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A Framework for Understanding the Role of Psychological Processes in Disease Development, Maintenance, and Treatment: The 3P-Disease Model.
Front Psychol
November 2019
Department of Psychology, West Virginia University, Morgantown, WV, United States.
Health psychology is multidisciplinary, with researchers, practitioners, and policy makers finding themselves needing at least some level of competency in a variety of areas from psychology to physiology, public health, and others. Given this multidisciplinary ontology, prior attempts have been made to establish a framework for understanding the role of biological, psychological, and socio-environmental constructs in disease development, maintenance, and treatment. Other models, however, do not explain factors may interact and develop over time.
View Article and Find Full Text PDFInsomnia research: 3Ps and beyond.
Sleep Med Rev
June 2014
Department of Psychology, Drexel University, USA.
[Pathophysiology of insomnia].
Nihon Rinsho
August 2009
Department of Psychophysiology, National Institute of Mental Health, NCNP.
Insomniacs generally report not only sleep-related symptoms such as difficulty in initiating, maintaining, obtaining sufficient restorative sleep, but also experience various daytime impairment reflective of sleep deficits. Although pathophysiology of insomnia remains to be explored, physiological hyperarousal evidenced by cognitive, endocrine, and neurophysiologic variables has been revealed to be involved in onset and development of insomnia. Patients with insomnia also suffer from cognitive impairment.
View Article and Find Full Text PDFMapping the parameters of prion-induced neuropathology.
Proc Natl Acad Sci U S A
September 2000
The Wellcome Trust Centre for the Epidemiology of Infectious Disease, Department of Zoology, South Parks Road, Oxford OX1 3PS, United Kingdom.
We present a theoretical framework that enables us to dissect out the parametric dependencies of the pathogenesis of prion diseases. We are able to determine the influence of both host-dependent factors (connectivity, cell density, protein synthesis rate, and cell death) and strain-dependent factors (cell tropism, virulence, and replication rate). We use a model based on a linked system of differential equations on a lattice to explore how the regional distribution of central nervous system pathology in Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker syndrome, and fatal familial insomnia relates to each of these factors.
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