TABLE OF CONTENTS
| | | | Volume 95, Issue 1 (January 2015) | | In this issue Inside the USCAP Journals Pathobiology in Focus Mini Reviews Research Articles Technical Report Also new AOP | | | | Inside the USCAP Journals | Top | | Inside the USCAP Journals 2015 95: 2-3; 10.1038/labinvest.2014.152 Full Text | | Pathobiology in Focus | Top | | A practical guide to induced pluripotent stem cell research using patient samples This review article assesses the impact of patient induced pluripotent stem cells (iPSCs) on human pathobiology, with a focus on the practical applications and limitations of iPSCs in the research laboratory. Katherine E Santostefano, Takashi Hamazaki, Nikolett M Biel, Shouguang Jin, Akihiro Umezawa and Naohiro Terada 2014 95: 4-13; advance online publication, August 4, 2014; 10.1038/labinvest.2014.104 Abstract | Full Text | | Mini Reviews | Top | | Regulation of autophagy by protein post-translational modification Autophagy is a lysosome-mediated intracellular protein degradation process that is important for quality control of macromolecules and organelles. Identification of the full spectrum of post-translational modifications of autophagy proteins, and determination of their impact on autophagy is crucial for a better understanding of autophagy regulation, its deficits in diseases, and how to exploit this process for disease therapies. Willayat Yousuf Wani, Michaël Boyer-Guittaut, Matthew Dodson, John Chatham, Victor Darley-Usmar and Jianhua Zhang 2014 95: 14-25; advance online publication, November 3, 2014; 10.1038/labinvest.2014.131 Abstract | Full Text | | | | Generation of pluripotent stem cells without the use of genetic material Induced pluripotent stem cells (iPSCs) provide a platform for acquisition of patient-specific cells for use in regenerative medicine. In this review, the authors discuss what types of small molecules (chemicals) or large molecules (proteins) could be used to replace viral transduction of genes and/or genetic reprogramming in order to obtain human iPSCs. Akon Higuchi, Qing-Dong Ling, S Suresh Kumar, Murugan A Munusamy, Abdullah A Alarfaj, Yung Chang, Shih-Hsuan Kao, Ke-Chen Lin, Han-Chow Wang and Akihiro Umezawa 2014 95: 26-42; advance online publication, November 3, 2014; 10.1038/labinvest.2014.132 Abstract | Full Text | | Research Articles | Top | | HEPATIC AND PANCREATIC SYSTEMS | Proteins associated with pancreatic cancer survival in patients with resectable pancreatic ductal adenocarcinoma Pancreatic ductal adenocarcinoma is a highly lethal disease with a dismal prognosis. Aiming to improve pancreatic cancer treatment through personalized medicine, the authors compared the proteomes of individual pancreatic adenocarcinomas from very long-term survivors and short-term survival patients. The study identified significant prognostic factors and potential therapeutic targets to improve pancreatic cancer survival. Ru Chen, David W Dawson, Sheng Pan, Niki A Ottenhof, Roeland F de Wilde, Christopher L Wolfgang, Damon H May, David A Crispin, Lisa A Lai, Anna R Lay, Meghna Waghray, Shouli Wang, Martin W McIntosh, Diane M Simeone, Anirban Maitra and Teresa A Brentnall 2014 95: 43-55; advance online publication, October 27, 2014; 10.1038/labinvest.2014.128 Abstract | Full Text | | | | ANGIOGENESIS, CARDIOVASCULAR AND PULMONARY SYSTEMS | Overexpression of stathmin 1 is a poor prognostic biomarker in non-small cell lung cancer Stathmin 1 (STMN1) is a microtubule-depolymerizing protein involved in cell cycle progression and motility. This paper shows that STMN1 is overexpressed in non-small cell lung cancer (NSCLC). High STMN1 expression correlates with poor tumor differentiation, large tumor size and advanced stages. Knockdown of STMN1 in lung cancer cells decreases proliferation and invasion. Therefore, STMN1 may be prognostic marker for NSCLC. Wei Nie, Mi-die Xu, Lu Gan, Hai Huang, Qingyu Xiu and Bing Li 2014 95: 56-64; advance online publication, November 10, 2014; 10.1038/labinvest.2014.124 Abstract | Full