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.

Elasticity of α-Cristobalite: A Silicon Dioxide with a Negative Poisson's Ratio

Abstract: Laser Brillouin spectroscopy was used to determine the adiabatic single-crystal elastic stiffness coefficients of silicon dioxide (SiO 2 ) in the α-cristobalite structure. This SiO 2 polymorph, unlike other silicas and silicates, exhibits a negative Poisson9s ratio; α-cristobalite contracts laterally when compressed and expands laterally when stretched. Tensorial analysis of the elastic coefficients shows that Poisson9s ratio reaches a maximum value of –0.5 in some directions, whereas averaged values for the single-phased aggregate yield a Poisson9s ratio of –0.16.

A test of spatial autocorrelation analysis using an isolation-by-distance model

Abstract: Using the isolation-by-distance model as an example, we have examined several assumptions of spatial autocorrelation analysis applied to gene frequency surfaces. Gene frequency surfaces generated by a simulation of Wright's isolation-by-distance model were shown to exhibit spatial autocorrelation, except in the panmictic case. Identical stochastic generating processes result in surfaces with characteristics that are functions of the process parameters, such as parental vagility and neighborhood size. Differences in these parameters are detectable as differences in spatial autocorrelations after only a few generations of the simulations. Separate realizations of processes with identical parameters yield similar spatial correlograms. We have examined the inferences about population structure that could have been made from these observations if they had been real, rather than simulated, populations. From such inferences, we could have drawn conclusions about the presence of selection, migration and drift in given natural systems.

Energetic cost of brain functional connectivity.

Abstract: The brain's functional connectivity is complex, has high energetic cost, and requires efficient use of glucose, the brain's main energy source. It has been proposed that regions with a high degree of functional connectivity are energy efficient and can minimize consumption of glucose. However, the relationship between functional connectivity and energy consumption in the brain is poorly understood. To address this neglect, here we propose a simple model for the energy demands of brain functional connectivity, which we tested with positron emission tomography and MRI in 54 healthy volunteers at rest. Higher glucose metabolism was associated with proportionally larger MRI signal amplitudes, and a higher degree of connectivity was associated with nonlinear increases in metabolism, supporting our hypothesis for the energy efficiency of the connectivity hubs. Basal metabolism (in the absence of connectivity) accounted for 30% of brain glucose utilization, which suggests that the spontaneous brain activity accounts for 70% of the energy consumed by the brain. The energy efficiency of the connectivity hubs was higher for ventral precuneus, cerebellum, and subcortical hubs than for cortical hubs. The higher energy demands of brain communication that hinges upon higher connectivity could render brain hubs more vulnerable to deficits in energy delivery or utilization and help explain their sensitivity to neurodegenerative conditions, such as Alzheimer's disease.

Control of Confounding and Reporting of Results in Causal Inference Studies. Guidance for Authors from Editors of Respiratory, Sleep, and Critical Care Journals

