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Paresh D. Patel

Researcher at University of Michigan

Publications -  36
Citations -  2749

Paresh D. Patel is an academic researcher from University of Michigan. The author has contributed to research in topics: Hippocampal formation & Mineralocorticoid receptor. The author has an hindex of 17, co-authored 33 publications receiving 2558 citations. Previous affiliations of Paresh D. Patel include Molecular and Behavioral Neuroscience Institute.

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Variant Brain-Derived Neurotrophic Factor (BDNF) (Met66) Alters the Intracellular Trafficking and Activity-Dependent Secretion of Wild-Type BDNF in Neurosecretory Cells and Cortical Neurons

TL;DR: Findings indicate that components of the regulated secretory machinery interacts specifically with a signal in the BDNF prodomain and that perturbations in BDNF trafficking may lead to selective impairment in CNS function.
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Polycistronic RNA polymerase II expression vectors for RNA interference based on BIC/miR-155

TL;DR: New RNA polymerase II expression vectors for RNAi are developed, designated SIBR vectors, based upon the non-coding RNA BIC, and it is found that expression of a short region of the third exon of mouse BIC is sufficient to produce miR-155 in mammalian cells.
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Glucocorticoid and mineralocorticoid receptor mRNA expression in squirrel monkey brain.

TL;DR: Receptor expression for corticosteroids in deep brain structures and the hippocampal formation was similar to that previously reported in rodents, but GR and MR mRNA were expressed at higher levels in squirrel monkey cerebral cortex.
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Mineralocorticoid Receptor Antagonism in Experimental Atherosclerosis

TL;DR: MR antagonism improves endothelial function and reduces O2·− generation in diet-induced atherosclerosis and Targeting aldosterone by blocking its receptor has potential antiatherosclerotic effects.
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Robust and tissue-specific expression of TPH2 versus TPH1 in rat raphe and pineal gland.

TL;DR: Almost exclusively, TPH2 mRNA is expressed in raphe, in a pattern overlapping the histologically defined raphe nuclei, and is likely to be the gene giving rise to the majority of TPH activity in these cells.