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X-WR-CALNAME:The Advanced Science Research Center
X-ORIGINAL-URL:https://asrc.gc.cuny.edu
X-WR-CALDESC:Events for The Advanced Science Research Center
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BEGIN:VEVENT
DTSTART;TZID=America/New_York:20190507T130000
DTEND;TZID=America/New_York:20190507T143000
DTSTAMP:20260528T081234
CREATED:20190125T193625Z
LAST-MODIFIED:20190503T211037Z
UID:10000878-1557234000-1557239400@asrc.gc.cuny.edu
SUMMARY:Neuroscience Work-in-Progress Seminar
DESCRIPTION:Neurodegeneration in multiple sclerosis: a role for ceramide C16?\nSpeaker:\n Mario Amatruda\nCasaccia Lab\, Advanced Science Research Center \nAbstract\nMultiple Sclerosis (MS) is an inflammatory\, demyelinating disease of the central nervous system. Major progress has been made to understand and modulate the inflammatory component of MS\, but the concomitant mechanisms contributing to neurodegeneration\, which causes irreversible disability\, remain largely unknown. We have recently discovered that ceramide C16 (a sphingolipid) is enriched in the cerebrospinal fluid of patients with MS\, and that it is sufficient to induce mitochondrial respiration impairment and degeneration of neurons in vitro (Vidaurre et al.\, 2014). Here\, we further examined the neurotoxic effect of ceramide C16. We show that ceramide C16 can readily enter into cultured neurons and accumulates in mitochondria changing their membrane potential and morphology. Furthermore\, we found that neurons exposed to pro-inflammatory cytokines and oxidative stress are characterized by increased expression of the ceramide C16 synthetic enzymes (CerS5 and CerS6)\, suggesting that the endogenous\, de novo synthesis of ceramide C16 could play a role in neurodegeneration during inflammation. Importantly\, we discovered that transgenic mice (tg: CamKIIaCre;CerS5fl/flCerS6fl/fl) in which the neuronal synthesis of ceramide C16 is genetically inhibited\, are protected during experimental autoimmune encephalomyelitis (EAE\, a model of MS) from neurological deficit and neurodegeneration compared with wild type controls. \nThese findings raise the possibility that ceramide C16 can contribute\, at least in part\, to the mitochondrial dysfunction and neurodegeneration occurring in MS and the modulation of its synthesis may represent a novel therapeutic target. \n\nThe ASRC Neuroscience Work-in-Progress Seminars consist of an hour-long presentation on research relevant to the fields of neurobiology and translational neuroscience. Talks will be given by senior Ph.D. students\, postdoctoral and faculty researchers. Anyone interested is encouraged to attend and actively participate in discussions. \nWork-in-Progress Seminars are presented in collaboration with The City College of New York.
URL:https://asrc.gc.cuny.edu/event/neuroscience-work-in-progress-seminar-2019-05-14/
LOCATION:ASRC 1st Floor Seminar Room\, 85 St. Nicholas Terrace\, New York\, NY\, 10031\, United States
CATEGORIES:Neuroscience
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/New_York:20190513T090000
DTEND;TZID=America/New_York:20190514T140000
DTSTAMP:20260528T081234
CREATED:20190123T214444Z
LAST-MODIFIED:20190513T204154Z
UID:10000948-1557738000-1557842400@asrc.gc.cuny.edu
SUMMARY:First Annual Manhattan Glia Spring Meeting
DESCRIPTION:Inaugural meeting for the Center of Glial Biology at Mount Sinai and CUNY\nThis two-day meeting is based on the growing interest in glia biology and in its contribution to neurological and psychiatric disorders. It will bring together leading scientists in the fields of CNS metabolism\, epigenetics and glia function. \nMay 13\, 9:00 a.m.-6:00 p.m. & May 14\, 9:00 a.m.-2:00 p.m. \nLearn more » \nPresented by The Center for Glial Biology\, a collaborative initiative of the Advanced Science Research Center and the Icahn School of Medicine at Mount Sinai
URL:https://asrc.gc.cuny.edu/event/first-annual-manhattan-glia-spring-meeting/
LOCATION:Leon and Norma Hess Center for Science and Medicine\, 1470 Madison Avenue\, New York\, NY\, United States
CATEGORIES:Neuroscience
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/New_York:20190515T140000
