{"title":"siRNA of ADAM17 gene induces apoptosis, proliferation inhibition and enhances the effects of genistein on HepG2 cells","authors":"Yongcun Liu, Zuo-ren Wang, Yu Ji, Feng Li","doi":"10.1016/S1007-4376(09)60040-X","DOIUrl":"https://doi.org/10.1016/S1007-4376(09)60040-X","url":null,"abstract":"","PeriodicalId":100807,"journal":{"name":"Journal of Nanjing Medical University","volume":"6 1","pages":"127-131"},"PeriodicalIF":0.0,"publicationDate":"2009-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82485288","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}
{"title":"Recombinant adenovirus-mediated shRNA silencing of midkine gene in BxPC-3 cells","authors":"Mingyue Xiong, Kunzheng Wang","doi":"10.1016/S1007-4376(09)60041-1","DOIUrl":"https://doi.org/10.1016/S1007-4376(09)60041-1","url":null,"abstract":"","PeriodicalId":100807,"journal":{"name":"Journal of Nanjing Medical University","volume":"46 1","pages":"132-136"},"PeriodicalIF":0.0,"publicationDate":"2009-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80596436","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}
Guoqiang Wang , Shuyu Wang , Qun Shen , Shiwei Yin , Chunping Li , Aiping Li , Jianyong Li , Jianwei Zhou , Qizhan Liu
{"title":"Polymorphisms in XRCC5, XRCC6, XRCC7 genes are involved in DNA double-strand breaks(DSBs) repair associated with the risk of acute myeloid leukemia(AML) in Chinese population","authors":"Guoqiang Wang , Shuyu Wang , Qun Shen , Shiwei Yin , Chunping Li , Aiping Li , Jianyong Li , Jianwei Zhou , Qizhan Liu","doi":"10.1016/S1007-4376(09)60034-4","DOIUrl":"10.1016/S1007-4376(09)60034-4","url":null,"abstract":"<div><h3>Objective</h3><p>To investigate the association between the X-ray repair cross complementing(XRCC) group 5, XRCC6 and XRCC7 polymorphisms and risk of acute myeloid leukemia(AML).</p></div><div><h3>Methods</h3><p>This hospital-based case-control study included 120 AML patients and 210 cancer-free controls in a Chinese population. Three polymorphisms of XRCC5, XRCC6 and XRCC7 were genotyped using the polymerase chain reaction(PCR) or polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP) method.</p></div><div><h3>Results</h3><p>We found that there was a significant decrease in risk of AML associated with the XRCC6 −61 CG/GG genotype(adjusted odd ratio (OR) = 0.55; 95% confident interval(CI) = 0.34-0.89) compared with the −61CC genotype. For the novel tandem repeat polymorphism (VNTR) in the XRCC5 promoter, we found when the XRCC5 six genotypes were dichotomized(i.e., 2R/2R, 2R/1R versus 2R/0R, 1R/1R, 1R/0R and 0R/0R), the latter group was associated with increased risk of AML(adjusted OR = 1.67; 95% CI = 1.00∼2.79) compared to 2R/2R+2R/1R genotype. However, the XRCC7 6721G > T polymorphism had no effect on risk of AML.</p></div><div><h3>Conclusion</h3><p>The XRCC6 −61C > G and XRCC5 2R/1R/0R polymorphisms, but not XRCC7 6721G > T polymorphism, could play an important role in the development of AML. Larger scale studies with more detailed data on environment exposure are needed to verify these findings.</p></div>","PeriodicalId":100807,"journal":{"name":"Journal of Nanjing Medical University","volume":"23 2","pages":"Pages 93-99"},"PeriodicalIF":0.0,"publicationDate":"2009-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1007-4376(09)60034-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86666606","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}
{"title":"In vitro effects of sodium hyaluronate on the proliferation and the apoptosis in chondrocytes from patients with Kashin-Beck disease and osteoarthritis","authors":"Zongqiang Gao , Xiong Guo , Chen Duan , Weijuan Ma , Peng Xu , Ruiyu Liu , Qisheng Gu , Junchang Chen","doi":"10.1016/S1007-4376(09)60036-8","DOIUrl":"10.1016/S1007-4376(09)60036-8","url":null,"abstract":"<div><h3>Objective</h3><p>To identify the <em>in vitro</em> effects of sodium hyaluronate(HA) on the proliferation and the apoptosis of chondrocytes from patients with Kashin-Beck disease(KBD) and osteoarthritis(OA).</p></div><div><h3>Methods</h3><p>Samples of articular cartilages from KBD and OA patients, as well as healthy volunteers(6 subjects in each of the 3 groups) were dissected, digested with collagenase and the cells cultured in monolayers. Chondrocytes from each sample were assigned to an untreated group and two HA-treated groups: H0(no HA), H100(HA, 0.1 g/L) and H500(HA, 0.5 g/L). The first passage chondrocytes were used to observe proliferation using the MTT assay, and apoptosis by flow cytometry through Annexin V/PI staining.