Publications by authors named "P Senguttuvan"

Topochemical reactions are powerful pathways to modify inorganic extended structures, but the present approaches are limited by the degrees of freedom to tune the structural connectivity and dimensionality. In this work, we unveil a new topochemical bottom-up approach to tailor three-dimensional (3D) iron fluoride frameworks from the same one-dimensional (1D) FeF.3HO (IF) precursor upon reacting with iodide-based reagents (AI; A = Na, K, and NH).

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Single-phase three-dimensional vanadium oxide (VO) was synthesized by reduction of VO using a gas stream of ammonia/argon (NH/Ar). The as-synthesized oxide, prepared by this simple gas reduction method was subsequently electrochemically transformed into a disordered rock salt type-"Li3.7V4O9" phase while cycling over the voltage window 3.

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Background: Congenital anomalies of the kidneys and urinary tract (CAKUT) are the most common cause of chronic kidney disease among children and adults younger than 30 yr. In our previous study, whole-exome sequencing (WES) identified a known monogenic cause of isolated or syndromic CAKUT in 13% of families with CAKUT. However, WES has limitations and detection of copy number variations (CNV) is technically challenging, and CNVs causative of CAKUT have previously been detected in up to 16% of cases.

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Sodium superionic conductor (NASICON)-Na VMn(PO ) (NVMP) cathode is attractive for sodium-ion battery application due to its reduced cost and toxicity, and high energy density (≈425 Wh kg ). However, it exhibits significant polarization, limited rate and cycling performances due to its lower electronic conductivity and formation of Jahn-Teller active Mn during cycling. In this report, a chemical approach is presented to partially replace Mn of the NVMP framework by Mg and Al substitutions.

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Congenital anomalies of the kidney and urinary tract (CAKUT) constitute one of the most frequent birth defects and represent the most common cause of chronic kidney disease in the first three decades of life. Despite the discovery of dozens of monogenic causes of CAKUT, most pathogenic pathways remain elusive. We performed whole-exome sequencing (WES) in 551 individuals with CAKUT and identified a heterozygous de novo stop-gain variant in ZMYM2 in two different families with CAKUT.

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