Li anodes have been rapidly developed in recent years owing to the rising demand for higher‐energy‐density batteries. However, the safety issues induced by dendrites hinder the practical applications ...of Li anodes. Here, Li metal anodes stabilized by regulating lithium plating/stripping in vertically aligned microchannels are reported. The current density distribution and morphology evolution of the Li deposits on porous Cu current collectors are systematically analyzed. Based on simulations in COMSOL Multiphysics, the tip effect leads to preferential deposition on the microchannel walls, thus taking full advantage of the lightening rod theory of classical electromagnetism for restraining growth of Li dendrites. The Li anode with a porous Cu current collector achieves an enhanced cycle stability and a higher average Coulombic efficiency of 98.5% within 200 cycles. In addition, the resultant LiFePO4/Li full battery demonstrates excellent rate capability and stable cycling performance, thus demonstrating promise as a current collector for high‐energy‐density, safe rechargeable Li batteries.
A new strategy to restrain lithium dendrite growth is proposed and demonstrated using vertically aligned microchannel Cu current collectors for Li metal anodes. Most of the lithium is preferentially deposited into the microchannels. The current‐density distribution, deposition behavior, and electrochemical performance are simulated and investigated experimentally to understand the effectiveness of the microchannel structure.
Bioprinting is the most convenient microfabrication method to create biomimetic three‐dimensional (3D) cardiac tissue constructs, that can be used to regenerate damaged tissue and provide platforms ...for drug screening. However, existing bioinks, which are usually composed of polymeric biomaterials, are poorly conductive and delay efficient electrical coupling between adjacent cardiac cells. To solve this problem, a gold nanorod (GNR)‐incorporated gelatin methacryloyl (GelMA)‐based bioink is developed for printing 3D functional cardiac tissue constructs. The GNR concentration is adjusted to create a proper microenvironment for the spreading and organization of cardiac cells. At optimized concentrations of GNR, the nanocomposite bioink has a low viscosity, similar to pristine inks, which allows for the easy integration of cells at high densities. As a result, rapid deposition of cell‐laden fibers at a high resolution is possible, while reducing shear stress on the encapsulated cells. In the printed GNR constructs, cardiac cells show improved cell adhesion and organization when compared to the constructs without GNRs. Furthermore, the incorporated GNRs bridge the electrically resistant pore walls of polymers, improve the cell‐to‐cell coupling, and promote synchronized contraction of the bioprinted constructs. Given its advantageous properties, this gold nanocomposite bioink may find wide application in cardiac tissue engineering.
A gold nanorod‐incorporated gelatin methacryloyl‐based bioink for printing of 3D cardiac tissue constructs is developed. The rapid deposition of the cell‐laden fibers at a high resolution is achieved, while reducing the shear stress on the encapsulated cells. The incorporated gold nanorods improve the electrical propagation between cardiac cells and promote their functional improvement in the printed cardiac construct.
Physical or mental stress leads to neuroplasticity in the brain and increases the risk of depression and anxiety. Stress exposure causes the dysfunction of peripheral T lymphocytes. However, the ...pathological role and underlying regulatory mechanism of peripheral T lymphocytes in mood disorders have not been well established. Here, we show that the lack of CD4+ T cells protects mice from stress-induced anxiety-like behavior. Physical stress-induced leukotriene B4 triggers severe mitochondrial fission in CD4+ T cells, which further leads to a variety of behavioral abnormalities including anxiety, depression, and social disorders. Metabolomic profiles and single-cell transcriptome reveal that CD4+ T cell-derived xanthine acts on oligodendrocytes in the left amygdala via adenosine receptor A1. Mitochondrial fission promotes the de novo synthesis of purine via interferon regulatory factor 1 accumulation in CD4+ T cells. Our study implicates a critical link between a purine metabolic disorder in CD4+ T cells and stress-driven anxiety-like behavior.
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•Peripheral CD4+ T cells control stress-induced anxiety-like behavior•Mitochondrial fission in peripheral CD4+ T cell causes severe anxiety symptoms•T cell-derived xanthine acts on the oligodendrocytes in the left amygdala•IRF-1 controls purine synthesis in CD4+ T cells and triggers the onset of anxiety
Xanthine metabolism in CD4+ T cells is found to be central to mediating the effects of stress-induced anxiety like behavior in mice through its effects on oligodendrocyte proliferation and neuronal hyperactivation.
Abstract
Lithium garnets have been widely studied as promising electrolytes that could enable the next-generation all-solid-state lithium batteries. However, upon exposure to atmospheric moisture and ...carbon dioxide, insulating lithium carbonate forms on the surface and deteriorates the interfaces within electrodes. Here, we report a scalable solid sintering method, defined by lithium donor reaction that allows for complete decarbonation of Li
6.4
La
3
Zr
1.4
Ta
0.6
O
12
(LLZTO) and yields an active LiCoO
2
layer for each garnet particle. The obtained LiCoO
2
coated garnets composite is stable against air without any Li
2
CO
3
. Once working in a solid-state lithium battery, the LiCoO
2
-LLZTO@LiCoO
2
composite cathode maintains 81% of the initial capacity after 180 cycles at 0.1 C. Eliminating CO
2
evolution above 4.0 V is confirmed experimentally after transforming Li
2
CO
3
into LiCoO
2
. These results indicate that Li
2
CO
3
is no longer an obstacle, but a trigger of the intimate solid-solid interface. This strategy has been extended to develop a series of LLZTO@active layer materials.
