CV Jessica Payne
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REWARD LIST ‐ RANK C JCR 2018 ‐CiteScore 2018 WOS Edition/ Scopus Main Rank Subject Category Journal Title ISSN Subject Area code IEEE TRANSACTIONS ON ULTRASONICS SCIE ACOUSTICS 08853010 C FERROELECTRICS AND FREQUENCY SCIE ACOUSTICS JOURNAL OF VIBRATION AND CONTROL 10775463 C SCIE AGRICULTURAL ECONOMICS & POLICY JOURNAL OF AGRICULTURAL ECONOMICS 0021857X C SCIE AGRICULTURAL ENGINEERING BIOMASS & BIOENERGY 09619534 C SCIE AGRICULTURE, DAIRY & ANIMAL SCIENCE ANIMAL REPRODUCTION SCIENCE 03784320 C SCIE AGRICULTURE, DAIRY & ANIMAL SCIENCE APPLIED ANIMAL BEHAVIOUR SCIENCE 01681591 C SCIE AGRICULTURE, DAIRY & ANIMAL SCIENCE ARCHIVES OF ANIMAL NUTRITION 1745039X C JOURNAL OF ANIMAL PHYSIOLOGY AND SCIE AGRICULTURE, DAIRY & ANIMAL SCIENCE 09312439 C ANIMAL NUTRITION SCIE AGRICULTURE, DAIRY & ANIMAL SCIENCE Animals 20762615 C SCIE AGRICULTURE, MULTIDISCIPLINARY Journal of Land Use Science 1747423X C RENEWABLE AGRICULTURE AND FOOD SCIE AGRICULTURE, MULTIDISCIPLINARY 17421705 C SYSTEMS SCIE AGRICULTURE, MULTIDISCIPLINARY ANNALS OF APPLIED BIOLOGY 00034746 C SCIE AGRICULTURE, MULTIDISCIPLINARY CALIFORNIA AGRICULTURE 00080845 C SCIE AGRONOMY PLANT PATHOLOGY 00320862 C SCIE AGRONOMY IRRIGATION SCIENCE 03427188 C SCIE AGRONOMY Rice Science 16726308 C SCIE AGRONOMY Agronomy‐Basel 20734395 C SCIE AGRONOMY CROP PROTECTION 02612194 C SCIE AGRONOMY EXPERIMENTAL AGRICULTURE 00144797 C JOURNAL OF PLANT NUTRITION AND SOIL SCIE AGRONOMY 14368730 C SCIENCE SCIE ALLERGY CONTACT DERMATITIS 01051873 C SCIE ALLERGY Allergy Asthma & Immunology Research 20927355 C Advances -
SCIENCE CITATION INDEX EXPANDED - JOURNAL LIST Total Journals: 8631
SCIENCE CITATION INDEX EXPANDED - JOURNAL LIST Total journals: 8631 1. 4OR-A QUARTERLY JOURNAL OF OPERATIONS RESEARCH 2. AAPG BULLETIN 3. AAPS JOURNAL 4. AAPS PHARMSCITECH 5. AATCC REVIEW 6. ABDOMINAL IMAGING 7. ABHANDLUNGEN AUS DEM MATHEMATISCHEN SEMINAR DER UNIVERSITAT HAMBURG 8. ABSTRACT AND APPLIED ANALYSIS 9. ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY 10. ACADEMIC EMERGENCY MEDICINE 11. ACADEMIC MEDICINE 12. ACADEMIC PEDIATRICS 13. ACADEMIC RADIOLOGY 14. ACCOUNTABILITY IN RESEARCH-POLICIES AND QUALITY ASSURANCE 15. ACCOUNTS OF CHEMICAL RESEARCH 16. ACCREDITATION AND QUALITY ASSURANCE 17. ACI MATERIALS JOURNAL 18. ACI STRUCTURAL JOURNAL 19. ACM COMPUTING SURVEYS 20. ACM JOURNAL ON EMERGING TECHNOLOGIES IN COMPUTING SYSTEMS 21. ACM SIGCOMM COMPUTER COMMUNICATION REVIEW 22. ACM SIGPLAN NOTICES 23. ACM TRANSACTIONS ON ALGORITHMS 24. ACM TRANSACTIONS ON APPLIED PERCEPTION 25. ACM TRANSACTIONS ON ARCHITECTURE AND CODE OPTIMIZATION 26. ACM TRANSACTIONS ON AUTONOMOUS AND ADAPTIVE SYSTEMS 27. ACM TRANSACTIONS ON COMPUTATIONAL LOGIC 28. ACM TRANSACTIONS ON COMPUTER SYSTEMS 29. ACM TRANSACTIONS ON COMPUTER-HUMAN INTERACTION 30. ACM TRANSACTIONS ON DATABASE SYSTEMS 31. ACM TRANSACTIONS ON DESIGN AUTOMATION OF ELECTRONIC SYSTEMS 32. ACM TRANSACTIONS ON EMBEDDED COMPUTING SYSTEMS 33. ACM TRANSACTIONS ON GRAPHICS 34. ACM TRANSACTIONS ON INFORMATION AND SYSTEM SECURITY 35. ACM TRANSACTIONS ON INFORMATION SYSTEMS 36. ACM TRANSACTIONS ON INTELLIGENT SYSTEMS AND TECHNOLOGY 37. ACM TRANSACTIONS ON INTERNET TECHNOLOGY 38. ACM TRANSACTIONS ON KNOWLEDGE DISCOVERY FROM DATA 39. ACM TRANSACTIONS ON MATHEMATICAL SOFTWARE 40. ACM TRANSACTIONS ON MODELING AND COMPUTER SIMULATION 41. ACM TRANSACTIONS ON MULTIMEDIA COMPUTING COMMUNICATIONS AND APPLICATIONS 42. ACM TRANSACTIONS ON PROGRAMMING LANGUAGES AND SYSTEMS 43. ACM TRANSACTIONS ON RECONFIGURABLE TECHNOLOGY AND SYSTEMS 44. -
Jennifer I. Luebke 1 Curriculum Vitae Jennifer I. Luebke, Ph.D. Associate
Jennifer I. Luebke Curriculum Vitae Jennifer I. Luebke, Ph.D. Associate Professor of Anatomy & Neurobiology Associate Professor of Psychiatry Director, Laboratory of Cellular Neurobiology Boston University School of Medicine 85 East Newton Street, M949 Boston, Massachusetts 02118 Voice: 617-638-4930 Email: [email protected] Education and Employment History: 1980-1984: B.S. (Biology) Randolph-Macon College, Ashland, Virginia 1984-1986: Laboratory Technician (Laboratory of Cell Biology and Genetics, NIDDK) National Institutes of Health, Bethesda, Maryland 1986-1990: Ph.D. Student (Anatomy & Neurobiology), Boston University School of Medicine, Boston, Massachusetts (Linda L. Wright, mentor) 1990-1992: Postdoctoral Fellow, Department of Psychiatry, Harvard