Michelle J. Hansen

ORCID: 0000-0002-2607-461X
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About
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Research Areas
  • Regulation of Appetite and Obesity
  • Chronic Obstructive Pulmonary Disease (COPD) Research
  • Biochemical Analysis and Sensing Techniques
  • Neuropeptides and Animal Physiology
  • Nutrition and Health in Aging
  • Respiratory Support and Mechanisms
  • Adipose Tissue and Metabolism
  • Adipokines, Inflammation, and Metabolic Diseases
  • Pediatric health and respiratory diseases
  • Asthma and respiratory diseases
  • Retinoids in leukemia and cellular processes
  • Hypothalamic control of reproductive hormones
  • Vitamin C and Antioxidants Research
  • Respiratory viral infections research
  • Immune Response and Inflammation
  • Exercise and Physiological Responses
  • Apelin-related biomedical research
  • Cancer, Stress, Anesthesia, and Immune Response
  • Healthcare Operations and Scheduling Optimization
  • Metabolism, Diabetes, and Cancer
  • Amyloidosis: Diagnosis, Treatment, Outcomes
  • Macrophage Migration Inhibitory Factor
  • Fibroblast Growth Factor Research
  • Obesity, Physical Activity, Diet
  • Animal Nutrition and Physiology

The University of Melbourne
2005-2018

UNSW Sydney
2006

The Royal Melbourne Hospital
2006

Cigarette smoke exposure is a major determinant of adverse lung health, but the molecular processes underlying its effects on inflammation and immunity remain poorly understood. Therefore, we sought to understand whether inflammatory host defense determinants are affected during subchronic cigarette exposure. Dose-response time course studies lungs from Balb/c mice exposed generated 3, 6, 9 cigarettes/day for 4 days showed macrophage- S100A8-positive neutrophil-rich in tissue bronchoalveolar...

10.1152/ajplung.00201.2005 article EN AJP Lung Cellular and Molecular Physiology 2005-12-17

Cigarette smoke has both pro-inflammatory and immunosuppressive effects. Both active passive cigarette exposure are linked to an increased incidence severity of respiratory virus infections, but underlying mechanisms not well defined. We hypothesized, based on prior gene expression profiling studies, that upregulation mediators by short term would be protective against a subsequent influenza infection. BALB/c mice were subjected whole body with 9 cigarettes/day for 4 days. Mice then infected...

10.1186/1465-9921-9-53 article EN cc-by Respiratory Research 2008-07-15

Cigarette smoke (CS) is the major cause of chronic obstructive pulmonary disease (COPD). Interleukin-17A (IL-17A) a pivotal cytokine that regulates lung immunity and inflammation. The aim present study was to investigate how IL-17A CS-induced inflammation in vivo. knockout (KO) mice neutralization wild-type (WT) reduced macrophage neutrophil recruitment chemokine (C-C motif) ligand 2 (CCL2), CCL3 matrix metalloproteinase (MMP)-12 mRNA expression response acute CS exposure. increased...

10.1042/cs20140703 article EN cc-by Clinical Science 2015-07-02

Abstract While a dysregulation in neuropeptide Y (NPY) signaling has been described rodent models of obesity, few studies have investigated the time‐course changes NPY content and responsiveness during development diet‐induced obesity. Therefore we effect differing lengths (2–17 weeks) high‐fat diet on hypothalamic peptide content, release NPY‐induced hyperphagia. Male Sprague–Dawley rats (211 ± 3 g) were fed either (30% fat) or laboratory chow (5% fat). Animals implanted with...

10.1046/j.1471-4159.2003.02217.x article EN Journal of Neurochemistry 2004-01-14

Rationale: Despite irrefutable epidemiologic evidence, cigarette smoking remains the major preventable cause of lung disease morbidity worldwide. The appetite-suppressing effect tobacco is a behavioral determinant smoking, but underlying molecular and neuronal mechanisms are not understood. Neuropeptide Y (NPY) an orexigenic neuropeptide, whose activity in hypothalamic paraventricular nucleus governs appetite.Objectives: To compare effects smoke exposure equivalent food restriction on body...

10.1164/rccm.200506-977oc article EN American Journal of Respiratory and Critical Care Medicine 2006-03-11

Chronic obstructive pulmonary disease (COPD) is an incurable inflammatory lung that afflicts millions of people worldwide, and it the fourth leading cause death. Systemic comorbidities affecting heart, skeletal muscle, bone, metabolism are major contributors to morbidity mortality. Given surprising finding in large prospective clinical biomarker studies peripheral white blood cell count more closely associated with than biomarkers, we probed role growth factors. Using SHIP-1-deficient COPD...

