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Liu P.,Shanghai JiaoTong University | Xie Q.,Shanghai Jiading District Central Hospital | Wei T.,Shanghai JiaoTong University | Chen Y.,Shanghai JiaoTong University | And 2 more authors.
Biochemical and Biophysical Research Communications | Year: 2015

Objective Obesity-induced vascular dysfunction is related to chronic low-grade systemic inflammation. Recent studies indicate that NLRP3, a multiprotein complex formed by NOD-like receptor (NLR) family members, is a key component mediating internal sterile inflammation, but the role in obesity-related vascular dysfunction is largely unknown. In the present study, we investigate whether NLRP3 activation is involved in vascular inflammation in obese Otsuka Long-Evans Tokushima Fatty rats (OLETF). Methods and results Male OLETF with their control Long-Evans Tokushima Otsuka rats (LETO) were studied at 3 and 12 months of age. Aortic relaxation in response to acetylcholine decreased gradually with age in both strains, with early and persistent endothelium dysfunction in obese OLETF compared with age-matched LETO controls. These changes are associated with parallel changes of aortic endothelial nitric oxide synthase (eNOS) content, macrophage accumulation and intimal thickening. NLRP3 increased in OLETF rats compared to LETO. Consistent with inflammasome activation, the conversion of procaspase-1 to cleaved and activated forms as well as IL-1β markedly increased in OLETF rats. Additionally, we observed increased expression of dynamin-related protein-1 (Drp1) and decreased fusion-relative protein optic atropy-1(OPA1). Altered mitochondrial dynamics was associated with elevated oxidative stress level in OLETF aortas. Conclusions These results demonstrate that obesity seems to accelerate endothelial dysfunction in OLETFs via the activation of NLRP3 and mitochondrial dysfunction. © 2015 Elsevier Inc. All rights reserved.

Yan J.,Shanghai Jiading District Central Hospital | Wang C.,Shanghai Jiading District Central Hospital | Zhang Q.,Shanghai Jiading District Central Hospital | Chen X.,Shanghai Jiading District Central Hospital | And 2 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2015

In this case, an old man was diagnosed as lung cancer, clinical stage IV. In order to alleviate cancer, this patient was treated with gefitinib. Three months later, symptoms such as a significant weakness, chest tightness and shortness of breath after sports arised and intensifying. Implosive therapy with high dose methylprednisolone is used to control the weakness caused by gefitinib. Eight days after treatment, patient’s condition significantly improved. The use of methylprednisolone can effectively treat interstitial pneumonia induced by gefitinibin, help patients get better from critical condition such as type I respiratory failure. This new discovery is a good guidance for clinical treatment of gefitinibin caused interstitial pneumonia. © 2015, E-Century Publishing Corporation. All rights reserved.

Xu Y.,Shanghai JiaoTong University | Xu Y.,Fudan University | Phillips M.R.,Shanghai JiaoTong University | Phillips M.R.,Emory University | And 4 more authors.
Archives of Suicide Research | Year: 2013

The objective of this study was to assess the feasibility of using currently available emergency department (ED) records to retrospectively ascertain the prevalence and characteristics of episodes of medically treated deliberate self-harm (DSH). Discussions with ED staff identified 10 ED diagnoses in persons 12 years of age or older that were commonly used for episodes of DSH and another 7 injury-related diagnoses that could, under specific conditions, be acts of DSH. A retrospective analysis of the ED registry of one large general hospital in Shanghai for 2007 to 2010 identified all cases with one of these diagnoses. Diagnosis-specific algorithms based on the characteristics of each case were applied to classify cases as "probable DSH," "possible DSH" or "probably not DSH." The 1,495 cases of DSH identified accounted for 0.2% of all ED admissions over the 4 years; only 6 of them (0.4%) had an ED diagnosis of "suicide attempt." Three ED diagnoses-overdose of medication, fall from height, and pesticide ingestion-accounted for 1,275 (85.3%) of the DSH cases. There were substantial differences in the characteristics of male and female cases of DSH and a 43% drop in the proportion of ED admissions for DSH over the 4 years. In locations where it is not feasible to develop prospective registries of suicide attempts treated in EDs, retrospective analysis of ED records that use algorithms to classify the intentionality of injuries can provide estimates of the prevalence and characteristics of medically treated episodes of DSH. © 2013 Copyright International Academy for Suicide Research.

Chen X.,Shanghai Jiading District Central Hospital | Zhang L.,Shanghai Jiading District Central Hospital | Wu G.,Shanghai Jiading District Central Hospital | Li H.,Shanghai Jiading District Central Hospital | And 2 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2016

The objective of the study was to investigate the effect of kaempferol on angiotensin II (Ang II)-induced vascular fibrosis. In vascular smooth muscle cells (VSMCs), Ang II induced cell proliferation in dose- and time-dependent manners. Ang II up-regulated the expression of collagen I (Coll I) and fibronectin (FN), and increased intracellular ROS production and expression of gp91phox. Kaempferol attenuated the effects of Ang II on VSMCs. Ang II significantly induced the JNK and ERK1/2 pathways in VSMCs, and the activation was inhibited by kaempferol treatment. In addition, Ang II induced high blood pressure in rats. Expression of Coll I and FN in aorta, and ROS and MDA levels in serum and aorta were also increased in the Ang II-infused rats. Treatment with kaempferol prevented vascular fibrosis of Ang II induced hypertension in rats. These findings demonstrated that kaempferol attenuated Ang II-induced vascular fibrosis. The JNK and ERK1/2 pathways were involved in the protective effect of kaempferol. © 2016, E-Century Publishing Corporation. All rights reserved.

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