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Tongshan, China

Huang X.,Nanjing Medical University | Ji J.,Xuzhou Medical University | Xue H.,Nanjing Medical University | Zhang F.,Nanjing Medical University | And 4 more authors.
European Journal of Gastroenterology and Hepatology

Objectives: The aim of this study was to investigate the relationship between fascin and cortactin protein expression and clinicopathological parameters and survival time in patients with hepatocellular carcinoma (HCC). Methods: A total of 77 specimens of HCC and seven specimens of normal liver tissues were collected. The expressions of fascin and cortactin were examined by immunohistochemical staining. The patients from whom the HCCs were taken were also followed up. In these 74 patients, Kaplan-Meier was used to assess survival outcomes. Results: The data revealed that fascin and cortactin expressions were upregulated in the HCC samples. The positive expression of fascin significantly correlated with histological differentiation and metastasis. The positive expression of cortactin significantly correlated with histological differentiation, metastasis, and T stage (International Union Against Cancer). Survival time of the patients with positive fascin expression and positive cortactin expression was significantly decreased, and the median survival duration was short. Conclusion: Fascin and cortactin might be important indicators of the malignancy and metastasis of liver cancer, and may have predictive value in the prognosis of HCC. © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins. Source

Yang L.-J.,Nanjing Medical University | Wang J.,Xuzhou Medical University | Tian Z.-F.,Nanjing Medical University | Yuan Y.-F.,Nanjing Medical University
Neurological Sciences

Perinatal hypoxia-ischemia remains the most important cause of brain injury in the newborn. However, there is still no effective cure for neonatal hypoxic-ischemic brain damage (HIBD). In the present study, we aimed to examine the neuroprotective effects of Shenfu injection (SFI) on HIBD of neonatal rat. Sprague-Dawley rats were divided randomly into three groups (n = 8): S group: the rats were sham operated; C group: the rats were operated for HIBD modeling and received intraperitoneal injection of saline; SFI group: the rats were operated for HIBD modeling and received intraperitoneal injection of SFI (10 ml/kg days) for 7 days. Flow cytometry analysis showed that apoptosis rate of neuron in hippocampal CAI region in SFI group was significantly less than in NC group at 3 and 7 days after HI insult (P < 0.05). Immunohistochemical staining demonstrated that Bcl-2 expression was markedly higher while Bax expression was significantly lower in SFI group than in the C group at 24, 72 h and 7 days after HI insult (P < 0.05). Our findings suggest that SFI exhibits neuroprotective effects for neonatal hypoxic-ischemic brain injury by preventing neuron apoptosis and has potential to be used in the clinical for the treatment of perinatal hypoxia-ischemia. © 2013 Springer-Verlag Italia. Source

Zhang H.,Xuzhou Medical University | Wang G.,Affiliated Hospital of Xuzhou Medical University | Yin R.,Nanjing Medical University | Qiu M.,Nanjing Medical University | Xu L.,Nanjing Medical University
Chinese Journal of Lung Cancer

Background and objective Long non-coding RNA (lncRNA) plays important regulatory roles in the development and invasion of various cancers. The aim of current study is to comprehensively identify microRNAs (miRNA) regulated by lncRNA MALAT1 via experimental and bioinformatics methods. Methods Antisense oligonucleotides (ASO) specifically targeting MALAT1 were designed and synthesized. After knockdown of MALAT1 by ASO in A549 cells, miRNA expression changes were profiled by TqaMan Low Density Array (TLDA). Gene set enrichment analysis (GSEA) was used to search enriched miRNAs among differentially expressed genes after knockdown of MALAT1. Results After efficient knockdown of MALAT1 by ASO, 153 miRNAs were differentially expressed, 131 up-regulated and 22 down-regulated. Among the 458 differentially expressed genes after MALAT1 silence, GSEA results revealed lots of enriched miRNAs. There were 28 overlapped miRNAs between TLDA and GSEA results, suggesting these 28 miRNAs are regulated by MALAT1. Conclusion This study comprehensively identified MALAT1 regulated miRNAs, providing resources for further research. © 2016, Chinese Journal of Lung Cancer. All rights reserved. Source

