988 resultados para Wigan, Arthur Cleveland, b. 1815,


Relevância:

30.00% 30.00%

Publicador:

Resumo:

Appendices: A. Chronological summary of principal events related to Mexican history.--B. Bibliography.--C. Notes on the historical geography of Mexico.

Relevância:

30.00% 30.00%

Publicador:

Resumo:

Polish and French.

Relevância:

30.00% 30.00%

Publicador:

Resumo:

Mode of access: Internet.

Relevância:

30.00% 30.00%

Publicador:

Resumo:

pt. 1. Introduction and text and appendices.--pt. 2. Translation and notes.

Relevância:

30.00% 30.00%

Publicador:

Resumo:

Mode of access: Internet.

Relevância:

30.00% 30.00%

Publicador:

Resumo:

<b>Top Row:b> Charles Smeltzer, asst. mngr. C.L. Thomas, William Pearson, Edmund Sheilds, Holbrook Cleveland, Charles MacPherran

<b>Middle Row:b> Edward Spurney, Sherman Spitzer, Albert Jefferis, Frank Crawford, George Rich, Arthur Seymour

<b>Front Row:b> (on ground) Ralph Russell, Martin Banks, Herman Krogman, Thomas Griffin

Relevância:

30.00% 30.00%

Publicador:

Resumo:

Bound with Berton, J. B. Précis historique, militaire et critique des batailles de Fleurus et de Waterloo. Paris, 1818. Grouchy, E. Observations sur la relation de la campagne de 1815. Paris, 1819. Gérard, E. M. Quelques documens, sur la bataille de Waterloo. Paris, 1829. Grouchy, E. Fragments historiques relatifs a la campagne de 1815 et a la bataille de Waterloo. Paris, 1829. Gérard, É. M. Dernières observations sur les opérations de l'aile droite de l'armée française a la bataille de Waterloo. Paris, 1830.

Relevância:

30.00% 30.00%

Publicador:

Resumo:

"First edition."

Relevância:

30.00% 30.00%

Publicador:

Resumo:

The glucagon-like peptide 1 (GLP-1) receptor is a class B G protein-coupled receptor (GPCR) that is a key target for treatments for type II diabetes and obesity. This receptor, like other class B GPCRs, displays biased agonism, though the physiologic significance of this is yet to be elucidated. Previous work has implicated R2.60190 , N3.43240 , Q7.49394 , and H6.52363 as key residues involved in peptide-mediated biased agonism, with R2.60190 , N3.43240 , and Q7.49394 predicted to form a polar interaction network. In this study, we used novel insight gained from recent crystal structures of the transmembrane domains of the glucagon and corticotropin releasing factor 1 (CRF1) receptors to develop improved models of the GLP-1 receptor that predict additional key molecular interactions with these amino acids. We have introduced E6.53364 A, N3.43240 Q, Q7.49493N, and N3.43240 Q/Q7.49 Q/Q7.49493N mutations to probe the role of predicted H-bonding and charge-charge interactions in driving cAMP, calcium, or extracellular signal-regulated kinase (ERK) signaling. A polar interaction between E6.53364 and R2.60190 was predicted to be important for GLP-1- and exendin-4-, but not oxyntomodulin-mediated cAMP formation and also ERK1/2 phosphorylation. In contrast, Q7.49394 , but not R2.60190 /E6.53364 was critical for calcium mobilization for all three peptides. Mutation of N3.43240 and Q7.49394 had differential effects on individual peptides, providing evidence for molecular differences in activation transition. Collectively, this work expands our understanding of peptide-mediated signaling from the GLP-1 receptor and the key role that the central polar network plays in these events.

Relevância:

30.00% 30.00%

Publicador:

Resumo:

Clostridium difficile is a leading cause of nosocomial infections, causing a spectrum of diseases ranging from diarrhoea to pseudomembranous colitis triggered by a range of virulence factors including C. difficile toxins A (TcdA) and B (TcdB). TcdA and TcdB are monoglucosyltransferases that irreversibly glycosylate small Rho GTPases, inhibiting their ability to interact with their effectors, guanine nucleotide exchange factors, and membrane partners, leading to disruption of downstream signalling pathways and cell death. In addition, TcdB targets the mitochondria, inducing the intrinsic apoptotic pathway resulting in TcdB-mediated apoptosis. Modulation of apoptosis is a common strategy used by infectious agents. Recently, we have shown that the enteropathogenic Escherichia coli (EPEC) type III secretion system effector NleH has a broad-range anti-apoptotic activity. In this study we examined the effects of NleH on cells challenged with TcdB. During infection with wild-type EPEC, NleH inhibited TcdB-induced apoptosis at both low and high toxin concentrations. Transfected nleH1 alone was sufficient to block TcdB-induced cell rounding, nuclear condensation, mitochondrial swelling and lysis, and activation of caspase-3. These results show that NleH acts via a global anti-apoptotic pathway.