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Wang C.,Nantong University | Wang Y.,Nantong University | Wu J.,Third Peoples Hospital of Nantong | Liu S.,Nantong University | And 8 more authors.
Journal of Diabetes Research | Year: 2015

The aim of this study was to evaluate the associations between chronic smoking and insulin resistance and β-cell function in Chinese men without diabetes. A total of 1,568 participants were recruited by multistage sampling. Using homeostatic model assessment (HOMA), geometric means of insulin resistance (HOMA-IR) and β-cell function (HOMA-β) with 95% confidence interval (CI) were calculated by general linear model. Odds ratios (ORs) with 95% CI were estimated to evaluate the associations between smoking status and insulin resistance and β-cell deficiency under a logistic regression model. Current smokers had higher levels of 2 h glucose (6.66 versus 6.48 mmol/L) for oral glucose tolerance test and lower levels of fasting insulin (5.68 versus 6.03 mU/L) than never smokers. The adjusted means for HOMA-β (%) were 54.86 in current smokers and 58.81 in never smokers (P=0.0257). Current smoking was associated with β-cell deficiency (OR 1.29, 95% CI 1.01-1.64) compared to never smoking. The β-cell function gradually decreased with increasing smoking intensity (Ptrend=0.0026), and the differences were statistically significant when the pack-year of smoking was 20 or above. No association was observed between smoking status and HOMA-IR. Our study suggested that chronic smoking may dose-dependently suppress insulin secretion in Chinese men. Copyright © 2015 Chun Wang et al.


Su Y.-M.,Nantong University | Li J.,Jiangnan University | Guo Y.-F.,Jiangnan University | Cai F.,Third Peoples Hospital Of Nantong | And 4 more authors.
Clinical Laboratory | Year: 2015

Background: MicroRNAs are small, single-stranded, non-protein-coding RNAs of about 22 nucleotides. Micro- RNA molecules have been identified to play key roles in a broad range of physiologic and pathologic processes. Polymorphisms in the corresponding sequence space are likely to make a significant contribution to phenotypic variation. A T/C genetic variant (rsll614913) in the pre-miR-196a2 sequence could alter mature miR-196a expression and target mRNA binding. The aim of the present study is to evaluate the relationship between this polymorphism and atrial fibrillation (AF). Methods: A total of 123 participants were enrolled, 65 AF patients were confirmed with electrocardiogram (ECG) or dynamic electrocardiography, 58 normal individuals were assigned to the control group. Genotypes of the pre- miR-196a2 were distinguished using the method of polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. Results: The distribution of the pre-miR-196a2 genotypes (TT, TC, and CC) was 15.38%, 46.15%, and 38.46% in the AF group and 39.66%, 46.55%, and 13.79% in the controls, respectively (p = 0.0011). Compared with the TT genotype, the C allele carriers (TC+CC genotypes) had a 3.968-fold increased risk of AF (adjusted OR = 3.968, 95% CI = 1.633 - 9.644, p = 0.002). AF patients with the TC+CC genotype had greater left atrial dimension than did patients with the TT genotype (42.10 ± 8.74 vs. 35.13 ± 8.16, p = 0.0224). Conclusions: Our data support that the pre-miR-196a2 polymorphism is associated with AF, and the C allele is a risk factor for AF.


Zhang J.,Nantong University | Jiang W.,Third Peoples Hospital of Nantong | Liu W.,Nantong University | Wu J.-J.,Nantong University | And 5 more authors.
Future Oncology | Year: 2016

Aim: We investigated the effects of TORC1/2 kinase inhibitors on colorectal cancer (CRC) cell lines. Materials & methods: Using selective TORC1/2 inhibitors, rapamycin and PP242, we assessed their effect on the growth of CRC cells in vitro and tumor growth in vivo. Results: Rapamycin and PP242 inhibit proliferation and induce apoptosis of CRC cells. They also enhance proapoptotic effect of conventional chemo drug doxorubicin in CRC cells in vitro. When combined with doxorubicin, rapamycin and PP242 almost completely inhibit tumor growth in vivo. Rapamycin and PP242 inhibit phosphorylation of Akt, ribosomal S6 kinase, 4EBP1 and mTOR. Conclusion: Our study suggests rapamycin and PP242 may be a useful therapeutic agent and inhibiting mTOR signaling pathway represents a new targeted therapy for CRC. © 2016 Future Medicine Ltd.