DTEND;TZID=America/New_York:20190515T150000
DTSTAMP:20260528T081234
CREATED:20190412T203413Z
LAST-MODIFIED:20190513T204856Z
UID:10000881-1557928800-1557932400@asrc.gc.cuny.edu
SUMMARY:Neuroscience Seminar: Klaus-Armin Nave\, Ph.D.\, Max Planck Institute of Experimental Medicine
DESCRIPTION:Myelin lipids as metabolic energy reserves in white matter tracts\nSpeaker:\nKlaus-Armin Nave\, Ph.D.\nDirector\, Deptartment of Neurogenetics\nMax Planck Institute of Experimental Medicine \nAbstract\nIn the central nervous system of vertebrates\, oligodendrocytes synthesize myelin\, a lipid-rich multilayered membrane sheath that electrically insulates axons for fast impulse propagation. As glycolytic cells\, oligodendrocytes provide spiking axons with lactate\, a metabolic support function of glia that precedes the evolution of myelin. In non-myelinating species\, glial cells harbor “lipid droplets”\, an energy source that may have evolved into the lipid-rich myelin compartment of higher vertebrates. We thus hypothesized that myelin itself can be a source of energy that is utilized during a metabolic crisis. Using the myelinated optic nerve as a model system\, we found that glucose deprived oligodendrocytes readily metabolize myelin lipids and survive\, unlike astrocytes\, for 24 hours which depends on fatty acid beta-oxidation. Using ex vivo recordings of the optic nerve and metabolic sensors neuronally expressed in transgenic mice\, we found that myelin lipid metabolization even supports ATP levels of the underlying axon. Deleting the glucose transporter (GLUT1) gene from mature oligodendrocytes causes a gradual loss of myelin in vivo\, as determined by g-ratio analysis. We suggest that myelin is a lipid based metabolic reserve that can prolong oligodendrocyte survival and axonal integrity upon energy deprivation\, a finding relevant for myelin disorders and potentially neurodegenerative diseases. \nAbout the Speaker\nKlaus-Armin Nave studied Biology obtained his Ph.D. in Neuroscience from the University of California\, San Diego\, followed by postdoctoral work at the Salk Institute for Biological Studies. He became an independent research group leader at the Center for Molecular Biology (ZMBH) of the University of Heidelberg\, where he was promoted to Full Professor in 1998. In 1999\, he was recruited by the Max Planck Society to direct the Department of Neurogenetics at the Max Planck Institute of Experimental Medicine in Goettingen. His current research focusses on mechanisms of neuron-glia signaling\, glial support of axonal energy metabolism and function\, and models of human neuropsychiatric diseases.
URL:https://asrc.gc.cuny.edu/event/neuroscience-seminar-klaus-armin-nave-ph-d-max-planck-institute-of-experimental-medicine/
LOCATION:ASRC 1st Floor Seminar Room\, 85 St. Nicholas Terrace\, New York\, NY\, 10031\, United States
CATEGORIES:Neuroscience
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/New_York:20190516T110000
DTEND;TZID=America/New_York:20190516T120000
DTSTAMP:20260528T081234
CREATED:20190412T203624Z
LAST-MODIFIED:20190513T205001Z
UID:10000882-1558004400-1558008000@asrc.gc.cuny.edu
SUMMARY:Neuroscience Seminar: Francesco De Angelis\, Ph.D.\, Italian Institute of Technology
DESCRIPTION:3D nanostructures for biosensing in living tissues\nSpeaker:\nFrancesco De Angelis\, Ph.D.\nItalian Institute of Technology \nAbstract\nThe ability to interact with neuronal cells and to monitor their status plays a pivotal role in neuroscience\, pharmacology and cell biology. Despite the efforts of a very large community\, progresses in this field remain slow because of a dense multi-scale dynamics involving signaling at the molecular\, cellular and large network levels. Therefore\, observing cell signaling within large networks is a major challenge that can revolutionize our capability of studying the brain and its physio-pathological functions\, as well as of deriving bio-inspired concepts to implement artificial systems based on neuronal circuits. \nIn the last years\, we deeply investigated both theoretically and experimentally the interactions of 3D nanostructured sensors with living cells such as human neurons and cardiomyocytes. The aim is to make