Abstract: Control of Confounding and Reporting of Results in Causal Inference Studies Guidance for Authors fromEditors of Respiratory, Sleep, andCritical Care Journals David J. Lederer*, Scott C. Bell*, Richard D. Branson*, James D. Chalmers*, Rachel Marshall*, David M. Maslove*, David E. Ost*, Naresh M. Punjabi*, Michael Schatz*, Alan R. Smyth*, Paul W. Stewart*, Samy Suissa*, Alex A. Adjei, Cezmi A. Akdis, Élie Azoulay, Jan Bakker, Zuhair K. Ballas, Philip G. Bardin, Esther Barreiro, Rinaldo Bellomo, Jonathan A. Bernstein, Vito Brusasco, Timothy G. Buchman, Sudhansu Chokroverty, Nancy A. Collop, James D. Crapo, Dominic A. Fitzgerald, Lauren Hale, Nicholas Hart, Felix J. Herth, Theodore J. Iwashyna, Gisli Jenkins, Martin Kolb, Guy B. Marks, Peter Mazzone, J. Randall Moorman, ThomasM.Murphy, Terry L. Noah, Paul Reynolds, Dieter Riemann, Richard E. Russell, Aziz Sheikh, Giovanni Sotgiu, Erik R. Swenson, Rhonda Szczesniak, Ronald Szymusiak, Jean-Louis Teboul, and Jean-Louis Vincent Department of Medicine and Department of Epidemiology, Columbia University Irving Medical Center, New York, New York; Editor-inChief, Annals of the American Thoracic Society; Department of Thoracic Medicine, The Prince Charles Hospital, Brisbane, Queensland, Australia; Editor-in-Chief, Journal of Cystic Fibrosis; Department of Surgery, University of Cincinnati, Cincinnati, Ohio; Editor-in-Chief, Respiratory Care; University of Dundee, Dundee, Scotland; Deputy Chief Editor, European Respiratory Journal; London, England; Deputy Editor, The Lancet Respiratory Medicine; Department of Medicine, Queen’s University, Kingston, Ontario, Canada; Associate Editor for Data Science, Critical Care Medicine; Department of Pulmonary Medicine, University of Texas MD Anderson Cancer Center, Houston, Texas; Editor-in-Chief, Journal of Bronchology and Interventional Pulmonology; Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland; Deputy Editor-in-Chief, SLEEP; Department of Allergy, Kaiser Permanente Medical Center, San Diego, California; Editor-in-Chief, The Journal of Allergy & Clinical Immunology: In Practice; Division of Child Health, Obstetrics, and Gynecology, University of Nottingham, Nottingham, England; Joint Editor-in-Chief, Thorax; Department of Biostatistics, University of North Carolina, Chapel Hill, North Carolina; Associate Editor, Pediatric Pulmonology; Department of Epidemiology, Biostatistics, and Occupational Health, McGill University, Montreal, Quebec, Canada; Advisor, COPD: Journal of Chronic Obstructive Pulmonary Disease; Department of Oncology, Mayo Clinic, Rochester, Minnesota; Editor-in-Chief, Journal of Thoracic Oncology; Swiss Institute of Allergy and Asthma Research, University of Zurich, Davos, Switzerland; Editor-in-Chief, Allergy; St. Louis Hospital, University of Paris, Paris, France; Editor-in-Chief, Intensive Care Medicine; Department of Medicine, Columbia University Irving Medical Center, and Division of Pulmonary, Critical Care, and Sleep, NYU Langone Health, New York, New York; Department of Intensive Care Adults, Erasmus MC University Medical Center, Rotterdam, the Netherlands; Department of Intensive Care, Pontificia Universidad Católica de Chile, Santiago, Chile; Editor-in-Chief, Journal of Critical Care; Department of Internal Medicine, University of Iowa and the Iowa City Veterans Affairs Medical Center, Iowa City, Iowa; Editor-in-Chief, The Journal of Allergy and Clinical Immunology; Monash Lung and Sleep, Monash Hospital and University, Melbourne, Victoria, Australia; Co-Editor-in-Chief, Respirology; Pulmonology Department, Muscle and Lung Cancer Research Group, Research Institute of Hospital del Mar and Centro de Investigación Biomédica en Red Enfermedades Respiratorias Instituto de Salud Carlos III, Barcelona, Spain; Editor-in-Chief, Archivos de Bronconeumologia; Department of Intensive Care Medicine, Austin Hospital and University of Melbourne, Melbourne, Victoria, Australia; Editor-in-Chief, Critical Care & Resuscitation; Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio; Editor-in-Chief, Journal of Asthma; Department of Internal Medicine, University of Genoa, Genoa, Italy; Editor-in-Chief, COPD: Journal of Chronic Obstructive Pulmonary Disease; Department of Surgery, Department of Anesthesiology, and Department of Biomedical Informatics, Emory University School of Medicine, Atlanta, Georgia; Editor-in-Chief,Critical CareMedicine; JFKNewJersey Neuroscience Institute, HackensackMeridian Health–JFKMedical Center, Edison, New Jersey; Editor-in-Chief, Sleep Medicine; Department of Medicine and Department of Neurology, Emory University School of Medicine, Atlanta, Georgia; Editor-in-Chief, Journal of Clinical Sleep Medicine; Department of Medicine, National Jewish Hospital, Denver, Colorado; Editor-in-Chief, Journal of the COPD Foundation; The Children’s Hospital at Westmead, Sydney Medical School, University of

Regulation of phospholipase D2: selective inhibition of mammalian phospholipase D isoenzymes by alpha- and beta-synucleins.

Abstract: Two widely expressed mammalian phosphatidylcholine (PC)-specific phospholipases D (PLD), PLD1 and PLD2, have been identified. Recombinantly expressed PLD2 has high basal activity and is insensitive to GTP-binding protein activators of PLD1 [Colley, W. C., et al. (1997) Curr. Biol. 7, 191-201]. To investigate the regulation of PLD2 we isolated PLD2, from mouse brain by immunoaffinity chromatography. The native and recombinant proteins have indistinguishable properties: PLD2 is potently activated by phosphoinositides with a vicinal 4,5-phosphate pair but is not stimulated by guanosine 5'-O-(3-thio triphosphate)-activated ADP-ribosylation factor-1, Rho family GTP-binding proteins, or protein kinases C-alpha, or -beta1. We used recombinant PLD2 in a reconstitution assay to search for regulators in cell and tissue extracts. Bovine brain contains a heat-stable protein factor that inhibits PLD2 activity in vitro. This factor was purified to homogeneity and identified as a mixture of alpha- and beta-synucleins by microsequencing and Western blotting. Recombinantly expressed alpha- and beta-synucleins inhibit PLD2 activity in vitro (K0.5 10 nM). Inhibition is not overcome by the protein or lipid activators of PLD1. Synucleins have been implicated in Parkinson's and Alzheimer's diseases. Our findings suggest that inhibition of PLD2 may be a function of synucleins. Modulation of PLD2 activity by synucleins may play a role in some aspects of the pathophysiologies that characterize these neurodegenerative diseases.