Laboratory Investigation - Table of Contents alert Volume 95 Issue 2

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TABLE OF CONTENTS Volume 95, Issue 2 (February 2015) In this issue Inside the USCAP Journals Mini Review Research Articles Also new AOP Sign up for e-alerts Recommend to your library Web feed Subscribe Inside the USCAP Journals Top Inside the USCAP Journals 2015 95: 122-123; 10.1038/labinvest.2014.164 Full Text Mini Review Top Cholesterol gallstone disease: focusing on the role of gallbladder The gallbladder plays an important role in the pathogenesis of cholesterol gallstone disease. In this article, various conditions affecting the formation of cholesterol gallstones are discussed, such as gallbladder motility, concentrating function, lipid transport, and an imbalance between pro-nucleation and nucleation inhibiting proteins. Yongsheng Chen, Jing Kong and Shuodong Wu 2015 95: 124-131; advance online publication, December 15, 2014; 10.1038/labinvest.2014.140 Abstract | Full Text Research Articles Top ANGIOGENESIS, CARDIOVASCULAR AND PULMONARY SYSTEMS Hemoglobin-associated oxidative stress in the pericardial compartment of postoperative cardiac surgery patients This study reveals that postoperative pericardial fluid contains high levels of cell-free hemoglobin, isoprostanes and prostaglandins, as well as infiltrating leukocytes, which all contribute to the highly pro-oxidant and pro-inflammatory environment within the pericardium following cardiac surgery. These alterations may promote the oxidative modification of cardiac proteins and lead to postoperative complications such as cardiomyocyte injury and loss of cardiac function. Philip A Kramer, Balu K Chacko, Saranya Ravi, Michelle S Johnson, Tanecia Mitchell, Stephen Barnes, Alireza Arabshahi, Louis J Dell'Italia, David J George, Chad Steele, James F George, Victor M Darley-Usmar and Spencer J Melby 2015 95: 132-141; advance online publication, December 1, 2014; 10.1038/labinvest.2014.144 Abstract | Full Text Endogeous sulfur dioxide protects against oleic acid-induced acute lung injury in association with inhibition of oxidative stress in rats An animal model was established to examine the role of the gasotransmitter SO2 in the pathogenesis of acute lung injury (ALI). The authors found that the SO2/aspartate aminotransferase 1 (AAT1) /AAT2 pathway protects against the development ALI by inhibiting oxidative stress, resulting in the improvement of gas exchange. Siyao Chen, Saijun Zheng, Zhiwei Liu, Chaoshu Tang, Bin Zhao, Junbao Du and Hongfang Jin 2015 95: 142-156; advance online publication, January 12, 2015; 10.1038/labinvest.2014.147 Abstract | Full Text BLOOD, LYMPHATICS, IMMUNE SYSTEM AND STEM CELLS Inactivation of Notch signaling reverses the Th17/Treg imbalance in cells from patients with immune thrombocytopenia Notch signaling is a critical factor in the imbalance of the Th17/Treg ratio seen in immune thrombocytopenia (ITP). In this study the authors show that inactivation of Notch signaling subsequently downregulates interleukin17 and the transcription factor RORγt, reducing Th17 levels. Therefore, inactivation of Notch signaling might be a potential immunoregulatory strategy for ITP. Shuang Yu, Chuanfang Liu, Lanhua Li, Tian Tian, Min Wang, Yu Hu, Cunzhong Yuan, Lei Zhang, Chunyan Ji and Daoxin Ma 2015 95: 157-167; advance online publication, December 8, 2014; 10.1038/labinvest.2014.142 Abstract | Full Text Remodeling of epithelial cells and basement membranes in a corneal deficiency model with long-term follow-up Irreversible injury of corneal epithelial stem cells cause conjunctival tissue to cover the ocular surface, leading to visual loss. In this study, an animal model of corneal deficiency is described, and the remodeling of the corneal epithelium and basement membrane are observed over time. This model may be useful in the development of regenerative therapies for corneal epithelium. Sumako Kameishi, Hiroaki Sugiyama, Masayuki Yamato, Yoshikazu Sado, Hideo Namiki, Takashi Kato and Teruo Okano 2015 95: 168-179; advance online publication, December 22, 2014; 10.1038/labinvest.2014.146 Abstract | Full Text Low doses of CMV induce autoimmune-mediated and inflammatory responses in bile duct epithelia of regulatory T cell-depleted neonatal mice Treg-depleted neonatal mice were infected with low-dose cytomegalovirus (LD-CMV) as a model to study biliary atreisa (BA). In this model, LD-CMV infection induced autoimmune-mediated inflammatory responses that resulted in extensive