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Hong Y.,Yixing Peoples Hospital | Ge Z.,Yixing Peoples Hospital | Jing C.,Wuxi No2 Peoples Hospital | Shi J.,Yixing Peoples Hospital | And 7 more authors.
PLoS ONE | Year: 2013

Background: Tumor necrosis factor-α (TNF-α) plays a crucial role in the development and progression of gastric cancer. A functional polymorphism, -308 G>A (rs1800629), which is located in the promoter of TNFA gene, has been suggested to alter the production of TNF-α and influence cancer risk. In the present study, we sought to investigate whether this polymorphism has effects on the risk and progression of gastric cancer in a Chinese population. Methods: We genotyped the TNFA -308 G>A polymorphism using the TaqMan method in a two-stage case-control study comprising a total of 1686 gastric cancer patients and 1895 cancer-free subjects. The logistic regression was used to assess the genetic associations with occurrence and progression of gastric cancer. Results: We found a significant association between the variant genotypes and increased risk of gastric cancer [P = 0.034, odds ratio (OR) = 1.39, 95% confidence interval (CI) = 1.01-1.67, GA/AA vs. GG]. Similar results were observed in the follow-up replication study. When combined the data from the two studies, we found a more significant association (P = 0.001, OR = 1.34, 95%CI = 1.13-1.59), especially for older subjects (>65 years). Furthermore, the patients carrying the variant genotypes had a significantly greater prevalence of T4 stage of disease (P = 0.001, OR = 2.19, 95%CI = 1.39-3.47) and distant metastasis (P = 0.013, OR = 1.61, 95%CI = 1.10-2.35). Conclusions: Our results suggest that the functional promoter -308 G>A polymorphism in TNFA influence the susceptibility and progression of gastric cancer in the Chinese population. © 2013 Hong et al.


PubMed | Shandong University, Guangzhou University, Peoples Hospital of Huangshan, Shanghai Sixth Peoples Hospital and 5 more.
Type: | Journal: Journal of hazardous materials | Year: 2016

This multi-centered study was designed to evaluate the biological effects of exposure to antineoplastic drugs (ADs) at PIVAS (Pharmacy Intravenous Admixture Service) across ten Chinese hospitals. 8-hydroxy-2-deoxyguanosine (8-OHdG) was used as a biomarker of DNA oxidative damage and lymphocyte apoptosis assays using peripheral lymphocyte cells were used to detect primary DNA damage. The mutagenicity activity was estimated with the Ames fluctuation test. 158 exposed and 143 unexposed workers participated in this study. The urinary 8-OHdG/Cr concentrations of the exposed group was 22.0517.89ng/mg Cr, which was significantly higher than controls of 17.3613.50ng/mg Cr (P<0.05). The rate of early lymphocyte apoptosis was slightly increased in exposed group than that of the control group (P=0.087). The mutagenic activity was significantly higher in the exposed group relative to the control group (P<0.05). Moreover, while no statistically significant difference was observed, higher concentrations of 8-OHdG/Cr in urine and an early lymphocyte apoptosis rate were found in exposed group II as compared to exposed group I. In addition, a significant correlation between early lymphocyte apoptosis and exposure time to ADs was also observed (P<0.05). In conclusion, our study identified elevated biomarkers in PIVAS workers exposed to ADs. However whether these findings could lead to increased incidence of genotoxic responses remains to be further investigated.


PubMed | Wuxi Peoples Hospital and Wuxi No2 Peoples Hospital
Type: Journal Article | Journal: PloS one | Year: 2016

Brain-derived neurotrophic factor (BDNF) protects retinal ganglion cells against ischemia in ocular degenerative diseases. We aimed to determine the effect of BDNF-AS on the ischemic injury of retinal ganglion cells.The levels of BDNF and BDNF-AS were measured in retinal ganglion cells subjected to oxygen and glucose deprivation. The lentiviral vectors were constructed to either overexpress or knock out BDNF-AS. The luciferase reporter gene assay was used to determine whether BDNF-AS could target its seed sequence on BDNF mRNA. The methyl thiazolyl tetrazolium assay was used to determine cell viability, and TUNEL staining was used for cell apoptosis.The levels of BDNF-AS were negatively correlated with BDNF in ischemic retinal ganglion cells. BDNF-AS directly targeted its complementary sequences on BDNF mRNA. BDNF-AS regulated the expression of BDNF and its related genes in retinal ganglion cells. Down-regulation of BDNF-AS increased cell viability and decreased the number of TUNEL-positive retinal ganglion cells under oxygen and glucose deprivation conditions.Inhibition of BDNF-AS protected retinal ganglion cells against ischemia by increasing the levels of BDNF.


