654 resultados para Henninger, Frederick


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William Frederick Haile was born in Putney, Windham County, Vermont on November 4th, 1791. He was raised in Fairfield, Herkimer County, New York. At the age of 21 he entered the United States Army. He served in the War of 1812 as a lieutenant in the 11th United States Infantry. He was severely wounded in the Battle of Lundy’s Lane [not mentioned in this memoir]. After the war he settled in Plattsburgh, New York and became a lawyer. He was a judge from April 1837 to March of 1843. He was also the fifth collector of customs for the District of Champlain. He died on October 1861 at the age of 69. This document was written for the children of William Frederick Haile in January of 1859 [as noted on p.23]. The memoir ends in July of 1814 before the Battle of Lundy’s Lane. Haile’s memoir is laced with names of military personnel and he expresses his opinions freely.

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UANL

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UANL

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UANL

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UANL

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UANL

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UANL

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UANL

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UANL

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UANL

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La méthode de subdivision Catmull-Clark ainsi que la méthode de subdivision Loop sont des normes industrielle de facto. D'autre part, la méthode de subdivision 4-8 est bien adaptée à la subdivision adaptative, parce que cette méthode augmente le nombre de faces ou de sommets par seulement un facteur de 2 à chaque raffinement. Cela promet d'être plus pratique pour atteindre un niveau donné de précision. Dans ce mémoire, nous présenterons une méthode permettant de paramétrer des surfaces de subdivision de la méthode Catmull-Clark et de la méthode 4-8. Par conséquent, de nombreux algorithmes mis au point pour des surfaces paramétriques pourrant être appliqués aux surfaces de subdivision Catmull-Clark et aux surfaces de subdivision 4-8. En particulier, nous pouvons calculer des bornes garanties et réalistes sur les patches, un peu comme les bornes correspondantes données par Wu-Peters pour la méthode de subdivision Loop.

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HIV upregulates cell-surface expression of specific ligands for the activating NKG2D receptor, including ULBP-1, -2, -3, but not MICA or MICB, in infected cells both in vitro and in vivo. However, the viral factor(s) involved in NKG2D ligand expression still remains undefined. HIV-1 Vpr activates the DNA damage/stress-sensing ATR kinase and promotes G2 cell-cycle arrest, conditions known to upregulate NKG2D ligands. We report here that HIV-1 selectively induces cell-surface expression of ULBP-2 in primary CD4+ T-lymphocytes by a process that is Vpr-dependent. Importantly, Vpr enhanced the susceptibility of HIV-1-infected cells to NK cell-mediated killing. Strikingly, Vpr alone was sufficient to upregulate expression of all NKG2D ligands and thus promoted efficient NKG2D-dependent NK cell-mediated killing. Delivery of virion-associated Vpr via defective HIV-1 particles induced analogous biological effects in non-infected target cells, suggesting that Vpr may act similarly beyond infected cells. All these activities relied on Vpr ability to activate the ATR-mediated DNA damage/stress checkpoint. Overall, these results indicate that Vpr is a key determinant responsible for HIV-1-induced upregulation of NKG2D ligands and further suggest an immunomodulatory role for Vpr that may not only contribute to HIV-1-induced CD4+ T-lymphocyte depletion but may also take part in HIV-1-induced NK cell dysfunction.

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While high levels of Pkd1 expression are detected in tissues of patients with autosomal dominant polycystic kidney disease (ADPKD), it is unclear whether enhanced expression could be a pathogenetic mechanism for this systemic disorder. Three transgenic mouse lines were generated from a Pkd1-BAC modified by introducing a silent tag via homologous recombination to target a sustained wild type genomic Pkd1 expression within the native tissue and temporal regulation. These mice specifically overexpressed the Pkd1 transgene in extrarenal and renal tissues from approximately 2- to 15-fold over Pkd1 endogenous levels in a copy-dependent manner. All transgenic mice reproducibly developed tubular and glomerular cysts leading to renal insufficiency. Interestingly, Pkd1(TAG) mice also exhibited renal fibrosis and calcium deposits in papilla reminiscent of nephrolithiasis as frequently observed in ADPKD. Similar to human ADPKD, these mice consistently displayed hepatic fibrosis and approximately 15% intrahepatic cysts of the bile ducts affecting females preferentially. Moreover, a significant proportion of mice developed cardiac anomalies with severe left ventricular hypertrophy, marked aortic arch distention and/or valvular stenosis and calcification that had profound functional impact. Of significance, Pkd1(TAG) mice displayed occasional cerebral lesions with evidence of ruptured and unruptured cerebral aneurysms. This Pkd1(TAG) mouse model demonstrates that overexpression of wildtype Pkd1 can trigger the typical adult renal and extrarenal phenotypes resembling human ADPKD.

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Thèse numérisée par la Division de la gestion de documents et des archives de l'Université de Montréal