an effective interface between living tissues and different classes of nano-sensors hence enabling multiscale and multivariable observation of cell dynamics. In particular\, we developed a method for opening transient nanopores into the cell membrane that is in close proximity with the nanosensor. After the membrane poration the tip of the sensor is in direct contact with the intracellular compartment thus enabling intracellular investigations which include Raman traces of biomolecules\, electrical recording of action potentials of human neurons and cardiomyocytes\, and controlled delivery of single nanoparticles into selected cells. We demonstrated the possibility of non-invasively testing the effect of relevant drugs on human cells with particular regards to cardio-toxicity\, that is a fundamental step before the clinical trials. Due to its robustness and ease of use\, we expect the method will be rapidly adopted by the scientific community and by pharmaceutical companies. In fact\, the field suffers the lack of reliable approaches for pharmacological screening of drugs devoted to the central nervous system. \nAlso\, we will take this opportunity to give a short overview of different types of optical and plasmonic biosensors we are currently developing. The latter includes single molecule Raman Sensors\, DNA detection\, and Protein sequencing. \nAbout the Speaker\nDr. Francesco De Angelis carried out his Ph.D. studies in Physics at the Institute of Photonics and Nanotechnologies (CNR\, Rome\, 2004). Currently\, he is Tenured Senior Researcher at Istituto Italiano di Tecnologia where he leads the Plasmon Nanotechnology Unit. The main goal of his research activity is to exploit advanced nanofabrication techniques for controlling the properties of materials at the nanoscales. The majority of the activity concerns the applications of photonic and plasmonic devices to biology and bio-sensing through enhanced spectroscopies (Raman\, IR\, Fluorescence) and electrical measurements. Different interdisciplinary projects are carried out in collaboration with Biologists and Neuroscientists. Among them\, the development of hybrid interfaces between 3D nanostructured devices and living neuronal networks and the development of next-generation optical methods for DNA and protein sequencing.
URL:https://asrc.gc.cuny.edu/event/neuroscience-seminar-francesco-de-angelis-ph-d-italian-institute-of-technology/
LOCATION:ASRC 1st Floor Seminar Room\, 85 St. Nicholas Terrace\, New York\, NY\, 10031\, United States
CATEGORIES:Neuroscience
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/New_York:20190520T140000
DTEND;TZID=America/New_York:20190520T160000
DTSTAMP:20260528T081234
CREATED:20190510T162331Z
LAST-MODIFIED:20190513T205324Z
UID:10000973-1558360800-1558368000@asrc.gc.cuny.edu
SUMMARY:Brain & Body
DESCRIPTION:Patrizia Casaccia\, founding director of the Neuroscience Initiative at the Advanced Science Research Center at The Graduate Center\, CUNY and her research team have joined together with the National Multiple Sclerosis Society to bring this wellness program to the Harlem Community. \nAgenda\n2:00 p.m. – Brain\nDr. Patrizia Casaccia will discuss how brain & body health are interconnected and share her latest research on how body weight may affect the disease course in ms. \n2:30 p.m. – Body\nThe ultimate exercise practice to feed your brain & body with fitness expert Raven. \n3:15 p.m. – Light refreshments & chat with the scientists \n4:00 p.m. – Farewell \nRegistration\nRegister by May 15: \nJoEllen Zembruski-Ruple\nManager\, Healthcare Provider Engagement\n212.453.3261\nJoEllen.Zembruskiruple@nmss.org
URL:https://asrc.gc.cuny.edu/event/brain-body/
LOCATION:CUNY Graduate School of Public Health & Health Policy\, 55 West 125 St. 7th floor\, New York\, NY\, 10027\, United States
CATEGORIES:Neuroscience
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/New_York:20190521T130000
DTEND;TZID=America/New_York:20190521T143000
DTSTAMP:20260528T081234
CREATED:20190125T193625Z
LAST-MODIFIED:20190520T164736Z
UID:10000879-1558443600-1558449000@asrc.gc.cuny.edu
SUMMARY:Neuroscience Work-in-Progress Seminar
