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Raj G. Kumar

Researcher at Icahn School of Medicine at Mount Sinai

Publications -  73
Citations -  1288

Raj G. Kumar is an academic researcher from Icahn School of Medicine at Mount Sinai. The author has contributed to research in topics: Traumatic brain injury & Medicine. The author has an hindex of 16, co-authored 55 publications receiving 928 citations. Previous affiliations of Raj G. Kumar include University of Pittsburgh & Chandka Medical College.

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Chronic Inflammation After Severe Traumatic Brain Injury: Characterization and Associations With Outcome at 6 and 12 Months Postinjury.

TL;DR: The authors' subacute cytokine load score classifies individuals at risk for unfavorable outcomes following injury as higher proinflammatory burden with IL-6, relative to the anti-inflammatory marker IL-10, is significantly associated with outcome.
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Acute CSF interleukin-6 trajectories after TBI: associations with neuroinflammation, polytrauma, and outcome.

TL;DR: Evidence is provided that sustained, elevated levels of CSF IL-6 are associated with an increased inflammatory load, and these increases areassociated with increased odds for unfavorable global outcomes in the first year following TBI.
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Acute inflammatory biomarker profiles predict depression risk following moderate to severe traumatic brain injury

TL;DR: Acute CSF IBR scores show promise for identifying individuals at risk forPTD and should explore anti-inflammatory treatments for PTD, as well as prevention and screening protocols, and link inflammatory biomarkers to symptom tracking.
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Exploratory associations with tumor necrosis factor-α, disinhibition and suicidal endorsement after traumatic brain injury.

TL;DR: Preliminary data suggest a biological to behavioral pathway of suicidality after TBI, from TNFα to disinhibition to suicidal endorsement.
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Variation in the BDNF gene interacts with age to predict mortality in a prospective, longitudinal cohort with severe TBI

TL;DR: Data suggest complex relationships between BDNF and TBI mortality that interact with age to influence survival predictions beyond clinical variables alone, and evidence supporting dynamic, temporal balances of pro-survival/pro-apoptotic target receptors may explain injury and age-related gene associations.