Spelling suggestions: "subject:"enternal medicine"" "subject:"enternal edicine""
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Physicians' Role in Research Including Self-ExperimentationEnck, Robert E. 01 October 2012 (has links)
No description available.
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"Good Medicine Always Has a Bitter Taste"Enck, Robert E. 01 August 2012 (has links)
No description available.
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The OODA LoopEnck, Robert E. 01 June 2012 (has links)
No description available.
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Respect for Home Care: A New DirectionEnck, Robert E. 01 February 2012 (has links)
No description available.
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Interesting EKG: All That Looks Saw-Toothed Is Not Flutter.Singh, Balraj, Ramu, Vijay K. 01 February 2012 (has links)
No description available.
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Pacemakers Are for Living--Not for Fiddling!Gangadharan, Venkataramanan, Der, Tatyana, Ramu, Vijay 01 January 2012 (has links)
No description available.
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On Being a Doctor: Rounding up the Usual Suspects.Peiris, Alan N., Atia, Antwan 01 January 2012 (has links)
No description available.
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A Word From the EditorHamdy, Ronald C. 01 April 2012 (has links)
No description available.
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Chronic Organizing Retroperitoneal Abscess Caused by Klebsiella Oxytoca Masquerading as Sarcoma: Recognition by Diff-Quik Stain on Fna MaterialYoussef, Dima, Shams, Wael, Kareem Abu Malouh, Abdel, Al-Abbadi, Mousa A. 01 August 2012 (has links)
No description available.
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Cross-Talk Between Programmed Death-1 and Suppressor of Cytokine Signaling-1 in Inhibition of IL-12 Production by Monocytes/Macrophages in Hepatitis C Virus InfectionZhang, Ying, Ma, Cheng J., Ni, Lei, Zhang, Chun L., Wu, Xiao Y., Kumaraguru, Uday, Li, Chuan F., Moorman, Jonathan P., Yao, Zhi Q. 01 March 2011 (has links)
Hepatitis C virus (HCV) dysregulates innate immune responses and induces persistent viral infection. We previously demonstrated that HCV core protein impairs IL-12 expression by monocytes/macrophages (M/MΦs) through interaction with a complement receptor gC1qR. Because HCV core-mediated lymphocyte dysregulation occurs through the negative immunomodulators programmed death-1 (PD-1) and suppressor of cytokine signaling-1 (SOCS-1), the aim of this study was to examine their role in HCV core-mediated IL-12 suppression in M/MΦs. We analyzed TLR-stimulated, primary CD14+ M/MΦs from chronically HCV-infected and healthy subjects or the THP-1 cell line for PD-1, SOCS-1, and IL-12 expression following HCV core treatment. M/MΦs from HCV-infected subjects at baseline exhibited comparatively increased PD-1 expression that significantly correlated with the degree of IL-12 inhibition. M/MΦs isolated from healthy and HCV-infected individuals and treated with HCV core protein displayed increased PD-1 and SOCS-1 expression and decreased IL-12 expression, an effect that was also observed in cells treated with gC1qR's ligand, C1q. Blocking gC1qR rescued HCV core-induced PD-1 upregulation and IL-12 suppression, whereas blocking PD-1 signaling enhanced IL-12 production and decreased the expression of SOCS-1 induced by HCV core. Conversely, silencing SOCS-1 expression using small interfering RNAs increased IL-12 expression and inhibited PD-1 upregulation. PD-1 and SOCS-1 were found to associate by coimmunoprecipitation studies, and blocking PD-1 or silencing SOCS-1 in M/MΦ led to activation of STAT-1 during TLR-stimulated IL-12 production. These data suggested that HCV core/gC1qR engagement on M/MΦs triggers the expression of PD-1 and SOCS-1, which can associate to deliver negative signaling to TLR-mediated pathways controlling expression of IL-12, a key cytokine linking innate and adaptive immunity.
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