Medical School, Boston, Massachusetts (Robert W. McCarley and Robert W. Greene mentors) 1992-1995: Postdoctoral Fellow, Department of Physiology, Tufts University Medical School, Boston, Massachusetts (Kathleen Dunlap, mentor) 1995-2003: Assistant Professor, Department of Anatomy & Neurobiology and Department of Psychiatry, Boston University School of Medicine, Boston, Massachusetts 2004-Present: Associate Professor, Department of Anatomy & Neurobiology and Department of Psychiatry, Boston University School of Medicine, Boston, Massachusetts 2010-Present: Adjunct Associate Professor, Department of Neuroscience, Mount Sinai School of Medicine, New York, New York Research Summary: Research is directed toward understanding alterations in the structure and function of individual cortical pyramidal cells in a rhesus monkey model of normal aging and in transgenic mouse models of neurodegenerative disease. Using whole-cell patch-clamp methods and ultra-high resolution confocal microscopy, Dr. Luebke has demonstrated marked alterations in action potential firing patterns (and underlying ionic currents), glutamatergic and GABAergic synaptic response properties and detailed dendritic and spine architecture in cortical pyramidal cells both in normal aging and in mouse models of neurodegenerative disease. -
Predicting Cognitive Decline: Genetic, Environmental and Lifestyle Risk Factors
Predicting Cognitive Decline: Genetic, Environmental and Lifestyle Risk Factors Shea J. Andrews April 2017 A thesis by compilation submitted for the degree of Doctor of Philosophy of The Australian National University © Copyright by Shea John Frederick Andrews 2017 All Rights Reserved i Declaration This work was conducted from February 2013 to August 2016 at the Genome Diversity and Health Group, John Curtin School of Medical Research, The Australian National University, Canberra, ACT. This thesis by compilation consists of five original publications describing the analyses I have performed during my candidature investigating the role of genetic, environmental and lifestyle risk factors in normal cognitive aging. All five publications have been published in Q1 ranked journals according to the SCImago Journal & Country Rankings in the fields of neurology, genetics, psychiatry and mental health, and geriatric and gerontology. My specific contribution to each manuscript is detailed in the subsequent pages in the form of a statement signed by the senior author of each publication. This document has not been submitted for qualifications at any other academic institution. Shea Andrews Canberra, Australia April 2017 ii Published Papers Andrews, SJ, Das, D., Anstey, KJ., Easteal, S. (2015). Interactive effect of APOE genotype and blood pressure on cognitive decline: The PATH through life project. Journal of Alzheimer's Disease. 44(4): 1087-98. DOI: 10.3233/JAD- 140630 For this publication, I designed and performed all statistical analyses and wrote the manuscript. A slightly modified version of this paper is presented in Chapter 3. ____________________ Simon Easteal Senior Author April 2017 Andrews SJ, Das D, Cherbuin N, Anstey KJ, Easteal S. -
Brain Ageing in the New Millennium
Brain ageing in the new millennium Julian N. Trollor, Michael J. Valenzuela Objective: This paper examines the current literature pertaining to brain ageing. The objective of this review is to provide an overview of the effects of ageing on brain structure and function and to examine possible mediators of these changes. Methods: A MEDLINE search was conducted for each area of interest. A selective review was undertaken of relevant articles. Results: Although fundamental changes in fluid intellectual abilities occur with age, global cognitive decline is not a hallmark of the ageing process. Decline in fluid intellectual ability is paralleled by regionally specific age related changes apparent from both structural and functional neuroimaging studies. The histopathological mediators of these changes do not appear to be reduction in neuronal number, which, with the exception of selected hippo- campal regions, remain relatively stable across age. At the molecular level, several mech- anisms of age related change have been postulated. Such theoretical models await refinement and may eventually provide a basis for therapy designed to reduce effects of the ageing process. The role of possible protective factors such as ‘brain reserve’, neuro- protective agents and hormonal factors in modifying individual vulnerability to the ageing process has been the focus of a limited number of studies. Conclusion: Our understanding of the functional and structural changes associated with both healthy and pathological ageing is rapidly gaining in sophistication and complexity. An awareness of the fundamental biological substrates underpinning the ageing process will allow improved insights into vulnerability to neuropsychiatric disease associated with advancing age. Key words: brain ageing, cognition, dementia, neuroimaging. -
