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TABLE OF CONTENTS
|  |  |  | Volume 94, Issue 4 (April 2014) |  | In this issue Inside the Uscap Journals Research Articles
Also new    AOP | |  |  | Inside the Uscap Journals | Top |  | Inside the USCAP Journals2014 94: 360-361; 10.1038/labinvest.2014.49 Full Text |  | Research Articles | Top |  | ANGIOGENESIS, CARDIOVASCULAR AND PULMONARY SYSTEMS | Inhibition of TBK1 attenuates radiation-induced epithelial–mesenchymal transition of A549 human lung cancer cells via activation of GSK-3β and repression of ZEB1In this study, the authors examined tank-binding kinase-1 (TBK1) signaling in radiation-induced epithelial-mesenchymal transition (EMT) with the hope of developing more effective radiotherapy. They found that silencing of TBK1 by siRNA overrides the radiation-induced EMT via activation of glycogen synthase kinase-3β and repression of transcriptional factor ZEB1. Wen Liu, Yi-Juan Huang, Cong Liu, Yan-Yong Yang, Hu Liu, Jian-Guo Cui, Ying Cheng, Fu Gao, Jian-Ming Cai and Bai-Long Li 2014 94: 362-370; advance online publication, January 27, 2014; 10.1038/labinvest.2013.153 Abstract | Full Text |  |  |  | Colony-stimulating factor 1 potentiates lung cancer bone metastasisThe authors examine the role of colony stimulating factor 1 (CSF1) in a model of lung cancer bone metastasis. They determine that CSF1 potentiates tumor cell proliferation, cancer-like stem cells and osteoclastic bone resorption. In lung cancer, CSF1 levels are elevated, therefore, inhibition of CSF1 may be useful for preventing complications of metastatic bone disease. Jaclyn Y Hung, Diane Horn, Kathleen Woodruff, Thomas Prihoda, Claude LeSaux, Jay Peters, Fermin Tio and Sherry L Abboud-Werner 2014 94: 371-381; advance online publication, January 27, 2014; 10.1038/labinvest.2014.1 Abstract | Full Text |  |  |  | Low-molecular-weight fucoidan protects endothelial function and ameliorates basal hypertension in diabetic Goto-Kakizaki ratsFucoidan, a sulfated polysaccharide extracted from brown seaweed, is shown in this study to protect vasoendothelial function and reduce basal blood pressure in type 2 diabetic rats, via preservation of endothelial NO synthase function. Fucoidan is therefore a potential candidate drug for alleviation of diabetic cardiovascular complications. Wentong Cui, Yuanyuan Zheng, Quanbin Zhang, Jing Wang, Limin Wang, Wenzhe Yang, Chenyang Guo, Weidong Gao, Xiaomin Wang and Dali Luo 2014 94: 382-393; advance online publication, March 10, 2014; 10.1038/labinvest.2014.12 Abstract | Full Text |  |  |  | HEPATIC AND PANCREATIC SYSTEMS | Increased expression of c-Jun in nonalcoholic fatty liver diseaseIn order to determine the mechanisms of non-alcoholic steatohepatitis (NASH), the authors developed a murine model. Livers of mice fed a NASH-inducing diet (ND) exhibit the pathological changes found in human NASH. Transcriptome-wide gene expression analysis identified AP-1 as a key factor causing transcriptional changes seen in NASH mice. Additionally, analysis of differentially expressed genes and proteins identified c-Jun as the hub in the largest deregulated network in ND-livers. Christoph Dorn, Julia C Engelmann, Michael Saugspier, Andreas Koch, Arndt Hartmann, Martina Müller, Rainer Spang, Anja Bosserhoff and Claus Hellerbrand 2014 94: 394-408; advance online publication, February 3, 2014; 10.1038/labinvest.2014.3 Abstract | Full Text |  |  |  | Fibrogenesis in pancreatic cancer is a dynamic process regulated by macrophage–stellate cell interactionThe authors describe the dynamic remodeling that occurs in pancreatic ductal adenocarcinoma, highlighting similarities and differences between benign and malignant disease. Fibrosis in pancreatic cancer involves a complex interplay of stellate cells, macrophages and matrices that regulate not only the tumor epithelium but the composition of the microenvironment itself. Chanjuan Shi, M Kay Washington, Rupesh Chaturvedi, Yiannis Drosos, Frank