High-Performance Microsized Si Anodes for Lithium-Ion Batteries: Insights into the Polymer Configuration Conversion Mechanism.

Microsized silicon particles are desirable Si anodes because of their low price and abundant sources. However, it is challenging to achieve stable electrochemical performances using a traditional microsized silicon anode due to the poor electrical conductivity, serious volume expansion, and unstable solid electrolyte interface. Herein, a composite microsized Si anode is designed and synthesized by constructing a unique polymer, poly(hexaazatrinaphthalene) (PHATN), at a Si/C surface (PCSi). The Li+ transport mechanism of the PCSi is elucidated by using in situ characterization and theoretical simulation. During the lithiation of the PCSi anode, CN groups with high electron density in the PHATN first coordinate Li+ to form CNLi bonds on both sides of the PHATN molecule plane. Consequently, the original benzene rings in the PHATN become active centers to accept lithium and form stable Li-rich PHATN coatings. PHATN molecules expand due to the change of molecular configuration during the consecutive lithiation process, which provides controllable space for the volume expansion of the Si particles. The PCSi composite anode exhibits a specific capacity of 1129.6 mAh g-1 after 500 cycles at 1 A g-1 , and exhibits compelling rate performance, maintaining 417.9 mAh g-1 at 16.5 A g-1 .

Novel Gene Mutations Regulating Immune Responses in Autoimmune Polyglandular Syndrome With an Atypical Course.

CONTEXT: Autoimmune polyglandular syndrome (APS) is a cluster of endocrine disorders arising from immune dysregulation, often combined with damage to nonendocrine organs. There are 2 types of APS: type 1 and type 2 (APS-1 and APS-2, respectively). In clinical practice, an atypical course of APS is often observed. OBJECTIVE: This work aims to find a novel genetic predictor of APS. METHODS: We performed exome sequencing in 2 patients with an atypical clinical APS picture and members of their families. Patient A presented with a manifestation of APS-2 in early childhood and patient B with a late manifestation of the main components of APS-1. RESULTS: In patient B, we identified inherited compound mutations as a novel combination of the c.769C > T and c.821delG alleles of AIRE and genetic variation in the CIITA gene. No homozygous or compound mutations in AIRE were found in patient A, but we did reveal mutations in genes encoding regulatory proteins of innate and acquired immunity in this patient. CONCLUSION: Our data revealed novel combination of mutations in the AIRE gene in atypical APS and imply that mutations in immune-related genes may modify the clinical manifestation of APS in AIRE-mutation carriers and contribute to the development of autoimmune pathology in non-AIRE carriers with atypical APS.