Luo L.-L.,Nanjing University | Luo L.-L.,Third Peoples Hospital of Nantong | Chen J.,Third Peoples Hospital of Nantong | Shao J.-G.,Third Peoples Hospital of Nantong
Academic Journal of Second Military Medical University | Year: 2010

The differential diagnosis of benign and malignant ascites is of great significance in clinic; the early diagnosis of malignant ascites is especially difficult. Definite diagnosis is usually based on conventional cytology to find cancer cells in the ascites in clinic, but the rate of missed diagnosis is high, and the negative outcome cannot exclude the presence of tumors. Currently, many new laboratory methods and indicators have been used clinically and have demonstrated primary efficiency in providing evidences for differential diagnosis of benign and malignant ascites. This article reviews the progress in laboratory indicators for differential diagnosis of benign and malignant ascites.


Sun L.,Nantong University | Qiang R.,Third Peoples Hospital of Nantong | Yang Y.,Nantong University | Jiang Z.-L.,Nantong University | And 5 more authors.
PLoS ONE | Year: 2014

The present study was conducted to clarify whether treatment with L-serine can improve the brain repair and neurorestoration of rats after permanent middle cerebral artery occlusion (pMCAO). After pMCAO, the neurological functions, brain lesion volume, and cortical injury were determined. GDNF, NGF, NCAM L1, tenascin-C, and Nogo-A levels were measured. Proliferation and differentiation of the neural stem cells (NSCs) and proliferation of the microvessels in the ischemic boundary zone of the cortex were evaluated. Treatment with L-serine (168 mg/kg body weight, i.p.) began 3 h after pMCAO and was repeated every 12 h for 7 days or until the end of the experiment. L-Serine treatment: 1) reduced the lesion volume and neuronal loss; 2) improved the recovery of neurological functions; 3) elevated the expression of nerve growth-related factors; and 4) facilitated the proliferation of endogenous NSCs and microvessels activated after pMCAO and increased the number of new-born neurons. 5) D-cycloserine, an inhibitor of serine hydroxymethyltransferase, blunted the effects of L-serine on NSC proliferation, differentiation, microvascular proliferation. In conclusions, L-serine treatment in pMCAO rats can reduce brain injury and facilitate neurorestoration which is partly associated with the improvement of proliferation of NSCs and microvessels, reconstruction of neurovascular units and resultant neurorepair. The effects of L-serine on endogenous NSC proliferation and microvascular proliferation are partly mediated by the action of L-serine as a substrate for the production of one-carbon groups used for purine and pyrimidine synthesis and modulation of the expression of some nerve growth-related factors. © 2014 Sun et al.


Zhang J.-D.,Third Peoples Hospital of Nantong | Cai C.-P.,Third Peoples Hospital of Nantong
Zhonghua Shiyan Yanke Zazhi/Chinese Journal of Experimental Ophthalmology | Year: 2012

