A convergence on Boolean algebras generalizing the convergence on the Aleksandrov cube

We compare the forcing related properties of a complete Boolean algebra B with the properties of the convergences $\lambda_s$ (the algebraic convergence) and $\lambda_{ls}$ on B generalizing the convergence on the Cantor and Aleksandrov cube respectively. In particular we show that $\lambda_{ls}$ is a topological convergence iff forcing by B does not produce new reals and that $\lambda_{ls}$ is weakly topological if B satisfies condition $(\hbar)$ (implied by the ${\mathfrak t}$-cc). On the other hand, if $\lambda_{ls}$ is a weakly topological convergence, then B is a $2^{\mathfrak h}$-cc algebra or in some generic extension the distributivity number of the ground model is greater than or equal to the tower number of the extension. So, the statement "The convergence $\lambda_{ls}$ on the collapsing algebra B=\ro ((\omega_2)^{<\omega}) is weakly topological" is independent of ZFC

On two-dimensional surface attractors and repellers on 3-manifolds

We show that if $f: M^3\to M^3$ is an $A$-diffeomorphism with a surface two-dimensional attractor or repeller $\mathcal B$ and $M^2_ \mathcal B$ is a supporting surface for $\mathcal B$, then $\mathcal B = M^2_{\mathcal B}$ and there is $k\geq 1$ such that: 1) $M^2_{\mathcal B}$ is a union $M^2_1\cup...\cup M^2_k$ of disjoint tame surfaces such that every $M^2_i$ is homeomorphic to the 2-torus $T^2$. 2) the restriction of $f^k$ to $M^2_i$ $(i\in\{1,...,k\})$ is conjugate to Anosov automorphism of $T^2$

A Sterol-Regulatory Element Binding Protein Is Required for Cell Polarity, Hypoxia Adaptation, Azole Drug Resistance, and Virulence in Aspergillus fumigatus

At the site of microbial infections, the significant influx of immune effector cells and the necrosis of tissue by the invading pathogen generate hypoxic microenvironments in which both the pathogen and host cells must survive. Currently, whether hypoxia adaptation is an important virulence attribute of opportunistic pathogenic molds is unknown. Here we report the characterization of a sterol-regulatory element binding protein, SrbA, in the opportunistic pathogenic mold, Aspergillus fumigatus. Loss of SrbA results in a mutant strain of the fungus that is incapable of growth in a hypoxic environment and consequently incapable of causing disease in two distinct murine models of invasive pulmonary aspergillosis (IPA). Transcriptional profiling revealed 87 genes that are affected by loss of SrbA function. Annotation of these genes implicated SrbA in maintaining sterol biosynthesis and hyphal morphology. Further examination of the SrbA null mutant consequently revealed that SrbA plays a critical role in ergosterol biosynthesis, resistance to the azole class of antifungal drugs, and in maintenance of cell polarity in A. fumigatus. Significantly, the SrbA null mutant was highly susceptible to fluconazole and voriconazole. Thus, these findings present a new function of SREBP proteins in filamentous fungi, and demonstrate for the first time that hypoxia adaptation is likely an important virulence attribute of pathogenic molds

Liver-Specific Expression of Transcriptionally Active SREBP-1c Is Associated with Fatty Liver and Increased Visceral Fat Mass

The pathogenesis of fatty liver is not understood in detail, but lipid overflow as well as de novo lipogenesis (DNL) seem to be the key points of hepatocyte accumulation of lipids. One key transcription factor in DNL is sterol regulatory element-binding protein (SREBP)-1c. We generated mice with liver-specific over-expression of mature human SREBP-1c under control of the albumin promoter and a liver-specific enhancer (alb-SREBP-1c) to analyze systemic perturbations caused by this distinct alteration. SREBP-1c targets specific genes and causes key enzymes in DNL and lipid metabolism to be up-regulated. The alb-SREBP-1c mice developed hepatic lipid accumulation featuring a fatty liver by the age of 24 weeks under normocaloric nutrition. On a molecular level, clinical parameters and lipid-profiles varied according to the fatty liver phenotype. The desaturation index was increased compared to wild type mice. In liver, fatty acids (FA) were increased by 50% (p<0.01) and lipid composition was shifted to mono unsaturated FA, whereas lipid profile in adipose tissue or serum was not altered. Serum analyses revealed a ∼2-fold (p<0.01) increase in triglycerides and free fatty acids, and a ∼3-fold (p<0.01) increase in insulin levels, indicating insulin resistance; however, no significant cytokine profile alterations have been determined. Interestingly and unexpectedly, mice also developed adipositas with considerably increased visceral adipose tissue, although calorie intake was not different compared to control mice. In conclusion, the alb-SREBP-1c mouse model allowed the elucidation of the systemic impact of SREBP-1c as a central regulator of lipid metabolism in vivo and also demonstrated that the liver is a more active player in metabolic diseases such as visceral obesity and insulin resistance

On realcompact topological vector spaces

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Biodiversity inventories in high gear: DNA barcoding facilitates a rapid biotic survey of a temperate nature reserve

Comprehensive biotic surveys, or ‘all taxon biodiversity inventories’ (ATBI), have traditionally been limited in scale or scope due to the complications surrounding specimen sorting and species identification. To circumvent these issues, several ATBI projects have successfully integrated DNA barcoding into their identification procedures and witnessed acceleration in their surveys and subsequent increase in project scope and scale. The Biodiversity Institute of Ontario partnered with the rare Charitable Research Reserve and delegates of the 6th International Barcode of Life Conference to complete its own rapid, barcode-assisted ATBI of an established land trust in Cambridge, Ontario, Canada