Kinetic Control of the Li0.9Mn1.6Ni0.4O4 Spinel Structure with Enhanced Electrochemical Performance.

The development of more sustainable societies has become an urgent goal worldwide. Electrical batteries are currently seen as one of the most important energy storage technologies for the development of decarbonized societies. However, many lithium-ion battery manufacturers currently utilize cobalt, a toxic and hazardous mineral, in their batteries. Lithium-deficient manganese nickel oxide spinels are considered promising candidates owing to their high potential and environmental friendliness. Their electrochemical performance highly depends on their average and local structures, such as phase purities, lattice parameters, and cation sites. Thus, a synthesis protocol should be designed to control these structural parameters to improve their electrochemical performance. In this study, we controlled the average and local structures of Li0.9Mn1.6Ni0.4O4 spinels obtained by co-precipitation by optimizing their cooling rates. High-resolution techniques, including transmission electron microscopy, synchrotron X-ray diffraction, and Auger-composition analysis combined with density functional theory calculations, X-ray absorption spectroscopy, and electrochemical analysis, were used to understand the average and local structural variations and their effects on the electrochemical properties. As a result, the control of oxygen diffusion at different cooling rates can promote the rearrangement of the structure, resulting in a cation-disordered spinel with minimal variations in lattice parameters and composition. Excellent electrochemical properties were noted in the cation-disordered spinel with high crystallinity and a slightly oxygen-rich surface produced via optimized cooling rates.

A Caucasian family with the 3271 mutation in mitochondrial DNA.

The second most common mutation associated with MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) in Japan is the 3271 mutation. This mutation was found in a Brazilian family of Portuguese and Italian descent, indicating that this mutation also exists in a race other than Japanese. The propositus had mild clinical manifestations atypical of MELAS, suggesting that patients with the 3271 mutation exhibit heterogeneous phenotypic expression as seen in the 3243 mutation.

Urinary excretion of human growth hormone in children with short stature: correlation with pituitary secretion of human growth hormone.

Thirty-five children with short-stature underwent insulin-loading and sleep tests for assessment of secretion of human growth hormone. Correlations between the levels of human growth hormone in the serum and urine during the tests were examined to elucidate the clinical significance of urinary human growth hormone levels in short children. The concentration and total amount of human growth hormone in the urine correlated significantly with the peak concentration of serum human growth hormone (r = 0.81, p less than 0.001 and r = 0.80, p less than 0.001, respectively) and the integrated concentration of human growth hormone (r = 0.85, p less than 0.001 and r = 0.85, p less than 0.001, respectively) in the insulin-loading test. The concentration and total amount of human growth hormone in the morning urine also correlated significantly with the peak concentration of serum human growth hormone (r = 0.80, p less than 0.001 and r = 0.70, p less than 0.001, respectively) and the integrated concentration of serum human growth hormone (r = 0.80, p less than 0.001 and r = 0.72, p less than 0.001, respectively) in the sleep test. The concentration or total amount of human growth hormone in the urine differed significantly among children with human growth hormone deficiency, those with nonendocrine short stature, and those with normal stature (p less than 0.05). These data suggest that measurement of human growth hormone in the urine may be used to assess secretion of human growth hormone, serving as a screening test for human growth hormone deficiency in children.

Renal tubular involvement mimicking Bartter syndrome in a patient with Kearns-Sayre syndrome.

A 10-year-old boy had short stature, external ophthalmoplegia, atypical retinal pigmentary degeneration, and sensorineural hearing loss (Kearns-Sayre syndrome). In addition to ragged-red fibers observed on modified Gomori trichrome staining, there were scattered fibers exhibiting no cytochrome c oxidase activity, indicating a focal deficiency. Cytochrome c oxidase and other respiratory chain enzyme activities were normal biochemically. The patient also had renal tubular dysfunction, including isosthenuria, decreased urine-concentrating ability, and excessive excretion of potassium and magnesium. In addition, he had hyperreninemia and hyperaldosteronism but no hypertension. The renal dysfunction was thought to have resulted from a primary defect in the thick ascending limb of the loop of Henle, mimicking Bartter syndrome. In contrast to previously described cases of cytochrome c oxidase deficiency with de Toni-Fanconi Debré syndrome, the patient had less intensive muscle abnormalities. A renal biopsy specimen showed ultrastructural changes in mitochondria that were similar to those seen in biopsy specimens of muscle. A large-scale deletion (8.8 kilobases) in mitochondrial DNA was found in biopsy specimens of muscle and kidney.