40 research outputs found

    Reactive Quenching Of Od A (2)ÎŁ(+) By H-2: Translational Energy Distributions For H- And D-Atom Product Channels

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    The H- and D-atom products from collisional quenching of OD A (2)Sigma(+) by H-2 are characterized through Doppler spectroscopy using two-photon (2 S-2 \u3c-\u3c- 1 S-2) laser-induced fluorescence. Partial deuteration enables separation of the channel forming H + HOD products, which accounts for 75% of reactive quenching events, from the D + H2O product channel. The Doppler profiles, along with those reported previously for other isotopic variants, are transformed into product translational energy distributions using a robust fitting procedure based on discrete velocity basis functions. The product translational energy distribution for the H- atom channel is strongly peaked at low energy (below 0.5 eV) with a long tail extending to the energetic limit. By contrast, the D-atom channel exhibits a small peak at low translational energy with a distinctive secondary peak at higher translational energy (approximately 1.8 eV) before falling off to higher energy. In both cases, most of the available energy flows into internal excitation of the water products. Similar distributions are obtained upon reanalysis of D- and H- atom Doppler profiles, respectively, from reactive quenching of OH A (2)Sigma(+) by D-2. The sum of the translational energy distributions for H- and D- atom channels is remarkably similar to that obtained for OH A (2)Sigma(+) + H-2, where the two channels cannot be distinguished from one another. The product translational energy distributions from reactive quenching are compared with those obtained from a previous experiment performed at higher collision energy, quasiclassical trajectory calculations of the post-quenching dynamics, and a statistical model. (C) 2011 American Institute of Physics. [doi: 10.1063/1.3644763

    Application of a Theory-Driven Approach to Detect Cognitively Disengaged Test-Taker Behavior

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    Bottom-up, data-driven response filtering methods that exclude unrealistically fast responses from calculating test scores have been successfully applied to improve test validity. We introduce a top-down, theory-driven method to detect cognitively disengaged behavior, compare it with a data-driven method using data from a nationally representative reading assessment, and discuss its potential and limitations

    RIP kinase 1-dependent endothelial necroptosis underlies systemic inflammatory response syndrome

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    Receptor interacting protein kinase 1 (RIPK1) has important kinase-dependent and kinase-independent scaffolding functions that activate or prevent apoptosis or necroptosis in a cell context-dependent manner. The kinase activity of RIPK1 mediates hypothermia and lethality in a mouse model of TNF-induced shock, reflecting the hyperinflammatory state of systemic inflammatory response syndrome (SIRS), where the proinflammatory cytokine storm has long been viewed as detrimental. Here, we demonstrate that cytokine and chemokine levels did not predict survival and, importantly, that kinase-inactive Ripk1D138N/D138N hematopoietic cells afforded little protection from TNF- or TNF/zVAD-induced shock in reconstituted mice. Unexpectedly, RIPK1 kinase-inactive mice transplanted with WT hematopoietic cells remained resistant to TNF-induced shock, revealing that a nonhematopoietic lineage mediated protection. TNF-treated Ripk1D138N/D138N mice exhibited no significant increases in intestinal or vascular permeability, nor did they activate the clotting cascade. We show that TNF administration damaged the liver vascular endothelium and induced phosphorylated mixed lineage kinase domain-like (phospho-MLKL) reactivity in endothelial cells isolated from TNF/zVAD-treated WT, but not Ripk1D138N/D138N, mice. These data reveal that the tissue damage present in this SIRS model is reflected, in part, by breaks in the vasculature due to endothelial cell necroptosis and thereby predict that RIPK1 kinase inhibitors may provide clinical benefit to shock and/or sepsis patients
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