonathan D Wren, Ralf Janknecht
{"title":"Upregulation of PSMD10 caused by the JMJD2A histone demethylase.","authors":"Tae-Dong Kim, Sangphil Oh, Stan A Lightfoot, Sook Shin, Jonathan D Wren, Ralf Janknecht","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>PSMD10, also known as gankyrin, is associated with the proteasome and has been shown to be an oncoprotein in the liver. Here, we report that PSMD10 expression is stimulated by the histone demethylase JMJD2A/KDM4A and its interaction partner, the ETV1 transcription factor, in LNCaP prostate cancer cells. Global analysis of expression patterns revealed that PSMD10 mRNA levels are positively correlated with those of both JMJD2A and ETV1. In human prostate tumors, PSMD10 is highly overexpressed at the protein level and correlates with JMJD2A overexpression; further, PSMD10 expression is enhanced in the prostates of transgenic JMJD2A mice. Moreover, PSMD10 is particularly overexpressed in high Gleason score prostate tumors. Downregulation of PSMD10 in LNCaP prostate cancer cells impaired their growth, indicating that PSMD10 may exert a pro-oncogenic function in the prostate. Lastly, we observed that PSMD10 expression is correlated to YAP1, a component of the Hippo signaling pathway and whose gene promoter is regulated by JMJD2A, and that PSMD10 can cooperate with YAP1 in stimulating LNCaP cell growth. Altogether, these data indicate that PSMD10 is a novel downstream effector of JMJD2A and suggest that inhibition of the JMJD2A histone demethylase by small molecule drugs may be effective to curtail the oncogenic activity of PSMD10 in various PSMD10-overexpressing tumors.</p>","PeriodicalId":13892,"journal":{"name":"International journal of clinical and experimental medicine","volume":"9 6","pages":"10123-10134"},"PeriodicalIF":0.1,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5584593/pdf/nihms884312.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35388264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Role of autophagy in chronic kidney diseases.","authors":"Song Mao, Jianhua Zhang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Chronic kidney diseases (CKD), a common pathway of various glomerular diseases, which carries great morbidity and mortality to people. CKD is characterized by progressive kidney fibrosis and remodeling. CKD is also associated with the depletion of glomerular and tubular cells. Autophagy is a highly conserved process that degrades cellular long-lived proteins and organelles. It plays an important role in both normal and disease states, including immunity, inflammation, and adaptation to stress. Evidence has indicated that impaired autophagic activity is involved in the development of CKD. Here, we review the progress in our understanding of the role of autophagy in the development and progression of CKD. Targeting the autophagic signaling pathways may be a therapeutic strategy for CKD. </p>","PeriodicalId":13892,"journal":{"name":"International journal of clinical and experimental medicine","volume":"8 12","pages":"22022-9"},"PeriodicalIF":0.1,"publicationDate":"2015-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4729962/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141081272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Differences of prevalence of dyslipidemia and risk factors related to LDL-c in the patients with abnormal fasting glucose between Uygur and Han in Xinjiang.","authors":"Li Quan, Lin Hu, Li Zhang, Sheng Jiang","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Aims: </strong>To evaluate the incidence of dyslipidemia among Uygur and Han patients with impaired fasting glucose (IFG). To investigate the influence factors on LDL-c in this population.</p><p><strong>Methods: </strong>This cross-sectional study included a total of 4709 participants, consisting of Uygurs patients (n=2053) and Han patients (n=2656) from Xinjiang province, who were screened for diabetes mellitus. A stratified multistage sampling design was used to collect the participants. The influence factors on LDL-c were analyzed by Logistic regression analysis.</p><p><strong>Results: </strong>Among the IFG patients (n=1757), Uighur IFG group had a higher prevalence of dyslipidemia than that of Han IFG group, 99.8% vs. 63.7%, P<0.05. Similar trends were existed in the prevalence of hypercholesteremia, hypertriglyceridemia, high LDL-c and low HDL-c (all P<0.05). Among the Uighur groups, IFG group had higher dyslipidemia rate than that of euglycemia group (74%). However, there was no such difference in the Han groups. Logistic regression analysis revealed that risk factors associated with LDL-c were age, total cholesterol and 2 h postprandial blood glucose for the Uighur IFG patients. However, gender and total cholesterol were risk factors for Han IFG patients.</p><p><strong>Conclusions: </strong>Uighur IFG patients had higher incidence of dyslipidemia than that of Han IFG patients. For Uyghur IFG patients, closing follow-up of total cholesterol and 2 h postprandial blood glucose were necessary. As to the Han IFG patients, we should pay more attention to male and total cholesterol in order to lower LDL-c levels. So, appropriately preventive and therapeutic measures should be chosen based on the characteristics of abnormal lipid profiles in different nationality.