DESCRIPTION:AFM profiling of lesions in animal and human models of CNS demyelination\nSpeaker:\n Matt Urbanski\nMelendez-Vasquez Lab\, Hunter College \nAbstract\nMechanical cues delivered by the extracellular matrix\, and mediated by myosin II activity\, have been shown to regulate cell morphology and gene expression independent of chemical signaling. \nWork from our laboratory has demonstrated that increased ECM stiffness inhibits oligodendrocyte differentiation in a myosin II-dependent manner in vitro\, and that ablation of myosin II results in enhanced myelin repair in a mouse model of focal CNS demyelination. These findings suggest that changes in ECM stiffness\, sensed in a myosin II dependent-manner\, may contribute to the poor remeyelination observed following traumatic injury\, or in disorders such as multiple sclerosis (MS). \nHowever\, the mechanical properties of injured CNS tissue have not been well characterized. In addition\, most studies were performed at low spatial resolution\, and do not accurately reflect the mechanical properties of tissue at the cellular level. Our recent work addresses this by using a combined atomic force microscopy (AFM) and histological approach. We have analyzed the mechanical properties of acutely and chronically demyelinated mouse brain\, as well as human MS tissue\, and show that acute and chronic lesions display opposite mechanical properties. \n\nThe ASRC Neuroscience Work-in-Progress Seminars consist of an hour-long presentation on research relevant to the fields of neurobiology and translational neuroscience. Talks will be given by senior Ph.D. students\, postdoctoral and faculty researchers. Anyone interested is encouraged to attend and actively participate in discussions. \nWork-in-Progress Seminars are presented in collaboration with The City College of New York.
URL:https://asrc.gc.cuny.edu/event/neuroscience-work-in-progress-seminar-2019-05-28/
LOCATION:ASRC 1st Floor Seminar Room\, 85 St. Nicholas Terrace\, New York\, NY\, 10031\, United States
CATEGORIES:Neuroscience
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/New_York:20190523T110000
DTEND;TZID=America/New_York:20190523T120000
DTSTAMP:20260528T081234
CREATED:20190123T214625Z
LAST-MODIFIED:20190520T164518Z
UID:10000949-1558609200-1558612800@asrc.gc.cuny.edu
SUMMARY:Neuroscience Seminar: Mark Ansorge\, Ph.D.\, Columbia University
DESCRIPTION:Monoaminergic circuit mechanisms mediating developmental malleability of emotional and cognitive function\nSpeaker:\nMark Ansorge\, Ph.D.\nAssistant Professor\, The Sackler Institute for Developmental Psychobiology\nColumbia University\nNew York\, NY \nAbstract\nWe have identified two sensitive developmental periods during which the strength of monoaminergic signaling affects adult behavior: (1) an early postnatal serotonin-sensitive period that impacts cognition\, anxiety and depression-related behaviors\, and (2) a later peri-adolescent dopamine- and serotonin-sensitive period affecting aggression\, impulsivity and behavioral response to psychostimulants. Our findings indicate that neuropsychiatric disorders characterized by alterations in these behavioral domains may have developmental origins. Thus\, genetic\, epigenetic and environmental factors that impact serotonin and/or dopamine signaling during specific periods of development might mediate the risk for depression\, anxiety disorders\, schizophrenia and substance abuse. Which neural circuits are sensitive to monoaminergic signaling during restricted developmental periods? What functional circuit parameters are affected? How do changes in circuit function relate to behavior? These questions currently guide most projects in the lab. While providing a general conceptual overview relating most projects in the lab\, the talk will largely focus on two monoaminergic pathways\, the median raphe to CA1 pathway and the ventral tegmental are to lateral septum pathway\, and their roles in memory formation and aggression\, respectively.
URL:https://asrc.gc.cuny.edu/event/neuroscience-seminar-mark-ansorge-2019-05-16/
LOCATION:ASRC 1st Floor Seminar Room\, 85 St. Nicholas Terrace\, New York\, NY\, 10031\, United States
CATEGORIES:Neuroscience
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