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I am not able to find the file with supplementary methods of the present paper. Can somebody help me to find it ?
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i could not find the supplementary data for this paper. please help me find them. thank you
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Articles from this Volume

Hanna Schierbeck, Peter Lundbäck, Karin Palmblad, Lena Klevenvall, Helena Erlandsson-Harris, Ulf Andersson, and Lars Ottosson

Chronic arthritides are inflammatory diseases associated with decreased quality of life and disability due to fatigue, pain and articular tissue destruction. Despite advances in the treatment of chronic arthritis, there are still many patients with unmet needs. HMGB1 is a DNA-binding nuclear protein that has been demonstrated as a pathogenic factor in many inflammatory conditions including arthritis. HMGB1-specific polyclonal antibody treatment has been shown to alleviate disease and protect against cartilage and bone destruction. Schierbeck et al. conducted the first study to evaluate the potential of a monoclonal anti-HMGB1 antibody to ameliorate arthritis. Their results showed administration of anti-HMGB1 mAb therapy to two different models significantly ameliorated the clinical course of both types of arthritis and partially prevented joint destruction. This study may aid in further development of an anti-HMGB1 mAb, which can help diverse conditions including arthritis, sepsis, organ transplantation, and stroke.

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Posted by Leah Caracappa on Oct 6, 2011 12:00 AM CDT
Christoph L Menzel, Qian Sun, Patricia A Loughran, Hans-Christoph Pape, Timothy R Billiar, and Melanie J Scott

Adaptive immune responses are induced in the liver after major stresses such as hemorrhagic shock (HS) and trauma. There is emerging evidence that the inflammasome, the multiprotein platform that induces caspase-1 activation and promotes IL1β and IL18 processing, is activated in response to cellular oxidative stress. Menzel et al. investigated inflammatory responses and end-organ injury in a model of HS with trauma.  Their results demonstrated that a lack of caspase-1 led to an increased proinflammatory cytokine profile, increased hepatocellular death and cellular damage.  These data suggest that caspase-1 balances the posttraumatic inflammatory response and is an important component of hepatocellular survival.  These findings shed new light on the role of caspase-1 in the setting of severe trauma and may lead to new therapeutic approaches for severely injured patients who are prone to multiple organ failure.

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Posted by Leah Caracappa on Oct 5, 2011 12:00 AM CDT
Valérie Vingtdeux, Pallavi Chandakkar, Haitian Zhao, Peter Davies, and Philippe Marambaud

Obesity is an increasing problem in today's world, particularly in the United States. AMP-activated protein kinase (AMPK) is a sensor and regulator of cellular energy metabolism and a potential drug target in metabolic diseases, such as diabetes and obesity. Studies show pharmacological activation of AMPK can be achieved using resveratrol, a natural polyphenol associated with protective effects against the deregulation of energy homeostasis. Vingtdeux et al. evaluated the antiadipogenic potential of resveratrol analogues. Their work identified novel-small molecules with potent inhibitory effects against adipocyte differentiation in vitro and weight gain. The analogues triggered early activation of AMPK in proliferating preadipocytes without inducing toxicity. These results identify novel small-molecule activators of AMPK as potent inhibitors of adipogenesis and thus show therapeutic potential against obesity.

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Posted by Leah Caracappa on Oct 4, 2011 12:00 AM CDT
Stefano Toldo, Mariarosaria Boccellino, Barbara Rinaldi, Ignacio M Seropian, Eleonora Mezzaroma, Anna Severino, Lucio Quagliuolo, Benjamin W Van Tassell, Raffaele Marfella, Giuseppe Paolisso, Francesco Rossi, Ramesh Natarajan, Norbert Voelkel, Antonio Abbate, Filippo Crea, and Alfonso Baldi

Ischemic heart disease is the most frequent cause of cardiovascular mortality worldwide. Individuals with diabetes have an increased risk of heart failure, in part explained by endoplasmic reticulum stress and apoptosis. Studies have shown protein disulfide isomerase (PDI) prevents stressed cardiomyocytes apoptosis. Toldo et al. used a model of diabetes to study PDI expression and its red-ox state in order to provide information regarding the lack of protective action of PDI during diabetes. Their results illustrated that diabetic models had a greater number of TUNEL positive cells than non-diabetic controls despite a greater myocardial PDI expression, suggesting altered PDI function. Diabetic models also showed signs of an altered PDI redox state. However, the authors found that restoration of the normal redox state of PDI by strategies like dehyrdoascorbate (DHA) administration may result in a more favorable cardiac remodeling.

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Posted by Leah Caracappa on Oct 3, 2011 12:00 AM CDT
Galit Shahaf, Hadas Moser, Eyal Ozeri, Mark Mizrahi, Avishag Abecassis, and Eli C Lewis

With current treatments, type 1 diabetes patients often endure uncontrolled glucose spikes and the risk of long-term complications. Pancreatic islet transplantation has been evaluated as a procedure that could enable patients to regain physiological glucose control, but the immunosuppressive protocol that accompanies this procedure results in the exposure of grafted cells to an unopposed inflammatory environment. Alpha-1 antitrypsin (AAT), the primary protease inhibitor in circulation, rises during acute phase responses and possesses anti-inflammatory properties. Shahaf et al. used gene-based human-AAT (hAAT) therapy in preclinical models to examine the ability of circulating single-isoform gene-delivered hAAT to protect islet allografts from acute rejection. Their results suggest that human AAT, both as the injectable clinical-grade material and also as a gene-delivered product, is able to diminish the alloimmune response by diminishing inflammatory mediators in the graft tissue. This study may aid future studies in examining the structure-function attributes of the islet protective activities of AAT.