Xu C.,Soochow University of China | Wu C.,Nanjing Medical University | Xia Y.,Nanjing Medical University | Zhong Z.,Nanjing Medical University | And 7 more authors.
PLoS ONE | Year: 2013

The Wilms' tumor suppressor gene (WT1) has been identified as an oncogene in many malignant diseases such as leukaemia, breast cancer, mesothelioma and lung cancer. However, the role of WT1 in non-small-cell lung cancer (NSCLC) carcinogenesis remains unclear. In this study, we compared WT1 mRNA levels in NSCLC tissues with paired corresponding adjacent tissues and identified significantly higher expression in NSCLC specimens. Cell proliferation of three NSCLC cell lines positively correlated with WT1 expression; moreover, these associations were identified in both cell lines and a xenograft mouse model. Furthermore, we demonstrated that up-regulation of Cyclin D1 and the phosphorylated retinoblastoma protein (p-pRb) was mechanistically related to WT1 accelerating cells to S-phase. In conclusion, our findings demonstrated that WT1 is an oncogene and promotes NSCLC cell proliferation by up-regulating Cyclin D1 and p-pRb expression. © 2013 Xu et al.


Huang H.,Wuxi No2 Peoples Hospital
Medical Journal of Wuhan University | Year: 2012

Objective: To compare and analyze the survival quality between peritoneal dialysis and hemodialysis patients. Methods: A total of 105 cases of end-stage renal disease (ESRD) patients were enrolled in this study, and all the patients received peritoneal dialysis (PD group, n=27) or hemodialysis (HD group, n=78) from January 2010 to January 2012 in our hospital. Mental health and quality of life between the two groups were compared. The Karnofsky function condition index was adopted to assess the body function condition, and HAMD was adopted to evaluate the mental state of these patients. Results: The ESRD severity index was significantly different between HD group and PD group (P<0.05). The karnofsky functional status score was respectively 69.3±3.8 in PD group and 72.1±4.6 in HD group, without statistically significant differences. HAMD factor analysis showed that the PD group patients were better in anxiety, somatization, and despair than in HD group (P<0.05). Conclusion: HD patients with severe renal diseases have higher quality of life than PD patients, although no significant difference was found in body function condition between the two groups. However, PD patients have better mental state than HD patients.


Xu W.,Suzhou University | Zhou Y.,Wuxi No2 Peoples Hospital | Hang X.,Suzhou University | Shen D.,Suzhou University
Molecular Biology Reports | Year: 2012

Abstract The association between single-nucleotide polymorphisms (SNPs) of the CYP1B1 gene and lung cancer risk is still ambiguous. In this meta analysis, we assessed 10 case-control studies included 7,067 cases and 9,374 controls of the association between CYP1B1 SNPs of Leu432Val (rs1056836, 432C[G), Asn453Ser (rs1800440, 453A[G), Ala119Ser (rs1056827, 119G[T), Arg48Gly (rs10012, 48C[G) and the risk of lung cancer. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to evaluate the strength of association between the polymorphism and lung cancer risk under codominant model, dominant model and additive model respectively. Although there were limitations, this meta analysis indicated that individuals with 432GG genotype had a 39.7% higher risk of having lung cancer than those with the 432CC genotype, and individuals with the 432G allele had a 26.3% increased risk as well. An increased risk of lung cancer of 2.13 fold was observed in individuals with 119TT genotype. For Arg48Gly, individuals with 48GG genotype had a significantly increased risk of lung cancer compared with individuals with 48CC (OR 3.859; 95% CI 2.536-5.87). Elevated risk of lung cancer were observed in dominant model (OR 2.115; 95% CI 1.653-2.705) as well. The risk of lung cancer was elevated as the frequency of G allele increased in additive model (P = 0.000). For individuals with the polymorphism at codon 453, no evidence of such association was observed. Furthermore, a possible association between the CYP1B1 polymorphism at codon 432 and the lung cancer could be detected in individuals of Caucasian origin, while a negative association was suggested in Asians and African-Americans. An increased lung cancer risk was also found in women with polymorphism at codon 453. These results are supportive for the hypothesis that the CYP1B1 432GG, 119TT and 48GG genotypes are low-penetrance risk factors for developing lung cancer, and further studies are needed to validate these associations.© Springer Science+Business Media B.V. 2011.


