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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

Frieda A Koopman, Susanne P Stoof, Rainer H Straub, Marjolein A van Maanen, Margriet J Vervoordeldonk, and Paul P Tak

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 9, 2011 12:00 AM CDT
Abid A Kazi, Ly Hong-Brown, Susan M Lang, and Charles H Lang

Skeletal muscle serves as the largest protein reservoir in the body balancing between rates of protein synthesis and degradation. This carefully regulated process is disrupted in muscle wasting associated with catabolic insults such as sepsis, alcohol abuse and aging. Deptor is an mTOR (mammalian target of rapamycin) kinase–binding protein that affects cell metabolism. Kazi et al. used a Deptor knockdown (KD) model to investigate its role in myocytes and in muscle. Data show Deptor is an important negative regulator of protein metabolism in myocytes and decreased expression was sufficient to ameliorate muscle atrophy caused by immobilization. Understanding the role of Deptor in myocyte cell cycle and proliferation and the ability of this protein to regulate protein synthesis may prove important in designing new strategies to manage muscle wasting.

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Supplemental Data


Posted by Leah Caracappa on Sep 8, 2011 12:00 AM CDT
Saman Eghtesad, Siddharth Jhunjhunwala, Steven R Little, and Paula R Clemens

Duchenne muscular dystrophy (DMD) is an X-linked, lethal degenerative disease caused by mutations in the dystrophin gene. This results in the absence of a functional dystrophin protein and leads to necrosis and inflammation in skeletal muscle tissue. Research suggests that down-regulation of the immune system in a dystrophic setting may have therapeutic effects. Eghtesad et al. studied the effect of rapamycin (RAPA) treatment on dystrophic pathology as well as the activation of mTOR (the mammalian target of RAPA) in tibialis anterior (TA) and diaphragm (Dia) muscles. Their work showed that RAPA treatment decreased inflammation and decreased necrosis in dystrophic muscle tissue. Their results also showed differences in mTOR activation between TA and Dia muscles, adding to the molecular understanding of the dystrophic phenotype.

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Posted by Leah Caracappa on Sep 7, 2011 12:00 AM CDT
Diahnn Futalan, Chien-Tze Huang, Ingo G H Schmidt-Wolf, Marie Larsson, and Davorka Messmer

Dendritic cells (DCs) are potent antigen-presenting cells that are crucial for immune responses. While DC-based adoptive tumor immunotherapy approaches have shown promising results, the incidence of tumor regression is low and DCs with more potent Th1 potential are needed. DCs are commonly differentiated under atmospheric oxygen conditions in incubators; however, in this work Futalan et al. investigated whether differentiation and maturation under physiological levels could produce more potent DCs. They found immature DCs differentiated in this manner showed a small but significant reduction in their endocytic capacity. There was no difference in T cell activation, but DCs did secrete higher levels of IL-12(p70). This may have implications for the use of ex vivo generated DCs in clinical studies since DCs differentiated at the physiological level could increase Th1 potential in vivo.

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Posted by Leah Caracappa on Sep 6, 2011 12:00 AM CDT
Alessandro Michelutti, Elisa Gremese, Francesca Morassi, Luca Petricca, Vincenzo Arena, Barbara Tolusso, Stefano Alivernini, Giusy Peluso, Silvia Laura Bosello, and Gianfranco Ferraccioli

Rheumatoid arthritis (RA) is a systemic autoimmune chronic inflammatory disease that attacks the joints, synovial  tissue and internal organs. RAcan lead to long periods of fatigue, severe pain, and decreased mobility. Research indicates that B cells are central in autoimmune diseases and that depletion of these B cells can play a therapeutic role. Michelutti et al. studied B-cell subset distribution in the peripheral blood and synovial fluid of seropositive, seronegative, and non-RA patients in order to determine whether there was a compartmentalization of subsets, specifically in seropositive subjects. Their work showed a subset of B cells expressing memory markers (CD27/IgD) and ZAP70 accumulate preferentially in the joints of RA patients but that no difference exists between seropositive and seronegative RA patients. This work may aid understanding of how B-cell depletion therapy could be used in RA.

