New York University

About: New York University is a education organization based out in New York, New York, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 72380 authors who have published 165545 publications receiving 8334030 citations. The organization is also known as: NYU & University of the City of New York.

Transcatheter Aortic-Valve Replacement with a Balloon-Expandable Valve in Low-Risk Patients

Abstract: Background Among patients with aortic stenosis who are at intermediate or high risk for death with surgery, major outcomes are similar with transcatheter aortic-valve replacement (TAVR) an...

NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals

Abstract: The inflammatory nature of atherosclerosis is well established but the agent(s) that incite inflammation in the artery wall remain largely unknown. Germ-free animals are susceptible to atherosclerosis, suggesting that endogenous substances initiate the inflammation. Mature atherosclerotic lesions contain macroscopic deposits of cholesterol crystals in the necrotic core, but their appearance late in atherogenesis had been thought to disqualify them as primary inflammatory stimuli. However, using a new microscopic technique, we revealed that minute cholesterol crystals are present in early diet-induced atherosclerotic lesions and that their appearance in mice coincides with the first appearance of inflammatory cells. Other crystalline substances can induce inflammation by stimulating the caspase-1-activating NLRP3 (NALP3 or cryopyrin) inflammasome, which results in cleavage and secretion of interleukin (IL)-1 family cytokines. Here we show that cholesterol crystals activate the NLRP3 inflammasome in phagocytes in vitro in a process that involves phagolysosomal damage. Similarly, when injected intraperitoneally, cholesterol crystals induce acute inflammation, which is impaired in mice deficient in components of the NLRP3 inflammasome, cathepsin B, cathepsin L or IL-1 molecules. Moreover, when mice deficient in low-density lipoprotein receptor (LDLR) were bone-marrow transplanted with NLRP3-deficient, ASC (also known as PYCARD)-deficient or IL-1alpha/beta-deficient bone marrow and fed on a high-cholesterol diet, they had markedly decreased early atherosclerosis and inflammasome-dependent IL-18 levels. Minimally modified LDL can lead to cholesterol crystallization concomitant with NLRP3 inflammasome priming and activation in macrophages. Although there is the possibility that oxidized LDL activates the NLRP3 inflammasome in vivo, our results demonstrate that crystalline cholesterol acts as an endogenous danger signal and its deposition in arteries or elsewhere is an early cause rather than a late consequence of inflammation. These findings provide new insights into the pathogenesis of atherosclerosis and indicate new potential molecular targets for the therapy of this disease.

Pragmatics of measuring recognition memory: applications to dementia and amnesia.

Abstract: SUMMARY This article has two purposes. The first is to describe four theoretical models of yesno recognition memory and present their associated measures of discrimination and response bias. These models are then applied to a set of data from normal subjects to determine which pairs of discrimination and bias indices show independence between discrimination and bias. The following models demonstrated independence: a two-highthreshold model, a signal detection model with normal distributions using d' and C (rather than beta), and a signal detection model with logistic distributions and a bias measure analogous to C. Cis defined as the distance of criterion from the intersection of the two underlying distributions. The second purpose is to use the indices from the acceptable models to characterize recognition memory deficits in dementia and amnesia, \bung normal subjects, Alzheimer's disease patients, and parkinsonian dementia patients were tested with picture recognition tasks with repeated study-test trials. Huntington's disease patients, mixed etiology amnesics, and age-matched normals were tested by Butters, Wolfe, Martone, Granholm, and Cermak (1985) using the same paradigm with word stimuli. Demented and amnesic patients produced distinctly different patterns of abnormal memory performance. Both groups of demented patients showed poor discrimination and abnormally liberal response bias for words (Huntington's disease) and pictures (Alzheimer's disease and parkinsonian dementia), whereas the amnesic patients showed the worst discrimination but normal response bias for words. Although both signal detection theory and twohigh-threshold discrimination parameters showed identical results, the bias measure from the two-high-threshold model was more sensitive to change than the bias measure (C) from signal detection theory. Three major points are emphasized. First, any index of recognition memory performance assumes an underlying model. Second, even acceptable models can lead to different conclusions about patterns of learning and forgetting. Third, efforts to characterize and ameliorate abnormal memory should address both discrimination and bias deficits.

Investor Sentiment and the Cross-Section of Stock Returns

Abstract: We examine how investor sentiment affects the cross-section of stock returns. Theory predicts that a broad wave of sentiment will disproportionately affect stocks whose valuations are highly subjective and are difficult to arbitrage. We test this prediction by studying how the cross-section of subsequent stock returns varies with proxies for beginning-of-period investor sentiment. When sentiment is low, subsequent returns are relatively high on smaller stocks, high volatility stocks, unprofitable stocks, non-dividend-paying stocks, extreme-growth stocks, and distressed stocks, consistent with an initial underpricing of these stocks. When sentiment is high, on the other hand, these patterns attenuate or fully reverse. The results are consistent with predictions and appear unlikely to reflect an alternative explanation based on compensation for systematic risk.