10.1172/jci98224 article EN Journal of Clinical Investigation 2018-04-29

Apelin, the endogenous peptide ligand of APJ receptor, is expressed in brain regions implicated food and water intake. This study reports for first time, effect apelin-12, one most potent apelin peptides, on spontaneous (nocturnal) feeding. Randomised intracerebroventricular injection 1, 3 10 nmol apelin-12 or saline vehicle, min prior to lights out, led dose-dependent reductions intake 2-4 h after (n=7; p<0.05). suggests that exerts a delayed inhibitory nocturnal Relative saline, no was...

10.1080/1028415031000111273 article EN Nutritional Neuroscience 2003-05-01

Aim: The aim of this study was to further explore the time‐dependent changes in leptin sensitivity using a rat model dietary fat–induced obesity and investigate potential mechanisms governing these changes. Methods: We used male, adult Sprague‐Dawley rats that were fed either standard laboratory chow diet (3% fat) or high–saturated fat (HF) (60% for 2 5 weeks. Energy balance (body weight, energy intake expenditure); central α‐melanin stimulating hormone (α‐MSH) administration expression...

10.1111/j.1463-1326.2006.00653.x article EN Diabetes Obesity and Metabolism 2006-08-29

Serum amyloid A (SAA) is expressed locally in chronic inflammatory conditions such as obstructive pulmonary disease (COPD), where macrophages that do not accord with the classic M1/M2 paradigm also accumulate. In this study, role of SAA regulating macrophage differentiation was investigated vitro using human blood monocytes from healthy subjects and patients COPD vivo an airway challenge model BALB/c mice. Differentiation stimulated proinflammatory monokines IL-6 IL-1β concurrently M2...

10.1096/fj.14-250332 article EN The FASEB Journal 2014-05-20

Obesity and cigarette smoking are both important risk factors for insulin resistance, cardiovascular disease, cancer. Smoking reduces appetite, which makes many people reluctant to quit. Few studies have documented the metabolic impact of combined smoke exposure (se) high-fat-diet (HFD). Neuropeptide Y (NPY) is a powerful hypothalamic feeding stimulator that promotes obesity. We investigated how chronic se affects caloric intake, adiposity, plasma hormones, inflammatory mediators, NPY...

10.1152/ajpendo.00442.2007 article EN AJP Endocrinology and Metabolism 2007-10-17

Skeletal muscle wasting is an important comorbidity of Chronic Obstructive Pulmonary Disease (COPD) and strongly correlated with morbidity mortality. Patients who experience frequent acute exacerbations COPD (AECOPD) have more severe reduced recovery mass function after each exacerbation. Serum levels the pro-inflammatory phase protein Amyloid A (SAA) can rise than 1000-fold in AECOPD are predictively exacerbation severity. The direct effects SAA on skeletal poorly understood. Here we...

10.1371/journal.pone.0146882 article EN cc-by PLoS ONE 2016-01-19

While global success in cessation advocacy has seen smoking rates fall many developed countries, persistent lung inflammation ex-smokers is an increasingly important clinical problem whose mechanistic basis remains poorly understood. In this study, candidate effector mechanisms were assessed mice exposed to cigarette smoke (CS) for 4 months following from long term CS exposure. BALF neutrophils, CD4+ and CD8+ T cells innate NK remained significantly elevated cessation. Analysis of neutrophil...

10.1371/journal.pone.0113180 article EN cc-by PLoS ONE 2014-11-18

Obesity and cigarette smoking independently constitute major preventable causes of morbidity mortality obesity is known to worsen lung inflammation in asthma. Paradoxically, higher body mass index (BMI) associated with reduced induced COPD whereas low BMI increases risk. To date, no study has investigated the effect a dietary-induced smoke exposure on loss skeletal muscle mice. Male BALB/c mice were exposed 4 cigarettes/day, 6 days/week for 7 weeks, or sham handled. Mice consumed either...

10.1371/journal.pone.0080471 article EN cc-by PLoS ONE 2013-11-19

<b>Introduction:</b> Oxidative stress and reactive oxygen species (ROS) have been implicated in COPD skeletal muscle wasting. <b>Aim:</b> To determine whether inhibiting ROS production reduces cigarette smoke (CS)-induced lung inflammation wasting mice. <b>Methods:</b> Male Balb/C mice were exposed to CS generated from 6 cigs/day, 5 days/week for 8 weeks. Sham air. Mice treated daily with apocynin (5mg/kg, i.p.) or vehicle (0.1% DMSO). Food intake was measured body weights recorded 3 times a...

10.1183/13993003.congress-2016.oa3310 article EN 05.01 - Airway pharmacology and treatment 2016-09-01
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