Xu Q.,Xuzhou Medical College | Jiang C.,Wuxi No2 Peoples Hospital | Rong Y.,Xuzhou Medical College | Yang C.,Xuzhou Medical College | And 2 more authors.
Journal of Molecular Neuroscience | Year: 2014

Cerebral ischemic injury involves a variety of cellular and molecular events. Signal transducers and activators of transcription-1 (STAT-1) activation is associated with neuronal cell death and contributes to ischemic injury. The effects of fludarabine, a specific inhibitor of STAT1 protein, on cerebral ischemic/reperfusion (I/R) injury were studied in a rat model. Rats subjected to I/R injury were either treated with intra-cerebroventricular injection of fludarabine (5,000 μM, 10 μl) or saline 20 min before middle cerebral artery occlusion (MCAO). MR examinations including T2-weighted imaging (T2WI), diffusion-weighted imaging (DWI), and perfusion-weighted imaging (PWI) were performed after I/R period. Then rat brains were sectioned for triphenyltetrazolium chloride (TTC) stains, analyzed by Western blot and TUNEL staining of apoptosis. It was found that fludarabine treatment decreased the infarct volume of the cerebrum and the number of apoptotic neural cells in the ischemic brain. Compared to saline-treated group, the apparent diffusion coefficient (ADC) and cerebral blood volume (CBV) in the ischemic region were greater, and the mean transit time (MTT) was shortened in the fludarabine-treated group. Moreover, fludarabine inhibited the expression level of phosphorylated STAT1 (P-STAT1) in neural cells after I/R injury, whereas the expression of phosphorylated STAT3 (P-STAT3) was increased. Therefore, we concluded that fludarabine administrated in early stage of cerebral ischemia had neuroprotective effects, and the underlying mechanism could be mediated through inhibiting STAT1 phosphorylation and activating the cross regulation between STAT1 and STAT3 in neural cells. © 2014, Springer Science+Business Media New York.


PubMed | Wuxi No2 Peoples Hospital
Type: Journal Article | Journal: Kidney & blood pressure research | Year: 2016

Triptolide (TPL), a main active ingredient of Tripterygium wilfordii has been shown to exert anti-inflammatory effect. The role of TPL on glomerular diseases remains unclear.This study aims to investigate the potential anti-inflammatory effect of TPL in rats with membranous glomerulonephritis (MGN).Our data showed that the pathological kidney damage was significantly alleviated by TPL treatment in MGN rats. We also found that MGN rats exhibited significantly higher (p < 0.01) level of inflammatory cytokines (TNF-, IL-1 and MCP-1) than those in normal group, while these inflammatory cytokines levels were significantly reduced in TPL treatment group compared with model group. Additionally, we found that TPL treatment could significantly decrease the malondialdehyde (MDA) level while enhanced superoxide dismutase (SOD) activity. Meanwhile, we also found that IB kinase inhibitor (IMD-0354) could significantly reduce the accumulation of inflammation damage and oxidative lesions. Furthermore, we observed that both TPL and IMD-0354 treatment could block IB degradation and suppress mRNA and protein level of nuclear factor (NF) -B p65.Together, all above results suggest that inflammatory response could be attenuated by TPL and this is partly due to the inhibition of NF- B signaling pathway.


PubMed | Nanjing Medical University, Wuxi No2 Peoples Hospital and Soochow University of China
Type: | Journal: Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie | Year: 2016

We aimed to examine the association between the 5-min Apgar score and reduced vision in children 3 to 6years of age.A total of 5834 preschool children aged 3 to 6years participated in this school-based eye survey. Reduced vision was defined as unaided distance vision of 6/12 or worse in the better-seeing eye. The 5-min Apgar scores of the participants were retrieved from medical records.The overall prevalence of reduced vision in this population was 6.63% (95% confidence interval [CI] 5.99-7.27). In multivariate analysis, the presence of reduced vision was associated with a low 5-min Apgar score at birth (<7 vs. 7-10; odds ratio [OR]=1.66, 95% CI 1.48-3.05) after adjusting for age, gender, parental history of myopia, maternal age, gestational age, and birth weight. In addition, both myopia and amblyopia were associated with Apgar scores of less than 7 in multivariate analyses.Children with 5-min Apgar scores of less than 7 were more likely to have reduced vision at the age of 3 to 6years.


PubMed | Wuxi No2 Peoples Hospital and Soochow University of China
Type: | Journal: Biochemical and biophysical research communications | Year: 2016

Pancreatic cancer (PC) is one of the most aggressive malignancies, with a high mortality. Distant metastasis and recurrence are the main causes of PC-related deaths. MicroRNAs (miRNAs) have been reported in the serum or tumor tissue of cancer patients, including PC, which makes them potential biomarkers. The dysfunction of many miRNAs has been linked to PC occurrence and metastasis. In the current study, we found that miR-601 expression was significantly lower in PC samples, especially in metastatic compared to non-metastatic PC tissues. Gain-of-function and loss-of-function analysis showed that miR-601 suppressed PC cell proliferation and migration. One potential mechanism is that miR-601 inhibited the expression of Sirtuin 1 (SIRT1), which is a well-known regulator of PC development. We found that overexpression of SIRT1 could reverse the effect of miR-601 on PC cells. Our investigation therefore suggests that both miR-601 and SIRT1 are possible biomarkers for the early detection, and targets for the treatment of PC.

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