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Anuwat Dinudom

Researcher at University of Sydney

Publications -  43
Citations -  2991

Anuwat Dinudom is an academic researcher from University of Sydney. The author has contributed to research in topics: Epithelial sodium channel & Amiloride. The author has an hindex of 25, co-authored 43 publications receiving 2702 citations.

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Pathogenesis of chytridiomycosis, a cause of catastrophic amphibian declines.

TL;DR: It is shown that Bd infection is associated with pathophysiological changes that lead to mortality in green tree frogs (Litoria caerulea), and in diseased individuals, electrolyte transport across the epidermis was inhibited by >50, plasma sodium and potassium concentrations were respectively reduced by ~20% and ~50%, and asystolic cardiac arrest resulted in death.
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Increased Gut Permeability and Microbiota Change Associate with Mesenteric Fat Inflammation and Metabolic Dysfunction in Diet-Induced Obese Mice

TL;DR: The current results implicate gut dysfunction, and attendant inflammation of contiguous adipose, as salient features of the metabolic dysregulation of diet-induced obesity.
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Effects of dietary fat profile on gut permeability and microbiota and their relationships with metabolic changes in mice

TL;DR: To distinguish the effects of dietary fat profile on gut parameters and their relationships with metabolic changes and to determine the capacity of n‐3 fatty acids to modify gut variables in the context of diet‐induced metabolic dysfunctions.
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The Nedd4-like protein KIAA0439 is a potential regulator of the epithelial sodium channel.

TL;DR: It is proposed that KIAA0439 and Nedd4 proteins either play a redundant role in ENaC regulation or function in a tissue- and/or signal-specific manner to down-regulate ENac.
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Nedd4 mediates control of an epithelial Na+ channel in salivary duct cells by cytosolic Na+

TL;DR: It is concluded that Nedd4 normally mediates feedback control of epithelial Na+ channels by intracellular Na+, and is suggested that the increased Na+ channel activity observed in Liddle's syndrome is attributable to the loss of this regulatory feedback system.