Jiangsu Province Geriatric Hospital
Jiangsu Province Geriatric Hospital
Zhu Y.,Jiangsu Province Geriatric Hospital |
Chen J.,Nanjing Medical University |
Cheng H.,Shanghai JiaoTong University |
Cai W.,Nanjing Medical University
International Journal of Clinical and Experimental Medicine | Year: 2017
Objective: The association between estrogen receptor alpha (ESR1) gene PvuII polymorphism and fracture risk is still ambiguous and inconclusive. Furthermore, this relationship in postmenopausal women with heart failure (HF) is rarely reported. The aim of the present study was to evaluate the effect of the PvuII polymorphism (rs2234693, C>T) of the ESR1 gene on fragility fractures in elderly postmenopausal women with HF. Methods: This was a hospital-based case-control study of postmenopausal women >60 years of age with HF, including 80 fracture patients and 80 controls between January 2009 and January 2014. The PvuII genotype was determined using a polymerase chain reaction-restriction fragment length polymorphism assay. Results: Fragility fracture was more common in smokers and those with a history of fragility fracture and less common in subjects who exercised daily. The PvuII T allele was present in 83.75% of patients with fractures vs. 62.50% of controls. Carriers of the variant rs2234693T allele had increased risk of fracture (P<0.05). Compared with the common genotype, the CT+TT rs2234693 genotype was associated with significantly increased risk of fracture (P = 0.036, adjusted odds ratio = 1.323, 95% confidence interval = 1.263-2.787). In stratified analyses, the association between the risk of fracture and the rs2234693 variant was more prominent in younger individuals (≤67 years) and non-smokers. Conclusion: The PvuII polymorphism (rs2234693, C>T) of the ESR1 gene may contribute to the development of fragility fractures in elderly postmenopausal women with HF. © 2017, E-Century Publishing Corporation. All rights reserved.
Wu Y.,Jiangsu Province Geriatric Hospital |
Liu H.-B.,Nanjing University |
Ding M.,Jiangsu Province Geriatric Hospital |
Liu J.-N.,Jiangsu Province Geriatric Hospital |
And 3 more authors.
Molecular Biology Reports | Year: 2012
E-cadherin has been implicated in invasiveness and metastasis. However, the clinical prognostic value of decreased E-cadherin expression in patients with non-small cell lung cancer (NSCLC) remains unsettled. A metaanalysis of eligible studies was performed to quantitatively review the correlation of decreased E-cadherin expression with survival in patients with NSCLC. Thirteen studies, including 2,274 patients, were subjected to final analysis. The rate of decreased E-cadherin expression was 47.6 % overall and 41.4 % for stage I disease. The combined hazard ratio (HR) was 1.41 (95 % CI 0.18-1.65; P = 0.001), indicating that decreased E-cadherin expression had an unfavorable impact on the survival of patients with NSCLC. Further, in the stratified analysis by ethnicity, the combined HR in Asians was 1.49 (95 % CI 1.27-1.71) and in non-Asians was 1.01 (95 % CI 1.00-1.02). However, when only the stage I studies were considered, the combined HR was 1.19 (95 % CI 0.90-1.47; P = 0.576), suggesting that decreased E-cadherin expression has no impact on survival. Decreased E-cadherin expression was associated with poor survival in patients with NSCLC, especially among Asians, but was not significantly correlated with survival for stage I NSCLC patients. © Springer Science+Business Media B.V. 2012.
