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Ncement in 39 cardiac transplant patients: prevalence, pattern, and extent Craig RL Butler1, Andreas Kumar2, Mustafa Toma1, Richard Thompson1, Matthias Friedrich3 and David Ian Paterson1 1 University of Alberta, Edmonton, AB, Canada 2 University of Calgary, Calgary, AB, Canada 3 Stephenson Cardiovascular MR Center, Calgary, AB, CanadaJournal of Cardiovascular Magnetic Resonance 2009, 11(Suppl 1):O
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Inase suppressor of Ras 1 (CNKSR1)* Correspondence: rudloffu@mail.nih.gov Equal contributors 1 Thoracic and Gastrointestinal Oncology Branch, Gastrointestinal Oncology Section, Investigator Center for Cancer Research, National Cancer Institute, Building 10 - Hatfield CRC, Room 4-5950, Bethesda, MD 20892, USA Full list of author information is available at the end of the article?The Author(s). 201
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Inase suppressor of Ras 1 (CNKSR1)* Correspondence: rudloffu@mail.nih.gov Equal contributors 1 Thoracic and Gastrointestinal Oncology Branch, Gastrointestinal Oncology Section, Investigator Center for Cancer Research, National Cancer Institute, Building 10 - Hatfield CRC, Room 4-5950, Bethesda, MD 20892, USA Full list of author information is available at the end of the article?The Author(s). 201
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Infection, typically increases, in both strains of mice (Table 3). The first group of note includes betaactin, myosin IIB (a non-muscle myosin), creatine kinase M, and Rho GDP dissociation inhibitor-alpha. All of these are proteins that play a role in phagocytosis [36] and are increased in both strains. These increases could be related to the presence of increased numbers of phagocytic cells to co
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BMed PMID: 25633035; PMCID: PMC4333488. 37. Golebski K, van Egmond D, de Groot EJ, Roschmann KI, Fokkens WJ, van Drunen CM. EGR-1 and DUSP-1 are important negative regulators of proallergic responses in airway epithelium. Mol Immunol. 2015;65(1):43-50. doi: 10.1016/j.molimm.2014.12.011. PubMed 38. Salotti J, Sakchaisri K, Tourtellotte WG, Johnson PF. An Arf-Egr-C/EBPbeta pathway linked to ras-indu
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Inase suppressor of Ras 1 (CNKSR1)* Correspondence: rudloffu@mail.nih.gov Equal contributors 1 Thoracic and Gastrointestinal Oncology Branch, Gastrointestinal Oncology Section, Investigator Center for Cancer Research, National Cancer Institute, Building 10 - Hatfield CRC, Room 4-5950, Bethesda, MD 20892, USA Full list of author information is available at the end of the article?The Author(s). 201
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Mbocytes, and endothelial cells[43]. NS1 is a glycoprotein that is secreted by infected cells, heavily present in patient serum supernatants, lacks a membrane spanning motif, but is not, itself, present in the virus. NS1 is known to be a major immune target and high concentrations of antiNS1 antibodies have been found in severe disease in patient studies[44]. When cells are exposed to NS1 antibodi
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Hway begins with the formation of an antibody C1q complex on the surface of a pathogen or pathogen infected cell. This complex, in turn, activates C2 via serine proteases and is itself also a serine protease[49]. The protein C2a combines with newly cleaved protein C4a to generate a C3 convertase, C2aC4b. C3b forms the central protein complex of the complement system either by binding to complement