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Melissa Behr

Researcher at University of Wisconsin-Madison

Publications -  34
Citations -  3604

Melissa Behr is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: Pseudogymnoascus destructans & Toxicity. The author has an hindex of 27, co-authored 34 publications receiving 3302 citations. Previous affiliations of Melissa Behr include New York State Department of Health & Behr.

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Journal ArticleDOI

Bat White-Nose Syndrome: An Emerging Fungal Pathogen?

TL;DR: Direct microscopy and culture analyses demonstrated that the skin of WNS-affected bats is colonized by a psychro-philic fungus that is phylogenetically related to Geomyces spp.
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Experimental infection of bats with Geomyces destructans causes white-nose syndrome

TL;DR: It is demonstrated that exposure of healthy little brown bats to pure cultures of G. destructans causes white-nose syndrome and that the recent emergence of WNS in North America may represent translocation of the fungus to a region with a naive population of animals.
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Liver-specific Deletion of the NADPH-Cytochrome P450 Reductase Gene: IMPACT ON PLASMA CHOLESTEROL HOMEOSTASIS AND THE FUNCTION AND REGULATION OF MICROSOMAL CYTOCHROME P450 AND HEME OXYGENASE *

TL;DR: The data indicate the absence of significant alternative redox partners for liver microsomal CYP and HO, provide in vivo evidence for the significance of hepatic CPR-dependent enzymes in cholesterol homeostasis and systemic drug clearance, and reveal novel regulatory pathways of CYP expression associated with altered cellularHomeostasis.
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In vivo mechanisms of tissue-selective drug toxicity: effects of liver-specific knockout of the NADPH-cytochrome P450 reductase gene on acetaminophen toxicity in kidney, lung, and nasal mucosa.

TL;DR: The results indicate that acetaminophen toxicity in the nasal mucosa is not dependent on hepatic microsomal P450-catalyzed metabolic activation and thatacetaminophenoxicity in the lung, kidney, and lateral nasal glands is at least partly caused by liver-derived acetaminphen metabolites.