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Karen Oliva, Gillian Barker, Clyde Riley, Mark J Bailey, Michael Permezel, Gregory E Rice and Martha Lappas

. The roles of these proteins in the regulation of placental function, and how they may influence fetus, are discussed below. Inflammation Exposure of the fetus to an intrauterine inflammatory environment may have short and long-term consequences

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Gilberto Paz-Filho, Claudio Alberto Mastronardi, Brian J Parker, Ainy Khan, Antonio Inserra, Klaus I Matthaei, Monika Ehrhart-Bornstein, Stefan Bornstein, Ma-Li Wong and Julio Licinio

) to non-alcoholic steatohepatitis (NASH) and cirrhosis ( Neuschwander-Tetri & Caldwell 2003 ). Approximately 23% of patients with NAFLD progress to NASH ( Wong et al . 2010 ), which is histologically characterized by steatosis, lobular inflammation

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Krisztina Pohóczky, József Kun, Bálint Szalontai, Éva Szőke, Éva Sághy, Maja Payrits, Béla Kajtár, Krisztina Kovács, József László Környei, János Garai, András Garami, Anikó Perkecz, Levente Czeglédi and Zsuzsanna Helyes

Introduction Transient receptor potential ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1) are non-selective cation channels predominantly localized in capsaicin-sensitive peptidergic sensory neurons and mediate pain and inflammation ( Szallasi et al

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Fabio Arturo Grieco, Andrea Alex Schiavo, Flora Brozzi, Jonas Juan-Mateu, Marco Bugliani, Piero Marchetti and Décio L Eizirik

systems taking place during insulitis ( Eizirik et al. 2009 , 2012 , Santin & Eizirik 2013 , Floyel et al. 2015 ). Islets inflammation triggers endoplasmic reticulum (ER) stress in beta cells exacerbating inflammation and contributing to beta cell

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Qi Zhang, Jing Liu, Jia Liu, Wenhui Huang, Limin Tian, Jinxing Quan, Yunfang Wang and Ruilan Niu

Introduction Type 2 diabetes mellitus (T2DM) is potentially complicated by hepatic microangiopathy and liver inflammation ( Hudacko et al . 2009 ) and is an independent risk factor for the formation and development of non-alcoholic fatty liver

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Lingyun Zhang, Takashi Sugiyama, Nao Murabayashi, Takashi Umekawa, Ning Ma, Yuki Kamimoto, Yoshihiro Ogawa and Norimasa Sagawa

Investigation 116 1494 – 1505 . doi:10.1172/JCI26498 . Kawanishi N Yano H Yokogawa Y Suzuki K 2010 Exercise training inhibits inflammation in adipose tissue via both suppression of macrophage infiltration and acceleration of phenotypic switching

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Qun Cheng, Weipin Dong, Lei Qian, Jingcheng Wu and Yongde Peng

( Li et al . 2008 ). Visfatin also participates in cellular resistance to genotoxic/oxidative stress, and enhances immune cell survival during stressful situations such as inflammation ( Rongvaux et al . 2008 ). In normal pregnancy, increased SIRT1

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R Buettner, K G Parhofer, M Woenckhaus, C E Wrede, L A Kunz-Schughart, J Schölmerich and L C Bollheimer

livers than the other high-fat and the SC animals ( P ≤ 0.05; Table 1 ). The histologic examination (hematoxylin–eosin staining) showed mainly microvesicular fat depositions in the HF-L, HF-O and HF-C livers (Fig. 3 ). No signs of inflammation or

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I M Adcock, M Peters, C Gelder, H Shirasaki, C R Brown and P J Barnes

ABSTRACT

Substance P has several inflammatory effects on the airways mediated via neurokinin 1 receptors (NK1Rs) and, if released from sensory nerves, may amplify the chronic inflammation seen in asthma. Northern blot analysis of NK1R mRNA in lung showed a 52 ± 10% (s.e.m.; P<0·01) increase in mRNA in the asthmatic lung compared with non-asthmatic control tissue. NK1R mRNA was reduced by 84·5 ± 1·9% after incubation with dexamethasone (1 μm) for 3 h (P<0·01). In contrast, NK2R mRNA was unaltered in asthmatic lungs and dexamethasone treatment had no effect on the level of NK2R mRNA. These results suggest that chronic inflammation in asthma may result in increased NK1R gene expression and that this effect is reversed by glucocorticosteroids.

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MK O'Bryan, KL Sebire, O Gerdprasert, MP Hedger, MT Hearn and DM de Kretser

Using a combination of polymerase chain reaction (PCR) procedures, we have cloned and sequenced the rat activin beta(E) subunit cDNA. The putative protein corresponding to the prepro-activin beta(E) subunit was predicted to comprise 350 amino acids which, when cleaved between amino acid residues 236 and 237, would yield a mature polypeptide of approximately M(r) 12 500 with a predicted pI of 5.1. Two cDNA transcripts for activin beta(E) were identified; these differed by 738 bp in the 3'-untranslated region. Activin beta(E) mRNA transcripts were expressed only in rat liver and lung tissue as assessed by Northern blotting and PCR analysis. Relatively higher levels of both transcripts were found in the liver, whereas the lung contained lower levels that were detectable by PCR only. In situ hybridisation data showed that, within the liver, activin beta(E) mRNA was localised to hepatocytes. In vivo treatment with lipopolysaccharide as a means of activating the immune system and the hepatic acute-phase response resulted in stimulated activin beta(E) mRNA levels, compared with untreated, control rats. This increased expression was accompanied by a preferential increase in the amount of the long activin beta(E) transcript over the shorter transcript. These findings suggested that the two activin beta(E) mRNA transcripts may be products of alternative splicing events or use alternative polyadenylation sites which are differentially regulated during inflammation. These data provide evidence of a role for activin beta(E) in liver function and inflammation in the rat.