Z
Zhenmin Ni
Researcher at University of California, Irvine
Publications - 36
Citations - 3735
Zhenmin Ni is an academic researcher from University of California, Irvine. The author has contributed to research in topics: Nitric oxide synthase & Nitric oxide. The author has an hindex of 27, co-authored 36 publications receiving 3379 citations. Previous affiliations of Zhenmin Ni include University of Zulia & University Medical Center Utrecht.
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Journal ArticleDOI
Chronic kidney disease alters intestinal microbial flora
Nosratola D. Vaziri,Jakk Wong,Madeleine V. Pahl,Yvette M. Piceno,Jun Yuan,Todd Z. DeSantis,Zhenmin Ni,Tien-Hung Nguyen,Gary L. Andersen +8 more
TL;DR: Uremia profoundly alters the composition of the gut microbiome and the biological impact of this phenomenon is unknown and awaits further investigation.
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Disintegration of colonic epithelial tight junction in uremia: a likely cause of CKD-associated inflammation
TL;DR: It is revealed, for the first time, that uremia results in depletion of the key protein constituents of the colonic tight junction, a phenomenon which can account for the impaired intestinal barrier function and contribute to the systemic inflammation in CKD.
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Upregulation of Renal and Vascular Nitric Oxide Synthase in Young Spontaneously Hypertensive Rats
TL;DR: Male SHR were studied during the early phase of evolution of hypertension to distinguish the primary changes of NO metabolism from those caused by advanced hypertension, vasculopathy, and aging late in the course of the disease.
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Enhanced Nitric Oxide Inactivation and Protein Nitration by Reactive Oxygen Species in Renal Insufficiency
TL;DR: Antioxidant therapy ameliorated the CRF-induced hypertension, improved vascular tissue NO production, lowered tissue nitrotyrosine burden, and reversed downregulations of NOS isoforms, and antioxidant therapy had no effects in the controls.
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Effect of Antioxidant Therapy on Blood Pressure and NO Synthase Expression in Hypertensive Rats
TL;DR: The role of oxidative stress in the genesis and/or maintenance of hypertension and compensatory upregulation of the expression of eNOS and iNOS in SHR is supported.