Macroautophagy (hereafter called autophagy) is a highly conserved physiological process that degrades over-abundant or damaged organelles, large protein aggregates and invading pathogens via the ...lysosomal system (the vacuole in plants and yeast). Autophagy is generally induced by stress, such as oxygen-, energy- or amino acid-deprivation, irradiation, drugs,
. In addition to non-selective bulk degradation, autophagy also occurs in a selective manner, recycling specific organelles, such as mitochondria, peroxisomes, ribosomes, endoplasmic reticulum (ER), lysosomes, nuclei, proteasomes and lipid droplets (LDs). This capability makes selective autophagy a major process in maintaining cellular homeostasis. The dysfunction of selective autophagy is implicated in neurodegenerative diseases (NDDs), tumorigenesis, metabolic disorders, heart failure,
. Considering the importance of selective autophagy in cell biology, we systemically review the recent advances in our understanding of this process and its regulatory mechanisms. We emphasize the 'cargo-ligand-receptor' model in selective autophagy for specific organelles or cellular components in yeast and mammals, with a focus on mitophagy and ER-phagy, which are finely described as types of selective autophagy. Additionally, we highlight unanswered questions in the field, helping readers focus on the research blind spots that need to be broken.
Recent advances in the pathophysiologic understanding of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has indicated that patients with severe coronavirus disease 2019 ...(COVID-19) might experience cytokine release syndrome (CRS), characterized by increased interleukin (IL)-6, IL-2, IL-7, IL-10, etc. Therefore, the treatment of cytokine storm has been proposed as a critical part of rescuing severe COVID-19. Several of the cytokines involved in COVID-19 employ a distinct intracellular signaling pathway mediated by Janus kinases (JAKs). JAK inhibition, therefore, presents an attractive therapeutic strategy for CRS, which is a common cause of adverse clinical outcomes in COVID-19. Below, we review the possibilities and challenges of targeting the pathway in COVID-19.
Recent advances in the pathophysiologic understanding of COVID-19 infection have suggested a critical role of cytokine release syndrome (CRS) in severe COVID-19 patients.Several inflammatory cytokines that are involved in CRS and correlate with adverse clinical outcomes in COVID-19 employ a distinct intracellular signaling pathway mediated by Janus kinases (JAKs).JAK-STAT signaling may be an excellent therapeutic target for the development of much needed therapies for COVID-19.
Viral infection triggers host innate immune responses, which primarily include the activation of type I interferon (IFN) signaling and inflammasomes. Here, we report that Zika virus (ZIKV) infection ...triggers NLRP3 inflammasome activation, which is further enhanced by viral non‐structural protein NS1 to benefit its replication. NS1 recruits the host deubiquitinase USP8 to cleave K11‐linked poly‐ubiquitin chains from caspase‐1 at Lys134, thus inhibiting the proteasomal degradation of caspase‐1. The enhanced stabilization of caspase‐1 by NS1 promotes the cleavage of cGAS, which recognizes mitochondrial DNA release and initiates type I IFN signaling during ZIKV infection. NLRP3 deficiency increases type I IFN production and strengthens host resistance to ZIKVin vitro and in vivo. Taken together, our work unravels a novel antagonistic mechanism employed by ZIKV to suppress host immune response by manipulating the interplay between inflammasome and type I IFN signaling, which might guide the rational design of therapeutics in the future.
Synopsis
Zika virus promotes NLRP3 inflammasome activation by stabilizing caspase‐1 to suppress cGAS‐mediated type I IFN signaling.
The non‐structural protein NS1 enhances ZIKV‐induced NLRP3 inflammasome activation.
NS1 stabilizes caspase‐1 by blocking its proteasomal degradation.
NS1 recruits USP8 to cleave K11‐linked poly‐ubiquitin chains from caspase‐1 at Lys134.
ZIKV enhances inflammasome activation to benefit its infection by inhibiting type I IFN signaling.
NS1‐mediated stabilization of caspase‐1 promotes the cleavage of cGAS.
The Zika virus promotes NLRP3 inflammasome activation by stabilizing caspase‐1 to suppress cGAS‐mediated type I IFN signaling.
Popularize the concept: A novel piezochromic luminescence (PIEL) system has been developed from a donor–acceptor binary complex. The complex is non‐fluorescent, but pressure‐induced phase separation ...leads to a crystalline fluorescent donor. This quenching–recovering mechanism ensures a high contrast ratio and popularizes the concept of PIEL.
Abstract We initiate the study of the nonlocal correlations in generic asymmetric quantum networks in a star configuration. Therein, the diverse unrelated sources can emit either partially or ...maximally entangled states, while the observers employ varying numbers of measurement settings. We propose nonlinear Bell inequalities tailored to the distributed entangled states. Specifically, we demonstrate that the algebraic maximal violations of the proposed nonlinear Bell inequalities are physically achievable within the quantum region. To achieve this, we construct the segmented Bell operators through the cut-graft-mix method applied to the Bell operators in the standard Bell tests. Furthermore, we devise the fitting Bell operators using the sum-of-square approach.
Atherosclerosis develops preferentially at branches and curvatures of the arterial tree, where blood flow pattern is disturbed rather than being laminar, and wall shear stress has an irregular ...distribution without defined directions. The endothelium in the atherosusceptible regions, in comparison to that in atheroresistant regions, shows activation of proproliferative and proinflammatory gene expressions, reduced production of nitric oxide (NO), increased leukocyte adhesion, and permeability, as well as other atheroprone phenotypes. Differences in gene expressions and cell phenotypes have been detected in endothelia residing in native atherosusceptible and atheroresistant regions of the arteries, or in arteries from animal models with artificial creation of disturbed flow. Similar results have also been shown in in vitro systems that apply controlled shear stresses with or without clear directions to cultured endothelial cells in fluid-dynamically designed flow-loading devices. The available evidence indicates that the coordination of multiple signaling networks, rather than individual separate pathways, links the mechanical signals to specific genetic circuitries in orchestrating the mechanoresponsive networks to evoke comprehensive genetic and functional responses.
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