نتایج جستجو برای: درصد حمایت از مصرفکنندگان cse

تعداد نتایج: 705849  

2013
Venkata Rami Reddy C. K. Suresh Babu D. G. Sudhakar

A. K.Rachel Praveena, B. Dr. G. Venkata Rami Reddy, C. K. Suresh Babu, D. G. Sudhakar M.TECH (CSE), School of IT, JNTUH,Hyderabad, India, [email protected] Associate Professor in CSE,School of IT,JNTUH,Hyderabad,India, [email protected] Assistant Professor in CSE, School of IT, JNTUH, Hyderabad, India, [email protected] Lecturer in CSE, School of IT, JNTUH,Hyderabad, India,...

2013
Luciana Gomes Menezes Juliana Alves Uzuelli Cristiane Tefé-Silva Simone Gusmão Ramos José Eduardo Tanus dos Santos José Antônio Baddini Martinez

OBJECTIVE To investigate the acute effects of intravenous administration of cigarette smoke extract (CSE) on histological, inflammatory, and respiratory function parameters in rats, as well as to compare this potential acute lung injury (ALI) model with that with the use of oleic acid (OA). METHODS We studied 72 Wistar rats, divided into four groups: control (those injected intravenously with...

2011
Marian C. Aldhous Kimberley Soo Lesley A. Stark Agata A. Ulanicka Jennifer E. Easterbrook Malcolm G. Dunlop Jack Satsangi

BACKGROUND Genetic and environmental factors influence susceptibility to Crohn's disease (CD): NOD2 is the strongest individual genetic determinant and smoking the best-characterised environmental factor. Carriage of NOD2 mutations predispose to small-intestinal, stricturing CD, a phenotype also associated with smoking. We hypothesised that cigarette smoke extract (CSE) altered NOD2 expression ...

2017
Yeong Ok Song Mijeong Kim Minji Woo Jang-Mi Baek Keon-Hee Kang Sang-Ho Kim Seong-Soo Roh Chan Hum Park Kap-Seop Jeong Jeong-Sook Noh

The protective effects of a chondroitin sulfate-rich extract (CSE) from skate cartilage against lipopolysaccharide (LPS)-induced hepatic damage were investigated, and its mechanism of action was compared with that of chondroitin sulfate (CS) from shark cartilage. ICR mice were orally administrated 200 mg/kg body weight (BW) of CS or 400 mg/kg BW of CSE for 3 consecutive days, followed by a one-...

Journal: :Toxicological sciences : an official journal of the Society of Toxicology 2013
Yue Zhao Yuan Xu Yuan Li Wenchao Xu Fei Luo Bairu Wang Ying Pang Quanyong Xiang Jianwei Zhou Xinru Wang Qizhan Liu

Cigarette smoking constitutes a major human health hazard because it is the most important risk factor for lung cancer. Although evidence for smoking-induced lung cancer in humans is strong, the molecular mechanisms by which smoking causes cancer remain to be established. In this investigation, we evaluated the roles of inflammation and the epithelial-mesenchymal transition (EMT) in cigarette s...

2011
Wenyue Sun Steven S. Chang Yumei Fu Yan Liu Joseph A. Califano

BACKGROUND Exposure to cigarette smoke is a major risk factor for head and neck squamous cell carcinoma (HNSCC). We have previously established a chronic cigarette smoke extract (CSE)-treated human oral normal keratinocyte model, demonstrating an elevated frequency of mitochondrial mutations in CSE treated cells. Using this model we further characterized the mechanism by which chronic CSE treat...

Journal: :Anaesthesia 2006

Journal: :International immunopharmacology 2015
Naixing Kang Ping Chen Yan Chen Huihui Zeng Xue He Yingqun Zhu

Cigarette smoke extract (CSE) induces apoptosis and inflammation, but the mechanism is unknown. Arginine methyltransferase (PRMT6) catalyzes the asymmetric di-methylation of histone H3 arginine 2 (H3R2me2a) to control global level transcription. We hypothesized that PRMT6 mediates CSE induced apoptosis and inflammation through H3R2me2a. The apoptosis after CSE treatment in human umbilical vein ...

2014
VuQuynhAnh Le Yang-Hoon Kim Jiho Min

OBJECTIVES Cigarette smoking had been recorded as the main cause of impaired endothelium- dependent vasodilation in smokers by reducing nitric oxide (NO), a production of endothelial nitric oxide synthase (eNOS). However, the mechanism of NO impairment via eNOS activity is unclear until now. In this study, cell passage is suggested to be a relevant factor to eNOS expression under cigarette smok...

2016
Ailing Liu Jinxiang Wu Aijun Li Wenxiang Bi Tian Liu Liuzhao Cao Yahui Liu Liang Dong

OBJECTIVES Cellular senescence is a state of irreversible growth arrest induced either by telomere shortening (replicative senescence) or stress. The bronchial epithelial cell is often injured by inhaled toxic substances, such as cigarette smoke. In the present study, we investigated whether exposure to cigarette smoke extract (CSE) induces senescence of bronchial epithelial cells; and Cordycep...

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