Reciprocal irreversibility compensation of LiNi0.2Co0.2Al0.1Mn0.45O2 cathode and silicon oxide anode in new Li-ion battery

A layered LiNi0.2Co0.2Al0.1Mn0.45O2 cathode is herein synthetized and investigated. Scanning electron micro- scopy (SEM) shows the layered morphology of the composite powder, while energy dispersive X-ray spectroscopy (EDS) and Inductively Coupled Plasma-Mass Spectrometry (ICP-MS) confirm the achieved stoichiometry. X-ray diffraction (XRD) well identifies the layered structure unit cell, and Raman spectroscopy displays the corre- sponding M-O bonds motions. The cycling voltammetry (CV) of LiNi0.2Co0.2Al0.1Mn0.45O2 in lithium half-cell reveals an electrochemical process characterized by a remarkable irreversible oxidation taking place at 4.6 V vs. Li+/Li during the first scan, and subsequent reversible Li (de)intercalation centered at 3.8 V vs. Li+/Li with interphase resistance limited to 16 Ω upon activation as indicated by electrochemical impedance spectroscopy (EIS). The relevant irreversibility during first charge is also detected by galvanostatic cycling in a lithium half-cell subsequently operating at an average voltage of 3.8 V with a stable trend, and a maximum specific capacity of 130 mAh g− 1. The initial irreversible capacity of the layered cathode is advantageously exploited for compen- sating the pristine inefficiency of the Li-alloying composite anode in a proof-of-concept Li-ion battery achieved by combining the LiNi0.2Co0.2Al0.1Mn0.45O2 with a silicon oxide composite (SiOx-C) without any preliminary pre- treatment of the electrodes. The full-cell displays a cycling behavior strongly influenced by the anode/cathode ratio, and the corresponding EIS performed both on the single electrodes and on the Li-ion cell by using an additional lithium reference suggests a controlling role of the anode interphase and possible enhancements through a slight excess of cathode material

Testicular dysfunction in 47, XXY boys: when it all begins. A semi-longitudinal study

Objective: Klinefelter syndrome is the most common chromosomal disorder in males, and the most common cause of hypergonadotropic hypogonadism. We describe the natural history of testicular dysfunction in patients with Klinefelter syndrome through the integration of clinical, hormonal and quantitative ultrasound data in a life-course perspective. Design: Prospective semi-longitudinal study. Methods: We included 155 subjects with 47, XXY karyotype (age range: 7 months - 55 years) naïve to testosterone replacement therapy. Subjects were divided according to pubertal stage and age group (transition age and adults). Serial clinical, hormonal and testicular ultrasound assessments were performed. Results: Testicular development progresses until Tanner stage 4, with subsequent regression, whereas Sertoli and germ cell impairment is not hormonally detected before Tanner stages 3-4, as reflected by normal inhibin B values until stage 4 and the fall in the inhibin B/FSH ratio thereafter. The Testosterone/LH ratio peaks during Tanner stages 2-3 and declines from Tanner stage 4 onward, preceding the development of overt hypogonadism. US echotexture progressively worsens until transition age, reflecting ongoing gonadal compromise, whereas quantitative US echotexture measures and the presence of both hypoechoic lesions and microlithiasis independently and significantly predict a lower circulating testosterone level. Conclusions: The findings from this large prospective study contribute to our understanding of the natural history of testicular dysfunction in Klinefelter syndrome, underlining the importance of quantitative testicular US in infancy and childhood, as well as during pubertal development and transition age, for the optimal care of Klinefelter syndrome patients