Lou P.,Xuzhou Medical University | Zhang P.,Xuzhou Medical University | Zhang L.,U.S. Center for Disease Control and Prevention | Chen P.,U.S. Center for Disease Control and Prevention | And 4 more authors.
Diabetes Research and Clinical Practice

Objective: To explore the interactions of sleep quality and sleep duration on the development of type 2 diabetes mellitus (DM2) in Chinese adults. Research design and methods: We randomly selected 11,842 Chinese subjects from the Xuzhou community of China and obtained self-reported quality and duration of sleep by questionnaire. DM2 was assessed by fasting blood glucose. Sleep quality was categorized as good, common, or poor. Sleep duration was measured by average hours of sleep per night. We evaluated interaction, relative excess risk of interaction (RERI), the attributable proportion (AP), and the synergy index (S) using a logistic regression model. Results: The relative risk for the development of DM2 was higher in subjects with short sleep duration (1.67 [1.34-2.16]) or poor sleep quality (1.91 [1.31-2.74]) or long sleep duration (1.45 [1.02-1.77]). DM2 occurred more frequently with poor sleep quality combined with short sleep duration (odds ratio: 6.21; 95% confidence interval (CI): 2.78-11.81). RERI, AP, and S values (and their 95% CI) were 3.99 (1.41-7.76), 0.64 (0.45-0.76), and 5.15 (3.74-7.89) for the interaction between poor sleep quality and short sleep duration. In subjects with poor sleep quality combined with long sleep duration, the RERI, AP, and S values (and 95% CI) were 0.13 (-0.19 to 0.66), 0.07 (-0.35 to 0.18), and 1.19 (0.85-2.11). Conclusions: Interactions between poor sleep quality and short sleep duration were additive. Preventive measures should focus on short sleep duration and poor sleep quality. © 2015 Elsevier Ireland Ltd. Source

Tang W.,Nanjing Medical University | Qin J.,Nanjing Medical University | Qin J.,Xuzhou Medical University | Tang J.,Nanjing Medical University | And 7 more authors.
Cellular Physiology and Biochemistry

Background: MiR-141 has been confirmed to be associated with various human diseases. However, whether miR-141 is involved in the pathogenesis of Hirschsprung's disease (HSCR) remains unknown. Here, we design the experiment to reveal the relationship between miR-141 and HSCR. Methods: Quantitative real-time PCR and Western blot were used to detect the expression levels of miR-141 and its potential genes in 70 tissues of HSCR compared with 60 controls. Bisulfite sequencing PCR (BSP) assay was applied to explain the possible mechanism of the aberrant expression level of miR-141. We employed a dual-luciferase reporter assay to validate the regulation relation between miR-141 and CD47/CUL3. Cell migration, proliferation, apoptosis, and cell cycle progression were examined by transwell assay, MTT assay, and flow cytometry, respectively. Results: MiR-141 was down-regulated whereas CD47 and CUL3 expression was increased in colon tissues from patients with HSCR compared with control group, The increased level of CD47 and CUL3 induced by miR-141 reduced proliferation and migration of 293T and SH-SY5Y cells. Furthermore, this suppression was reversed by reducing of CD47 and CUL3. Hypermethylation of a CpG Island in the promoter region of miR-141 gene was confirmed in HSCR tissues. Conclusion: Aberrant reduction of miR-141 may play an important role in the pathogenesis of HSCR with the inhibiting affection on cell migration and proliferation abilities. The present study demonstrates for the first time the role of miR-141 and its target genes in the occurrence of HSCR, and provides us a new direction for the study of the pathogenesis of Hirschsprung's disease. © 2013 S. Karger AG, Basel. Source

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