Cation Disorder and Large Tetragonal Supercell Ordering in the Li-Rich Argyrodite LiZnSiS.

A tetragonal argyrodite with >7 mobile cations, LiZnSiS, is experimentally realized for the first time through solid state synthesis and exploration of the Li-Zn-Si-S phase diagram. The crystal structure of LiZnSiS was solved from high-resolution X-ray and neutron powder diffraction data and supported by solid-state NMR. LiZnSiS adopts a tetragonal 4 structure at room temperature with ordered Li and Zn positions and undergoes a transition above 411.

Biallelic variants in YRDC cause a developmental disorder with progeroid features.

The highly conserved YrdC domain-containing protein (YRDC) interacts with the well-described KEOPS complex, regulating specific tRNA modifications to ensure accurate protein synthesis. Previous studies have linked the KEOPS complex to a role in promoting telomere maintenance and controlling genome integrity. Here, we report on a newborn with a severe neonatal progeroid phenotype including generalized loss of subcutaneous fat, microcephaly, growth retardation, wrinkled skin, renal failure, and premature death at the age of 12 days.

Activation of anionic redox in d transition metal chalcogenides by anion doping.

Expanding the chemical space for designing novel anionic redox materials from oxides to sulfides has enabled to better apprehend fundamental aspects dealing with cationic-anionic relative band positioning. Pursuing with chalcogenides, but deviating from cationic substitution, we here present another twist to our band positioning strategy that relies on mixed ligands with the synthesis of the LiTiSSe solid solution series. Through the series the electrochemical activity displays a bell shape variation that peaks at 260 mAh/g for the composition x = 0.

Blood RNA biomarkers in prodromal PARK4 and rapid eye movement sleep behavior disorder show role of complexin 1 loss for risk of Parkinson's disease.

Parkinson's disease (PD) is a frequent neurodegenerative process in old age. Accumulation and aggregation of the lipid-binding SNARE complex component α-synuclein (SNCA) underlies this vulnerability and defines stages of disease progression. Determinants of SNCA levels and mechanisms of SNCA neurotoxicity have been intensely investigated.