A5005282344- Chronic Obstructive Pulmonary Disease (COPD) Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Respiratory Support and Mechanisms
- Stress Responses and Cortisol
- Congenital gastrointestinal and neural anomalies
- Eicosanoids and Hypertension Pharmacology
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
- Pulmonary Hypertension Research and Treatments
- Muscle Physiology and Disorders
- Respiratory and Cough-Related Research
- Olfactory and Sensory Function Studies
- Helicobacter pylori-related gastroenterology studies
- Sodium Intake and Health
- High Altitude and Hypoxia
- Asthma and respiratory diseases
- Genetics and Neurodevelopmental Disorders
- Heme Oxygenase-1 and Carbon Monoxide
- Inflammation biomarkers and pathways
- Adipose Tissue and Metabolism
- Exercise and Physiological Responses
- Gastrointestinal motility and disorders
- Tryptophan and brain disorders
- Nicotinic Acetylcholine Receptors Study
- Autism Spectrum Disorder Research
RMIT University
2020-2024
MIT University
2020-2023
Background and Objective Neurocognitive dysfunction is present in up to ∼61% of people with chronic obstructive pulmonary disease (COPD), symptoms including learning memory deficiencies, negatively impacting the quality life these individuals. As mechanisms responsible for neurocognitive deficits COPD remain unknown, we explored whether cigarette smoke (CS) exposure causes mice this associated neuroinflammation an altered neuropathology. Methods Male BALB/c were exposed room air (sham) or CS...
Cigarette smoking (CS) is the leading cause of chronic obstructive pulmonary disease (COPD). The "spill-over" inflammation into systemic circulation may damage brain, to cognitive dysfunction. Cessation CS can improve and neurocognitive outcomes, however, its benefit on neuroinflammatory profile remains uncertain. Here, we investigate how exposure impairs neurocognition whether this be reversed with cessation or an antioxidant treatment.Male BALB/c mice were exposed (9 cigarettes/day for 8...
Background and Purpose Cardiovascular disease affects up to half of the patients with chronic obstructive pulmonary (COPD), exerting deleterious impact on health outcomes survivability. Vascular endothelial dysfunction marks onset cardiovascular disease. The present study examined effect a potent NADPH Oxidase (NOX) inhibitor free‐radical scavenger, apocynin, COPD‐related Experimental Approach Male BALB/c mice were exposed either room air (Sham) or cigarette smoke (CS) generated from 9...
Chronic obstructive pulmonary disease (COPD) is a major, incurable respiratory condition that primarily caused by cigarette smoking (CS). Neurocognitive disorders including cognitive dysfunction, anxiety and depression are highly prevalent in people with COPD. It understood increased lung inflammation oxidative stress from CS exposure may 'spill over' into the systemic circulation to promote onset of these extra-pulmonary comorbidities, thus impacts quality life The precise role 'spill-over'...
Background and Purpose Skeletal muscle dysfunction is a major comorbidity of chronic obstructive pulmonary disease (COPD). This type may be direct consequence oxidative insults evoked by cigarette smoke (CS) exposure. The present study examined the effects potent Nox inhibitor reactive oxygen species (ROS) scavenger, apocynin, on CS‐induced dysfunction. Experimental Approach Male BALB/c mice were exposed to either room air (sham) or CS generated from nine cigarettes per day, 5 days week for...
People with chronic obstructive pulmonary disease (COPD) are susceptible to respiratory infections which exacerbate and/or cardiovascular complications, increasing their likelihood of death. The mechanisms driving these complications remain unknown but increased oxidative stress has been implicated. Here we investigated whether influenza A virus (IAV) infection, following cigarette smoke (CS) exposure, worsens vascular function and if so, the antioxidant ebselen alleviates this dysfunction....
Abstract Gastrointestinal (GI) dysfunction is a common comorbidity of chronic obstructive pulmonary disease (COPD) for which major cause cigarette smoking (CS). The underlying mechanisms and precise effects CS on gut contractility, however, are not fully characterised. Therefore, the aim present study was to investigate whether impacts GI function structure in mouse model CS-induced COPD. We also aimed presence ebselen, an antioxidant that has shown beneficial lung inflammation resulting...
Individuals with autism often experience gastrointestinal issues but the cause is unknown. Many gene mutations that modify neuronal synapse function are associated and therefore may impact enteric nervous system regulates function. A missense mutation in Nlgn3 encoding cell adhesion protein, Neuroligin-3, was identified two brothers who both experienced severe dysfunction. Mice expressing this (Nlgn3R451C mice) a well-studied preclinical model of show autism-relevant characteristics,...
Chronic Obstructive Pulmonary Disease (COPD) is a multifaceted respiratory disorder characterized by progressive airflow limitation and systemic implications. It has become increasingly apparent that COPD exerts its influence far beyond the system, extending impact to various organ systems. Among these, musculoskeletal system emerges as central player in both pathogenesis management of associated comorbidities. Muscle dysfunction osteoporosis are prevalent disorders patients, leading...
Individuals with autism often experience gastrointestinal issues but the cause is unknown. Many gene mutations that modify neuronal synapse function are associated and therefore may impact enteric nervous system regulates function. A missense mutation in Nlgn3 encoding cell adhesion protein Neuroligin-3 was identified two brothers who both experienced severe dysfunction. Mice expressing this (Nlgn3R451C mice) a well-studied preclinical model of show autism-relevant characteristics, including...
Limb muscle dysfunction is a hallmark of Chronic Obstructive Pulmonary Disease (COPD) which further worsened following viral-induced acute exacerbation COPD (AECOPD). An amplified airway inflammation underlies the aggravated respiratory symptoms seen during AECOPD, however, its contributory role to limb unclear. The present study examined impact influenza A virus (IAV)-induced on hind parameters. Airway was established in male BALB/c mice by exposure cigarette smoke (CS) for 8 weeks....
Background and Purpose: Cigarette smoking (CS) is the major risk factor for developing COPD related skeletal muscle dysfunction. It has been postulated that CS exposure may directly causes dysfunction via induction of oxidative stress. The present study examined effect a potent Nox inhibitor ROS scavenger, apocynin on CS-induced Experimental Approach: Male BALB/c mice were exposed to either room air (sham) or generated from 9 cigarettes per day, 5 days week 8 weeks with without treatment (5...
Background and Purpose: People with COPD are susceptible to respiratory infections which exacerbate pulmonary and/or cardiovascular complications, increasing their likelihood of death. The mechanisms driving these complications remain unknown but increased oxidative stress has been implicated. Here we investigated whether influenza A virus (IAV) infection, following chronic cigarette smoke (CS) exposure, worsens vascular function if so, the antioxidant ebselen alleviates this dysfunction....
Background and Purpose: Cardiovascular disease (CVD) affects up to half of the patients with chronic obstructive pulmonary (COPD), which exerts deleterious impact on health outcomes survivability. Vascular endothelial dysfunction marks onset cardiovascular disease. The present study examined effect a potent NADPH Oxidase (NOX) inhibitor free-radical scavenger, apocynin, COPD-related CVD. Experimental Approach: Male BALB/c mice were exposed either room air (Sham) or cigarette smoke (CS)...
Abstract Background: Cigarette smoking (CS) is the leading cause of chronic obstructive pulmonary disease (COPD). The “spill-over” inflammation into systemic circulation may damage brain, to cognitive dysfunction. Cessation CS can improve and neurocognitive outcomes, however, its benefit on neuroinflammatory profile remains uncertain. Here, we investigate how exposure impairs neurocognition whether this be reversed with cessation or an antioxidant treatment. Methods: Male BALB/c mice were...