Bryan S. Richardson

ORCID: 0000-0002-0067-8298
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About
Contact & Profiles
Research Areas
  • Neonatal and fetal brain pathology
  • Neonatal Respiratory Health Research
  • Birth, Development, and Health
  • Neuroscience of respiration and sleep
  • Pregnancy and preeclampsia studies
  • Gestational Diabetes Research and Management
  • Metabolism and Genetic Disorders
  • Preterm Birth and Chorioamnionitis
  • Infant Development and Preterm Care
  • Prenatal Substance Exposure Effects
  • Diet and metabolism studies
  • Congenital Diaphragmatic Hernia Studies
  • Vagus Nerve Stimulation Research
  • Fetal and Pediatric Neurological Disorders
  • Sleep and Wakefulness Research
  • Hyperglycemia and glycemic control in critically ill and hospitalized patients
  • Heart Rate Variability and Autonomic Control
  • Adipose Tissue and Metabolism
  • Neurogenesis and neuroplasticity mechanisms
  • Infant Health and Development
  • Cardiac Arrest and Resuscitation
  • Neuroendocrine regulation and behavior
  • Reproductive Physiology in Livestock
  • Mesenchymal stem cell research
  • Anesthesia and Neurotoxicity Research

Western University
2015-2025

Children’s Health Research Institute
2008-2023

Lawson Health Research Institute
2005-2021

London Health Sciences Centre
2018

Victoria Hospital
2018

Health Sciences Centre
2017

St Joseph's Health Centre
1988-2015

Institute of Physiology and Basic Medicine
2014

Université de Montréal
2013

UCLA Medical Center
2013

10.1016/0002-9378(78)90744-5 article EN American Journal of Obstetrics and Gynecology 1978-11-01

Abstract Over 30 years ago Professor David Barker first proposed the theory that events in early life could explain an individual's risk of non‐communicable disease later life: developmental origins health and (DOHaD) hypothesis. During 1990s validity DOHaD hypothesis was extensively tested a number human populations mechanisms underpinning it characterised range experimental animal models. past decade, researchers have sought to use this mechanistic understanding develop therapeutic...

10.1113/jp274948 article EN The Journal of Physiology 2018-04-10

Neuroinflammation in utero may contribute to brain injury resulting life-long neurological disabilities. The pivotal role of the efferent cholinergic anti-inflammatory pathway (CAP) controlling inflammation, e.g., by inhibiting HMGB1 release, via macrophages' α7 nicotinic acetylcholine receptor (α7nAChR) has been described adults, but its importance fetus is unknown. Moreover, it unknown whether CAP also exert effects on anatomically predominant afferent component vagus nerve.We measured...

10.1186/s12974-016-0567-x article EN cc-by Journal of Neuroinflammation 2016-05-10

10.1016/j.ajog.2004.06.034 article EN American Journal of Obstetrics and Gynecology 2005-01-01

10.1016/0002-9378(79)90674-4 article EN American Journal of Obstetrics and Gynecology 1979-02-01

This study explored arterial remodelling in fetuses growth restricted by hypoxia. Chronically catheterized fetal sheep were made moderately or severely hypoxic placental embolization for 15 days starting at gestational age 116-118 (term ∼147 days). Cross-sections of the aorta analysed collagen and elastin content using histological procedures, while immunofluorescence was applied to measure markers vascular smooth muscle cell (VSMC) type. In frozen aortae quantitative PCR used mRNA levels...

10.1113/jphysiol.2011.210625 article EN The Journal of Physiology 2011-05-04

Fetal growth restriction is implicated in the programming of later-life neurodegeneration. We hypothesized that growth-restricted offspring would show accelerated changes to microglial white matter morphology, relative controls. Control guinea pig sows were fed ad libitum, while maternal nutrient received 70% control diet switched 90% from mid-gestation. Offspring sacrificed at ∼26 days (neonate) or ∼110 (adult) postpartum. Coronal brain sections frontal cortex subject IBA1 staining for...

10.1139/cjpp-2024-0275 article EN Canadian Journal of Physiology and Pharmacology 2025-04-17
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