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Robert A. Zinna

Researcher at Washington State University

Publications -  14
Citations -  281

Robert A. Zinna is an academic researcher from Washington State University. The author has contributed to research in topics: Bone resorption & Sexual dimorphism. The author has an hindex of 9, co-authored 14 publications receiving 225 citations. Previous affiliations of Robert A. Zinna include University of Arizona & Medical University of South Carolina.

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Anti-inflammatory effect of MAPK phosphatase-1 local gene transfer in inflammatory bone loss

TL;DR: Rat macrophages transduced with recombinant adenovirus and bone marrow cells of MKP-1 KO mice significantly decreased IL-6, IL-10, TNF-α and chemokine levels, and formed fewer osteoclasts induced by LPS than compared with control group of cells, indicating that MKp-1 is a key therapeutic target to control of inflammation-induced bone loss.
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Rhinoceros beetle horn development reveals deep parallels with dung beetles.

TL;DR: Deep parallels in the development of rhinoceros and dung beetle horns are highlighted, suggesting either that both horn types arose in the common ancestor of all scarabs, a surprising reconstruction of horn evolution that would mean the majority of scarab species actively repress horn growth, or that parallel origins of these extravagant structures resulted from repeated co-option of the same underlying developmental processes.
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Sexual dimorphism and heightened conditional expression in a sexually selected weapon in the Asian rhinoceros beetle.

TL;DR: RNAseq analysis is used to build on recent work exploring mechanisms in the exaggerated weapons of beetles, by examining patterns of differential gene expression in exaggerated and non‐exaggerated traits in the Asian rhinoceros beetle, Trypoxylus dichotomus, to suggest that sexually dimorphic expression of weaponry involves large‐scale changes in gene expression, relative to other traits, while nutrition‐driven changes inGene expression in these same weapons are less pronounced.
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Silencing mitogen-activated protein kinase-activated protein kinase-2 arrests inflammatory bone loss.

TL;DR: This proof-of-concept study suggests a novel target using an intraoral RNA interference strategy to control periodontal inflammation, and validated MK2 siRNA specificity and arrested LPS-induced inflammatory bone loss, decreased inflammatory infiltrate, and decreased osteoclastogenesis.