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Supplementary Data

Posted by Leah Caracappa on Oct 2, 2011 12:00 AM CDT
Juan Wang, Feng Shuang An, Wei Zhang, Lei Gong, Shu Jian Wei, Wei d*** Qin, Xu Ping Wang, Yu Xia Zhao, Yun Zhang, Cheng Zhang, and Ming-Xiang Zhang

Atherosclerosis begins as local inflammation of arterial walls at sites of disturbed flow. c-Jun NH2-terminal kinase (JNK) is a major regulator of flow-dependent gene expression in atherosclerosis. Wang et al. studied the effect of JNK on low shear stress-induced atherogenesis in preclinical models and investigated the potential mechanism in human umbilical vein endothelial cells (HUVECs). In HUVECs, downregulation of JNK by si-JNK or an inhibitior both attenuated NF-ĸB activity and VCAM-1 expression induced by low shear stress, suggesting that JNK may play a critical role in low shear stress-induced atherogenesis at least in part by modulating NF-ĸB activity and VCAM-1 expression. These findings may aid in the design of therapeutic tools to protect arteries against shear stress-induced inflammation in atherosclerosis.

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Posted by Leah Caracappa on Oct 1, 2011 12:00 AM CDT
Babett Bartling, Hans-Stefan Hofmann, Antonia Sohst, Yvonne Hatzky, Veronika Somoza, Rolf-Edgar Silber, and Andreas Simm

Despite surgical removal of non–small cell lung carcinomas (NSCLCs), many patients die after treatment due to recurring tumors. Staging of NSCLC patients by TNM classification is inadequate in determining proper prognosis and treatment options after surgery. Bartling et al. studied the prognostic relevance of a simple fluorescence spectrometry test of patient plasma samples that detects the fluorescence of AGEs (advanced glycation end-products). NSCLC patients with high AGE-related plasma fluorescence were characterized by later tumor recurrence after surgery as well as a higher survival rate compared with patients with low plasma fluorescence. The anti-tumorigenic effect of circulating AGEs on NSCLC growth was confirmed in vitro and in vivo. The authors suggest AGE-related plasma fluorescence is a simple predictor of NSCLC patient outcome after curative surgery, and that additional analyses of individual plasma fluorescence may support this assessment of patient health.

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Posted by Leah Caracappa on Sep 13, 2011 12:00 AM CDT
Jeremy Koppel, Fabien Campagne, Valérie Vingtdeux, Ute Dreses-Werringloer, Michael Ewers, Dan Rujescu, Harald Hampel, Marc L Gordon, Erica Christen, Julien Chapuis, Blaine S Greenwald, Peter Davies, and Philippe Marambaud

Alzheimer's disease (AD), which affects as many as 5.1 million Americans, is a progressive neurodegenerative disorder characterized by the presence of senile plaques in the brain.  Senile plaques result from the deposition of amyloid-β (Aβ), a series of peptides produced by sequential endoproteolysis of the amyloid precursor protein.  Research indicates the P86L polymorphism in the CLAHM1 gene may influence Aβ metabolism in vivo by increasing Aβ levels in human cerebrospinal fluid (CSF).Koppel et al. analyzed the association of CALHM1 P86L with CSF Aβ in samples from 203 AD cases and 46 young cognitively healthy individuals with a family history of AD. Their work showed CALHM1 modulates CSF Aβ levels in presymptomatic individuals, suggesting CALHM1 is involved in AD pathogenesis.  This work provides support for the use of CSF Aβ measurements as a quantitative endophenotype for identifying or validating AD risk genes in populations of individuals with pre-clinical AD.

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Posted by Leah Caracappa on Sep 12, 2011 12:00 AM CDT

Prithi Rajan

A more global understanding of the transcriptional, post-transcriptional and epigenetic events that orchestrate cellular events may lead to greater control over the management of human disease. An example of this comes with signal transducers and activators of transcription 3 (Stat3), a transcription factor implicated in the development and maintenance of the immune and nervous systems. Dr. Rajan discusses the effects of Stat3 in normal and pathological conditions within the mammalian nervous systems. Concentrations, activation states, and spatial distributions of signaling molecules may participate to create a context in which Stat3 activation can yield different outcomes. An analysis of the context in which Stat3 activation occurs in cellular differentiation, maintenance, cancer and regeneration shows potential as a predictive paradigm, through which new methods for intervention and regulation may be designed.

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Posted by Leah Caracappa on Sep 11, 2011 12:00 AM CDT
Murielle Mimeault and Surinder K Batra

Prostate cancer (PC) is among the most commonly diagnosed malignancies and the second leading cause of cancer-related deaths in men. Although progress in developing early detection tests has led to improved clinical treatments, the progression of locally advanced, invasive and metastatic castration-resistant prostate cancers (CRPCs) usually leads to disease relapse. Drs. Mimeault and Batra reviewed recent advancements in the establishment of the cellular origin of PC as well as key signal transduction elements that may contribute to the acquisition of more malignant phenotypes by PC stem/progenitor cells and their progenies during prostate carcinogenesis, metastases and treatment resistance.

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Posted by Leah Caracappa on Sep 10, 2011 12:00 AM CDT
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