L Revetta, Connie J Weaver, Emily Buzhardt, Fiona E Yull, Timothy S Blackwell, Beatriz Sosa-Pineda, Robert H Whitehead, R Daniel Beauchamp, Keith T Wilson and Anna L Means 2014 94: 409-421; advance online publication, February 17, 2014; 10.1038/labinvest.2014.10 Abstract | Full Text |  |  |  | BREAST, SKIN, SOFT TISSUE AND BONE | DNA aptamer raised against advanced glycation end products inhibits melanoma growth in nude miceIn this study, the authors found that an advanced glycation end products (AGE)-aptamer inhibits the AGE-AGE receptor axis in melanoma cells and results in suppression of tumor growth in nude mice by blocking angiogenesis. This AGE-aptamer might be a novel therapeutic strategy for preventing the progression of malignant melanoma in diabetes. Ayako Ojima, Takanori Matsui, Sayaka Maeda, Masayoshi Takeuchi, Hiroyoshi Inoue, Yuichiro Higashimoto and Sho-ichi Yamagishi 2014 94: 422-429; advance online publication, February 10, 2014; 10.1038/labinvest.2014.5 Abstract | Full Text |  |  |  | Apoptosis-associated tyrosine kinase 1 inhibits growth and migration and promotes apoptosis in melanomaThis is the first study to examine the roles of apoptosis-associated tyrosine kinase (AATK) in melanoma. AATK is a multi-functional protein that inhibits growth and migration and promotes apoptosis. The results of this study suggest that loss of AATK is important in tumor progression in melanoma. Shuang Ma and Brian P Rubin 2014 94: 430-438; advance online publication, March 3, 2014; 10.1038/labinvest.2014.13 Abstract | Full Text |  |  |  | GENITOURINARY AND REPRODUCTIVE SYSTEM | Na+/H+ exchanger-1 reduces podocyte injury caused by endoplasmic reticulum stress via autophagy activationIn this paper, the authors demonstrate that autophagy, which is activated by Na+/H+ exchanger-1 via the Akt pathway, plays a pivotal role in lessening podocyte injury induced by endoplasmic reticulum stress. This is a novel target for prevention of podocyte injury and amelioration of proteinuria during the course of glomerular disease. Zhe Feng, Li Tang, Lingling Wu, Shaoyuan Cui, Quan Hong, Guangyan Cai, Di Wu, Bo Fu, Ribao Wei and Xiangmei Chen 2014 94: 439-454; advance online publication, February 24, 2014; 10.1038/labinvest.2014.4 Abstract | Full Text |  |  |  | Activation of platelet-activating factor receptor exacerbates renal inflammation and promotes fibrosisThis study shows that platelet activating factor (PAF) receptor engagement by PAF or PAF-like molecules generated during unilateral ureter obstruction potentiates renal dysfunction. PAF receptor signaling promotes a pro-inflammatory environment, favoring the fibrotic process, which can eventually leads to renal dysfunction and progressive organ failure. Matheus Correa-Costa, Vinicius Andrade-Oliveira, Tarcio T Braga, Angela Castoldi, Cristhiane F Aguiar, Clarice ST Origassa, Andrea CD Rodas, Meire I Hiyane, Denise MAC Malheiros, Francisco JO Rios, Sonia Jancar and Niels OS Câmara 2014 94: 455-466; advance online publication, February 3, 2014; 10.1038/labinvest.2013.155 Abstract | Full Text |  |  |  | MODELS AND TECHNIQUES | A tissue quality index: an intrinsic control for measurement of effects of preanalytical variables on FFPE tissueA tissue quality index is defined as a molecular test that provides quantitative information on the suitability of a specimen for analysis by immunohistochemistry. This paper shows proof-of-concept for this index, along with pilot validation studies for a first version of a tissue quality index. Veronique M Neumeister, Fabio Parisi, Allison M England, Summar Siddiqui, Valsamo Anagnostou, Elizabeth Zarrella, Maria Vassilakopolou, Yalai Bai, Sasha Saylor, Anna Sapino, Yuval Kluger, David G Hicks, Gianni Bussolati, Stephanie Kwei and David L Rimm 2014 94: 467-474; advance online publication, February 17, 2014; 10.1038/labinvest.2014.7 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. 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