Highly Active Nanostructured CoS2/CoS Heterojunction Electrocatalysts for Aqueous Polysulfide/Iodide Redox Flow Batteries

Aqueous polysulfide/iodide redox flow batteries are attractive for scalable energy storage due to their high energy density and low cost. However, their energy efficiency and power density are usually limited by poor electrochemical kinetics of the redox reactions of polysulfide/iodide ions on graphite electrodes, which has become the main obstacle for their practical applications. Here, CoS2/CoS heterojunction nanoparticles with uneven charge distribution, which are synthesized in situ on graphite felt by a one-step solvothermal process, can significantly boost electrocatalytic activities of I−/I3− and S2−/Sx2−redox reactions by improving absorptivity of charged ions and promoting charge transfer. The polysulfide/iodide flow battery with the graphene felt-CoS2/CoS heterojunction can deliver a high energy efficiency of 84.5% at a current density of 10 mA cm−2, a power density of 86.2 mW cm−2 and a stable energy efficiency retention of 96% after approximately 1000 h of continuous operation

Exuberant fibroblast activity compromises lung function via ADAMTS4

© 2020, The Author(s), under exclusive licence to Springer Nature Limited. Severe respiratory infections can result in acute respiratory distress syndrome (ARDS)1. There are no effective pharmacological therapies that have been shown to improve outcomes for patients with ARDS. Although the host inflammatory response limits spread of and eventually clears the pathogen, immunopathology is a major contributor to tissue damage and ARDS1,2. Here we demonstrate that respiratory viral infection induces distinct fibroblast activation states, which we term extracellular matrix (ECM)-synthesizing, damage-responsive and interferon-responsive states. We provide evidence that excess activity of damage-responsive lung fibroblasts drives lethal immunopathology during severe influenza virus infection. By producing ECM-remodelling enzymes—in particular the ECM protease ADAMTS4—and inflammatory cytokines, damage-responsive fibroblasts modify the lung microenvironment to promote robust immune cell infiltration at the expense of lung function. In three cohorts of human participants, the levels of ADAMTS4 in the lower respiratory tract were associated with the severity of infection with seasonal or avian influenza virus. A therapeutic agent that targets the ECM protease activity of damage-responsive lung fibroblasts could provide a promising approach to preserving lung function and improving clinical outcomes following severe respiratory infections

Publisher Correction: Exuberant fibroblast activity compromises lung function via ADAMTS4 (Nature, (2020), 587, 7834, (466-471), 10.1038/s41586-020-2877-5)

© 2020, The Author(s), under exclusive licence to Springer Nature Limited. An amendment to this paper has been published and can be accessed via a link at the top of the paper

Mimicking Bone Nanostructure by Combining Block Copolymer Self-Assembly and 1D Crystal Nucleation

The orientation and spatial distribution of nanocrystals in the organic matrix are two distinctive structural characteristics associated with natural bone. Synthetic soft materials have been used to successfully control the orientation of mineral crystals. The spatial distribution of minerals in a synthetic scaffold, however, has yet to be reproduced in a biomimetic manner. Herein, we report using block copolymer-decorated polymer nanofibers to achieve biomineralized fibrils with precise control of both mineral crystal orientation and spatial distribution. Exquisite nanoscale structural control in biomimetic hybrid materials has been demonstrated

Mimicking Bone Nanostructure by Combining Block Copolymer Self-Assembly and 1D Crystal Nucleation

The orientation and spatial distribution of nanocrystals in the organic matrix are two distinctive structural characteristics associated with natural bone. Synthetic soft materials have been used to successfully control the orientation of mineral crystals. The spatial distribution of minerals in a synthetic scaffold, however, has yet to be reproduced in a biomimetic manner. Herein, we report using block copolymer-decorated polymer nanofibers to achieve biomineralized fibrils with precise control of both mineral crystal orientation and spatial distribution. Exquisite nanoscale structural control in biomimetic hybrid materials has been demonstrated

Endogenous controls of gene expression in N-methyl-N-nitrosourea-induced T-cell lymphoma in p53-deficient mice

Abstract Background Real-time polymerase chain reaction (PCR) has become an increasingly important technique for gene expression profiling because it can provide insights into complex biological and pathological processes and be used to predict disease or treatment outcomes. Although normalized data are necessary for an accurate estimation of mRNA expression levels, several pieces of evidence suggest that the expression of so-called housekeeping genes is not stable. This study aimed to validate reference genes for the normalization of real-time PCR in an N-methyl-N-nitrosourea (MNU)-induced T-cell lymphoma mouse model. Methods T-cell lymphomas were generated in p53-deficient mice by treatment with 37.5 mg/kg MNU. Thymus and spleen were identified as the primary target organs with the highest incidences of lymphomas. We analyzed the RNA expression levels of eight potential endogenous reference genes (Gapdh, Rn18s, Actb, Hprt, B2M, Rplp0, Gusb, Ctbp1). The expression stabilities of these reference genes were tested at different time points after MNU treatment using geNorm and NormFinder algorithms. Results A total of 65% of MNU-treated mice developed T-cell lymphomas, with the spleen and thymus as the major target organs. All candidate reference genes were amplified efficiently by quantitative reverse-transcription polymerase chain reaction (RT-qPCR). Gene stability evaluation after MNU treatment and during lymphomagenesis revealed that Ctbp1 and Rplp0 were the most stably expressed genes in the thymus and spleen, respectively. RT-PCR of thymus RNA using two additional sets of primer confirmed that Ctbp1 was the most stable of all the candidate reference genes. Conclusions We provided suitable endogenous controls for gene expression studies in the T-cell lymphoma model

PML/RARα fusion protein transactivates the tissue factor promoter through a GAGC-containing element without direct DNA association

A severe coagulopathy is a life-threatening complication of acute promyelocytic leukemia (APL) and is ascribable mainly to the excessive levels of tissue factor (TF) in APL cells regulated in response to the promyelocytic leukemia/retinoic acid receptor α (PML/RARα) fusion protein. The underlying molecular mechanisms for this regulation remain ill-defined. With U937-PR9 cell lines stably expressing luciferase reporter gene under the control of different mutants of the TF promoter, both luciferase and ChIP data allowed the localization of the PML/RARα-responsive sequence in a previously undefined region of the TF promoter at position −230 to −242 devoid of known mammalian transcription factor binding sites. Within this sequence a GAGC motif (−235 to −238) was shown to be crucial because deletion or mutation of these nucleotides impaired both PML/RARα interaction and promoter transactivation. However, EMSA results showed that PML/RARα did not bind to DNA probes encompassing the −230 to −242 sequences, precluding a direct DNA association. Mutational experiments further suggest that the activator protein 1 (AP-1) sites of the TF promoter are dispensable for PML/RARα regulation. This study shows that PML/RARα transactivates the TF promoter through an indirect interaction with an element composed of a GAGC motif and the flanking nucleotides, independent of AP-1 binding