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Liu Z.,Key Laboratory of Biological Cancer Therapy of Jiangsu Province | Liu Z.,Xuzhou Medical College | Liu Z.,Key Laboratory of Brain Disease Bioinformation of Jiangsu Province | Xu J.,Key Laboratory of Biological Cancer Therapy of Jiangsu Province | And 5 more authors.
Journal of the Neurological Sciences

The present study was performed to investigate the effects of Ca 2+/calmodulin-dependent protein kinase II (CaMKII) antisense oligodeoxynucleotides (ODNs) on the assembly of the CaMKII•GluR6•PSD- 95 signaling module, GluR6 serine phosphorylation and c-Jun N-terminal kinase 3 (JNK3) activation. A further aim was to determine the neuroprotective mechanism of CaMKII antisense ODNs against ischemia-reperfusion (I/R)-induced neuronal death in the rat hippocampus. CaMKII antisense ODNs were intracerebroventricularly infused to inhibit CaMKII expression once daily for 3 days prior to the induction of ischemia. Transient cerebral ischemia (15 min) and reperfusion were induced by four-vessel occlusion in Sprague-Dawley rats as an animal model for transient cerebral I/R. The expression of related proteins was examined by immunoprecipitation and immunoblotting. Neuronal death in the rat hippocampus was detected by histology and histochemistry. The results indicate that CaMKII antisense ODNs inhibit several of the processes that are normally induced by cerebral I/R, including CaMKII expression, increased CaMKII•GluR6•PSD-95 signaling module assembly, GluR6 serine phosphorylation and JNK3 activation. Alternatively, CaMKII antisense ODNs also exhibit a significant neuroprotective role against cerebral I/R-induced cell death. These results provide the first evidence that CaMKII antisense ODNs can exert neuroprotective effects on cerebral I/R-induced cell death. The possible molecular mechanisms underlying this effect include 1) an inhibition of CaMKII expression and subsequent suppression of the assembly of the CaMKII•GluR6•PSD-95 signaling module, 2) GluR6 serine phosphorylation, and 3) reduced JNK3 activation. © 2011 Elsevier B.V. All rights reserved. Source

Zhu Z.-S.,Xuzhou First Peoples Hospital | Wang H.-Y.,Nanjing Medical University | Wang D.-F.,Nanjing Medical University | Lu Y.-L.,Nanjing Medical University
Medical Journal of Chinese People's Liberation Army

Objective To investigate the effects of HMG-CoA reductase inhibitor rosuvastatin on atherosclerosis and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), and nuclear factor (NF)-kB p65 expressions in apolipoprotein E (ApoE)-deficient mice. Methods Twenty six-week-old ApoE-deficient male mice were randomly divided into hyperlipidemia model group (n=10) and rosuvastatin group (n=10), and they were fed high-fat diet for 13 weeks. Ten six-week-old C57BL/6J (wild type, WT) male mice were selected as normal control group, and were fed normal diet for 13 weeks. After 13 weeks, blood was drawn from the mice to determine serum levels of total cholesterol (TCH), triglyceride (TG), and low density lipoprotein cholesterol (LDL-C). These mice were sacrificed, and their aortas were obtained and examined with HE staining; Western blotting and RT-PCR were used to analyze LOX-1, NF-kB p65 expression intensity in aorta tissue quantitatively. Results The serum level of TCH, TG and LDL-C in rosuvastatin group were lower than those in hyperlipidemia model group (P<0.05). Pathological observation showed that atherosclerotic lesions of the aortas were aggravated significantly in hyperlipidemia model group but alleviated in rosuvastatin group compared with normal control group. Compared with normal control group, LOX-1, NF-kB p65 protein and mRNA expressions significantly increased in hyperlipidemia model group (P<0.05) and reduced in rosuvastatin group (P<0.05). Conclusions Rosuvastatin may lower blood lipid significantly, alleviate the degree of atherosclerotic lesions, and inhibit LOX-1, NF-kB p65 protein and mRNA expressions in the aortic tissue of ApoE-deficient mice. Its anti-athrosclerosis effect is related to down regulation of LOX-1 and NF-kB p65 expressions. © 2014, People's Military Medical Press. All rights reserved. Source

