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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 ?
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

Karla C S Queiroz, Cornelis van 't Veer, Yascha van den Berg, JanWillem Duitman, Henri H Versteeg, Hella L Aberson, Angelique P Groot, Marleen I Verstege, Joris J T H Roelofs, Anje A te Velde, and C Arnold Spek

Inflammatory bowel diseases are chronic disorders of the gastrointestinal tract which generally lead to mucosal disruption and ulceration. The etiology and pathogenesis of these diseases remain only moderately understood. Tissue factor (TF) traditionally initiates blood coagulation, but also serves an important role in the body's inflammatory process. Considering the pivotal role of coagulation in inflammatory bowel disease, Queiroz et al. assessed whether genetic ablation of TF might limit experimental colitis. Genetic ablation reduced colitis severity and data suggest TF plays a detrimental role in experimental colitis via enhancement of granulocyte migration into the colon. This process may have pivotal relevance in the clinical setting of inflammatory bowel disease.

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Posted by Leah Caracappa on Oct 14, 2011 12:00 AM CDT
Noemí Fabelo, Virginia Martín, Gabriel Santpere, Raquel Marín, Laia Torrent, Isidre Ferrer, and Mario Díaz

Parkinson's disease (PD) is a multisystemic, neurodegenerative disease. Classical PD is manifested as a complex motor disorder, while incidental PD (iPD) does not show motor symptoms, and is usually discovered post-mortem. Lipid rafts are microdomains that provide a microenvironment to promote protein-lipid and protein-protein interactions. Recent evidence has demonstrated molecular alterations in PD contribute to abnormal levels of fatty acids in the frontal cortex. Whether altered lipid composition affects highly specialized structures such as lipid rafts is not known. Fabelo et al. purified lipid rafts from the human frontal cortex of normal, early motor stages of PD and iPD subjects and analyzed the lipid composition. The data point to modification of fatty acid contents in polar lipids from lipid rafts in PD and iPD, and indicate these lipid raft abnormalities occur at early stages of PD pathology. Such physicochemical alterations could have a profound impact in lipid raft thermodynamic properties, spatial organization and signal transduction.

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Posted by Leah Caracappa on Oct 13, 2011 12:00 AM CDT
Sae-Won Lee, Joo-Yun Won, Hae-Young Lee, Ho-Jae Lee, Seock-Won Youn, Ji-Young Lee, Chung-Hyun Cho, Hyun-Jai Cho, Seil Oh, In-Ho Chae, and Hyo-Soo Kim

Prolonged periods of myocardial ischemia may lead to irreversible cardiomyocyte and vasculature loss, which can disrupt cardiac integrity and function. Early reperfusion is the dominant clinical strategy for myocardial salvage. Unfortunately, while early reperfusion is essential for tissue salvage, it also causes myocardial and vascular injury. Angopoietin-1 is an endothelial-specific angiogenic factor known to regulate vessel formation and maintenance of endothelial integrity. The possible effect of angiopoietin-1 on cardiomyocytes and vascular cells during reperfusion has not yet been investigated. To test the protective mechanism of angiopoietin-1, Lee et al. employed a model of myocardial ischemia/reperfusion. The authors show angiopoietin-1 promotes both endothelial integrity and cardiomyocyte survival. The data suggest angopoietin-1 is a prospective therapeutic candidate to preserve myocardial function after reperfusion injury.

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upplementary data PDF
Posted by Leah Caracappa on Oct 12, 2011 12:00 AM CDT
Fahim Atif, Iqbal Sayeed, Seema Yousuf, Tauheed Ishrat, Fang Hua, Jun Wang, Daniel J Brat, and Donald G Stein

Neuroblastoma is the most common tumor among children under one year, accounting for about 28% of all cancers diagnosed in European and US infants. A safe and effective drug without the adverse side effects associated with radiation or chemotherapy has not yet been found. Studies suggest that progesterone (P4) may have selectively toxic effects. Atif et al. investigated the antitumorogenic effects of P4 in a human neuroblastoma cell line and in a xenograft model of neuroblastoma. Their work showed that at high doses, P4 significantly decreased cell viability and did not induce cell death in healthy primary cortical neurons or human fibroblasts. These results indicate that at high doses, P4 effectively inhibits the growth of solid neuroblastoma tumors while having selective toxicity and a high margin of safety. This suggests P4 may be a possible candidate for clinical treatment of neuroblastoma.

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Posted by Leah Caracappa on Oct 11, 2011 12:00 AM CDT
Wayne W Chaung, Rongqian Wu, Youxin Ji, Zhimin Wang, Weifeng Dong, Cletus Cheyuo, Lei Qi, Xiaoling Qiang, Haichao Wang, and Ping Wang

Stroke is one of the foremost causes of death in the world and the main cause of acquired adult disability worldwide. Brain injury after acute stroke is mediated in part by ischemia-elicited inflammatory responses. Adrenomedullin (AM), a vasoactive hormone, counterbalances inflammatory responses, however, regulation of AM activity in ischemic stroke remains largely unexplored. Chaung et al. used a model of focal cerebral ischemia, induced by permanent middle cerebral artery occlusion, to investigate the possible benefits of AM. The authors found plasma levels of AM increased significantly after stroke, while plasma levels of AM binding protein (AMBP-1) decreased. Additional treatment with AM and AMBP-1 reduced neuron apoptosis and morphological damage. The data indicate human AM/AMBP-1 could be used to reduce stroke-induced brain injury and may warrant further development.

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Posted by Leah Caracappa on Oct 10, 2011 12:00 AM CDT
Yi-Chu Liao, Yung-Song Wang, Yuh-Cherng Guo, Kouichi Ozaki, Toshihiro Tanaka, Hsiu-Fen Lin, Ming-Hong Chang, Ku-Chung Chen, Ming-Lung Yu, Sheng-Hsiung Sheu, and Suh-Hang Hank Juo

Ultrasound measurements of intima-media thickness and plaque at the carotid arteries are predictors of future cardiovascular risks, including myocardial infarction (MI) and atherosclerosis. However, these two phenotypes represent distinct traits with unique relationships to atherosclerosis. The BRCA-1 associated protein gene (BRAP) was recently identified as a susceptibility gene for myocardial infarction. In this study, Liao et al. studied the association between BRAP polymorphism and carotid atherosclerosis as well as the mechanism beneath the pro-atherogenic effect. They studied the single nucleotide polymorphism (SNP) rs11066001 because it has been shown to correlate most strongly with MI risks. Inflammatory stimuli up-regulated BRAP expression, while BRAP activated the inflammatory cascades by regulating the NF-ĸB nuclear translocation. These results indicate that the SNP in BRAP confers a risk for carotid atherosclerosis. This work could aid further studies to identify treatment strategies for individuals at risk of atherosclerosis.

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Supplemental Data


Posted by Leah Caracappa on Oct 9, 2011 12:00 AM CDT
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
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