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Articles by S Moore
Total Records ( 4 ) for S Moore
  W Gu , K. A Winters , A. S Motani , R Komorowski , Y Zhang , Q Liu , X Wu , I. C Rulifson , G Sivits , M Graham , H Yan , P Wang , S Moore , T Meng , R. A Lindberg and M. M. Veniant
 

Antagonism of the glucagon receptor (GCGR) is associated with increased circulating levels of glucagon-like peptide-1 (GLP-1). To investigate the contribution of GLP-1 to the antidiabetic actions of GCGR antagonism, we administered an anti-GCGR monoclonal antibody (mAb B) to wild-type mice and GLP-1 receptor knockout (GLP-1R KO) mice. Treatment of wild-type mice with mAb B lowered fasting blood glucose, improved glucose tolerance, and enhanced glucose-stimulated insulin secretion during an intraperitoneal glucose tolerance test (ipGTT). In contrast, treatment of GLP-1R KO mice with mAb B had little efficacy during an ipGTT. Furthermore, pretreatment with the GLP-1R antagonist exendin-(9–39) diminished the antihyperglycemic effects of mAb B in wild-type mice. To determine the mechanism whereby mAb B improves glucose tolerance, we generated a monoclonal antibody that specifically antagonizes the human GLP-1R. Using a human islet transplanted mouse model, we demonstrated that pancreatic islet GLP-1R signaling is required for the full efficacy of the GCGR antagonist. To identify the source of the elevated GLP-1 observed in GCGR mAb-treated mice, we measured active GLP-1 content in pancreas and intestine from db/db mice treated with anti-GCGR mAb for 8 wk. Elevated GLP-1 in GCGR mAb-treated mice was predominantly derived from increased pancreatic GLP-1 synthesis and processing. All together, these data show that pancreatic GLP-1 is a significant contributor to the glucose-lowering effects observed in response to GCGR antagonist treatment.

  S Moore and J. Turnbull
 

The Court of Appeal for England and Wales provides the first clear guidance on the timing and substantive requirements for applying for and obtaining a paediatric extension to an existing Supplementary Protection Certificate (‘SPC’).

  S Moore and A. Bailey
 

The Court of Appeal confirms first instance decision that a patent application needs to disclose sufficiently specific and credible ways of exploiting the invention to satisfy the requirement for industrial applicability.

  N Goonetilleke , M. K.P Liu , J. F Salazar Gonzalez , G Ferrari , E Giorgi , V. V Ganusov , B. F Keele , G. H Learn , E. L Turnbull , M. G Salazar , K. J Weinhold , S Moore , Letvin CHAVI Clinical Core B , B. F Haynes , M. S Cohen , P Hraber , T Bhattacharya , P Borrow , A. S Perelson , B. H Hahn , G. M Shaw , B. T Korber and A. J. McMichael
 

Identification of the transmitted/founder virus makes possible, for the first time, a genome-wide analysis of host immune responses against the infecting HIV-1 proteome. A complete dissection was made of the primary HIV-1–specific T cell response induced in three acutely infected patients. Cellular assays, together with new algorithms which identify sites of positive selection in the virus genome, showed that primary HIV-1–specific T cells rapidly select escape mutations concurrent with falling virus load in acute infection. Kinetic analysis and mathematical modeling of virus immune escape showed that the contribution of CD8 T cell–mediated killing of productively infected cells was earlier and much greater than previously recognized and that it contributed to the initial decline of plasma virus in acute infection. After virus escape, these first T cell responses often rapidly waned, leaving or being succeeded by T cell responses to epitopes which escaped more slowly or were invariant. These latter responses are likely to be important in maintaining the already established virus set point. In addition to mutations selected by T cells, there were other selected regions that accrued mutations more gradually but were not associated with a T cell response. These included clusters of mutations in envelope that were targeted by NAbs, a few isolated sites that reverted to the consensus sequence, and bystander mutations in linkage with T cell–driven escape.

 
 
 
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