Years and Volumes

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Articles from this Volume

Hye-Soon Lee, Annette T Lee, Lindsey A Criswell, Michael F Seldin, Christopher I Amos, John P Carulli, Cristina Navarrete, Elaine F Remmers, Daniel L Kastner, Robert M Plenge, Wentian Li, and Peter K Gregersen

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease characterized by joint inflammation and progressive joint destruction. Recently, several new genes with modest levels of risk for RA have been identified in various populations. Nevertheless, the MHC remains the strongest region of genetic association with this disease, and until recently this has been assumed to be entirely due to the well-defined allelic associations with the class II HLA-DRB1 locus. However, it is likely that additional risk loci for RA are present WITHIN the major histocompatibility complex (MHC), independent of the HLA-DRB1 locus. Lee et al. (293-300) now provide evidence for several new risk loci for RA located in the Class I region of the MHC, as well as in the region centromeric to the DRB1 locus. These data emphasize the need for more detailed analysis of the MHC in RA, a theme that is also emerging for other autoimmune diseases such as type 1 diabetes.

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Posted by Leah Caracappa on Jan 28, 2014 8:35 AM CST

Margot Gallowitsch-Puerta

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Posted by Leah Caracappa on Mar 27, 2012 8:46 AM CDT

Review Article

Katja Rabe, Michael Lehrke, Klaus G Parhofer, and Uli C Broedl

Understanding the pathogenesis of obesity and its metabolic sequelae has advanced rapidly over the past decade.  Due to the dramatic rise of obesity, adipose tissue – traditionally considered to be an energy storage depot – has gained tremendous scientific interest.  Rabe et al. summarize current data on the effect of adipose tissue-derived hormones on insulin resistance.

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Posted by Leah Caracappa on Dec 5, 2008 12:00 AM CST

Review Article

Kathryn Beauchamp, Haitham Mutlak, Wade R Smith, Esther Shohami, and Philip F Stahel

Traumatic bran injury (TBI) – a major health care problem and significant socioeconomic challenge – is the leading cause of death and disability in young people.  Approximately 1.5 million patients in the United States are affected each year, and despite advances in research and improved neurointensive care, no specific pharmacological therapy for TBI patients is currently available.  Beauchamp et al. review the published prospective clinical trials on pharmacological treatment modalities for TBI patients and outline future promising therapeutic options in the field.

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Posted by Leah Caracappa on Dec 4, 2008 12:00 AM CST

Carla Q Feitoza, Giselle M Gonçalves, Patrícia Semedo,  Marcos A Cenedeze, Hélady S Pinheiro,  Felipe Caetano Beraldo, Oscar Fernando Pavão dos Santos, Vicente de Paula A Teixeira, Marlene A dos Reis, Marilda Mazzali, Alvaro Pacheco-Silva, and Niels O S Câmara

Ischemia and reperfusion injury (IRI) contributes to the development of chronic interstitial fibrosis/tubular atrophy in renal allograft patients. Cyclooxygenase (COX) 1 and 2 actively participate in acute ischemic injury by activating endothelial cells and inducing oxidative stress.  Blockade of COX 1 and 2 is associated with organ improvement after ischemic damage.  Feitoza et al. investigate the role of COX 1 and 2 in the development of fibrosis by performing COX 1 and 2 blockade immediately before IRI.  Inhibition of COX 1 and 2 resulted in less tissue fibrosis, which was associated with a decrease in proinflammatory cytokines and enhancement of the protective cellular response. The present work demonstrates that COXs play an important role in the development of sustained inflammation. There is no effective treatment for renal fibrosis and COX blockade prior to acute injury may represent a treatment strategy for renal damage associated with fibrosis.

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Posted by Leah Caracappa on Dec 3, 2008 12:00 AM CST

LaWanda H Thompson, Hyeong T Kim, Yuchen Ma, Natalia A Kokorina, and Joseph L Messina

Severe injuries such as surgical trauma, hemorrhage, thermal injury, and sepsis can lead to acute insulin resistance. The efficacy of intensive insulin therapy in these injuries suggests that understanding acute insulin resistance mechanisms may be important for development of new therapeutic strategies.  Thompson et al. used a surgical trauma and hemorrhage model to determine the development, timing and muscle selectivity of hemorrhage-induced skeletal muscle insulin resistance. The data indicate defects in insulin signaling occurred rapidly and were reversible. Additionally, insulin signaling was more severe in some skeletal muscles but did not occur in cardiac muscle. The mechanisms leading to recovering insulin responsiveness may be key in reducing morbidity and mortality in the intensive care environment.

