Let G -- Spec A be an affine K-group scheme and A = (w ∈ A* : dimK A*-w 〈 ∞, dimK w. A* 〈 ∞}. Let (-, -) : A* × A → K, (w, w) := tr(ww), be the trace form. We prove that G is linearly reductive if...
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Let G -- Spec A be an affine K-group scheme and A = (w ∈ A* : dimK A*-w 〈 ∞, dimK w. A* 〈 ∞}. Let (-, -) : A* × A → K, (w, w) := tr(ww), be the trace form. We prove that G is linearly reductive if and only if the trace form is non-degenerate on A*.
The activity of Lewis (Nb2O5) and Br nsted (Amberlyst 70) acid catalysts for the cyclodehydration of xylose to furfural was studied. The nature of the acidity resulted in significant changes in the reaction mechanism....
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The activity of Lewis (Nb2O5) and Br nsted (Amberlyst 70) acid catalysts for the cyclodehydration of xylose to furfural was studied. The nature of the acidity resulted in significant changes in the reaction mechanism. Lewis acid sites promote the formation of xylulose, while Br nsted acid sites are required to further dehydrate the sugar to furfural. Amberlyst 70 in water/toluene at 175 ℃ showed lower activity but gave a higher furfural yield. Using N2 as the stripping agent considerably improved the furfural yield and product purity in the stripped stream. Catalyst stability was also studied.
Identification of the precise molecular pathways involved in oncogene-induced transformation may help us gain a better understanding of tumor initiation and promotion. Here, we demonstrate that SOX2^+ foregut epitheli...
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Identification of the precise molecular pathways involved in oncogene-induced transformation may help us gain a better understanding of tumor initiation and promotion. Here, we demonstrate that SOX2^+ foregut epithelial cells are prone to oncogenic transformation upon mutagenic insults, such as Kras^G12D and p53 deletion. GFP-based lineage-tracing experiments indicate that SOX2^+ cells are the cells-of-origin of esophagus and stomach hyperplasia. Our observations indicate distinct roles for oncogenic KRAS mutation and P53 deletion. p53 homozygous deletion is required for the acquisition of an invasive potential, and Kras^G12D expression, but not p53 deletion, suffices for tumor formation. Global gene expression analysis reveals secreting factors upregulated in the hyperplasia induced by oncogenic KRAS and highlights a crucial role for the CXCR2 pathway in driving hyperplasia. Collectively, the array of genetic models presented here demonstrate that stratified epithelial cells are susceptible to oncogenic insults, which may lead to a better understanding of tumor initiation and aid in the design of new cancer therapeutics.
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