PubMed | Baker IDI Heart and Diabetes Institute, Tongji University, Xi'an Jiaotong University, Sun Yat Sen University and 12 more.
Type: Comparative Study | Journal: Diabetic medicine : a journal of the British Diabetic Association | Year: 2016
To evaluate the clinical profile of patients with diabetic ketoacidosis in tertiary hospitals in China.A retrospective study of patients hospitalized with diabetic ketoacidosis between 2010 and 2012 was carried out in 15 tertiary hospitals around China. Clinical and laboratory data were collected. Patients were classified based on clinical diagnosis and treatment history. Groups were compared for differences in vital statistics and biochemical profiles at presentation.The study comprised 643 patients with diabetic ketoacidosis: 308 patients (47.9%) with Type 1 diabetes, 294 patients (45.7%) with Type 2 diabetes and 41 patients (6.4%) with atypical diabetes. Three hundred and eighty-eight diabetic ketoacidosis episodes (60.3%) were in patients with known diabetes. The most common precipitating factor was infection (40.1%), followed by unknown causes (36.9%) and non-compliance with anti-diabetes treatment (16.8%). At presentation, gastrointestinal symptoms and dehydration were more common in the Type 1 diabetes group. For new-onset diabetes, only 74.4% and 55.9% of patients were evaluated for -cell function and autoantibodies for classification. Only 67% of patients with diabetic ketoacidosis received appropriate fluid therapy and 56% patients with severe acidosis received bicarbonate therapy. The length of hospital stay was 10.0 (7.0-14.0) days. The mortality rate was 1.7%, and was much higher in Type 2 diabetes than that in Type 1 diabetes (3.2% vs. 0.4%, P < 0.01).Type 2 and Type 1 diabetes contribute to a similar proportion of cases presenting with diabetic ketoacidosis in China. Admissions with diabetic ketoacidosis are still associated with significant mortality and prolonged hospitalization. The efficiency of diabetic ketoacidosis management needs to be improved by implementing the updated guidelines.
Shen H.,U.S. Center for Disease Control and Prevention |
Shen H.,Nanjing Medical University |
Cao J.,Nanjing Medical University |
Cao J.,Institute of Occupational Disease Prevention |
And 11 more authors.
PLoS ONE | Year: 2014
DNA damage to cochlear hair cells caused by 8-oxoguanine (8-oxoG) is essential for the development of noise-induced hearing loss (NIHL). Human 8-oxoG DNA glycosylase1 (hOGG1) is a key enzyme in the base excision repair (BER) pathway that eliminates 8-oxoG. Many epidemiological and functional studies have suggested that the hOGG1 Ser326Cys polymorphism (rs1052133) is associated with many diseases. The purpose of this investigation was to investigate whether the hOGG1 Ser326Cys polymorphism in the human BER pathway is associated with genetic susceptibility to NIHL in a Chinese population. This polymorphism was genotyped among 612 workers with NIHL and 615 workers with normal hearing. We found that individuals with the hOGG1 Cys/Cys genotype had a statistically significantly increased risk of NIHL compared with those who carried the hOGG1 Ser/Ser genotype (adjusted OR = 1.59, 95% CI = 1.13-2.25) and this increased risk was more pronounced among the workers in the 15- to 25- and >25-year noise exposure time, 85-92 dB(A) noise exposure level, ever smoking, and ever drinking groups, similar effects were also observed in a recessive model. In summary, our data suggested that the hOGG1 Cys/Cys genotype may be a genetic susceptibility marker for NIHL in the Chinese Han population. © 2014 Shen et al.
Zhu Y.,Second Hospital of Jiaxing |
Xiao X.,First Peoples Hospital of Kunshan |
Dong L.,Second Hospital of Jiaxing |
Liu Z.,Guangxi Medical University
Analytical Cellular Pathology | Year: 2012
MicroRNAs are small noncoding RNA molecules that control expression of target genes. Our previous studies show that let-7a decreased in gastric carcinoma and that up-regulation of let-7a by gene augmentation inhibited gastric carcinoma cell growth both in vitro and in vivo, whereas it remains largely unclear as to how let-7a affects tumor growth. In this study, proteins associated with the function of let-7a were detected by high throughout screening. The cell line of SGC-7901 stablely overexpressing let-7a was successfully established by gene cloning. Two-dimensional gel electrophoresis (2-DEy was used to separate the total proteins of SGC-7901/let-7a, SGC-7901/EV and SGC-7901, and PDQuest software was applied to analyze 2-DE images. Ten different protein spots were identified by MALDI-TOF-MS, and they may be the proteins associated with let-7a function. The overexpressed proteins included Antioxidant protein 2, Insulin-like growth factor binding protein 2, Protein disulfide isomerase A2, C-1-tetrahydrofolate synthase, Cyclin-dependent kinase inhibitor1 (CDKN1) and Rho-GTPase activating protein 4. The underexpressed proteins consisted of S-phase kinase-associated protein 2 (Spk2), Platelet membrane glycoprotein, Fibronectin and Cks1 protein. Furthermore, the different expression levels of the partial proteins (CDKN1, Spk2 and Fibronectin) were confirmed by western blot analysis. The data suggest that these differential proteins are involved in a novel let-7a signal pathway and these findings provide the basis to investigate the functional mechanisms of let-7a in gastric carcinoma. © 2012 - IOS Press and the authors. All rights reserved.