The Effects of Normal Aging on Myelin and Nerve Fibers: a Review∗
Journal of Neurocytology 31, 581–593 (2002) The effects of normal aging on myelin and nerve fibers: A review∗ ALAN PETERS Department of Anatomy and Neurobiology, Boston University School of Medicine, 715, Albany Street, Boston, MA 02118, USA [email protected] Received 7 January 2003; revised 4 March 2003; accepted 5 March 2003 Abstract It was believed that the cause of the cognitive decline exhibited by human and non-human primates during normal aging was a loss of cortical neurons. It is now known that significant numbers of cortical neurons are not lost and other bases for the cognitive decline have been sought. One contributing factor may be changes in nerve fibers. With age some myelin sheaths exhibit degenerative changes, such as the formation of splits containing electron dense cytoplasm, and the formation on myelin balloons. It is suggested that such degenerative changes lead to cognitive decline because they cause changes in conduction velocity, resulting in a disruption of the normal timing in neuronal circuits. Yet as degeneration occurs, other changes, such as the formation of redundant myelin and increasing thickness suggest of sheaths, suggest some myelin formation is continuing during aging. Another indication of this is that oligodendrocytes increase in number with age. In addition to the myelin changes, stereological studies have shown a loss of nerve fibers from the white matter of the cerebral hemispheres of humans, while other studies have shown a loss of nerve fibers from the optic nerves and anterior commissure in monkeys. It is likely that such nerve fiber loss also contributes to cognitive decline, because of the consequent decrease in connections between neurons. -
Technology and Aging in America (Part 14 Of
Appendix B The Cell Biology of Aging Introduction spans that seem to be “programmed” into them accord- ing to species. Mechanisms underlying this programmed The distinction between the effects of aging as a aging could involve an intrinsic genetic component of chronological process and diseases whose prevalence the tissues (24), and/or an extrinsic “neuroendocrine increase with advancing age remains blurred. Condi- pacemaker” (16,17). tions once thought to be inevitable companions of old The genetic version of the biological clock is bol- age are now known to in fact be pathological in origin stered by the observation that the survival time of and thus possibly treatable and preventable. One ex- tissues grafted (or transferred) from an older animal ample is senile dementia, no longer the mysterious fate into a younger one of the same species seems to de- of the very old, but often a clinical manifestation of pend on the age of the donor and is not influenced arteriosclerotic or biochemical brain disease. by the “younger” environment into which it has been Further research may elucidate the mechanisms introduced (24). Similarly, when nuclei from younger underlying aging and their possible connection to age- cells are transplanted into the cytoplasm of older cells, related diseases, leading to the development of medi- the recipients then live longer and regain the ability cal techniques that delay the onset and progression to replicate. These observations all suggest that a of symptoms. While it may not lead to actual exten- “clock” controlling aging does exist and may be located sion of the human life span, such knowledge could re- in the nucleus, possibly in the genetic material (24). -
Integrated Transcriptomic and Neuroimaging Brain Model Decodes
