Laboratory Investigation - Table of Contents alert Volume 93 Issue 6

TABLE OF CONTENTS Volume 93, Issue 6 (June 2013) In this issue Inside LI Research Articles Also new AOP Sign up for e-alerts Recommend to your library Web feed Subscribe Advertisement Take part in our reader survey for a chance to win a MacBook Air As a reader of NPG's clinical and society-owned journals, we invite you to take part in a survey on your use of our journals and their associated websites. Take the survey and be entered into a prize draw for a MacBook Air* *Terms & conditions apply   Inside LI Top Inside Lab Invest 2013 93: 624-625; 10.1038/labinvest.2013.68 Full Text Research Articles Top ANGIOGENESIS, CARDIOVASCULAR AND PULMONARY SYSTEMS Immune complexes activate human endothelium involving the cell-signaling HMGB1-RAGE axis in the pathogenesis of lupus vasculitis The pathogenesis of systemic lupus erythematosus (SLE) vasculitis is shown to involve immune complexes that activate endothelium cellular signaling via the high-mobility group box 1 protein (HMGB1)-receptor for advanced glycation end products (RAGE) axis. This mechanism may suggest new therapeutic management of SLE vasculitis. Wenping Sun, Yulian Jiao, Bin Cui, Xuejun Gao, Yu Xia and Yueran Zhao 2013 93: 626-638; advance online publication, April 29, 2013; 10.1038/labinvest.2013.61 Abstract | Full Text Autophagy mediates paracrine regulation of vascular endothelial cells This paper reveals a proliferative role for gastrin-releasing peptide in vascular endothelial cells via upregulation of the PI3K/ AKT/mTOR signaling pathway. A novel role for this neuropeptideis described; the inhibition of autophagy, which regulates tubule formation by vascular endothelial cells. These findings may aid in development of therapies targeting tumor angiogenesis. Kwang Woon Kim, Pritha Paul, Jingbo Qiao and Dai H Chung 2013 93: 639-645; advance online publication, April 22, 2013; 10.1038/labinvest.2013.57 Abstract | Full Text Lack of Cyp1b1 promotes the proliferative and migratory phenotype of perivascular supporting cells Cytochrome P450 1B1 (Cyp1B1) is constitutively expressed in retinal perivascular supporting cells. Deficiency of Cyp1B1 in these cells results in enhanced proliferation, decreased apoptosis, and attenuation of capillary morphogenesis of endothelial cells, as well as increased oxidative stress, sustained NF-κB activation, and increased thrombospondin-2 production. Thus, a lack of Cyp1B1 in pericytes may have a significant role in vascular dysfunction. Tammy L Palenski, Christine M Sorenson, Colin R Jefcoate and Nader Sheibani 2013 93: 646-662; advance online publication, April 8, 2013; 10.1038/labinvest.2013.55 Abstract | Full Text PERIPHERAL AND CENTRAL NERVOUS SYSTEM Elevated TRAF2/6 expression in Parkinson’s disease is caused by the loss of Parkin E3 ligase activity Parkin, an E3 ligase, suppresses inflammation and cytokine-induced cell death by promoting the proteasomal degradation of TNF-α receptor associated factor (TRAF) 2/6. Because TRAF6 is elevated in Parkin-deficient human Parkinson's disease samples, these results may provide the basic pathological mechanism of Parkinson's disease. Ji-Yun Chung, Hee Ra Park, Su-Jin Lee, Sun-Hye Lee, Jin Sik Kim, Youn-Sang Jung, Sang Hyun Hwang, Nam-Chul Ha, Won-Gi Seol, Jaewon Lee and Bum-Joon Park 2013 93: 663-676; advance online publication, April 22, 2013; 10.1038/labinvest.2013.60 Abstract | Full Text BLOOD, LYMPHATICS, IMMUNE SYSTEM, STEM CELLS RIP1 expression is necessary for CD30-mediated cell death induction in anaplastic large-cell lymphoma cells This paper identifies receptor-interacting protein 1 (RIP1) as a crucial mediator of CD30-induced cell death in anaplastic large-cell lymphoma (ALCL) cells. In these cells, CD30-induces cell death that bears features of apoptosis as well as necroptosis. RIP1 therefore appears to be a novel candidate molecule for ALCL therapy. Burkhard Hirsch, Edda von der Wall, Michael Hummel and Horst Dürkop 2013 93: 677-689; advance online publication, April 1, 2013; 10.1038/labinvest.2013.50 Abstract | Full Text Methods for defining distinct bioenergetic