Zhu Y.,Second Hospital of Jiaxing |
Xiao X.,First Peoples Hospital of Kunshan |
Dong L.,Second Hospital of Jiaxing |
Liu Z.,Guangxi Medical University
Tumor Biology | Year: 2012
MicroRNAs are small noncoding RNA molecules that control the expression of target genes. Our previous studies show that let-7a decreased in gastric carcinoma and that up-regulation of let-7a by gene augmentation inhibited gastric carcinoma cell growth both in vitro and in vivo, whereas it remains largely unclear as to how let-7a affects tumor growth. In this study, proteins associated with the function of let-7a were detected in high-throughput screening. The cell line of SGC-7901 stably overexpressing let-7a was successfully established by gene clone. Two-dimensional gel electrophoresis (2-DE) was used to separate the total proteins of SGC-7901/let-7a, SGC-7901/EV and SGC-7901, and PDQuest software was applied to analyze 2-DE images. Ten differential protein spots were identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry, and they may be the proteins associated with let-7a function. The overexpressed proteins include antioxidant protein 2, insulin-like growth factor binding protein 2, protein disulfide isomerase A2, C-1-tetrahydrofolate synthase, cyclin-dependent kinase inhibitor1 (CDKN1) and Rho-GTPase activating protein 4. The underexpressed proteins consisted of S-phase kinase-associated protein 2 (Spk2), platelet membrane glycoprotein, fibronectin and Cks1 protein. Furthermore, the different expression levels of the partial proteins (CDKN1,Spk2 and Fibronectin) were confirmed by Western blot analysis. The data suggest that these differential proteins are involved in novel let-7a signal pathway, and these findings provided the basis to comprehensively investigate the functional mechanisms of let-7a in gastric carcinoma. © 2012 International Society of Oncology and BioMarkers (ISOBM).
Chen J.,Nanjing University of Traditional Chinese Medicine |
Chen J.,First Peoples Hospital of Kunshan |
Wang B.-C.,Xi'an Jiaotong University |
Tang J.-H.,Nanjing University of Traditional Chinese Medicine |
Tang J.-H.,Jiangsu Province Tumor Hospital
Journal of Surgical Oncology | Year: 2012
Background The aim of this study is to investigate clinical significance of miR-155 expression in breast cancer. Methods TaqMan real-time RT-PCR was performed to detect miR-155 expression in breast cancer tissues. The correlation of miR-155 expression with clinicopathological factors and prognosis of breast cancer patients was analyzed. Then, the prognostic value of miR-155 expression was analyzed by univariate and multivariate analyses. Moreover, the effect of miR-155 expression on phenotypes of breast cancer cell was determined by antisense technology. Results The relative expression of miR-155 was significantly higher in breast cancer tissues than in corresponding nontumor tissues. High miR-155 expression was correlated with higher tumor grade, advanced tumor stage and lymph node metastasis (P=0.012, 0.001, and 0.003, respectively). Kaplan-Meier survival analysis indicated that the disease-free and overall survival rates of high miR-155 group were significantly lower than those of low miR-155 group (P=0.038 and 0.029, respectively). Multivariate analysis showed that high miR-155 expression was a poor prognostic factor (P=0.009). Furthermore, antisense targeting miR-155 could inhibit growth, induce cell arrest in G0/G1 phase, enhance apoptosis, and increase radiosensitivity in breast cancer cells. Conclusions MiR-155 expression might be an independent prognostic factor and a therapeutic target for human breast cancer. © 2011 Wiley Periodicals, Inc. Copyright © 2011 Wiley Periodicals, Inc.
Yan W.,Nanjing Medical University |
Qian C.,Nanjing Medical University |
Zhao P.,Nanjing Medical University |
Zhang J.,Nanjing Medical University |
And 7 more authors.