</p></div><div><h3>Results</h3><p>HA promoted proliferation of chondrocytes in all the three groups, and in KBD and OA groups, for cells cultured for 4 and 6 days, H500 significantly promoted the cell proliferation. The apoptotic rates of both KBD and OA group chondrocytes were in the order H500 < HA100 < H0.</p></div><div><h3>Conclusion</h3><p>Sodium hyaluronate administration has a dose-dependent <em>in vitro</em> effect to promote proliferation and inhibit apoptosis of chondrocytes from patients with KBD and OA.</p></div>","PeriodicalId":100807,"journal":{"name":"Journal of Nanjing Medical University","volume":"23 2","pages":"Pages 104-110"},"PeriodicalIF":0.0,"publicationDate":"2009-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1007-4376(09)60036-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86423471","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}
{"title":"The effect of methylseleninic acid on paclitaxel efficacy in A2780 ovarian cancer cells","authors":"Qiaoli Zhang , Rami G. Azrak","doi":"10.1016/S1007-4376(09)60037-X","DOIUrl":"10.1016/S1007-4376(09)60037-X","url":null,"abstract":"<div><h3>Objective</h3><p>The role of methylseleninic acid (MSeA), a selenium compound, has been documented in cancer chemoprevention. However, the therapeutic effect of MSeA in combination with paclitaxel, a chemotherapeutic agent used to treat ovarian cancer, is unknown. In this study, we investigated the effect of combination treatment of MSeA and paclitaxel against ovarian cancer cells.</p></div><div><h3>Methods</h3><p>Ovarian cancer cells(A2780) were treated with different concentrations of MSeA, paclitaxel alone or in combination. The individual and combined concentrations of drugs that achieved certain cells growth/death were determined using a sulforhodamine B(SRB) assay. Drug effects on cell viability were further confirmed using floating cell count and trypan blue exclusion assay. The mean values, standard deviation were calculated and compared between treatment groups using unpaired t test.</p></div><div><h3>Results</h3><p>The concentration of paclitaxel alone that inhibited 50% of cell growth(IC<sub>50</sub>) was 0.5 μmol/L. This concentration increased to 1.2 μmol/L when paclitaxel was given in sequential combination with MSeA. The number of dead cells after the combination treatment did not show a significance increase when compared with drug alone.</p></div><div><h3>Conclusion</h3><p>Pretreatment with MSeA did not enhance the paclitaxel effect against A2780 ovarian cancer cells.</p></div>","PeriodicalId":100807,"journal":{"name":"Journal of Nanjing Medical University","volume":"23 2","pages":"Pages 111-116"},"PeriodicalIF":0.0,"publicationDate":"2009-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1007-4376(09)60037-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72833675","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}
Liu Ou-yang, Yukun Zhang, Shuhua Yang, Shunan Ye, Weihua Xu
{"title":"Effect of the gap junction blocker 1-heptanol on chondrogenic differentiation of mouse bone marrow mesenchymal stem cells in vitro","authors":"Liu Ou-yang, Yukun Zhang, Shuhua Yang, Shunan Ye, Weihua Xu","doi":"10.1016/S1007-4376(09)60038-1","DOIUrl":"10.1016/S1007-4376(09)60038-1","url":null,"abstract":"<div><h3>Objective</h3><p>To investigate the effect of the gap junction blocker 1-heptanol on the <em>in vitro</em> chondrogenic differentiation of mouse bone marrow mesenchymal stem cells(MSCs) following induction by GDF-5.</p></div><div><h3>Methods</h3><p>MSCs were isolated from mouse bone marrow and cultured <em>in vitro</em>. After 3 passages cells were induced to undergo chondrogenic differentiation with recombinant human GDF-5(100 ng/ml), with or without 1-heptanol(2.5μ mol/L). The effect of 1-heptanol on MSCs proliferation was investigated using the MTT assay. Type, collagen mRNA and protein were examined by RT-PCR and immunocytochemistry respectively, and the sulfate glycosaminoglycan was assessed by Alcian blue dye staining. Connexin43(Cx43) protein was examined by western blotting.</p></div><div><h3>Results</h3><p>GDF-5 induced proliferation and chondrogenic differentiation of MSCs. While 1-heptanol treatment had no effect on this proliferation, it inhibited the expression of both type, collagen mRNA and protein. The Alcian blue staining revealed that 1-heptanol also inhibited the deposition of the typical cartilage extracellular matrix promoted by recombinant GDF-5. Western blotting demonstrated that 1-heptanol had no effect on the expression of Cx43.