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Articles 1 - 7 of 7
Full-Text Articles in Physiological Processes
A Rare Delayed Neuropsychiatric Encephalopathy After Hyperbaric Oxygen Treatment For Carbon Monoxide Poisoning: A Couple’S Case Report, Sabrina Kasha, William J. Naber Ii, Michael Reimer
A Rare Delayed Neuropsychiatric Encephalopathy After Hyperbaric Oxygen Treatment For Carbon Monoxide Poisoning: A Couple’S Case Report, Sabrina Kasha, William J. Naber Ii, Michael Reimer
Graduate Medical Education Research Journal
Background: Carbon monoxide (CO) poisoning is caused when carbon monoxide builds up in the blood, most specifically due to its high binding affinity for the heme structure in hemoglobin. This can lead to serious tissue damage and even be fatal. CO poisoning is primarily the result of incomplete combustion of fuels, with common sources domestically and internationally including furnaces, gas heaters, generators, and motor vehicles.2 Symptoms tend to present as neuropsychiatric symptoms, such as dementia, psychosis, parkinsonism, and incontinence. There are few well-researched CO poisoning specific treatments, which suggest supplemental oxygen and hyperbaric oxygen are most effective. We present a …
Novel Mechanisms For The Neural Control Of Breathing In Acute Lung Injury, Kajal Kamra
Novel Mechanisms For The Neural Control Of Breathing In Acute Lung Injury, Kajal Kamra
Theses & Dissertations
Acute lung injury (ALI) triggers inflammation that disrupts the normal alveolar-capillary endothelial barrier, impairing gas exchange and causing hypoxemia, which reflexively increases respiration. An elevated respiratory rate (fR) usually develops within hours to days following ALI. This acute respiratory failure disorder affects approximately 200,000 new cases annually in the US and accounts for 10% of ICU admissions, with high morbidity and mortality. The neural mechanisms underlying respiratory dysfunction post-ALI are not fully understood. My doctoral dissertation aimed to investigate the mediators of abnormal ventilation during ALI. Systemic hypoxia stimulates the carotid body (CB) chemoreflex, a crucial protective reflex that maintains …
The Role Of Calprotectin In T-Lymphocyte Driven Inflammation In A Mouse Model Of Psychological Trauma, Cassandra Moshfegh
The Role Of Calprotectin In T-Lymphocyte Driven Inflammation In A Mouse Model Of Psychological Trauma, Cassandra Moshfegh
Theses & Dissertations
Post-traumatic stress disorder (PTSD) is a debilitating psychological disorder that affects nearly 45 million Americans. This mental disorder is characterized by behavioral symptoms such as learned helplessness, hyperarousal, withdrawal, and flashbacks. The deleterious effects of PTSD are far-reaching and go beyond behavioral dysfunction, as these individuals are at a three-fold higher risk of comorbid inflammatory diseases. Autonomic, metabolic, and cardiovascular diseases plague these individuals later in their lifetime, however, the mechanistic link connecting psychological trauma to this systemic peripheral immunological dysfunction remains elusive. T-lymphocyte-induced inflammation plays a significant role in all these disease pathologies. Previous work from our laboratory demonstrated …
Neural Oscillatory Activity Serving Sensorimotor Control Is Regulated By The Mitochondrial Redox Environment In Health And Disease, Rachel Spooner
Neural Oscillatory Activity Serving Sensorimotor Control Is Regulated By The Mitochondrial Redox Environment In Health And Disease, Rachel Spooner
Theses & Dissertations
Despite effective regimens of combination antiretroviral therapy, individuals with HIV are still at higher risk for developing forms of cognitive impairment, with one of the most common behavioral abnormalities to manifest being motor dysfunction. This is an important consideration, as deficits in motor control likely contribute to higher-order cognitive impairments, which together, lead to functional dependencies in the ever-growing aging population of HIV-infected adults. While the neuroanatomical bases of motor dysfunction have recently been illuminated in people living with HIV (PLWH), there remains an open question regarding the molecular processes supporting the circuit-level neuronal dynamics that potentially serve these behavioral …
Multiquantal Glutamate Release From Rod Photoreceptors, Cassandra L. Hays
Multiquantal Glutamate Release From Rod Photoreceptors, Cassandra L. Hays
Theses & Dissertations
Neurons communicate via Ca2+-dependent release of neurotransmitters packaged into vesicles (quanta). Some CNS neurons, especially sensory synapses, can release multiple vesicles at a time, increasing information transmission and overcoming the unreliability of a stochastic process. Ribbon-bearing neurons, including retinal photoreceptors, face the challenge of encoding sensory receptor potentials into an ever-changing train of vesicle release events. We studied release of glutamate using voltage clamp to measure anion currents activated during glutamate reuptake into presynaptic terminals (IA(glu)) of salamander and mouse rods, finding that each employ distinct mechanisms for multiquantal release. In amphibian rods, we found that …
Alcohol Drives Oxidation-Dependent Desensitization Of Airway Cilia Motility Responsiveness, Michael Price
Alcohol Drives Oxidation-Dependent Desensitization Of Airway Cilia Motility Responsiveness, Michael Price
Theses & Dissertations
Alcohol abuse, which can impair clearance of pathogens and debris from the airway, is associated with an increase in complications and a higher mortality rate during the progression of pneumonia. With prolonged alcohol exposure, mucociliary clearance (MCC), which depends on the coordinated beating of cilia, is dysfunctional. Effective MCC relies on cAMP-dependent protein kinase (PKA) activation of ciliary beat frequency (CBF). PKA activation and stimulation of CBF are blunted with chronic exposure to alcohol. This phenomenon is known as alcohol-induced ciliary dysfunction (AICD). Previous studies have shown that concomitant feeding of mice with alcohol and antioxidants prevents AICD, suggesting a …
Mechanisms Of Lateral-Inhibitory Feedback From Horizontal Cells To Cone Photoreceptors At The First Synapse Of The Retina, Ted J. Warren
Mechanisms Of Lateral-Inhibitory Feedback From Horizontal Cells To Cone Photoreceptors At The First Synapse Of The Retina, Ted J. Warren
Theses & Dissertations
Polarization of the horizontal cell (HC) membrane potential causes changes in the synaptic cleft pH that result in inhibitory feedback from HCs to cone photoreceptors (PRs). HCs average signals from many PRs and so negative feedback onto PR terminals from HCs subtracts the average luminance of the visual scene from the light responses of an individual cone. This feedback operates by changing the voltage-dependence and amplitude of the L-type Ca2+ current (ICa) that regulates synaptic release. Feedback regulation of PR Ca2+ channels involves protons but the mechanism by which this pH change occurs is unclear. We …