Neuro-Oncology | Year: 2010
Osteopontin (OPN) is widely overexpressed in various cancers, including gliomas, and plays an important role in tumorigenesis. However, the expression pattern and functions of OPN splice variants expressed in gliomas remain unclear. The aims of our current study were to examine the expression pattern and functions of OPN splice variants in gliomas. In present study, the mRNA levels of OPN splice variants are markedly increased in gliomas tissues, and all OPN splice variants were also found in U251 and U87 cells. Furthermore, knock-down and regain of function experiments were designed to explore the functions of OPN splice variants in U251 and U87 cells. Lentiviral vectors of OPN small interference RNA (siRNA) targeting all three endogenous mRNAs of OPN and OPN splice variants synonymous mutant that were not silenced by OPN siRNA were constructed. Our results showed that all OPN splice variants synonymous mutant-protected glioma cells from apoptosis induced by OPN siRNA through alteration of the levels of Bcl-2 family proteins and OPN-b Mu elicted a significant effect. Both OPN-a Mu and -c Mu promoted glioma cell invasion through alteration of the levels of uPA, MMP-2, and MMP-9 expressions and the activities of MMP-2 and MMP-9 via activation PI-3K/AKT/NF-κB signaling pathway. Moreover, OPN-c Mu showed the strongest effect on glioma cell invasion, while OPN-b Mu showed no effect on the invasion of U251 and U87 cells. Thus, different splice variants of OPN have divergent functions in regulating apoptosis and invasion of glioma cells, which broadens their importance in glioma biotherapy. © The Author(s) 2010.
Zhong N.,First Peoples Hospital of Kunshan |
Jiang D.,Suzhou University |
Zheng S.-Y.,Suzhou University
2010 4th International Conference on Bioinformatics and Biomedical Engineering, iCBBE 2010 | Year: 2010
We investigate the anticancer effect of a traditional Chinese medicine gambogic acid (GA) in human gastric cancer line SGC-7901 and further study the mechanism of apoptosis induction of GA.Low differential human gastric cancer line SGC-7901 were treated with GA at different doses and different times, the inhibitory rates were detected by MTT assay. Apoptosis induced by GA in SGC-7901 cells was observed by Annexin-V/PI doubling staining flow cytometry assay. And T/C (%) was chosen to detect the inhibition of GA on human gastric adenocar-cinoma SGC-7901 nude mice xenografts. Apoptosis on nude mice xenografts was observed by Annexin-V/PI doubling staining flow cytometry assay and DNA fragmentation assay. To further determine the molecular mechanism of apoptosis induced by GA, the changes on the expression of bcl-2 and bax genes were detected by RT-PCR. After incubation with GA, low differential human gastric cancer line SGC-7901 was dramatically inhibited in a dose-dependent manner. After these cells were exposed to GA for 24, 48 and 72 h, the IC50 value was 1.02±0.05, 1.4±0.20 and 1.14± 0.19 μmol/L, respectively. Apoptosis in SGC-7901 cells induced by GA was observed by Annexin-V/PI doubling staining flow cytome-try assay. The apoptotic population of SGC-7901 cells was about 12.96% and 24.58%, respectively, when cells were incuba-ted with 1.2 μmol/L GA for 48 and 72 h. T/C (%) of human gastric carcinoma adeno-carcinoma SGC-7901 nude mice xenografts was 44.3, when the nude mice were treated with GA (8 mg/kg). Meanwhile, apoptosis induced by GA was observed in human gastric carcinoma adenocarcinoma SGC-7901 nude mice xenografts. The increase of bax gene and the decrease of bc1-2 gene expressions were found by RT-PCR.The inhibition of GA on human gastric cancer line SGC-7901 was confirmed. This effect connects with the inducing apoptosis in SGC-7901 cells and the molecular mechanism might be related to the reduction of expression of apoptosis-regulated gene bcl-2, and the improvement of the expression of apoptosis-regulated gene bax. The result was also confirmed in vivo. © 2010 IEEE.
Che J.,Fourth Peoples Hospital of Wuxi |
Che J.,Soochow University of China |
Lu Y.-W.,Soochow University of China |
Sun K.-K.,First Peoples Hospital of Kunshan |
And 3 more authors.