profiles in platelets, lymphocytes, monocytes, and neutrophils, and the oxidative burst from human blood Open A high throughput assay for measurement of oxygen consumption in cells isolated from human blood could give insights into cellular bioenergetics in a range of diseases. This study reveals how extracellular flux analysis can define a bioenergetic profile in platelets, monocytes, lymphocytes and measurement of the oxidative burst in monocytes and neutrophils from individual donors. Balu K Chacko, Philip A Kramer, Saranya Ravi, Michelle S Johnson, Robert W Hardy, Scott W Ballinger and Victor M Darley-Usmar 2013 93: 690-700; advance online publication, March 25, 2013; 10.1038/labinvest.2013.53 Abstract | Full Text MODELS AND TECHNIQUES Evaluating the repair of DNA derived from formalin-fixed paraffin-embedded tissues prior to genomic profiling by SNP–CGH analysis Pathology archives of formalin-fixed paraffin-embedded (FFPE) tissue samples are vast resources of clinical material. However, the integrity of DNA and RNA in FFPE tissue is compromised, and obtaining informative data regarding epigenetic, genomic, and expression alterations is challenging. This paper shows that DNA that is damaged during fixation and storage can be repaired, aiding genomic studies of large archival cohorts and study of rare cancer types. Abdel Nasser Hosein, Sarah Song, Amy E McCart Reed, Janani Jayanthan, Lynne E Reid, Jamie R Kutasovic, Margaret C Cummings, Nic Waddell, Sunil R Lakhani, Georgia Chenevix-Trench and Peter T Simpson 2013 93: 701-710; advance online publication, April 8, 2013; 10.1038/labinvest.2013.54 Abstract | Full Text The Justy mutant mouse strain produces a spontaneous murine model of salivary gland cancer with myoepithelial and basal cell differentiation Justy mice, with a mutant Gon4l gene, are proposed as a mouse model for human salivary gland neoplasia. These mice spontaneously develop carcinomas with myoepithelial and basaloid differentiation in salivary glands and exhibit dysregulation of epidermal growth factor receptor signaling. Andrean L Simons, Ping Lu, Katherine N Gibson-Corley, Robert A Robinson, David K Meyerholz and John D Colgan 2013 93: 711-719; advance online publication, April 22, 2013; 10.1038/labinvest.2013.62 Abstract | Full Text HEPATIC AND PANCREATIC SYSTEMS Transforming growth factor-α activates pancreatic stellate cells and may be involved in matrix metalloproteinase-1 upregulation This paper elucidates the role of transforming growth factor-α (TGF-α) in chronic pancreatitis and pancreatic cancer. Because TGF-α promotes the proliferation and migration of pancreatic stellate cells (PSC), its inhibition could decrease tumor cell invasion. Inhibition of TGF-α may also decrease the suitability of PSC-induced microenvironments for cancer growth, and affect the significant crosstalk between PSCs and pancreatic carcinoma cells. Hiroki Tahara, Ken Sato, Yuichi Yamazaki, Tatsuya Ohyama, Norio Horiguchi, Hiroaki Hashizume, Satoru Kakizaki, Hitoshi Takagi, Iwata Ozaki, Hideo Arai, Junko Hirato, Ralf Jesenofsky, Atsushi Masamune and Masatomo Mori 2013 93: 720-732; advance online publication, April 22, 2013; 10.1038/labinvest.2013.59 Abstract | Full Text Micro-computed tomography and nuclear magnetic resonance imaging for noninvasive, live-mouse cholangiography The cholangiopathies are an etiopathogenically diverse group of disorders affecting epithelial cells lining the tubular network of bile ducts. Noninvasive methods for assessing biliary disease in murine models are lacking. This paper describes a novel magnetic resonance-based technique for live-mouse cholangiography, which can be useful for longitudinal study of the cholangiopathies. James H Tabibian, Slobodan I Macura, Steven P O'Hara, Jeff L Fidler, James F Glockner, Naoki Takahashi, Val J Lowe, Bradley J Kemp, Prasanna K Mishra, Pamela S Tietz, Patrick L Splinter, Christy E Trussoni and Nicholas F LaRusso 2013 93: 733-743; advance online publication, April 15, 2013; 10.1038/labinvest.2013.52 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. 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