Pan Y.,Nanjing Medical University | Han Y.,Nanjing Medical University | Zhang H.,Xuzhou First Peoples Hospital | Zhou L.,Institute of environment disease prevention and control | And 5 more authors.
Environmental and Molecular Mutagenesis

A recent genome-wide meta-analysis identified six new susceptible genetic variants for nonsyndromic orofacial clefts (NSOC), but it was still unknown whether these newly identified variants were associated with NSOC susceptibility in Chinese populations. In this study, we genotyped these variants in a case-control study of 602 NSOC cases and 605 controls and found that four of these variants (rs7590268, rs7632427, rs12543318, and rs1873147) were associated with susceptibility to NSOC. We further investigated the cumulative effects of these four variants and found a dose-dependent increase in risk with the number of variant alleles. Furthermore, an association was observed between rs7590268 and a family history of NSOC. Our results provide confirmative evidence that these risk loci contribute to NSOC susceptibility in Chinese populations. © 2013 Wiley Periodicals, Inc. Source

Pan Y.,Nanjing Medical University | Zhang W.,Nanjing Medical University | Du Y.,Nanjing Medical University | Tong N.,Nanjing Medical University | And 6 more authors.
American Journal of Medical Genetics, Part A

Nonsyndromic orofacial clefts (NSOC) are the most common developmental anomalies in human beings. Recently, a large-scale genome-wide association study identified two novel NSOC susceptibility loci: rs13041247 near MAFB and rs560426 near ABCA4. In the present study, we recruited 396 NSOC cases and 384 healthy controls to replicate their associations with risk of NSOC as well as their subgroups in a Chinese Han population. We found the overall genotype and allele frequencies of rs13041247, but not rs560426 were significantly different between cases and controls. Further logistic regression analysis showed rs13041247 CT, CC, and CT/CC were associated with decreased NSOC susceptibility, compared with rs13041247 TT wide-type homozygote. Moreover, the apparent protection against cleft lip with or without cleft palate (CL/P), cleft lip with cleft palate (CLP), and cleft lip only (CLO) was also identified in stratified analysis. However, none of any rs560426 genotypes or alleles was associated with risk of NSOC or their subgroups. Taken together, our findings confirmed the contribution of MAFB in the etiology of NSOC in a Chinese Han population. © 2011 Wiley-Liss, Inc. Source

Zhang H.,Xuzhou First Peoples Hospital | Zhou L.,U.S. Center for Disease Control and Prevention | Han Y.,Nanjing Medical University | Cai Q.,Nanjing Medical University | And 3 more authors.
Oral Diseases

Objectives: CD14 is a causative gene for periodontitis. However, conflicting results had been achieved when evaluating the associations between CD14 -159 C>T and periodontitis, which warranted us to conduct this meta-analysis. Material and Methods: A meta-analysis based on eight relevant case-control studies was conducted to address this issue. Odds ratios (OR) with 95% confidence intervals (CIs) were applied to test the association. The statistical heterogeneity across studies was assessed by Chi-square-based Q-test. Results: Retrieved studies regarding CD14 -159 C>T and periodontitis susceptibility were put into the final analysis. Overall and subgroup analyses were performed. Finally, we did not find that this polymorphism could contribute to modified risk of periodontitis or in stratified analysis by ethnicity and type of disease. However, this polymorphism was associated with decreased risk of mild to moderate periodontitis (TT vs CC, OR = 0.42, 95% CI = 0.21-0.81, CT/CC vs TT, OR = 1.91, 95% CI = 1.09-3.35) but not severe periodontitis. Conclusion: The present meta-analysis provided confirmative evidence that CD14 -159 C>T was involved in the development of periodontitis. © 2013 John Wiley & Sons A/S. Source

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