Text | | | | Treatment with CA-074Me, a Cathepsin B inhibitor, reduces lung interstitial inflammation and fibrosis in a rat model of polymyositis Muscle cathepsin B (CB) levels are increased the connective tissue diseases polymyositis and dermatomyositis (PM/DM). This paper reveals the role of CB in the interstitial lung disease (ILD) associated with PM/DM. In an animal model of PM, a CB inhibitor decreases inflammation, fibrosis, and apoptosis in the lung through downregulation of TGF-β1. Therefore, CB may be a therapeutic target for ILD associated with PM/DM. Li Zhang, Xiao-Hong Fu, Yong Yu, Ruo-Hong Shui, Chun Li, Hai-Ying Zeng, Yu-Lei Qiao, Li-Yan Ni and Qiang Wang 2014 95: 65-77; advance online publication, November 10, 2014; 10.1038/labinvest.2014.135 Abstract | Full Text | | | | GENITOURINARY AND REPRODUCTIVE SYSTEMS | The pathological role of IL-18Rα in renal ischemia/reperfusion injury Acute kidney injury in mice with ischemia/reperfusion injury is more rapid and severe in IL-18 receptor (IL-18R)-deficient mice than wild type mice. The authors show that IL-18R affects T and B-cell responses, increases accumulation of leukocytes, and affects apoptosis via Fas/Fas ligand expression. Suppression of pro-inflammatory molecules and apoptosis through IL-18Rα represents a novel therapeutic strategy for ischemia-related renal injury. Tomohiro Yano, Yuji Nozaki, Koji Kinoshita, Shoichi Hino, Yasuaki Hirooka, Kaoru Niki, Hideki Shimazu, Kazuya Kishimoto, Masanori Funauch and Itaru Matsumura 2014 95: 78-91; advance online publication, October 20, 2014; 10.1038/labinvest.2014.120 Abstract | Full Text | | | | BREAST, SKIN, SOFT TISSUE AND BONE | Development of non-traumatic osteonecrosis of the femoral head requires toll-like receptor 7 and 9 stimulations and is boosted by repression on nuclear factor kappa B in rats OPEN Osteonecrosis of the femoral head (ONFH) commonly occurs after orticosteroid therapy for inflammation. It is known that toll-like receptor (TLR) signaling contributes to inflammation, and that corticosteroids reduce levels of NF-κB. In this study, the authors found that corticosteroid treatment after administration of TLR ligands to rats causes a decrease in NF-κB activity, resulting in ONFH. Shunichiro Okazaki, Satoshi Nagoya, Hiroshi Matsumoto, Keisuke Mizuo, Mikito Sasaki, Satoshi Watanabe, Toshihiko Yamashita and Hiromasa Inoue 2014 95: 92-99; advance online publication, November 10, 2014; 10.1038/labinvest.2014.134 Abstract | Full Text | | | | MODELS AND TECHNIQUES | Methods for detecting circulating cancer stem cells (CCSCs) as a novel approach for diagnosis of colon cancer relapse/metastasis This paper describes the development of a novel diagnostic assay for detecting circulating cancer stem cells (CSCs), using a combination of CSC and epithelial cell markers. This assay may prove useful as an early approach for more accurate prediction of the risk of cancer relapse and/or metastatic disease in colon cancer patients. Carla Kantara, Malaney Ravae O'Connell, Gurinder Luthra, Aakash Gajjar, Shubhashish Sarkar, Robert Leo Ullrich and Pomila Singh 2014 95: 100-112; advance online publication, October 27, 2014; 10.1038/labinvest.2014.133 Abstract | Full Text | | Technical Report | Top | | Diffuse large B-cell lymphoma: sub-classification by massive parallel quantitative RT-PCR A robust protocol for cell-of-origin classification of diffuse large B-cell lymphoma (DLBCL) was established using RNA samples from formalin-fixed paraffin-embedded tissues and massive parallel quantitative reverse transcription PCR. Machine learning classifiers correctly identified activated B-cell like and germinal center B-cell like DLBCL cases, indicating that this assay may be useful for routine diagnostic biopsies. Xuemin Xue, Naiyan Zeng, Zifen Gao and Ming-Qing Du 2014 95: 113-120; advance online publication, November 24, 2014; 10.1038/labinvest.2014.136 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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