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- Adaptive fetal programming (1)
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Articles 1 - 6 of 6
Full-Text Articles in Physiology
The Role Of Inflammatory Pathways In Development, Growth, And Metabolism Of Skeletal Muscle In Iugr Offspring; Blood Gene Expression Of Inflammatory Factors As Novel Biomarkers For Assessing Stress And Wellbeing In Exotic Species., Robert J. Posont
Department of Animal Science: Dissertations, Theses, and Student Research
Our first study identified the effects of maternal inflammation-induced intrauterine growth restriction (MI-IUGR) on growth and muscle glucose metabolism in offspring supplemented with curcumin. MI-IUGR lambs exhibited asymmetric growth restriction at birth and 30d of age, but normal glucose-stimulated insulin secretion. Hindlimb glucose oxidation was reduced by MI-IUGR and not improved by curcumin supplementation. Ex vivo muscle glucose oxidation was reduced by MI-IUGR but improved somewhat by curcumin. These finding indicate that fetal programming responses to MI contribute to neonatal growth and metabolic deficits. Neonatal curcumin supplementation had minimal effect on growth deficits but may improve glucose metabolism. …
Autonomic And Redox Imbalance Correlates With T-Lymphocyte Inflammation In A Model Of Chronic Social Defeat Stress, Cassandra M. Moshfegh, Safwan K. Elkhatib, Christopher W. Collins, Allison J. Kohl, Adam J. Case
Autonomic And Redox Imbalance Correlates With T-Lymphocyte Inflammation In A Model Of Chronic Social Defeat Stress, Cassandra M. Moshfegh, Safwan K. Elkhatib, Christopher W. Collins, Allison J. Kohl, Adam J. Case
Journal Articles: Cellular & Integrative Physiology
Patients diagnosed with post-traumatic stress disorder (PTSD) are at a significantly elevated risk of developing comorbid inflammatory conditions, but the mechanisms underlying this predilection remain unclear. Our previous work has shown that T-lymphocytes exposed to elevated levels of norepinephrine (NE) displayed a pro-inflammatory signature reminiscent of an autoreactive phenotype. With this, we hypothesized that the increased sympathetic tone observed during psychological trauma may be promoting pro-inflammatory T-lymphocytes, which causes a predisposition to comorbid inflammatory conditions. Here, we examined the consequences of psychological trauma on splenic T-lymphocytes using a mouse model of repeated social defeat stress. Social defeat led to anxiety-like …
Redox Biology In Physiology And Disease, Matthew C. Zimmerman, Adam J. Case
Redox Biology In Physiology And Disease, Matthew C. Zimmerman, Adam J. Case
Journal Articles: Cellular & Integrative Physiology
No abstract provided.
Central Glucagon-Like Peptide-1 Receptor Signaling Via Brainstem Catecholamine Neurons Counteracts Hypertension In Spontaneously Hypertensive Rats, Kenichi Katsurada, Masanori Nakata, Toshinobu Saito, Boyang Zhang, Yuko Maejima, Shyam Sundar Nandi, Neeru M. Sharma, Kaushik K. Patel, Kazuomi Kario, Toshihiko Yada
Central Glucagon-Like Peptide-1 Receptor Signaling Via Brainstem Catecholamine Neurons Counteracts Hypertension In Spontaneously Hypertensive Rats, Kenichi Katsurada, Masanori Nakata, Toshinobu Saito, Boyang Zhang, Yuko Maejima, Shyam Sundar Nandi, Neeru M. Sharma, Kaushik K. Patel, Kazuomi Kario, Toshihiko Yada
Journal Articles: Cellular & Integrative Physiology
Glucagon-like peptide-1 receptor (GLP-1R) agonists, widely used to treat type 2 diabetes, reduce blood pressure (BP) in hypertensive patients. Whether this action involves central mechanisms is unknown. We here report that repeated lateral ventricular (LV) injection of GLP-1R agonist, liraglutide, once daily for 15 days counteracted the development of hypertension in spontaneously hypertensive rats (SHR). In parallel, it suppressed urinary norepinephrine excretion, and induced c-Fos expressions in the area postrema (AP) and nucleus tractus solitarius (NTS) of brainstem including the NTS neurons immunoreactive to dopamine beta-hydroxylase (DBH). Acute administration of liraglutide into fourth ventricle, the area with easy access to …
Redox-Sensitive Calcium/Calmodulin-Dependent Protein Kinase Iiα In Angiotensin Ii Intra-Neuronal Signaling And Hypertension, Urmi Basu, Adam J. Case, Jinxu Liu, Jun Tian, Yulong Li, Matthew C. Zimmerman
Redox-Sensitive Calcium/Calmodulin-Dependent Protein Kinase Iiα In Angiotensin Ii Intra-Neuronal Signaling And Hypertension, Urmi Basu, Adam J. Case, Jinxu Liu, Jun Tian, Yulong Li, Matthew C. Zimmerman
Journal Articles: Cellular & Integrative Physiology
Dysregulation of brain angiotensin II (AngII) signaling results in modulation of neuronal ion channel activity, an increase in neuronal firing, enhanced sympathoexcitation, and subsequently elevated blood pressure. Studies over the past two decades have shown that these AngII responses are mediated, in part, by reactive oxygen species (ROS). However, the redox-sensitive target(s) that are directly acted upon by these ROS to execute the AngII pathophysiological responses in neurons remain unclear. Calcium/calmodulin-dependent protein kinase II (CaMKII) is an AngII-activated intra-neuronal signaling protein, which has been suggested to be redox sensitive as overexpressing the antioxidant enzyme superoxide dismutase attenuates AngII-induced activation of …
A Hybrid Cognitive Architecture With Primal Affect And Physiology, Christopher L. Dancy
A Hybrid Cognitive Architecture With Primal Affect And Physiology, Christopher L. Dancy
Faculty Journal Articles
Though computational cognitive architectures have been used to study several processes associated with human behavior, the study of integration of affect and emotion in these processes has been relatively sparse. Theory from affective science and affective neuroscience can be used to systematically integrate affect into cognitive architectures, particularly in areas where cognitive system behavior is known to be associated with physiological structure and behavior. I introduce a unified theory and model of human behavior that integrates physiology and primal affect with cognitive processes in a cognitive architecture. This new architecture gives a more tractable, mechanistic way to simulate affect-cognition interactions …