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Michael G. Wade

Researcher at Health Canada

Publications -  94
Citations -  3720

Michael G. Wade is an academic researcher from Health Canada. The author has contributed to research in topics: Hormone & Offspring. The author has an hindex of 34, co-authored 90 publications receiving 3251 citations. Previous affiliations of Michael G. Wade include University of Guelph.

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Loss-of-function mutations in IGSF1 cause an X-linked syndrome of central hypothyroidism and testicular enlargement

TL;DR: Observations delineate a new X-linked disorder in which loss-of-function mutations in IGSF1 cause central hypothyroidism, likely secondary to an associated impairment in pituitary TRH signaling.
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Environmental Hazards: Evidence for Effects on Child Health

TL;DR: This review summarizes knowledge of associations between child health and development outcomes and environmental exposures, including lead, methylmercury, polychlorinated biphenyls (PCBs), dioxins and related polyhalogenated aromatic hydrocarbons (PHAHs), certain pesticides, environmental tobacco smoke, aeroallergens, ambient air toxicants, and ETS.
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Thyroid toxicity due to subchronic exposure to a complex mixture of 16 organochlorines, lead, and cadmium.

TL;DR: It is demonstrated that low doses of ubiquitous environmental contaminants can alter HPT physiology in sexually mature male rats and with great variability between endpoints in the sensitivity.
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Effects of Subchronic Exposure to a Complex Mixture of Persistent Contaminants in Male Rats: Systemic, Immune, and Reproductive Effects

TL;DR: The data suggest that additive or synergistic effects of exposure to contaminants resulting in residue levels representative of contemporary human tissue levels are unlikely to result in adverse effects on immune function or reproductive physiology in male rats.
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Estrogenic exposure affects metamorphosis and alters sex ratios in the northern leopard frog (Rana pipiens): Identifying critically vulnerable periods of development

TL;DR: Tadpoles exposed to EE2 during mid-metamorphosis were developmentally delayed immediately following exposure and took 2 weeks longer to reach metamorphic climax, demonstrating that transient early life-stage exposure to estrogen can induce effects on the reproductive organs that persist into the beginning of adult life-stages.