S
Swarooparani Vadlamudi
Researcher at University of North Carolina at Chapel Hill
Publications - 28
Citations - 1575
Swarooparani Vadlamudi is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Genome-wide association study & Expression quantitative trait loci. The author has an hindex of 16, co-authored 24 publications receiving 1305 citations.
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Journal ArticleDOI
Prenatal infection and risk for schizophrenia: IL-1β, IL-6, and TNFα inhibit cortical neuron dendrite development
TL;DR: Investigating the effect of cytokines generated in response to infection on the dendritic development of cortical neurons indicates that inflammatory cytokines can significantly reduce dendrite development and complexity of developing cortical neurons, consistent with the neuropathology of schizophrenia.
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Genetic regulatory signatures underlying islet gene expression and type 2 diabetes
Arushi Varshney,Laura J. Scott,Ryan P. Welch,Michael R. Erdos,Peter S. Chines,Narisu Narisu,Ricardo D’Oliveira Albanus,Peter Orchard,Brooke N. Wolford,Romy Kursawe,Swarooparani Vadlamudi,Maren E Cannon,John P. Didion,John Hensley,Anthony Kirilusha,Lori L. Bonnycastle,D. Leland Taylor,D. Leland Taylor,Richard M. Watanabe,Karen L. Mohlke,Michael Boehnke,Francis S. Collins,Stephen C. J. Parker,Michael L. Stitzel +23 more
TL;DR: The largest integrated analysis to date of high-resolution, high-throughput human islet molecular profiling data is presented to characterize the genome, epigenome, and transcriptome and find that T2D genetic variants are enriched in regions of the genome where transcription Regulatory Factor X (RFX) is predicted to bind in an islet-specific manner.
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Maternal poly I:C exposure during pregnancy regulates TNFα, BDNF, and NGF expression in neonatal brain and the maternal–fetal unit of the rat
TL;DR: Changes in TNFalpha, BDNF, and NGF after maternal exposure to poly I:C represent a potential mechanism through which maternal infection increases risk for neurodevelopmental disorders.
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The genetic regulatory signature of type 2 diabetes in human skeletal muscle
Laura J. Scott,Michael R. Erdos,Jeroen R. Huyghe,Ryan P. Welch,Andrew T. Beck,Brooke N. Wolford,Peter S. Chines,John P. Didion,Narisu Narisu,Heather M. Stringham,D. Leland Taylor,D. Leland Taylor,Anne U. Jackson,Swarooparani Vadlamudi,Lori L. Bonnycastle,Leena Kinnunen,Jouko Saramies,Jouko Sundvall,Ricardo D’Oliveira Albanus,Anna Kiseleva,John Hensley,Gregory E. Crawford,Hui Jiang,Xiaoquan Wen,Richard M. Watanabe,Timo A. Lakka,Karen L. Mohlke,Markku Laakso,Jaakko Tuomilehto,Heikki A. Koistinen,Heikki A. Koistinen,Heikki A. Koistinen,Michael Boehnke,Francis S. Collins,Stephen C. J. Parker +34 more
TL;DR: In this article, the authors analyse skeletal muscle biopsies from 271 well-phenotyped Finnish participants with glucose tolerance ranging from normal to newly diagnosed Type 2 diabetes (T2D) to understand how T2D status, metabolic traits and genetic variation influence gene expression.
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Maternal infection regulates BDNF and NGF expression in fetal and neonatal brain and maternal-fetal unit of the rat.
TL;DR: Low levels of brain-derived neurotrophic factor and nerve growth factor expression in maternal plasma, placenta, amniotic fluid, fetal liver/spleen, fetal brain, and cerebral cortex after birth represents a potential mechanism through which maternal infection increases risk for neurodevelopmental disorders.