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Posted by Leah Caracappa on Dec 2, 2008 12:00 AM CST

Giovana S Di Marco, Antoine Alam, Frédéric Dol, Pierre Corvol, Jean-Marie Gasc, and Etienne Larger

Diabetic patients exhibit impaired angiogenesis often leading to difficulties in wound healing and organ transplantation. Therapeutic angiogenesis or arteriogenesis may represent a beneficial strategy for patients with diabetes as well as those with peripheral or coronary artery disease ineligible for surgical revascularization. Trials involving therapeutic angiogenesis have garnered negative responses due in part to the direct effect of hyperglycemia on neovascularization. To further investigate this, Di Marco et al. tested the activity of proangiogenic molecules under hyperglycemic conditions. Of the three molecules tested, results showed the negative effects of diabetes on capillary density could be overcome only by vascular endothelial growth factor (VEGF) overexpression. This suggests proangiogenic factors may play a role in patients with diabetes and future trials involving therapeutic angiogenesis should be monitored for hyperglycemic interference.

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Posted by Leah Caracappa on Dec 1, 2008 12:00 AM CST

L Jorge Gonez, Gaetano Naselli, Ilia Banakh, Hideo Niwa, and Leonard C Harrison

Steroid hormones have been shown to rapidly modify cell function by binding to surface membrane receptors. In a screen for genes differentially expressed in mouse pancreatic β-cells, Góñez et al. identified a candidate steroid membrane receptor, the progestin and adipoQ receptor (PAQR) 10. PAQR10 is structurally related to bacterial hemolysins, pore-forming virulence factors that target mitochondria and regulate apoptosis. Góñez et al.propose PAQR10 may act at the level of the mitochondrion to regulate pancreatic endocrine cell development and survival, and further studies are likely to establish a key role of PAQR10 in pancreatic β-cell biology.

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Posted by Leah Caracappa on Nov 5, 2008 12:00 AM CST

Fariba Moeinpour, Mashkoor A Choudhry, Luiz F Poli de Figueiredo, Kirby I Bland, and Irshad Chaudry

Sex hormones are known to modulate immune function in animals and humans under normal conditions as well as under stress.  Administration of estrogen following trauma-hemorrhage attenuates the elevation of cytokine production and mitogen-activated protein kinase.  Whether the beneficial effects of estrogen are mediated by estrogen receptor ER-α or ER-β remains unknown. In this work, Moeinpour et al. sought to determine which estrogen receptor was responsible for the salutary effects in a model of trauma-hemorrhage. Using an agonist strategy to isolate receptor subtypes, Moeinpour et al. determined that both ER-α and ER-β contribute to the beneficial effects of estrogen on keratinocytes after trauma-hemorrhage. 

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Posted by Leah Caracappa on Nov 4, 2008 12:00 AM CST

Manuela Mengozzi, Ilaria Cervellini, Paolo Bigini, Sara Martone, Antonella Biondi, Rosetta Pedotti, Barbara Gallo, Sara Barbera, Tiziana Mennini, Mariaserena Boraso, Marina Marinovich, Edwige Petit, Myriam Bernaudin, Roberto Bianchi, Barbara Viviani, and Pietro Ghezzi

Systemically administered erythropoietin (EPO) crosses the blood brain barrier and is protective in several animal models of disease. Endogenous EPO is induced by hypoxic or ischemic injury, however, little is known regarding the expression of endogenous EPO in central nervous system (CNS) diseases.  Mengozzi et al. investigated the expression of EPO in the spinal cord using models of experimental autoimmune encephalomyelitis (EAE), representative of multiple sclerosis.  Their findings indicate EPO is induced in EAE and is negatively regulated by interferon gamma and tumor necrosis factor. This cross-talk between EPO and inflammatory cytokines in the CNS may have important implications in disease pathogenesis. Therapeutic exploitation strategies could be aimed at upregulating the endogenous EPO-mediated protective response.

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Posted by Leah Caracappa on Nov 3, 2008 12:00 AM CST
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