</p></div><div><h3>Conclusion</h3><p>These results suggest that mouse bone marrow MSCs can be differentiated into a chondrogenic phenotype by GDF-5 administration <em>in vitro</em>. While the gap junction blocker, 1-heptanol, did not reduce gap junction Cx43, these intercellular communication pathways clearly played an important functional role in GDF-5-induced cartilage differentiation.</p></div>","PeriodicalId":100807,"journal":{"name":"Journal of Nanjing Medical University","volume":"23 2","pages":"Pages 117-121"},"PeriodicalIF":0.0,"publicationDate":"2009-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1007-4376(09)60038-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87376435","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}
Pu Huang , Wenli Gou , Mali Jiang , Rui Zhang , Yunping Sun
{"title":"Impairments of spatial learning and memory in rat offspring with fetal growth restriction","authors":"Pu Huang , Wenli Gou , Mali Jiang , Rui Zhang , Yunping Sun","doi":"10.1016/S1007-4376(09)60027-7","DOIUrl":"10.1016/S1007-4376(09)60027-7","url":null,"abstract":"<div><h3>Objective</h3><p>Throughout the world, fetal growth restriction(FGR) is one of the most severe complications occurring during pregnancy. It is subsequently associated with neurologic abnormalities in chldren. Our aim was to investigate the spatial learning and memory ability of rat offspring born with FGR.</p></div><div><h3>Methods</h3><p>A rat model of FGR was constructed using the method of passive smoking. Spatial learning and memory were studied in rat offspring born with FGR by assessing the animals' performance using the Morris water maze task.</p></div><div><h3>Results</h3><p>At 1- and 2-months of age, both female and male offspring rats showed impairment of performance, while at 4 months of age, only female rats showed impaired performance. The FGR offspring spent a longer time swimming and used inefficient strategies(<em>P</em> < 0.05, respectively). However, there were no significant maze performance FGR effects in the 4 month old male rats. In all groups of FGR offspring, irrespective of age or sex, the time spent in the platform quadrant by the rat was significantly less than that in the control group(<em>P</em> < 0.05).</p></div><div><h3>Conclusion</h3><p>The Morris water maze performance decreased in rat offspring born with FGR. It is suggested that FGR can cause impairments of spatial learning and memory in young animals.</p></div>","PeriodicalId":100807,"journal":{"name":"Journal of Nanjing Medical University","volume":"23 1","pages":"Pages 54-58"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1007-4376(09)60027-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90904416","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}
{"title":"Induction of interleukin-8 production by angiotensin II in rat vascular smooth muscle cells","authors":"Zhi Wang, Lili Zhang, Baogui Sun, Qiuyan Dai","doi":"10.1016/S1007-4376(09)60026-5","DOIUrl":"10.1016/S1007-4376(09)60026-5","url":null,"abstract":"<div><h3>Objective</h3><p>Interleukin-8(IL-8) represents the prototypical chemokine that is made by a wide variety of cell types. Previously studies have suggested that angiotensin II(Ang II) is involved in atherogenesis through induction of proinflammatory cytokines such as interleukin-6 or monocyte chemoattractant protein-1(MCP-1) in vascular smooth muscle cells(VSMCs), while the role of Ang II on IL-8 expression in VSMCs is poorly studied.</p></div><div><h3>Methods</h3><p>In this study, VSMCs were isolated from the thoracic aorta of Sprague-Dawley rats. The expression of smooth muscle α-actin was confirmed by an immunohistochemical method. Semi-quantitative RT-PCR and enzyme-linked immunosorbent assay (ELISA) analyses were conducted to detect IL-8 expression.</p></div><div><h3>Results</h3><p>In the present study we found that Ang II significantly increased the expression of IL-8 both at the mRNA and protein levels in rat VSMCs in a dose- and time-dependent manner.</p></div><div><h3>Conclusion</h3><p>These findings suggested that Ang II may participate in atherosclerosis through induction of inflammatory mediator in VSMCs.</p></div>","PeriodicalId":100807,"journal":{"name":"Journal of Nanjing Medical University","volume":"23 1","pages":"Pages 50-53"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1007-4376(09)60026-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91371381","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}
