Chemical modification at and within nanopowders: Synthesis of core‐shell Al2O3@TiON nanopowders via nitriding nano‐(TiO2)0.43(Al2O3)0.57 powders in NH3

Here, we demonstrate the potential utility of using chemical modification to reorganize metastable nanoparticles into nanostructured nanoparticles without coincidentally inducing extensive necking/sintering. The motivation for this effort derives from the concept that chemical reduction in a single component in a mixed‐metal nanoparticle will create segregated islands of a second immiscible phase. Given the very high chemical energies inherent in nanoparticles, the formation of even smaller islands of a second phase can be anticipated to lead to extremely high interfacial energies that may drive these islands to diffuse to cores or surfaces to form core‐shell structures that minimize such interfacial energies. Thus, ammonolysis of (TiO2)0.43(Al2O3)0.57 composition nanopowders where both elements are approximately uniformly mixed at atomic length scales, under selected conditions (1000°C) for various periods of time at constant NH3 flow rates leads primarily to the reduction in the Ti species to form TiN or TiON which then appears to diffuse to the surface of the particles. The final products consist of Al2O3@TiON core‐shell nanopowders that remain mostly unaggregated pointing to a new mechanism for modifying nanopowder chemistries and physical properties.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142336/1/jace15303_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/142336/2/jace15303.pd

Empagliflozin in Patients with Chronic Kidney Disease

Background The effects of empagliflozin in patients with chronic kidney disease who are at risk for disease progression are not well understood. The EMPA-KIDNEY trial was designed to assess the effects of treatment with empagliflozin in a broad range of such patients. Methods We enrolled patients with chronic kidney disease who had an estimated glomerular filtration rate (eGFR) of at least 20 but less than 45 ml per minute per 1.73 m(2) of body-surface area, or who had an eGFR of at least 45 but less than 90 ml per minute per 1.73 m(2) with a urinary albumin-to-creatinine ratio (with albumin measured in milligrams and creatinine measured in grams) of at least 200. Patients were randomly assigned to receive empagliflozin (10 mg once daily) or matching placebo. The primary outcome was a composite of progression of kidney disease (defined as end-stage kidney disease, a sustained decrease in eGFR to < 10 ml per minute per 1.73 m(2), a sustained decrease in eGFR of & GE;40% from baseline, or death from renal causes) or death from cardiovascular causes. Results A total of 6609 patients underwent randomization. During a median of 2.0 years of follow-up, progression of kidney disease or death from cardiovascular causes occurred in 432 of 3304 patients (13.1%) in the empagliflozin group and in 558 of 3305 patients (16.9%) in the placebo group (hazard ratio, 0.72; 95% confidence interval [CI], 0.64 to 0.82; P < 0.001). Results were consistent among patients with or without diabetes and across subgroups defined according to eGFR ranges. The rate of hospitalization from any cause was lower in the empagliflozin group than in the placebo group (hazard ratio, 0.86; 95% CI, 0.78 to 0.95; P=0.003), but there were no significant between-group differences with respect to the composite outcome of hospitalization for heart failure or death from cardiovascular causes (which occurred in 4.0% in the empagliflozin group and 4.6% in the placebo group) or death from any cause (in 4.5% and 5.1%, respectively). The rates of serious adverse events were similar in the two groups. Conclusions Among a wide range of patients with chronic kidney disease who were at risk for disease progression, empagliflozin therapy led to a lower risk of progression of kidney disease or death from cardiovascular causes than placebo