RESEARCH ARTICLE Integrated transcriptomic and neuroimaging brain model decodes biological mechanisms in aging and Alzheimer’s disease Quadri Adewale1,2,3, Ahmed F Khan1,2,3, Felix Carbonell4, Yasser Iturria-Medina1,2,3*, Alzheimer’s Disease Neuroimaging Initiative† 1Neurology and Neurosurgery Department, Montreal Neurological Institute, McGill University, Montreal, Canada; 2McConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Canada; 3Ludmer Centre for Neuroinformatics and Mental Health, McGill University, Montreal, Canada; *For correspondence: 4Biospective Inc, Montreal, Canada [email protected] †Data used in preparation of this article were partly obtained from the Alzheimer’s Disease Abstract Both healthy aging and Alzheimer’s disease (AD) are characterized by concurrent Neuroimaging Initiative (ADNI) alterations in several biological factors. However, generative brain models of aging and AD are database (adni.loni.usc.edu). As limited in incorporating the measures of these biological factors at different spatial resolutions. such, the investigators within the Here, we propose a personalized bottom-up spatiotemporal brain model that accounts for the ADNI contributed to the design direct interplay between hundreds of RNA transcripts and multiple macroscopic neuroimaging and implementation of ADNI modalities (PET, MRI). In normal elderly and AD participants, the model identifies top genes and/or provided data but did not modulating tau and amyloid-b burdens, vascular flow, glucose metabolism, functional activity, and participate in analysis or writing atrophy to drive cognitive decline. The results also revealed that AD and healthy aging share of this report. A complete listing specific biological mechanisms, even though AD is a separate entity with considerably more altered of ADNI investigators can be pathways. -
1 out of 25 ELIZABETH A. KENSINGER
ELIZABETH A. KENSINGER Boston College • 140 Commonwealth Avenue • Chestnut Hill, MA 02467 Department of PsyChology and Neuroscience • McGuinn Hall Room 300 Phone: 617-552-1350 • Fax: 617-552-0523 Email: [email protected] CV updated 2/15/21 EDUCATION 1998-2003 Massachusetts Institute of Technology, Ph.D., Neuroscience Advisor: Suzanne Corkin; Committee: Helen Barbas, Earl Miller, Anthony Wagner Dissertation title: Investigations of the cognitive and neural processes supporting memory for emotional and neutral information 1994-1998 Harvard University, B.A., Psychology and Biology, summa cum laude POSTDOCTORAL RESEARCH TRAINING 2003-06 Research fellow, Massachusetts General Hospital, Dept. of Radiology and Harvard University, Dept. of Psychology Advisor: Daniel Schacter PRIMARY ACADEMIC POSITION 2018-present Chair, Dept. of Psychology and Neuroscience*, Boston College 2013-present Professor, Dept. of Psychology and Neuroscience*, Boston College *name changed from Dept. of Psychology in 2020 2009-2013 Associate Professor, Dept. of Psychology, Boston College 2006-2009 Assistant Professor, Dept. of Psychology, Boston College RESEARCH SUPPORT Ongoing Research Grants Elizabeth A. Kensinger, co-P.I. (Jessica D. Payne, co-P.I.) Sleep and Selective Emotional Memory Consolidation from Young Adulthood through Middle Age: PSG an fMRI Investigations National Science Foundation (BCS-2001025) 09/01/2020-08/31/2024 Elizabeth A. Kensinger, co-I (Jaclyn H. Ford, P.I.) Age differences in when - not whether - sensory regions are recruited during memory retrieval (BCS- 1923173) National Science Foundation (BCS) 08/16/2019-08/15/2023 Elizabeth A. Kensinger, P.I. Links between affect, executive function, and prefrontal structure in aging: A longitudinal analysis National Institute on Aging (R03-AG060027) 09/01/2018-05/31/2021 Elizabeth A. -
Time-Dependent Effects of Cortisol on Selective Attention and Emotional Interference: a Functional MRI Study
ORIGINAL RESEARCH ARTICLE published: 28 August 2012 INTEGRATIVE NEUROSCIENCE doi: 10.3389/fnint.2012.00066 Time-dependent effects of cortisol on selective attention and emotional interference: a functional MRI study MarloesJ.A.G.Henckens1,2*, Guido A. van Wingen 1,3, Marian Joëls 2 and Guillén Fernández 1,4 1 Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen, Nijmegen, Netherlands 2 Department of Neuroscience and Pharmacology, Rudolf Magnus Institute, University Medical Center Utrecht, Utrecht, Netherlands 3 Department of Psychiatry, Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands 4 Department of Cognitive Neuroscience, Radboud University Nijmegen Medical Centre, Nijmegen, Netherlands Edited by: Acute stress is known to induce a state of hypervigilance, allowing optimal detection Florin Dolcos, University of Illinois at of threats. Although