</p>","PeriodicalId":13892,"journal":{"name":"International journal of clinical and experimental medicine","volume":"8 12","pages":"22403-10"},"PeriodicalIF":0.1,"publicationDate":"2015-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4730006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71434228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Human pituitary homeobox-3 gene in congenital cataract in a Chinese family.","authors":"Xiangyu Ye, Guangbin Zhang, Nuo Dong, Yan Meng","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objectives: </strong>Congenital cataract is the common cause of world blindness. It is generally inherited as an autosomal recessive trait and has various phenotypes. This study aimed to explore the gene responsible for autosomal recessive congenital cataract in a Chinese family, and to investigate the functional and cellular consequences of the mutation.</p><p><strong>Methods: </strong>A four-generation Chinese family with autosomal recessive congenital cataract was included in the study. A genome wide scan and linkage analysis were performed in the chromosomal region of Pituitary homeobox 3 (PITX3) to identify the linked region of the genome. And sequence analysis of PITX3 gene was also investigated using BigDye Terminator mix 3.0 and SeqScape Software 2.5.</p><p><strong>Results: </strong>The genome wide scan and linkage analysis identified a disease-haplotype interva. The maximum logarithm of odds LOD score was (Zmax) 3.11 at marker D10S1693 (θmax=0.00), flanked by D10S1680 and D10S467, which included the PITX3 gene. Sequencing revealed a splice site mutation, G→A, at D10S1680 and D10S467, which co-segregated with all the affected members of this family.</p><p><strong>Conclusions: </strong>The 543delG is a novel mutation in PITX3 causing an autosomal recessive congenital cataract.</p>","PeriodicalId":13892,"journal":{"name":"International journal of clinical and experimental medicine","volume":"8 12","pages":"22435-9"},"PeriodicalIF":0.1,"publicationDate":"2015-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4730011/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140193701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Extramedullary relapse in lumbar spine of patient with acute promyelocytic leukemia after remission for 16 years: a case report and literature review.","authors":"Zheng-mei He, Shan-dong Tao, Yuan Deng, Yue Chen, Lixiao Song, Bang-he Ding, Kankan Chen, Liang Yu, Chun-ling Wang","doi":"10.3760/CMA.J.ISSN.1671-7368.2016.01.018","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1671-7368.2016.01.018","url":null,"abstract":"Acute promyelocytic leukemia (APL) is a common myeloid leukemia. At the newly diagnosed stage, it can be fatal because of the serious complication-disseminated intravascular coagulation. With the advent and early application of all-trans retinoic acid, most APL patients can achieve a long-term survival, and only a minority of patients will develop extramedullary relapse after remission. The most common site of extramedullary relapse is central nervous system, while other sites are relatively rare. Here, we report a particularly rare APL patient who experienced extramedullary relapse with lumbar spine as the isolated site after a rather long time of remission for 16 years. At the time of relapse, the main clinical manifestations of the patient are obvious low back pain, weakness in lower limbs and limitation of activity. After treatment of local radiotherapy combined with ATRA and arsenic trioxide, the patient achieved and maintained a second complete remission by now.","PeriodicalId":13892,"journal":{"name":"International journal of clinical and experimental medicine","volume":"8 12 1","pages":"22430-4"},"PeriodicalIF":0.1,"publicationDate":"2015-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70001017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yu Bai, Feng Zhao, Yan Li, Lei Wang, Xiang-Jie Fang, Chen-Yu Wang
{"title":"Ginkgo biloba extract induce cell apoptosis and G0/G1 cycle arrest in gastric cancer cells.","authors":"Yu Bai, Feng Zhao, Yan Li, Lei Wang, Xiang-Jie Fang, Chen-Yu Wang","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objective: </strong>Previous studies have shown that the Ginkgo biloba extract (EGb761) can be used to anti-cancer. However, the mechanism by which EGb761 mediate this effect is still unclear. In the present study, EGb761 inhibited cell proliferation and induced cell apoptosis in gastric cancer cell was explored.</p><p><strong>Methods: </strong>The cell viability was detected by the CCK8 assay. The cell cycle and apoptosis was assessed by flow cytometry. The protein expression of caspase-3, p53 and Bcl-2 were analyzed by western blot.</p><p><strong>Results: </strong>Treatment of human gastric cancer cells with EGb761 induced cell death in a dose-dependent manner by using CCK8 assay. Consistent with the CCK8 assay, the flow cytometry results showed that gastric cancer cells were accumulated in G0/G1 phase when exposed to EGb761. Furthermore, the proportion of apoptosis cells was increased after EGb761 treatment as compared to untreated group. In addition, our results showed that the treatment of AGS cells with EGb761 significantly increased the expression of caspase3 and p53, and decreased the anti-apoptotic Bcl-2 level.</p><p><strong>Conclusions: </strong>Our results demonstrated that EGb761 could inhibit gastric cancer proliferation through adjusting cell cycle and inducing cell apoptosis.</p>","PeriodicalId":13892,"journal":{"name":"International journal of clinical and experimental medicine","volume":"8 11","pages":"20977-82"},"PeriodicalIF":0.1,"publicationDate":"2015-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4723873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140193728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}