intrahepatic and extrahepatic bile duct injury. These findings enhance our understanding of the progressive biliary injury and cirrhosis observed in BA. Jie Wen, Yongtao Xiao, Jun Wang, Weihua Pan, Ying Zhou, Xiaoling Zhang, Wenbin Guan, Yingwei Chen, Kejun Zhou, Yang Wang, Bisheng Shi, Xiaohui Zhou, Zhenghong Yuan and Wei Cai 2015 95: 180-192; advance online publication, December 22, 2014; 10.1038/labinvest.2014.148 Abstract | Full Text HEPATIC AND PANCREATIC SYSTEMS Anterior gradient 2 downregulation in a subset of pancreatic ductal adenocarcinoma is a prognostic factor indicative of epithelial–mesenchymal transition In this study, the authors demonstrate that downregulation of anterior gradient 2 (AGR2) correlates with induction of epithelial-mesenchymal transition (EMT) and adverse outcome in a subset of pancreatic ductal adenocarcinoma patients. In vitro analyses suggest that AGR2 downregulation is accompanied by EMT induction and is partially mediated by transforming growth factor-b1 secreted by cancer stromal cells. Yusuke Mizuuchi, Shinichi Aishima, Kenoki Ohuchida, Koji Shindo, Minoru Fujino, Masami Hattori, Tetsuyuki Miyazaki, Kazuhiro Mizumoto, Masao Tanaka and Yoshinao Oda 2015 95: 193-206; advance online publication, November 24, 2014; 10.1038/labinvest.2014.138 Abstract | Full Text Two-dimensional culture of human pancreatic adenocarcinoma cells results in an irreversible transition from epithelial to mesenchymal phenotype The authors developed new methods for the isolation and culture of human pancreatic ductal adenocarcinoma cells from murine xenografts of human tumors. These new cell lines have more mesenchymal phenotypic characteristics than the xenografts, along with accelerated growth rates and increasing sensitivity to chemotherapeutics with later passages. Ya'an Kang, Ran Zhang, Rei Suzuki, Shao-qiang Li, David Roife, Mark J Truty, Deyali Chatterjee, Ryan M Thomas, James Cardwell, Yu Wang, Huamin Wang, Matthew H Katz and Jason B Fleming 2015 95: 207-222; advance online publication, December 8, 2014; 10.1038/labinvest.2014.143 Abstract | Full Text TRAIL-producing NK cells contribute to liver injury and related fibrogenesis in the context of GNMT deficiency Glycine-N-methyltransferase (GNMT) is essential to liver homeostasis; it is low in cirrhosis and absent in hepatocellular carcinoma. GNMT-deficient hepatocytes express high levels of death receptor DR5, which binds the cytokine TRAIL. The authors elucidated the role of the TRAIL/DR5 axis in fibrogenesis in the context of GNMT deficiency. Their data demonstrate that TRAIL-producing NK cells contribute to liver injury and enhance fibrogenesis. Sara Fernández-Álvarez, Virginia Gutiérrez-de Juan, Imanol Zubiete-Franco, Lucia Barbier-Torres, Agustín Lahoz, Albert Parés, Zigmund Luka, Conrad Wagner, Shelly C Lu, José M Mato, María L Martínez-Chantar and Naiara Beraza 2015 95: 223-236; advance online publication, December 22, 2014; 10.1038/labinvest.2014.151 Abstract | Full Text ORAL AND GASTROINTESTINAL SYSTEMS Epigenetic modulation of the muscarinic type 3 receptor in salivary epithelial cells This paper shows that the muscarinic type 3 receptor (M3R), which plays a key role in exocrine secretion, is inactivated by hypermethylation in salivary gland cancer cell lines. M3R is also hypermethylated in salivary gland tumors from patients. The demethylating agent 5-aza-2′-deoxycytidine can restore M3R function in the cell lines, indicating it may have therapeutic use in salivary gland cancer. Yong-Hwan Shin, Meihong Jin, Sung-Min Hwang, Seul-Ki Choi, Eun Namkoong, Minkyoung Kim, Moon-Yong Park, Se-Young Choi, Jong-Ho Lee and Kyungpyo Park 2015 95: 237-245; advance online publication, December 8, 2014; 10.1038/labinvest.2014.150 Abstract | Full Text Please note that you need to be a subscriber or site-licence holder to enjoy full-text access to Laboratory Investigation. In order to do so, please purchase a subscription. You have been sent this Table of Contents Alert because you have opted in to receive it. You can change or discontinue your e-mail alerts at any time, by modifying your preferences on your nature.com account at: www.nature.com/nams/svc/myaccount (You will need to log in to be recognised as a nature.com registrant). For further technical assistance, please contact our registration department. For print subscription enquiries, please contact our subscription department. For other enquiries, please contact our customer feedback department. 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