Fioravanti M.,University of Rome La Sapienza |
Nakashima T.,Hiroshima University |
Xu J.,Jiangsu Province Geriatric Hospital
BMJ Open | Year: 2014
Objective: To evaluate the safety profile of nicergoline compared with placebo and other active agents from published randomised controlled trials. Design: Systematic review and meta-analysis of nicergoline compared with placebo and other active agents across various indications. Data sources: MEDLINE, Medline-in-process, Cochrane, EMBASE, EMBASE alerts, Cochrane Central Register of Controlled Trials (CENTRAL), Cochrane Database of Systematic Reviews (CDSR) and Cochrane Methodology Register (CMR) for all the randomised controlled trials, open-label or blinded, in adults treated with nicergoline. Studies published until August 2013 were included. Review method: 29 studies were included for data extraction. The studies included in this review were majorly from European countries and mostly in cerebrovascular disease (n=15) and dementia (n=8). Results: The treatment withdrawals were comparatively lower in the nicergoline group as compared with the placebo group (RR=0.92; 95% CI 0.7 to 1.21) and other active comparators (RR=0.45; 95% CI 0.10 to 1.95), but the difference was non-significant. Incidence of any adverse events (AEs) was slightly higher (RR=1.05; 95% CI 0.93 to 1.2) while incidence of serious AEs was lower (RR=0.85; 95% CI 0.50 to 1.45) in the nicergoline compared with placebo group. Frequency of anxiety was significantly lower in nicergoline as compared with placebo (p=0.01). Other AEs including diarrhoea, gastric upset, dizziness and drowsiness were less frequent in the nicergoline group when compared with placebo/active drugs, but the difference was non-significant. Frequency of hypotension and hot flushes was slightly higher in the nicergoline group but the difference was non-significant. None of the studies reported any incidence of fibrosis or ergotism with nicergoline treatment. Conclusions: Nicergoline is an ergot derivative, but its safety profile is better than other ergot derivatives like ergotamine and ergotoxine. This systematic review and meta-analysis suggests that nicergoline has a good safety profile. None of the studies included in this systematic review reported any incidence of fibrosis or ergotism with nicergoline.
Shao N.,Jiangsu Province Geriatric Hospital
Molecular biology reports | Year: 2012
Evidence is accumulating that cyclooxygenase-2 (COX-2) may play an important role in prostate cancer (PCa). Recently, gene polymorphisms in COX-2 have been implicated to alter the risk of PCa and overexpression of COX-2 may be associated with clinical and prognostic significance in PCa. However, the results of these studies are inconclusive or controversial. To derive a more precise estimation of the relationships, we performed an updated meta-analysis. A comprehensive search was conducted to examine all the eligible studies of COX-2 polymorphism and expression in PCa. We used odds ratios (ORs) to assess the strength of the association and the 95 % confidence intervals (CIs) give a sense of the precision of the estimate. Overall, no significant associations between COX-2 polymorphism and PCa risk were found. However, high expression of COX-2 was significantly higher in T3-T4 stages of PCa than in T1-T2 stages of PCa (OR = 2.33, 95 %CI: 1.54-3.53, P < 0.0001). COX-2 might play an important role in the progress of PCa, overexpression of COX-2 correlates with T3-T4 stages of PCa. COX-2 might be a potential therapy target for PCa and work as a prognostic factor for PCa patients.
Tan T.,Jiangsu Province Geriatric Hospital |
Zhang K.,Nanjing University |
Sun W.C.,Jiangsu Province Geriatric Hospital
Breast Cancer | Year: 2016
Background: The objective of this study was to investigate whether the genetic polymorphism rs12665607 of ESR1, rs10995190 of ZNF365, rs3817198 of LSP1 and rs17001868 of SGSM3/MKL1 are associated with the development of breast cancer (BC) in the Chinese women. Methods: The 4 SNPs were genotyped for 453 female BC patients and 750 controls. The differences of genotype and allele distributions between patients and controls were evaluated using the Chi-square test. The comparison of SGSM3 expression in the tumor and the adjacent normal breast tissues was carried out by the Student’s t test. One-way ANOVA test was used to analyze the relationship between genotypes of rs17001868 and the tissue expression of SGSM3. Results: Patients were found to have significantly higher allele T of rs12665607 and allele C of rs17001868 than that of the controls (35.2 % vs. 29.6 %, p = 0.004 for rs12665607; 23.1 % vs. 19.1 %, p = 0.02 for rs17001868). The OR values were 1.29 for rs12665607 and 1.27 for rs17001868, respectively. The mean expression level of SGSM3 was significantly lower in BC tumors than in the adjacent normal tissues (0.0082 ± 0.0038 vs. 0.0134 ± 0.0078; p < 0.001). Patients with genotype CC were found to have a remarkably lower SGSM3 expression in the tumors than those with genotype AA (p = 0.007). Conclusions: ESR1 gene and the SGSM3 gene are associated with the risk of BC in Chinese population. Besides, rs17001868 may be a putative functional variant that can affect the expression of SGSM3 in patients with BC. With the OR ranging from 1.27 to 1.29, variants of these 2 genes can only explain limited variance of BC. Further investigations into the functional role of the susceptible genes would be helpful to clarify the etiology of BC. © 2016 The Japanese Breast Cancer Society
Liu H.-B.,Nanjing University |
Wu Y.,Jiangsu Province Geriatric Hospital |
Lv T.-F.,Nanjing University |
Yao Y.-W.,Nanjing University |
And 3 more authors.