Background: To study diabetic retinopathy (DR) related risk factors is very important in the prevention of DR. Platelet endothelial cell adhesion molecule-1 (PECAM-1) is an important mediator that mediates high blood glucose-induced vascular diseases in diabetic patients. However, its mechanism is still below understood. Objective: This clinical study was to investigate the effect of serum level changes of PECAM-1 on DR in type 2 diabetic patients. Methods: Fifty-four patients with type 2 diabetes were enrolled from the endocrinology department of the Third People's Hospital of Nantong City. Fundus examination was performed using the ophthalmoscope and fundus fluorescence angiography (FFA) on all the patients, and these patients were grouped as the non-DR (NDR) group (18 cases), non-proliferative DR(NPDR) group (20 cases) and proliferative DR group (PDR) (16 cases) based on the DR staging criterion of the Chinese Medical Association (1987 version). Eighteen age- and gender-matched normal subjects served as the normal control group. Peripheral blood was collected, and serum PECAM-1 levels were assayed using ELISA. Serum HbA1c levels were detected using the high performance liquid colorimetric(HPLC) method. The correlation of serum PECAM-1 level with serum HbA1c level was analyzed. All results were compared among the groups. Results: The serum PECAM-1 levels were (10.907 ± 2.792), (7.024 ± 2.377), (5.231 ± 1.816) and(3.817± 1.045) μg/L, respectively, in the PDR group, NPDR group, NDR group and normal control group, showing a significant difference among the 4 groups (F= 12.630, P = 0.02). Serum PECAM-1 content was significantly higher in the PDR group when compared with the NPDR group, NDR group and normal control group (P<0.05). The serum HbA1c levels were (12.596 ± 3.148)%, (9.118 ± 3.356)%, (5.491 ± 1.017)% and (4.992 ± 0.725)% in the PDR group, NPDR group, NDR group and normal control group, respectively, with a significant difference among these 4 groups (F = 7.130, P = 0.015), and those in the PDR group and NPDR group were significantly elevated in comparison with the NDR group and normal control group (P<0.05). Significantly positive correlations were seen between serum PECAM-1 level and HbA1c level in the PDR group, NPDR group and NDR group (r = 0.799, P<0.01; r = 0.647, P<0.01; r = 0.685, P<0.01). Significantly more patients with a disease course of ≥ 10 years were in the NPDR group in comparison with the PDR group (P = 0.023). Conclusions: Increase of serum PECAM-1 level is closely associated with blood glucose level, and it is an important factor in the pathogenesis and development of DR. These results imply that control of blood glucose is crucial for the prevention of DR in patient with type 2 diabetes. Copyright © 2012 by the Chinese Medical Association.


Hu B.-Y.,Nantong University | Liu X.-J.,Third Peoples Hospital of Nantong | Qiang R.,Third Peoples Hospital of Nantong | Jiang Z.-L.,Nantong University | And 4 more authors.
Journal of Ethnopharmacology | Year: 2014

Ethnopharmacological relevance Ginseng, the root of Panax ginseng C.A. Meyer, is a traditional medicinal herb that has been widely used in Asia for the treatment of many diseases through its effects of reinforcing vitality, strengthening the bodily resistance to pathogenic factors, engendering body liquids and allaying thirst, relieving uneasiness of the body and mind and benefiting intelligence, reducing body weight and prolonging life. Ginsenosides are the most important biologically active substances in ginseng. Many reports have suggested that ginsenosides could exert prominent neuroprotective and neurotrophic effects, promote neural stem/progenitor cell (NSC) proliferation and promote neurite outgrowth and neuronal network formation. The present study aimed to investigate whether treatment with ginsenosides could facilitate NSC proliferation in the hippocampal formation after traumatic brain injury (TBI) and contribute to the recovery of neurological functions including learning and memory. Materials and methods The modified Feeneys method was used to induce a TBI in rats. Ginseng total saponins (GTS) were treated intraperitoneally twice a day for 1 week after the TBI. The neurological functions, morphology of the hippocampus, expression of nerve growth-related factors and number of NSCs in the hippocampal formation ipsilateral to the trauma were determined. Results We determined 1) GTS (5-80 mg/kg) treatment after a TBI improved the recovery of neurological functions, including learning and memory, and reduced cell loss in the hippocampal area. The effects of GTS at 20, 40, 60, and 80 mg/kg were better than the effects of GTS at 5 and 10 mg/kg. 2) GTS treatment (20 mg/kg) after a TBI increased the expression of NGF, GDNF and NCAM, inhibited the expression of Nogo-A, Nogo-B, TN-C, and increased the number of BrdU/nestin positive NSCs in the hippocampal formation. Conclusions GTS treatment in rats after a TBI alleviated the secondary brain injury and ameliorated the neurological functions with an effective dose limit of 5-80 mg/kg. GTS regulated the expression of nerve growth-related factors and improved the proliferation of neural stem/progenitor cells, which might facilitate neural regeneration and tissue repair, and might contribute to the recovery of neurological functions, including learning and memory. These effects of GTS might provide a foundation for the use of ginseng as a medicinal herb to enhance intelligence, reduce the aging process and prolong life in the traditional medicine. © 2014 Elsevier Ireland Ltd.

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