, BPA1, BPA2 and BPA3 groups respectively. The body weight (BW), liver weight (LW) and LW/BW were recorded and data are expressed as mean ± s.e.m. from 7 animals by each group. BPA-induced hepatic inflammation in CD1 mice To investigate
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Qiong Lv, Rufei Gao, Chuan Peng, Juan Yi, Lulu Liu, Shumin Yang, Danting Li, Jinbo Hu, Ting Luo, Mei Mei, Ying Song, Chaodong Wu, Xiaoqiu Xiao, and Qifu Li
Hassina Ould Hamouda, Bernadette Delplanque, Yacir Benomar, Delphine Crépin, Laure Riffault, Pascale LeRuyet, Cécile Bonhomme, and Mohammed Taouis
in the elderly ( Paz-Filho et al . 2008 , Cardoso et al . 2009 ). Thus, promoting overall insulin sensitivity in elderly subjects could contribute to a delay in the onset of some aging-related disorders, including eating disorders, inflammation
Jie Wei, Xia Sun, Yajie Chen, Yuanyuan Li, Liqiong Song, Zhao Zhou, Bing Xu, Yi Lin, and Shunqing Xu
population in Western countries and 9–40% of people in Asian countries ( Farrell & Larter 2006 ). A subset of patients with NAFLD may progress to nonalcoholic steatohepatitis (NASH), a more severe form of hepatic damage associated with inflammation, fibrosis
Michela Campolo, Akbar Ahmad, Rosalia Crupi, Daniela Impellizzeri, Rossana Morabito, Emanuela Esposito, and Salvatore Cuzzocrea
beneficial effect in an arthritis model reducing the dose; on the other hand, it reduces the degree of spinal cord inflammation, ameliorating the recovery of limb function. These results show the reduction of the side effects related to the use of steroids
Miriam Thomalla, Andreas Schmid, Elena Neumann, Petra Ina Pfefferle, Ulf Müller-Ladner, Andreas Schäffler, and Thomas Karrasch
steatosis, inflammation and fibrosis in mice fed a choline-deficient amino acid-defined (CDAA) diet, a murine model of non-alcoholic steatohepatitis (NASH). In this model, Tlr9 −/− mice are protected from CDAA-induced steatohepatitis and fibrosis and have
Daniel J Tobiansky, George V Kachkovski, Reilly T Enos, Kim L Schmidt, E Angela Murphy, and Kiran K Soma
interest to examine the effects of sucrose intake during this time period. We examined glucose regulation, hepatic lipogenesis, adipose inflammation, serum and brain steroid levels, and markers of DA synthesis and signalling in the mesocorticolimbic system
Jane J Reavey, Catherine Walker, Alison A Murray, Savita Brito-Mutunayagam, Sheona Sweeney, Moira Nicol, Ana Cambursano, Hilary O D Critchley, and Jacqueline A Maybin
women have no structural cause for their regular AUB and are assigned the AUB-E (AUB of endometrial origin) category. The cause of AUB-E remains undefined but current studies implicate excessive inflammation, delayed repair of the endometrium and
A D Dobrian, M A Hatcher, J J Brotman, E V Galkina, P Taghavie-Moghadam, H Pei, B A Haynes, and J L Nadler
inflammation emerge as key contributors to atherosclerosis. The Apoe −/− mouse model of atherosclerosis displays accelerated plaque formation on high cholesterol diet. However, this mouse model neither gains weight nor develops insulin resistance as a result
Maria Karsai, Richard A Zuellig, Roger Lehmann, Federica Cuozzo, Daniela Nasteska, Edlira Luca, Constanze Hantel, David J Hodson, Giatgen A Spinas, Guy A Rutter, and Philipp A Gerber
Duan JL Liu YQ 2015 The zinc ion chelating agent TPEN attenuates neuronal death/apoptosis caused by hypoxia/ischemia via mediating the pathophysiological cascade including excitotoxicity, oxidative stress, and inflammation . CNS Neuroscience and
Lisa D Madison, Jarrad M Scarlett, Peter Levasseur, XinXia Zhu, Kenneth Newcomb, Ayesha Batra, Darren Bowe, and Daniel L Marks
inflammation and malignancy act on the central nervous system (CNS) to alter the release and function of a number of key neurotransmitters, thereby altering both appetite and metabolic rate ( Plata-Salaman 1989 , 1999 , Tisdale 1997 , Inui 1999 b ). In