{"title":"Relationship between obstructive sleep apnea hypopnea syndrome and cardiovascular disorders in adult snorers","authors":"Rui Wu , Xilong Zhang , Ling Hu , Enzhi Jia","doi":"10.1016/S1007-4376(09)60028-9","DOIUrl":"10.1016/S1007-4376(09)60028-9","url":null,"abstract":"<div><h3>Objective</h3><p>To investigate the relationship between sleep apnea hypopnea syndrome(OSAHS) and some cardiovascular disorders in adult habitual snorers as well as the effectiveness of nasal continuous positive airway pressure(NCPAP) on those with OSAHS.</p></div><div><h3>Methods</h3><p>With the use of polysomnography, 262 adult habitual snorers were examined and divided into the OSAHS group and the Non-OSAHS group (control). Using ambulatory electrocardiogram and blood pressure measurement, daily nocturnal rhythm of blood pressure, hypertension, heart rate variability, some arrythmias and angina pectoris of coronary heart disease were monitored and compared between the two groups, before and after 14 days of treatment with NCPAP in the OSAHS group.</p></div><div><h3>Results</h3><p>This study indicated a higher incidence (39.6%) of OSAHS in adult snorers and demonstrated that there was a significantly higher incidence of hypertension, disappearance of the daily nocturnal rhythm of blood pressure, poor effectiveness of nitrate on angina pectoris of coronary heart disease, decreased heart rate variability during sleep, increased arrythmias and lower SpO<sub>2</sub> levels in the OSAHS group than in the Non-OSAHS group. After NCPAP treatment during sleep, snoring control, significantly higher SpO<sub>2</sub> and lower apnea hypopnea indices were achieved in the OSAHS group; heart rate variability and daily nocturnal rhythm of blood pressure returned to normal levels.</p></div><div><h3>Conclusion</h3><p>The results of this research suggested that there was a close relationship between the development of OSAHS and some cardiovascular disorders. Furthermore, NCPAP treatment was effective not only on OSAHS but also on coexisting cardiovascular disorders.</p></div>","PeriodicalId":100807,"journal":{"name":"Journal of Nanjing Medical University","volume":"23 1","pages":"Pages 59-63"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1007-4376(09)60028-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90930819","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}
{"title":"Effect of Rapamycin on TGF-β1-induced epithelial-mesenchymal transition in LoVo colonic adenocarcinoma cells","authors":"Renhu Sun, Jiang Li, Jing Cui, Qing Lv, Xinghua Liu, Guobin Wang","doi":"10.1016/S1007-4376(09)60020-4","DOIUrl":"10.1016/S1007-4376(09)60020-4","url":null,"abstract":"<div><h3>Objective</h3><p>To investigate the effect of Rapamycin on epithelial-mesenchymal transition(EMT) of LoVo colonic adenocarcinoma cells <em>in vitro</em>.</p></div><div><h3>Methods</h3><p>Cultured LoVo colonic adenocarcinoma cells were divided into three groups: negative control group, EMT-inducing group(TGF-β <sub>1</sub>) and EMT-interfering group(TGF-β <sub>1</sub> plus Rapamycin). E-cadherin expression in LoVo cells was detected by Western Blot, while the expression of vimentin was evaluated through immunocytochemistry. The Snail mRNA in LoVo cells was examined by RT-PCR.</p></div><div><h3>Results</h3><p>TGF-β <sub>1</sub> induced LoVo cell switching from polygonal to spindle-shaped. TGF-β <sub>1</sub> enhanced the expression of vimentin, but lowered the level of E-cadherin. In contrast, Rapamycin impaired the transition induced by TGF-β <sub>1</sub>. Rapamycin dramatically abrogated TGF-β <sub>1</sub>-induced vimentin expression and restored E-cadherin expression in LoVo cells. Rapamycin significantly repressed the up-regulation of Snail mRNA expression induced by TGF-β <sub>1</sub>.</p></div><div><h3>Conclusion</h3><p>Rapamycin dramatically abrogated TGF-β <sub>1</sub> induced Snail mRNA expression in LoVo cells, hence inhibiting EMT of these cells <em>in vitro</em>.</p></div>","PeriodicalId":100807,"journal":{"name":"Journal of Nanjing Medical University","volume":"23 1","pages":"Pages 15-19"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1007-4376(09)60020-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72983098","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}