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Full-Text Articles in Medicine and Health Sciences
Solution-Focused Therapy Changes Neurophysiological Activation In Collegiate Athletes: An Intervention Study, Kyler T. Shumway
Solution-Focused Therapy Changes Neurophysiological Activation In Collegiate Athletes: An Intervention Study, Kyler T. Shumway
Doctor of Psychology (PsyD)
Neurophysiological research has begun to uncover how therapy produces change in the brain. To examine this phenomenon, many studies have controlled for specific symptoms to identify where therapy has the greatest effect (Linden, 2006). In athletic performance, anxiety represents a significant struggle for college athletes (Mabweazara, Leach, & Andrews, 2017). The present study intended to examine the impact of brief therapy on brain activation and competition anxiety in college athletes. A sample of collegiate athletes (n = 17) participated in a pre-post intervention study. Pre- and post-intervention measures included electroencephalogram (EEG), galvanic skin response (GSR), self-report anxiety measures (SAS-2, GAD-7), …
Strad Pseudokinases Regulate Axogenesis And Lkb1 Stability, Biliana O. Veleva-Rotse, James L. Smart, Annette F. Baas, Benjamin Edmonds, Zi-Ming Zhao, Allyson Brown, Lillian R. Klug, Kelly Hansen, Gabrielle Rielly, Alexandria P. Gardner, Krishnaveni Subbiah, Eric A. Gaucher, Hans Clevers, Anthony P. Barnes
Strad Pseudokinases Regulate Axogenesis And Lkb1 Stability, Biliana O. Veleva-Rotse, James L. Smart, Annette F. Baas, Benjamin Edmonds, Zi-Ming Zhao, Allyson Brown, Lillian R. Klug, Kelly Hansen, Gabrielle Rielly, Alexandria P. Gardner, Krishnaveni Subbiah, Eric A. Gaucher, Hans Clevers, Anthony P. Barnes
Faculty Publications - Department of Biological & Molecular Science
No abstract provided.
Glucocorticoids Exacerbate Obesity And Insulin Resistance In Neuron-Specific Proopiomelanocortin-Deficient Mice, James L. Smart, Virgine Tolle, Malcolm J. Low
Glucocorticoids Exacerbate Obesity And Insulin Resistance In Neuron-Specific Proopiomelanocortin-Deficient Mice, James L. Smart, Virgine Tolle, Malcolm J. Low
Faculty Publications - Department of Biological & Molecular Science
Null mutations of the proopiomelanocortin gene (Pomc–/–) cause obesity in humans and rodents, but the contributions of central versus pituitary POMC deficiency are not fully established. To elucidate these roles, we introduced a POMC transgene (Tg) that selectively restored peripheral melanocortin and corticosterone secretion in Pomc–/– mice. Rather than improving energy balance, the genetic replacement of pituitary POMC in Pomc–/–Tg+ mice aggravated their metabolic syndrome with increased caloric intake and feed efficiency, reduced oxygen consumption, increased subcutaneous, visceral, and hepatic fat, and severe insulin resistance. Pair-feeding of Pomc–/–Tg+ mice to the daily intake of lean controls normalized their rate of …
Proopiomelanocortin Neurons In Nucleus Tractus Solitarius Are Activated By Visceral Afferents: Regulation By Cholecystokinin And Opioids, Suzanne M. Appleyard, Timothy W. Bailey, Mark W. Doyle, Young-Ho Jin, James L. Smart, Malcolm J. Low, Michael C. Andresen
Proopiomelanocortin Neurons In Nucleus Tractus Solitarius Are Activated By Visceral Afferents: Regulation By Cholecystokinin And Opioids, Suzanne M. Appleyard, Timothy W. Bailey, Mark W. Doyle, Young-Ho Jin, James L. Smart, Malcolm J. Low, Michael C. Andresen
Faculty Publications - Department of Biological & Molecular Science
The nucleustractus solitarius (NTS) receives dense terminations from cranial visceral afferents, including those from the gastrointestinal (GI) system. Although the NTS integrates peripheral satiety signals and relays this signal to central feeding centers, little is known about which NTS neurons are involved or what mechanisms are responsible. Proopiomelanocortin (POMC) neurons are good candidates for GI integration, because disruption of the POMC gene leads to severe obesity and hyperphagia. Here, we used POMC– enhanced green fluorescent protein (EGFP) transgenic mice to identify NTS POMC neurons. Intraperitoneal administration of cholecystokinin (CCK) induced c-fos gene expression in NTS POMC–EGFP neurons, suggesting that they …
Identification Of Neuronal Enhancers Of The Proopiomelanocortin Gene By Transgenic Mouse Analysis And Phylogenetic Footprinting, Flavio S. J. De Souza, Andrea M. Santangelo, Viviana Bumaschny, Marıa Elena Avale, James L. Smart, Malcolm J. Low, Marcelo Rubinstein
Identification Of Neuronal Enhancers Of The Proopiomelanocortin Gene By Transgenic Mouse Analysis And Phylogenetic Footprinting, Flavio S. J. De Souza, Andrea M. Santangelo, Viviana Bumaschny, Marıa Elena Avale, James L. Smart, Malcolm J. Low, Marcelo Rubinstein
Faculty Publications - Department of Biological & Molecular Science
The proopiomelanocortin (POMC) gene is expressed in the pituitary and arcuate neurons of the hypothalamus. POMC arcuate neurons play a central role in the control of energy homeostasis, and rare loss of function mutations in POMC cause obesity. Moreover, POMC is the prime candidate gene within a highly significant quantitative trait locus on chromosome 2 associated with obesity traits in several human populations. Here, we identify two phylogenetically conserved neuronal POMC enhancers designated nPE1 (600 bp) and nPE2 (150 bp) located approximately 10 to 12 kb upstream of mammalian POMC transcriptional units. We show that mouse or human genomic regions …
Activation Of Central Melanocortin Pathways By Fenfluramlne, Lora K. Heisler, Michael A. Cowley, Laurence H. Tecott, Wei Fan, Malcolm J. Low, James L. Smart, Marcelo Rubinstein, Jeffrey B. Tatro, Jacob N. Marcus, Henne Holstege, Charlotte E. Lee, Roger D. Cone, Joel K. Elmquist
Activation Of Central Melanocortin Pathways By Fenfluramlne, Lora K. Heisler, Michael A. Cowley, Laurence H. Tecott, Wei Fan, Malcolm J. Low, James L. Smart, Marcelo Rubinstein, Jeffrey B. Tatro, Jacob N. Marcus, Henne Holstege, Charlotte E. Lee, Roger D. Cone, Joel K. Elmquist
Faculty Publications - Department of Biological & Molecular Science
D-fenfluramine (d-FEN) was once widely prescribed and was among the most effective weight loss drugs, but was withdrawn from clinical use because of reports of cardiac complications in a subset of patients. Discerning the neurobiology underlying the anorexic action of d-FEN may facilitate the development of new drugs to prevent and treat obesity. Through a combination of functional neuroanatomy, feeding, and electrophysiology studies in rodents, we show that d-FEN-induced anorexia requires activation of central nervous system melanocortin pathways. These results provide a mechanistic explanation of d-FEN's anorexic actions and indicate that drugs targeting these downstream melanocortin pathways may prove to …