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Tatiana A. Vishnivetskaya

Researcher at University of Tennessee

Publications -  87
Citations -  21592

Tatiana A. Vishnivetskaya is an academic researcher from University of Tennessee. The author has contributed to research in topics: Permafrost & Arctic. The author has an hindex of 32, co-authored 81 publications receiving 19029 citations. Previous affiliations of Tatiana A. Vishnivetskaya include Oak Ridge National Laboratory & Russian Academy of Sciences.

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Structure, function and diversity of the healthy human microbiome

Curtis Huttenhower, +253 more
- 14 Jun 2012 - 
TL;DR: The Human Microbiome Project Consortium reported the first results of their analysis of microbial communities from distinct, clinically relevant body habitats in a human cohort; the insights into the microbial communities of a healthy population lay foundations for future exploration of the epidemiology, ecology and translational applications of the human microbiome as discussed by the authors.
Journal Article

Structure, function and diversity of the healthy human microbiome

Curtis Huttenhower, +247 more
- 01 Jun 2012 - 
TL;DR: The Human Microbiome Project has analysed the largest cohort and set of distinct, clinically relevant body habitats so far, finding the diversity and abundance of each habitat’s signature microbes to vary widely even among healthy subjects, with strong niche specialization both within and among individuals.
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A framework for human microbiome research

Barbara A. Methé, +253 more
- 14 Jun 2012 - 
TL;DR: The Human Microbiome Project (HMP) Consortium has established a population-scale framework which catalyzed significant development of metagenomic protocols resulting in a broad range of quality-controlled resources and data including standardized methods for creating, processing and interpreting distinct types of high-throughput metagenomics data available to the scientific community as mentioned in this paper.
Journal ArticleDOI

Calmodulin kinase II inhibition protects against structural heart disease

TL;DR: CaMKII inhibition substantially prevented maladaptive remodeling from excessive βAR stimulation and myocardial infarction, and induced balanced changes in excitation-contraction coupling that preserved baseline and βAR-stimulated physiological increases in cardiac function.