one may benefit from sensitive sensory processing, it comes at Urbana-Champaign, USA the cost of unselective attention and increased distraction by irrelevant information. Reviewed by: Corticosteroids, released in response to stress, have been shown to profoundly influence Barry Setlow, University of Florida, USA brain function in a time-dependent manner, causing rapid non-genomic and slow genomic Hao Zhang, Duke University, USA effects. Here, we investigated how these time-dependent effects influence the neural Florin Dolcos, University of Illinois at mechanisms underlying selective attention and the inhibition of emotional distracters Urbana-Champaign, USA in humans. Implementing a randomized, double-blind, placebo-controlled design, 65 Jessica Payne, University of Notre Dame, USA young healthy men received 10 mg hydrocortisone either 60 min (rapid effects) or *Correspondence: 270 min (slow effects), or placebo prior to an emotional distraction task, consisting Marloes J. -
The Effect of Cortisol on Emotional Responses Depends on Order of Cortisol and Placebo Administration in a Within-Subject Design
+ Models PNEC-1901; No. of Pages 10 Psychoneuroendocrinology (2011) xxx, xxx—xxx available at www.sciencedirect.com journal homepage: www.elsevier.com/locate/psyneuen The effect of cortisol on emotional responses depends on order of cortisol and placebo administration in a within-subject design Michelle M. Wirth a,*, Sean M. Scherer b, Roxanne M. Hoks c,1, Heather C. Abercrombie b,c a Department of Psychology, University of Notre Dame, United States b Department of Psychology, University of Wisconsin-Madison, United States c Department of Psychiatry, University of Wisconsin-Madison, United States Received 31 August 2010; received in revised form 29 November 2010; accepted 30 November 2010 KEYWORDS Summary Cortisol does not exhibit a straightforward relationship with mood states; adminis- Emotion; tration of glucocorticoids to human subjects has produced mixed effects on mood and emotional Negative affect; processing. In this study, participants (N = 46) received intravenous hydrocortisone (synthetic Cortisol; cortisol; 0.1 mg/kg body weight) and placebo in randomized order over two sessions 48 h apart. Glucocorticoids; Following the infusion, participants rated neutral and unpleasant pictures. In Session 1, parti- International Affective cipants reported elevated negative affect (NA) following the picture-rating task, regardless of Picture System (IAPS); treatment. In Session 2, however, only participants who received cortisol (and thus who had Learning received placebo in Session 1) reported elevated NA. Arousal ratings for unpleasant -
Learning, Memory, and Sleep in Humans
Author's personal copy Learning, Memory, and Sleep in Humans Jessica D. Payne, PhD KEYWORDS Slow wave sleep Memory Hippocampus Rapid eye movement sleep About one-third of a person’s life is spent sleeping, functional consequences but also makes it difficult yet in spite of the advances in understanding the to know which distinction is critical for memory processes that generate and maintain sleep, the processing: NREM versus REM sleep or early functional significance of sleep remains a mystery. versus late sleep. Numerous theories regarding the role of sleep Neurotransmitters, particularly the monoamines have been proposed, including homeostatic resto- serotonin (5-HT) and norepinephrine (NE), and ration, thermoregulation, tissue repair, and immune acetylcholine (ACh), play a critical role in switching control. A theory that has received enormous the brain from one sleep stage to another. REM support in the last decade concerns sleep’s role in sleep occurs when activity in the aminergic system processing and storing memories. This article has decreased enough to allow the reticular reviews some of the evidence suggesting that sleep system to escape its inhibitory influence.1 The is critical for long-lasting memories. This body of release from aminergic inhibition stimulates evidence has grown impressively large and covers cholinergic reticular neurons in the brainstem and a range of studies at the molecular, cellular, physio- switches the sleeping brain into the highly active logic, and behavioral levels of analysis. REM state, in which ACh levels are as high as in the waking state. Overall, REM sleep is also associated with higher levels of cortisol than DEFINING SLEEP AND MEMORY NREM sleep.