PLoS ONE | Year: 2013
Background: The aim of this study was to assess the role of skin rash in predicting the efficacy of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) and the prognosis of patients with non-small cell lung cancer (NSCLC). Method: We systematically searched for eligible articles investigating the association between rash and the efficacy of EGFR-TKIs and the prognosis of patients with NSCLC. The summary risk ratio (RR) and hazard ratio (HR) were calculated using meta-analysis. Results: We identified 33 eligible trials involving 6,798 patients. We used two different standards to group the patients [standard 1: rash vs. no rash, standard 2: rash (≥ stage 2) vs. rash (stage 0, 1)]. For standard 1, the objective response rate (ORR) and disease control rate (DCR) of the rash group were significantly higher than the no rash group [RR = 3.28; 95% CI: 2.41-4.47(corrected RR = 2.225, 95% CI: 1.658-2.986); RR = 1.96, 95% CI: 1.58-2.43]. The same results were observed for standard 2. For standards 1 and 2, the progression-free survival (PFS) (HR = 0.45, 95% CI: 0.37-0.53; HR = 0.57, 95% CI: 0.50-0.65) and overall survival (OS) (HR = 0.40, 95% CI: 0.28-0.52; HR = 0.53, 95% CI: 0.35-0.71) of the rash group were significantly longer than the control group, and the same results were observed in the subgroup analysis. Conclusions: skin rash after EGFR-TKI treatment may be an efficient clinical marker for predicting the response of patients with NSCLC to EGFR-TKIs. Furthermore, skin rash is also the prognostic factor of patients with NSCLC. Patients with skin rash have a longer PFS and OS. © 2013 Liu et al.
Ji N.-F.,Nanjing Medical University |
Ji N.-F.,Jiangsu Province Geriatric Hospital |
Xie Y.-C.,Jiangsu Province Geriatric Hospital |
Zhang M.-S.,Nanjing Medical University |
And 5 more authors.
International Immunopharmacology | Year: 2014
Asthma is an inflammatory disease closely associated with activated T cells in the lung. Imbalances in Th1/Th2 and Treg/Th17 have been found in asthmatic patients. Ligustrazine from the Chinese herb chuanxiong has been used in China in combination with glucocorticoids to treat asthma. Previous studies have proved that ligustrazine can modulate the expression of transcription factors for Th1 (T-bet) and Th2 (Gata-3) in asthma. In the present study, ligustrazine alleviated allergic airway inflammation in a mouse asthmatic model by reducing the influx of eosinophils and neutrophils, which was mediated, at least in part, by the regulation of Th1/Th2 and Treg/Th17 via the re-balance of cytokine profiles and of ratios of transcription factors, T-bet/Gata-3 and Foxp3/RORγt, thus providing new insights into the mechanisms of action for asthma treatment with ligustrazine. © 2014 Elsevier B.V.
