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Anand Swaroop

Researcher at National Institutes of Health

Publications -  528
Citations -  53580

Anand Swaroop is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Retinitis pigmentosa & Retinal degeneration. The author has an hindex of 89, co-authored 508 publications receiving 43170 citations. Previous affiliations of Anand Swaroop include Vision-Sciences, Inc. & Yale University.

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Multi-omics analyses reveal early metabolic imbalance and mitochondrial stress in neonatal photoreceptors leading to cell death in Pde6brd1/rd1 mouse model of retinal degeneration.

TL;DR: These studies provide a mechanistic framework with mitochondrial damage and metabolic disruptions as early drivers of photoreceptor cell death in retinal degeneration and implicate aberrant calcium signaling as an initiator of higher mitochondrial stress.
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High-resolution genome topology of human retina uncovers super enhancer-promoter interactions at tissue-specific and multifactorial disease loci

TL;DR: In this paper , the authors mapped chromatin contacts at high resolution and integrated with super-enhancers (SEs), histone marks, binding of CTCF and select transcription factors to elucidate genomic regulation in human retina, and uncover candidate genes for susceptibility variants linked to age-related macular degeneration and glaucoma.
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Transcriptome profiling of NIH3T3 cell lines expressing opsin and the P23H opsin mutant identifies candidate drugs for the treatment of retinitis pigmentosa.

TL;DR: Transcriptome profiling can provide essential information about the therapeutic potential of a candidate drug to restore normal gene expression in pathological conditions and revealed that different drugs targeted distinct molecular pathways that resulted in a similar phenotype selected by a cell‐based high‐throughput screen.
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Longitudinal Examination of Links Between Risk Factors for the Metabolic Syndrome and Both Age and Fasting Glucose Levels in Nondiabetic Subjects.

TL;DR: Current findings gathered over years are consistent with the original hypothesis that maintaining relatively low, stable circulating glucose levels during aging retards the development and intensity of many common manifestations of the metabolic syndrome.