Oncology Reports | Year: 2013
The aim of this study was to investigate the effects and mechanisms of antiproliferative transducer of erbB2, 1 (TOB1) on the radiosensitivity of the normal human bronchial epithelial cell line HBE. After exposure to different doses of irradiation or a certain dose for different time intervals, the expression of TOB1 mRNA and protein in HBE cells was determined by semi-quantitative RT-PCR and western blot analysis. Liposome-induced recombinant plasmid transfection and G418 selection were performed to establish a stably transfected TOB1-overexpressing HBE cell line. A clonogenic assay was used to determine the radiosensitivity of the HBE cells with different TOB1 expression statuses. The cell cycle distribution was detected by flow cytometry. The ionizing radiation (IR)-induced γ-H2AX foci formation was detected by immunofluorescence assay. The related mechanism was explored by western blot analysis. TOB1 expression in the HBE cells was not induced by IR, neither dose-dependently nor time-dependently. Compared to the parental or 'mock' transfected HBE cells, the radiosensitivity of HBE cells overexpressing TOB1 was significantly decreased (P<0.05). Exogenous TOB1 prevented HBE cells from apoptosis after IR, in contrast to the control cells (P<0.05), and significantly decreased the IR-induced γ-H2AX foci formation. After IR, the expression of DNA damage repair proteins such as XRCC1, MRE11, FEN1 and ATM was increased in the TOB1-overexpressing HBE cells when compared with the expression levels in the control cells. HBE/TOB1 cells presented a much higher phosphorylated ERK1/2 and phosphorylated p53 when compared with the levels in the control cell lines when receiving 6 Gy of X-rays. Notably, the increased expression of phosphorylated p53 in HBE/TOB1 cells after IR was sufficiently blocked by U0126, a specific inhibitor of MEK1/2. Different from its functions in several lung cancer cell lines, TOB1 demonstrated a radioprotective function in the immortalized normal human bronchial epithelial cell line HBE via the MAPK/ERK signaling pathway.
Wang H.-G.,Nanjing Medical University |
Huang X.-D.,Nanjing Medical University |
Shen P.,Nanjing Medical University |
Li L.-R.,Nanjing Medical University |
And 2 more authors.
International Journal of Molecular Medicine | Year: 2013
In the present study, we investigated the anticancer effects of sodium butyrate (NaBu) on hepatocellular carcinoma (HCC) cells in vitro. As a histone deacetylase (HDAC) inhibitor, NaBu upregulated Ac-H3 and inhibited HDAC4 protein expression in a time- and dose-dependent manner. MTT assays showed that treatment with NaBu at high concentrations significantly inhibited the growth of various HCC cells. Exposure to NaBu for 24 h induced cell cycle arrest in the SMMC-7721 and HepG2 cells. NaBu also induced the apoptosis of SMMC 7721 cells. The expression levels of cell cycle- and apoptosis-related proteins were further investigated by western blot analysis using specific antibodies. The results provided a possible mechanism responsible for the inhibitory effects of NaBu on the growth of HCC cells. To further analyze the role of NaBu in cell migration, wound healing and Transwell assays were performed, indicating that NaBu significantly inhibits cell migration/invasion in HCC cells. Transforming growth factor-β1 (TGF-β1)-induced epithelial to mesenchymal transition (EMT) has been associated with tumor cell migration and invasion. The EMT markers, E-cadherin, vimentin and N-cadherin, were regulated by TGF-β1, while NaBu inhibited this process in which HDAC4 and matrix metalloproteinase (MMP)7 may be involved. Based on our findings, we propose that NaBu may be useful as an anticancer drug for HCC therapy. Copyright © 2013 Spandidos Publications Ltd.
Yao J.,Nanjing Medical University |
Jiang M.,First Peoples Hospital of Kunshan |
Zhang Y.,Nanjing Medical University |
Liu X.,Nanjing Medical University |
And 2 more authors.
International Immunopharmacology | Year: 2016
Asthma is a chronic airway inflammatory disorder and progresses mainly due to airway remodeling. Chrysin, a natural flavonoid, has been reported to possess multiple biologic activities, including anti-inflammation, anti-oxidation and anti-proliferation. The present study aimed to investigate whether chrysin could relieve allergic airway inflammation and remodeling in a murine model of chronic asthma and the mechanism involved. The female BALB/c mice sensitized and challenged with ovalbumin (OVA) successfully developed airway hyperresponsiveness (AHR), inflammation and remodeling. The experimental data showed that chrysin could alleviate OVA-induced AHR. Chrysin could also reduce OVA-induced increases in the number of inflammatory cells, especially eosinophils, interleukin (IL) -4, and IL-13 in bronchoalveolar lavage fluid (BALF) and total IgE in serum. The decreased interferon-γ (IFN-γ) level in BALF was also upregulated by chrysin. In addition, inflammatory cell infiltration, goblet cell hyperplasia and the expression of α-smooth muscle actin (α-SMA) around bronchioles were suppressed by chrysin. Furthermore, the phosphorylation levels of Akt and extracellular signal-regulated kinase (ERK) could be decreased by chrysin, which are associated with airway smooth muscle cell (ASMC) proliferation. These results indicate the promising therapeutic effect of chrysin on chronic asthma, especially the progression of airway remodeling. © 2016 Elsevier B.V. All rights reserved.