Elaborate molecular design on cathodes is of great importance for rechargeable aqueous zinc-organic batteries' performance elevation. Herein, we design a novel orthoquinone-based covalent organic framework with an ordered channel structures (BT-PTO COF) cathode for an ultrahigh performance aqueous zinc-organic battery. The ordered channel structure facilitates ions transfer and makes the COF follow a redox pseudocapacitance mechanism. Thus, it delivers a high reversible capacity of 225 mAh g À 1 at 0.1 A g À 1 and an exceptional long-term cyclability (retention rate 98.0 % at 5 A g À 1 ( � 18 C) after 10 000 cycles). Moreover, a co-insertion mechanism with Zn 2 + first followed by two H + is uncovered for the first time. Significantly, this co-insertion behaviour evolves to more H + insertion routes at high current density and gives the COF ultra-fast kinetics thus it achieves unprecedented specific power of 184 kW kg À 1 (COF) and a high energy density of 92.4 Wh kg À 1 (COF) . Our work reports a superior organic material for zinc batteries and provides a design idea for future high-performance organic cathodes.

The lung is the primary organ targeted by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), making respiratory failure a leading coronavirus disease 2019 (COVID-19)-related mortality. However, our cellular and molecular understanding of how SARS-CoV-2 infection drives lung pathology is limited. Here we constructed multi-omics and single-nucleus transcriptomic atlases of the lungs of patients with COVID-19, which integrate histological, transcriptomic and proteomic analyses. Our work reveals the molecular basis of pathological hallmarks associated with SARS-CoV-2 infection in different lung and infiltrating immune cell populations. We report molecular fingerprints of hyperinflammation, alveolar epithelial cell exhaustion, vascular changes and fibrosis, and identify parenchymal lung senescence as a molecular state of COVID-19 pathology. Moreover, our data suggest that FOXO3A suppression is a potential mechanism underlying the fibroblast-to-myofibroblast transition associated with COVID-19 pulmonary fibrosis. Our work depicts a comprehensive cellular and molecular atlas of the lungs of patients with COVID-19 and provides insights into SARS-CoV-2-related pulmonary injury, facilitating the identification of biomarkers and development of symptomatic treatments.

Organismal aging is driven by interconnected molecular changes encompassing internal and extracellular factors. Combinational analysis of high-throughput ‘multi-omics’ datasets (gathering information from genomics, epigenomics, transcriptomics, proteomics, metabolomics and pharmacogenomics), at either populational or single-cell levels, can provide a multi-dimensional, integrated profile of the heterogeneous aging process with unprecedented throughput and detail. These new strategies allow for the exploration of the molecular profile and regulatory status of gene expression during aging, and in turn, facilitate the development of new aging interventions. With a continually growing volume of valuable aging-related data, it is necessary to establish an open and integrated database to support a wide spectrum of aging research. The Aging Atlas database aims to provide a wide range of life science researchers with valuable resources that allow access to a large-scale of gene expression and regulation datasets created by various high-throughput omics technologies. The current implementation includes five modules: transcriptomics (RNA-seq), single-cell transcriptomics (scRNA-seq), epigenomics (ChIP-seq), proteomics (protein–protein interaction), and pharmacogenomics (geroprotective compounds). Aging Atlas provides user-friendly functionalities to explore age-related changes in gene expression, as well as raw data download services. Aging Atlas is freely available at https://bigd.big.ac.cn/aging/index.