Stony Brook University

About: Stony Brook University is a education organization based out in Stony Brook, New York, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 32534 authors who have published 68218 publications receiving 3035131 citations. The organization is also known as: State University of New York at Stony Brook & SUNY Stony Brook.

Optimizing Binding Energies of Key Intermediates for CO2 Hydrogenation to Methanol over Oxide-Supported Copper.

Abstract: Rational optimization of catalytic performance has been one of the major challenges in catalysis. Here we report a bottom-up study on the ability of TiO2 and ZrO2 to optimize the CO2 conversion to methanol on Cu, using combined density functional theory (DFT) calculations, kinetic Monte Carlo (KMC) simulations, in situ diffuse reflectance infrared Fourier transform spectroscopy (DRIFTS) measurements, and steady-state flow reactor tests. The theoretical results from DFT and KMC agree with in situ DRIFTS measurements, showing that both TiO2 and ZrO2 help to promote methanol synthesis on Cu via carboxyl intermediates and the reverse water–gas-shift (RWGS) pathway; the formate intermediates, on the other hand, likely act as a spectator eventually. The origin of the superior promoting effect of ZrO2 is associated with the fine-tuning capability of reduced Zr3+ at the interface, being able to bind the key reaction intermediates, e.g. *CO2, *CO, *HCO, and *H2CO, moderately to facilitate methanol formation. This ...

Neuronal circuitry mechanism regulating adult quiescent neural stem-cell fate decision

Abstract: Adult neurogenesis arises from neural stem cells within specialized niches. Neuronal activity and experience, presumably acting on this local niche, regulate multiple stages of adult neurogenesis, from neural progenitor proliferation to new neuron maturation, synaptic integration and survival. It is unknown whether local neuronal circuitry has a direct impact on adult neural stem cells. Here we show that, in the adult mouse hippocampus, nestin-expressing radial glia-like quiescent neural stem cells (RGLs) respond tonically to the neurotransmitter γ-aminobutyric acid (GABA) by means of γ2-subunit-containing GABAA receptors. Clonal analysis of individual RGLs revealed a rapid exit from quiescence and enhanced symmetrical self-renewal after conditional deletion of γ2. RGLs are in close proximity to terminals expressing 67-kDa glutamic acid decarboxylase (GAD67) of parvalbumin-expressing (PV+) interneurons and respond tonically to GABA released from these neurons. Functionally, optogenetic control of the activity of dentate PV+ interneurons, but not that of somatostatin-expressing or vasoactive intestinal polypeptide (VIP)-expressing interneurons, can dictate the RGL choice between quiescence and activation. Furthermore, PV+ interneuron activation restores RGL quiescence after social isolation, an experience that induces RGL activation and symmetrical division. Our study identifies a niche cell–signal–receptor trio and a local circuitry mechanism that control the activation and self-renewal mode of quiescent adult neural stem cells in response to neuronal activity and experience.

NNLO corrections to the total cross section for Higgs boson production in hadron-hadron collisions

Abstract: We present the next-to-next-to-leading order (NNLO) corrections to the total cross section for (pseudo-) scalar Higgs boson production using an alternative method than those used in previous calculations. All QCD partonic subprocesses have been included and the computation is carried out in the effective Lagrangian approach which emerges from the standard model by taking the limit $m_t \to \infty$ where $m_t$ denotes the mass of the top quark. Our results agree with those published earlier in the literature. We estimate the theoretical uncertainties by comparing the $K$-factors and the variation with respect to the mass factorization/renormalization scales with the results obtained by lower order calculations. We also investigate the dependence of the cross section on several parton density sets provided by different groups. Further we study which part of the coefficient functions dominates the cross section. This is of interest for the resummation of large corrections which occur near the boundary of phase space. It turns out that depending on the definition of the total cross section the latter is dominated by the the soft-plus-virtual gluon corrections represented by $\delta(1-x)$ and $(\ln^i(1-x)/(1-x))_+$ terms. PACS numbers: 12.38.-t, 12.38.Bx, 13.85.-t, 14.80.Gt.

A complement–microglial axis drives synapse loss during virus-induced memory impairment

Abstract: Over 50% of patients who survive neuroinvasive infection with West Nile virus (WNV) exhibit chronic cognitive sequelae. Although thousands of cases of WNV-mediated memory dysfunction accrue annually, the mechanisms responsible for these impairments are unknown. The classical complement cascade, a key component of innate immune pathogen defence, mediates synaptic pruning by microglia during early postnatal development. Here we show that viral infection of adult hippocampal neurons induces complement-mediated elimination of presynaptic terminals in a murine WNV neuroinvasive disease model. Inoculation of WNV-NS5-E218A, a WNV with a mutant NS5(E218A) protein leads to survival rates and cognitive dysfunction that mirror human WNV neuroinvasive disease. WNV-NS5-E218A-recovered mice (recovery defined as survival after acute infection) display impaired spatial learning and persistence of phagocytic microglia without loss of hippocampal neurons or volume. Hippocampi from WNV-NS5-E218A-recovered mice with poor spatial learning show increased expression of genes that drive synaptic remodelling by microglia via complement. C1QA was upregulated and localized to microglia, infected neurons and presynaptic terminals during WNV neuroinvasive disease. Murine and human WNV neuroinvasive disease post-mortem samples exhibit loss of hippocampal CA3 presynaptic terminals, and murine studies revealed microglial engulfment of presynaptic terminals during acute infection and after recovery. Mice with fewer microglia (Il34(-/-) mice with a deficiency in IL-34 production) or deficiency in complement C3 or C3a receptor were protected from WNV-induced synaptic terminal loss. Our study provides a new murine model of WNV-induced spatial memory impairment, and identifies a potential mechanism underlying neurocognitive impairment in patients recovering from WNV neuroinvasive disease.

Role of the Kv4.3 K+ Channel in Ventricular Muscle: A Molecular Correlate for the Transient Outward Current

Abstract: The expression of 15 different K + channels in canine heart was examined, and a new K + channel gene (Kv4.3), which encodes a rapidly inactivating K + current, is described. The Kv4.3 channel was found to have biophysical and pharmacological properties similar to the native canine transient outward current (I to ). The Kv4.3 gene is also expressed in human and rat heart. It is concluded that the Kv4.3 channel underlies the bulk of the I to in canine ventricular myocytes, and probably in human myocytes. Both the Kv4.3 and Kv4.2 channels are likely to contribute to the I to in rat heart, and differential expression of these two channels can account for observed differences in the kinetic properties of the I to in different regions of rat ventricle. There are significant differences in the pattern of K + channel expression in canine heart, compared with rat heart, and these differences may be an adaptation to the different requirements for cardiac function in mammals of markedly different sizes. It is possible that the much longer ventricular action potential duration observed in canine heart compared with rat heart is due, in part, to the lower levels of Kv1.2, Kv2.1, and Kv4.2 gene expression in canine heart.