Anchoring Active Li Metal in Oriented Channel by In Situ Formed Nucleation Sites Enabling Durable Lithium-Metal Batteries.

Lithium metal is the ultimate anode material for pursuing the increased energy density of rechargeable batteries. However, fatal dendrites growth and huge volume change seriously hinder the practical application of lithium metal batteries (LMBs). In this work, a lithium host that preinstalled CoSe nanoparticles on vertical carbon vascular tissues (VCVT/CoSe) is designed and fabricated to resolve these issues, which provides sufficient Li plating space with a robust framework, enabling dendrite-free Li deposition. Their inherent N sites coupled with the in situ formed lithiophilic Co sites loaded at the interface of VCVT not only anchor the initial Li nucleation seeds but also accelerate the Li+ transport kinetics. Meanwhile, the Li2Se originated from the CoSe conversion contributes to constructing a stable solid-electrolyte interphase with high ionic conductivity. This optimized Li/VCVT/CoSe composite anode exhibits a prominent long-term cycling stability over 3000 h with a high areal capacity of 10 mAh cm-2. When paired with a commercial nickel-rich LiNi0.83Co0.12Mn0.05O2 cathode, the full-cell presents substantially enhanced cycling performance with 81.7% capacity retention after 300 cycles at 0.2 C. Thus, this work reveals the critical role of guiding Li deposition behavior to maintain homogeneous Li morphology and pave the way to stable LMBs.

Electromagnetic pulse induced blood-brain barrier breakdown through tight junction opening in rats.

The blood-brain barrier (BBB) is the main obstacle to hydrophilic and large molecules to enter the brain, maintaining the stability of the central nervous system (CNS). But many environmental factors may affect the permeability and structure of the BBB. Electromagnetic pulses (EMP) irradiation has been proven to enhance the permeability of the BBB, but the specific mechanism is still unclear. To explore the potential mechanism of EMP-induced BBB opening, this study investigated the permeability, fine structure and the proteins expression of the tight junction (TJ) of the BBB in the rats exposed to EMP. Using the leakage of fluorescein isothiocyanate-labeled dextran with different molecular mass under different field intensity of EMP exposure, we found that the tracer passing through the BBB is size-dependent in the rat exposed to EMP as field intensity increased. Transmission electron microscopy showed TJ of the endothelial cells in the EMP-exposed group was open, compared with the sham-irradiated group. But the levels of TJ proteins including ZO-1, claudin-5, or occludin were not changed as indicated by western blot. These data suggest that EMP induce BBB opening in a field intensity-dependent manner and probably through dysfunction of TJ proteins instead of their expression. Our findings increase the understanding of the mechanism for EMP working on the brain and are helpful for CNS protection against EMP.

A Novel circUBR4/miR-491-5p/NRP2 ceRNA Network Regulates Oxidized Low-density Lipoprotein-induced Proliferation and Migration in Vascular Smooth Muscle Cells.

ABSTRACT: Vascular smooth muscle cells (VSMCs) play critical roles in the progression of atherosclerosis. Circular RNA (circRNA) ubiquitin protein ligase E3 component n-recognin 4 (circUBR4) has been shown to regulate VSMC migration and proliferation. In this study, we sought to identify the mechanism in the regulation of circUBR4. CircUBR4, microRNA (miR)-491-5p, and Neuropilin-2 (NRP2) were quantified by quantitative real-time polymerase chain reaction (PCR) and western blot. Cell proliferation was evaluated by Cell Counting Kit-8 and 5-Ethynyl-2'-Deoxyuridine assays. Cell migration was examined by wound-healing and transwell invasion assays. The direct relationship between miR-491-5p and circUBR4 or NRP2 was validated by dual-luciferase reporter and RNA immunoprecipitation assays. Our data indicated that in VSMCs, ox-LDL induced circUBR4 expression. Silencing endogenous circUBR4 attenuated VSMC proliferation and migration induced by ox-LDL. Mechanistically, circUBR4 targeted miR-491-5p by pairing to miR-491-5p. Moreover, miR-491-5p was identified as a downstream mediator of circUBR4 function in ox-LDL-treated VSMCs. NRP2 was a direct target of miR-491-5p, and circUBR4 acted as a competing endogenous RNA for miR-491-5p to regulate NRP2 expression. In addition, NRP2 was a functionally downstream effector of miR-491-5p in regulating ox-LDL-evoked VSMC proliferation and migration. Our findings identify a new competing endogenous RNA network, the circUBR4/miR-491-5p/NRP2 axis, for the regulation of circUBR4 in VSMC migration and proliferation.

Circ-USP9X Inhibition Reduces Oxidized Low-density Lipoprotein-induced Endothelial Cell Injury via the microRNA 599/Chloride Intracellular Channel 4 Axis.

ABSTRACT: Atherosclerosis (AS) is the common pathological basis of cardiovascular disease. Circular RNA circ-USP9X (hsa_circ_0090231) has been discovered to be upregulated in oxidized low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cells (HUVECs), but the role of circ-USP9X in ox-LDL-induced endothelial cell injury is indistinct. The purpose of the research was to investigate the role and regulatory mechanism of circ-USP9X in ox-LDL--induced endothelial cell injury. Expression of circ-USP9X was examined by quantitative real-time polymerase chain reaction. Loss-of-function experiments were performed to assess the impacts of circ-USP9X inhibition on viability, cell cycle progression, apoptosis, and tube formation, inflammation, and oxidative stress of ox-LDL-induced HUVEC. The regulatory mechanism of circ-USP9X predicted by bioinformatics analysis and verified by dual-luciferase reporter or RNA immunoprecipitation assays. We observed that circ-USP9X was upregulated in AS patients' serum and ox-LDL-induced HUVEC. Inhibition of circ-USP9X elevated viability, promoted cell cycle progression and angiopoiesis, and decreased apoptosis, inflammation, and oxidative stress of ox-LDL-induced HUVEC. Mechanically, circ-USP9X regulated chloride intracellular channel 4 (CLIC4) messenger RNA expression by sponging microRNA (miR)-599. Furthermore, miR-599 inhibitor overturned circ-USP9X silencing-mediated influence on ox-LDL-induced HUVEC injury. Also, CLIC4 overexpression reversed miR-599 elevation-mediated effect on ox-LDL-induced HUVEC injury. In conclusion, circ-USP9X silencing decreased ox-LDL-induced endothelial cell injury via the miR-599/CLIC4 axis, which offered a novel molecular mechanism to comprehend the pathology of AS.

A body characteristic index to evaluate the level of risk of heat strain for a group of workers with a test.

The purpose of this study was to develop a body characteristic index (BCI) based on the distribution of maximal oxygen uptake per body mass (VO2max/mass), body surface area per body mass (BSA/mass), and percentage of body fat (Fat%) to evaluate the relative level of individual physiological responses to heat strain in a group of workers. BCI was based upon the data obtained from 10 males and 10 females exercising for 60 min on a treadmill at 2 relative exercise intensities of 25% and 45% VO2max in mild, warm wet, and hot dry climate condition, separately. BCI was developed into 2 formulas, which were proved to be better predictors for heat strain responses than each individual characteristic, and more sensitive than body type to describe the distributions of individual characteristics and distinguish the differences in physiological responses to heat.