Publications by authors named "G Vinothkumar"

Purpose: Environmental pollutant Bisphenol A (BPA) strongly interacts with insulin resistance, which leads to type 2 diabetes mellitus (T2DM). Uncontrolled glucose levels in both blood and urine develops vascular complications in T2DM patients. However, glucose-controlled diabetic patients are also affected by vascular complications due to vascular calcification, and there is a lack of clinically relevant data on BPA levels available in patients with T2DM-associated vascular complications due to vascular calcification.

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Background: Cognitive dysfunction potentially affecting up to 60% of CKD patients. GSK-3β plays a key role in the pathogenesis of AD and Cognitive dysfunction, contributing to Aβ production and Aβ-mediated neuronal death by phosphorylating tau inducing hyperphosphorylation in paired helical filaments. However, studies have shown that plasma p-Tau181 is more specific for AD and cognitive dysfunction.

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In the present work, we focus on the development of CePO-CeO composite nanorods with peroxidase mimetic activity for the sensitive detection of hydrogen peroxide and glucose. The Ce/PO molar ratio (CP10:1, CP5:1, CP2:1) in the hydrothermal reaction controlled the formation of pure CePO, CePO-CeO composite nanozymes with different percentages of CeO, and its crystal structure. A higher Ce/PO molar ratio (CP10:1 or CP5:1) was required to obtain CePO-CeO composite nanostructure, while a lower Ce/PO molar (CP2:1) ratio was sufficient to fabricate pure CePO nanorods.

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Rare earth phosphates have been used extensively in luminescent phosphors, bio-imaging, catalysis, and sensors. However, there is a need to correlate the structural-chemical changes associated with stability and performance. In the present work, hydrothermally synthesized CePO:Sm (x = 0, 5 and 10 mol%) nanorods were annealed at different temperatures to understand the modulations in structure as well as optical and enzyme mimetic properties.

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Background: Cognitive dysfunction is reported to be a major cause of morbidity in chronic kidney disease (CKD). The senile plaques (SPs) in the brain are one of the most pathophysiological characteristics of cognitive dysfunction and its major constituent amyloid β (Aβ) released from amyloid precursor protein (APP) by β (BACE1) and γ (presenilin 1) secretases . Platelets contain more than 95% of the circulating APP and implicate as a candidate biomarker for cognitive decline.

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