A Review on Engineering Transition Metal Compound Catalysts to Accelerate the Redox Kinetics of Sulfur Cathodes for Lithium-Sulfur Batteries.

Engineering transition metal compounds (TMCs) catalysts with excellent adsorption-catalytic ability has been one of the most effective strategies to accelerate the redox kinetics of sulfur cathodes. Herein, this review focuses on engineering TMCs catalysts by cation doping/anion doping/dual doping, bimetallic/bi-anionic TMCs, and TMCs-based heterostructure composites. It is obvious that introducing cations/anions to TMCs or constructing heterostructure can boost adsorption-catalytic capacity by regulating the electronic structure including energy band, d/p-band center, electron filling, and valence state. Moreover, the electronic structure of doped/dual-ionic TMCs are adjusted by inducing ions with different electronegativity, electron filling, and ion radius, resulting in electron redistribution, bonds reconstruction, induced vacancies due to the electronic interaction and changed crystal structure such as lattice spacing and lattice distortion. Different from the aforementioned two strategies, heterostructures are constructed by two types of TMCs with different Fermi energy levels, which causes built-in electric field and electrons transfer through the interface, and induces electron redistribution and arranged local atoms to regulate the electronic structure. Additionally, the lacking studies of the three strategies to comprehensively regulate electronic structure for improving catalytic performance are pointed out. It is believed that this review can guide the design of advanced TMCs catalysts for boosting redox of lithium sulfur batteries.

Using structural analysis to clarify the impact of single nucleotide variants in neurexin/neuroligin revealed in clinical genomic sequencing.

The synapse is a highly specialized and dynamic structure, which is involved in regulating neurotransmission. Nerve cell adhesion molecule is a kind of transmembrane protein that mediates the interaction between cells and cells, cells and extracellular matrix, and plays a role in cell recognition, metastasis, and transmembrane signal transduction. Among nerve cell adhesion molecules, Neurexins (NRXNs) and Neuroligins (NLGNs) have been focused due to the relation with autism and other neuropsychiatric diseases. The previous research discovered numerous variants in NRXNs and NLGNs reported in neurodevelopmental disorders by genomic sequencing. However, structural variants in synaptic molecules caused by genome variants still prevent us from understanding the molecular mechanism of diseases. Thus, we sought to conduct a comprehensive risk assessment of the known NRXN and NLGN gene variants by protein structure analysis. In this study, we analyzed the structural properties of the NRXN/NLGN complex by calculating free energy in residue scanning, in combination with existing risk evaluation tools to focus on candidate missense mutations. Our calculations show that five candidate missense mutations in NLGNs can reduce the stability of NLGNs and even prevent the formation of NRXN/NLGN complexes, namely R87W, R204H, R437H, R437C and R583W. In addition, we found that the affinity of the amino acid substitution (Leu593Phe) (ΔΔG(affinity)) changes the affinity of the NLGN dimer. Overall, we have identified important potential pathological variants that provide clues to biomarkers. Communicated by Ramaswamy H. Sarma.

Potential role of genomic imprinted genes and brain developmental related genes in autism.

BACKGROUND: Autism is a complex disease involving both environmental and genetic factors. Recent efforts have implicated the correlation of genomic imprinting and brain development in autism, however the pathogenesis of autism is not completely clear. Here, we used bioinformatic tools to provide a comprehensive analysis of the autism-related genes, genomic imprinted genes and the spatially and temporally differentially expressed genes of human brain, aiming to explore the relationship between autism, brain development and genomic imprinting. METHODS: This study analyzed the distribution correlation between autism-related genes and imprinted genes on chromosomes using sliding windows and statistical methods. The normal brains' gene expression microarray data were reanalyzed to construct a spatio-temporal coordinate system of gene expression during brain development. Finally, we intersected the autism-related genes, imprinted genes and brain spatio-temporally differentially expressed genes for further analysis to find the major biological processes that these genes involved. RESULTS: We found a positive correlation between the autism-related genes' and imprinted genes' distribution on chromosomes. Through the analysis of the normal brain microarray data, we constructed a spatio-temporal coordinate system of gene expression during human brain development, and obtained 13 genes that are differentially expressed in the process of brain development, which are both autism-related genes and imprinted genes. Furthermore, enrichment analysis illustrated that these genes are mainly involved in the biological processes, such as gamma-aminobutyric acid signaling pathway, neuron recognition, learning or memory, and regulation of synaptic transmission. Bioinformatic analysis implied that imprinted genes regulate the development and behavior of the brain. And its own mutation or changes in the epigenetic modification state of the imprinted control region could lead to some diseases, indicating that imprinted genes and brain development play an important role in diagnosis and prognosis of autism. CONCLUSION: This study systematically correlates brain development and genomic imprinting with autism, which provides a new perspective for the study of genetic mechanisms of autism, and selected the potential candidate biomarkers for early diagnosis of autism in clinic.