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Supplementary Data

Posted by Leah Caracappa on Sep 5, 2011 12:00 AM CDT
Hogyoung Kim, Amarjit S Naura, Youssef Errami, Jihang Ju, and A Hamid Boulares

Poly(ADP-ribose) polymerase-1 (PARP-1) is emerging as a viable therapeutic target for the treatment of inflammatory disease and numerous types of cancers. Kim et al. investigated whether cordycepin, a natural product derived from Cordyceps militaris, blocks acute lung injury–associated inflammatory responses and expression of related genes by testing whether such effects were related to PARP inhibition. They also examined whether the potential PARP inhibition trait promotes the killing of BRCA1-deficient breast cancer cells. Their results demonstrated that cordycepin differentially affects the expression of adhesion molecules, suggesting the drug may be acting as a PARP inhibitor.  This was confirmed using a cell-free system with purified recombinant PARP-1. The authors indicate cordycepin is a promising drug for the treatment of breast and ovarian cancers.  Furthermore, they suggest the antiinflammatory characteristics of cordycepin could counteract any inflammatory processes triggered by traditional chemotherapeutic drugs.

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Supplementary Data
Posted by Leah Caracappa on Sep 4, 2011 12:00 AM CDT
Nimesh SA Patel, Kiran K Nandra, Michael Brines, Massimo Collino, WS Fred Wong, Amar Kapoor, Elisa Benetti, Fera Y Goh, Roberto Fantozzi, Anthony Cerami, and Christoph Thiemermann

Severe hemorrhage accounts for nearly 40% of all trauma deaths and is the leading cause of preventable trauma death. Recent studies have shown erythropoietin (EPO) has cytoprotective effects in a wide variety of tissues. However, it has also been shown to have serious side effects. Patel et al. investigated the effect of pyroglutamate helix B-surface peptide (pHBSP) – a non-erythropoietic, tissue protective peptide that mimics the 3D structure of EPO – on organ injury/dysfunction and inflammation in a model of severe hemorrhagic shock. Their work showed that pHBSP protects against multiple organ injury/dysfunction and inflammation through a mechanism that may involve activation of Akt and endothelial nitric oxide synthase, and inhibition of glycogen synthase kinase-3β and nuclear factor-ĸB. This suggests non-hematopoietic analogues of EPO may be viable treatment tools to mimic the tissue-protective effects of EPO without causing the serious well-documented side effects.

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Posted by Leah Caracappa on Sep 3, 2011 12:00 AM CDT
Florian Barthélémy, Nicolas Wein, Martin Krahn, Nicolas Lévy, and Marc Bartoli

Dysferlinopatheies are autosomal recessive disorders caused by mutations in the DYSF gene, encoding the dysferlin protein. DYSF mutations lead to a wide range of muscular phenotypes, many resulting in muscular dystrophy. Symptoms generally appear at the end of childhood, and while disease progression is typically slow, walking impairments eventually result in all cases. In this review, Barthélémy et al. summarize the pathopsysiology of dysferlinopathies and evaluate the therapeutic potential for treatments currently under development. The authors predict advancements in this area will lead to a better understanding of these diseases, enabling the development of appropriate therapeutic strategies based on clinical observations.

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Posted by Leah Caracappa on Sep 2, 2011 12:00 AM CDT
Mariam Al-Omari, Elena Korenbaum, Matthias Ballmaier, Ulrich Lehmann, Danny Jonigk,
Dietmar J Manstein, Tobias Welte, Ravi Mahadeva, and Sabina Janciauskiene

An inflammatory response often relies on rapid neutrophil recruitment to sites of injury or infection. While essential for host defense against pathogenic stimuli, this recruitment may cause chronic tissue destruction. Understanding the mechanisms underlying neutrophil recruitment and regulation is important for the prevention of neutrophil-induced tissue injury and the resulting organ dysfunction. Al-Omari et al. examined mechanisms related to the effect of acute phase protein α1-antitrypsin (AAT) on neutrophil responses. They found a previously unknown function of AAT, which inactivates calpain I and induces a rapid cell polarization and random migration. This inactivation may offer substantial protection against neutrophilic inflammation. These results broaden our understanding of the regulation of calpain-related neutrophil functional activities, and provide the impetus for new studies to define the role of AAT and other acute phase proteins in health and disease.

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Posted by Leah Caracappa on Sep 1, 2011 12:00 AM CDT

Mary Leung, David Rosen, Scott Fields, Alessandra Cesano, and Daniel R Budman

The BRCA genes are commonly linked with hereditary breast and ovarian cancers with a potential lifetime risk as high as 50% and 40% respectively. Hereditary breast cancers linked to these genes exhibit defective homologous DNA repair (HR) and patients with either BRCA-1 or BRCA-2 defective genes have genomic instability. As a result, the cell depends on alternate DNA repair processes, such as base excision repair (BER), which requires Poly(ADP-ribose) polymerase 1 (PARP-1). In this review, Leung et al. discuss the current state of PARP-1 understanding and suggest ways in which inhibition of this gene may contribute to enhanced efficacy of a wide range of chemotherapeutics.

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Posted by Leah Caracappa on Aug 16, 2011 12:00 AM CDT
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