An association study of severity of intellectual disability with peripheral biomarkers of disabled children in a rehabilitation home, Kolkata, India

International audienceThe current investigation has identified the biomarkers associated withseverity of disability and correlation among plethora of systemic,cellular and molecular parameters of intellectual disability (ID) in arehabilitation home. The background of study lies with the recentclinical evidences which identified complications in ID. Variousindicators from blood and peripheral system serve as potentialsurrogates for disability related changes in brain functions. IDsubjects (Male, age 10 ± 5 yrs, N = 45) were classified as mild,moderate and severe according to the severity of disability usingstandard psychometric analysis. Clinical parameters including stressbiomarkers, neurotransmitters, RBC morphology, expressions ofinflammatory proteins and neurotrophic factor were estimated from PBMC,RBC and serum. The lipid peroxidation of PBMC and RBC membranes, levelsof serum glutamate, serotonin, homocysteine, ROS, lactate and LDH-Aexpression increased significantly with severity of ID whereas changesin RBC membrane ?-actin, serum BDNF, TNF-? and IL-6 was found non-significant. Structural abnormalities of RBC were more in severelydisabled children compared to mildly affected ones. The oxidative stressremained a crucial factor with severity of disability. This is confirmednot only by RBC alterations but also with other cellular dysregulations.The present article extends unique insights of how severity ofdisability is correlated with various clinical, cellular and molecularmarkers of blood. This unique study primarily focuses on the strongpredictors of severity of disability and their associations via brain-blood axis

Gossypetin ameliorates ionizing radiation-induced oxidative stress in mice liver—a molecular approach

<div><p></p><p>Radioprotective action of gossypetin (GTIN) against gamma (γ)-radiation-induced oxidative stress in liver was explored in the present article. Our main aim was to evaluate the protective efficacy of GTIN against radiation-induced alteration of liver in murine system. To evaluate the effect of GTIN, it was orally administered to mice at a dose of 30 mg/kg body weight for three consecutive days prior to γ-radiation at a dose of 5 Gy. Radioprotective efficacy of GTIN were evaluated at physiological, cellular, and molecular level using biochemical analysis, comet assay, flow cytometry, histopathology, immunofluorescence, and immunoblotting techniques. Ionizing radiation was responsible for augmentation of hepatic oxidative stress in terms of lipid peroxidation and depletion of endogenous antioxidant enzymes. Immunoblotting and immunofluorescence studies showed that irradiation enhanced the nuclear translocation of nuclear factor kappa B (NF-κB) level, which leads to hepatic inflammation. To investigate further, we found that radiation induced the activation of stress-activated protein kinase/c-Jun NH2-terminal kinase (SAPK/JNK)-mediated apoptotic pathway and deactivation of the NF-E2-related factor 2 (Nrf2)-mediated redox signaling pathway, whereas GTIN pretreatment ameliorated these radiation-mediated effects. This is the novel report where GTIN rationally validated the molecular mechanism in terms of the modulation of cellular signaling system’ instead of ‘ This is the novel report where GTIN is rationally validated in molecular terms to establish it as promising radioprotective agents. This might be fruitful especially for nuclear workers and defense personnel assuming the possibility of radiation exposure.</p></div