Sun S.Z.,Jiangsu Province Geriatric Hospital
Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine / Zhongguo Zhong xi yi jie he xue hui, Zhongguo Zhong yi yan jiu yuan zhu ban | Year: 2013
To study effects of Yishen Kangxian Compound (YKC) and benazepril containing serums on HK-2 cells (human renal proximal tubule epithelial cells) in the process of renal tubular epithelial cells to mesenchymal myofibroblasts transdifferentiation (TEMT) by gene chip. YKC and benazepril containing serums were prepared. Their inhibitory effects on HK-2 cells in the transforming growth factor-beta1 (TGF-beta1)-induced TEMT process were observed. HK-2 cells were randomly divided into four groups, i.e., the blank control group, the model group, the benazepril group, and the YKC group. The gross RNAs were extracted and purified by taking advantage of the HumanHT-12 v4 of IlluminaBeadChip. Differentially expressed genes were obtained after they were reversely transcribed to cDNA, incorporating biotin labeling probe, hybridized with GeneChip, picture signals of fluorescence in gene array scanned and compared with differential genes by computer analysis. Differentially expressed genes were successfully identified by gene chip. Compared with the model group, there were 227 differentially expressed genes in the benazepril group, including 118 up-regulated genes and 109 downregulated genes. Compared with the model group, there were 97 differentially expressed genes in the YKC group, including 69 up-regulated genes and 28 down-regulated genes. The Gene Ontology (GO) analysis indicated that YKC was more actively involved in the regulatory process than benazepril in terms of cell damage, apoptosis, growth, NF-KB, protein kinase, neuron, and blood vessel growth. YKC and benazepril could inhibit the TEMT process of HK-2 cells. But YKC also had taken part in cell damage, apoptosis, growth,and more pathways of early stage TEMT.
PubMed | Nanjing Medical University and Jiangsu Province Geriatric Hospital
Type: Journal Article | Journal: Molecular medicine reports | Year: 2016
Jatrorrhizine hydrochloride (JH) is an active component of the traditional Chinese herb Coptis chinensis, which has been used to prevent and treat metabolic disorders. Hyperlipidemia is one of the principal factors underlying numerous metabolic diseases, including diabetes and obesity. Therefore, the aim of the present study was to investigate the lipid lowering effects of JH treatment invivo in an obesity mouse model. JH-treated hyperlipidemic mice exhibited a reduction in body weight, as well as improved glucose tolerance and insulin sensitivity. In addition, JHtreated hyperlipidemic mice exhibited reduced serum triglyceride, total cholesterol and lowdensity lipoprotein cholesterol levels, as well as increased highdensity lipoprotein cholesterol levels compared with untreated mice fed a highfat diet. Notably, JH treatment ameliorated the pathophysiological changes observed in the livers of hyperlipidemic mice. At the molecular level, JH downregulated the hepatic mRNA expression levels of SREBP1c and FAS, and induced PPAR and CPT1A mRNA expression in hyperlipidemic mice. These findings suggest that JH ameliorates hyperlipidemia via the suppression of lipogenesis and the enhancement of lipid oxidation in the liver.
PubMed | Jiangsu Cancer Hospital, Nanjing Medical University, Zhengzhou University, Huadong Medical Institute of Biotechniques and Jiangsu Province Geriatric Hospital
Type: | Journal: Oncotarget | Year: 2016
Latent membrane protein 1 (LMP1), which is associated with the development of different types of Epstein-Barr virus (EBV) related lymphoma, has been suggested to be an important oncoprotein. In this study, a human anti-LMP1 IgG antibody (LMP1-IgG) was constructed and characterized by ELISA, western blotting (WB), affinity and immunohistochemistry (IHC) analyses. CCK-8, MTT, apoptosis assays, antibody-dependent cell-mediated cytotoxicity (ADCC) and CDC (complement-dependent cytotoxicity) assays were performed to evaluate the inhibitory effects of LMP1-IgG on extranodal nasal-type natural killer (NK)/T-cell lymphoma (ENKTL). Then, the influence of LMP1-IgG on the JAK/STAT signaling pathway was investigated. The results showed that the successfully constructed LMP1-IgG inhibited proliferation, induced apoptosis, and activated ADCC and CDC of ENKTL in a concentration- and time- dependent manner. Moreover, phosphorylation of JAK3 and STAT3 was inhibited by LMP1-IgG. Our data indicate that LMP1-IgG may provide a novel and promising therapeutic strategy for the treatment of LMP1-positive ENKTL.