2,248 research outputs found

    Density of States in Landau Level Tails of GaAs-AlxGa1-xAs Heterostructures

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    From an analysis of the thermally activated resistivity as a function of the magnetic field in the quantum Hall regime we deduced the position of the Fermi energy in the mobility gap as a function of the filling factor and therefore the density of states. The measured density of states is best described by a Gaussian like profile superimposed on a constant background

    The Strategic Assessment Model (STRATAM): Studying and Preventing Strategic Failure

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    The purpose of this study is to introduce the Strategic Assessment Model (STRATAM), a model designed to assist in the prevention of strategic failure. STRATAM aids firstly in the assessment of a strategy, as well as its crafting and evolution; secondly, it aims to enable and possibly streamline civil-military strategic debates on military operations. It is argued that strategic blunders in many cases result from latent organizational failures on one’s own side. Therefore, STRATAM combines Clausewitz’ theory of war and strategy with organizational failure theory. To demonstrate the use of this model, this paper uses Operation Cast Lead (or the Gaza War) of 2008-2009 as a case study. The paper’s findings include that the ultimate reasons for strategic failure were on one hand Clausewitzian; on the other hand, the Israeli Defense Force’s failure in organizational learning from a previous war two years earlier. The timely, strategic assessment and an effective civil-military debate about the effects of ongoing military operations might have prevented this failure. STRATAM would have provided the necessary language, structure, and relevance to identify actual and potential strategic failures with the goal to evolve the strategy

    Early protection against pathogenic virus infection at a mucosal challenge site after vaccination with attenuated simian immunodeficiency virus

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    Atraumatic application of attenuated SIVmac23Δnef vaccine to the tonsils of rhesus macaques provided protection against challenge 26 weeks later with infectious SIVmac251 applied through this route. Early events at the mucosal portal of entry of challenge virus were followed. Wild-type virus was detected in nonvaccinated controls by day 4, and then simian immunodeficiency virus (SIV) replicated vigorously at days 7 and 14. In contrast, a challenge of 10 of 10 vaccinees with SIV did not significantly raise RNA levels in the plasma or increase infected cells in lymphoid tissues, as assessed by single-cell labeling for viral RNA and nef protein. Vaccine virus was found in the tonsils of all vaccinees, but challenge virus was only detected at this portal of entry in 4 of 10 monkeys. In the tonsil, the challenge virus did not induce an expansion of perforin+ killer cells. However, there was a significant increase in γδ T cells and mature dendritic cells relative to unvaccinated controls. Therefore, during tonsillar SIVΔnef vaccination, infection is blocked early at the entry portal, which we propose is due in part to innate functions of γδ T and dendritic cells

    Modulating flowering time and prevention of pod shatter in oilseed rape

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    Floral induction is a key developmental switch in plants that leads to the production of flowers, fruits and seeds, which are of paramount importance for human life. To meet the demands of several crop harvests per year, or the growth of crop plants in regions with short vegetation times and for the production of ornamental plants, the timing of the floral transition is very important. The discovery of genes that are involved in flowering time control in model plants should allow the modulation of this developmental switch also in plants with economic value. By using a transgenic approach, we showed that a single MADS box gene accelerated flowering and seed ripening in summer rape plants. The MADSB transgene also partially substituted for the strict temperature requirements for flowering in winter rape plants. Transgenic winter rape plants expressing the MADSB transgene also produced more rigid siliques than wild type winter rape plants, and this prevented precocious seed dispersa

    Flow-dependent regulation of endothelial Tie2 by GATA3 in vivo

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    BACKGROUND Reduced endothelial Tie2 expression occurs in diverse experimental models of critical illness, and experimental Tie2 suppression is sufficient to increase spontaneous vascular permeability. Looking for a common denominator among different critical illnesses that could drive the same Tie2 suppressive (thereby leak inducing) phenotype, we identified "circulatory shock" as a shared feature and postulated a flow-dependency of Tie2 gene expression in a GATA3 dependent manner. Here, we analyzed if this mechanism of flow-regulation of gene expression exists in vivo in the absence of inflammation. RESULTS To experimentally mimic a shock-like situation, we developed a murine model of clonidine-induced hypotension by targeting a reduced mean arterial pressure (MAP) of approximately 50% over 4 h. We found that hypotension-induced reduction of flow in the absence of confounding disease factors (i.e., inflammation, injury, among others) is sufficient to suppress GATA3 and Tie2 transcription. Conditional endothelial-specific GATA3 knockdown (B6-Gata3tm1−Jfz^{tm1-Jfz} VE-Cadherin(PAC)-cerERT2) led to baseline Tie2 suppression inducing spontaneous vascular leak. On the contrary, the transient overexpression of GATA3 in the pulmonary endothelium (jet-PEI plasmid delivery platform) was sufficient to increase Tie2 at baseline and completely block its hypotension-induced acute drop. On the functional level, the Tie2 protection by GATA3 overexpression abrogated the development of pulmonary capillary leakage. CONCLUSIONS The data suggest that the GATA3-Tie2 signaling pathway might play a pivotal role in controlling vascular barrier function and that it is affected in diverse critical illnesses with shock as a consequence of a flow-regulated gene response. Targeting this novel mechanism might offer therapeutic opportunities to treat vascular leakage of diverse etiologies
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