Lithium (Li)‐metal anodes are of great promise for next‐generation batteries due to their high theoretical capacity and low redox potential. However, Li‐dendrite growth during cycling imposes a tremendous safety concern on the practical application of Li‐metal anodes. Herein, an effective approach to suppress Li‐dendrite growth by coating a polypropylene (PP) separator with a thin layer of ultrastrong diamond‐like carbon (DLC) is reported. Theoretical calculations indicate that the DLC coating layer undergoes in situ chemical lithiation once assembled with the lithium‐metal anode, transforming the DLC/PP separator into an excellent 3D Li‐ion conductor. This in situ lithiated DLC/PP separator can not only mechanically suppress Li‐dendrite growth by its intrinsically high modulus (≈100 GPa), but also uniformly redistributes Li ions to render dendrite‐free lithium deposition. The twofold effects of the DLC/PP separator result in stable cycling of lithium plating/stripping (over 4500 h) at a high current density of 3 mA cm−2. Remarkably, this approach enables more than 1000 stable cycles at 5 C with a capacity retention of ≈71% in a Li || LiFePO4 coin cell and more than 200 stable cycles at 0.2 C in a Li || LiNi0.5Co0.3Mn0.2O2 pouch cell with cathode mass loading of ≈9 mg cm−2.
Objective: Multiple mechanisms including vascular endothelial cell damage have a critical role in the formation and development of atherosclerosis (AS), but the specific molecular mechanisms are not exactly clarified. This study aims to determine the possible roles of proline-rich tyrosine kinase 2 (Pyk2)/mitochondrial calcium uniporter (MCU) pathway in AS mouse model and H2O2-induced endothelial cell damage model and explore its possible mechanisms.Approach and Results: The AS mouse model was established using apolipoprotein E-knockout (ApoE–/–) mice that were fed with a high-fat diet. It was very interesting to find that Pyk2/MCU expression was significantly increased in the artery wall of atherosclerotic mice and human umbilical vein endothelial cells (HUVECs) attacked by hydrogen peroxide (H2O2). In addition, down-regulation of Pyk2 by short hairpin RNA (shRNA) protected HUVECs from H2O2 insult. Furthermore, treatment with rosuvastatin on AS mouse model and H2O2-induced HUVEC injury model showed a protective effect against AS by inhibiting the Pyk2/MCU pathway, which maintained calcium balance, prevented the mitochondrial damage and reactive oxygen species production, and eventually inhibited cell apoptosis.Conclusion: Our results provide important insight into the initiation of the Pyk2/MCU pathway involved in AS-related endothelial cell damage, which may be a new promising target for atherosclerosis intervention.
Dual-ion batteries (DIBs) are one of the promising candidates to meet the low-cost requirements of commercial applications because of their high working voltage, excellent safety, and environmental friendliness. In addition to the electrolyte, the research on DIBs mainly focuses on the electrode materials, especially the high-performance anodes. Alloy-type materials, such as Si, Sn, Al, and so forth, are promising alternative anodes owing to their large abundance, excellent conductivity, and especially high specific capacity. However, the alloy-type anodes tend to pulverize due to the excessive volume expansion during the alloying/dealloying process, along with repeated growth/fracture of the solid electrolyte interphase (SEI) layer and continuous consumption of the electrolyte. Herein, we have successfully developed an amorphous carbon nanointerface (ACNI) (<10 nm) coated on an Al anode that acts as an artificial SEI to prevent the continuous growth of the formed SEI layer and maintain its structural stability. Further, pairing this ultrathin ACNI/Al anode with the graphite cathode constructs proof-of-concept DIBs, exhibiting significantly improved performances with a specific capacity of 115 mA h g −1 and a capacity retention ratio of ∼94% after 1000 cycles.
Glucagon-like peptide-1 (GLP-1) regulates energy homeostasis via activation of the GLP-1 receptors (GLP-1Rs) in the central nervous system. However, the mechanism by which the central GLP-1 signal controls blood glucose levels, especially in different nutrient states, remains unclear. Here, we defined a population of glucose-sensing GLP-1R neurons in the dorsomedial hypothalamic nucleus (DMH), by which endogenous GLP-1 decreases glucose levels via the cross-talk between the hypothalamus and pancreas. Specifically, we illustrated the sufficiency and necessity of DMH GLP-1R in glucose regulation. The activation of the DMH GLP-1R neurons is mediated by a cAMP-PKA–dependent inhibition of a delayed rectifier potassium current. We also dissected a descending control of DMH GLP-1R –dorsal motor nucleus of the vagus nerve (DMV)–pancreas activity that can regulate glucose levels by increasing insulin release. Thus, our results illustrate how central GLP-1 action in the DMH can induce a nutrient state–dependent reduction in blood glucose level.
Anterior circulation large artery occlusion (Ac-LAo) related acute ischemic stroke (AiS) is particularly common in clinics in China. We retrospectively analyzed 787 consecutively hospitalized AIS patients with AC-LAO in Hebei Province, China. AC-LAO was defined as a complete occlusion of at least one intracranial internal carotid artery (icA) or middle cerebral artery (McA) based on computed tomography or magnetic resonance angiography. Among eight subtypes of Ac-LAo, unilateral McA occlusion is the most common one (49.8%, n = 392), while bilateral ICA/unilateral MCA occlusion is the least (0.3%, n = 2). Compared with unilateral MCA and unilateral ICA occlusion, patients with tandem ICA/MCA and bilateral ICA/MCA occlusion had poor outcomes after suffering AIS. Age (OR 1.022; 95%CI, 1.007 to 1.036) was an independent risk factor for single artery progressed to multiple artery occlusion, while ApoA1 (OR 0.453; 95% CI, 0.235 to 0.953) was a protective factor. Patients with unilateral MCA occlusion were prone to artery-to-artery embolism infarction subtype, unilateral icA occlusion group were the most vulnerable to hypoperfusion/impaired emboli clearance subtype. Our results suggested various AC-LAO subtypes have different clinical characteristics and prognosis and were prone to different subtypes of infarction. Customized preventive measures based on AC-LAO subtypes may be more targeted preventions of stroke recurrences for AiS patients and could improve their prognoses.Anterior circulation large artery occlusion (AC-LAO) is the most common cause of ischemic strokes 1,2 , especially in Chinese population 3 . For the treatment of those patients, thrombolytic therapy has a time window, and endovascular intervention treatment requires advanced surgical equipment and intensive care. Due to the large differences in medical conditions and levels across China, endovascular intervention treatment is available only in major stroke centers in cities, which means it cannot be applied to all patients with acute infarction, especially in rural areas 4-6 . Previous study showed intravenous thrombolysis and endovascular intervention treatments may not be effective in most patients with high clot burden LAO, and the resulting emboli may cause a worse prognosis 7 . Thus, there is still no treatment much more effective for patients with LAO suffering acute ischemic stroke (AIS) currently. By reviewing the literature, we found that most studies focusing on single unilateral middle cerebral artery (MCA), unilateral internal carotid artery (ICA), or tandem ICA/MCA occlusion, showing that a thrombus in the more proximal intracranial vasculature were more likely to have a poor outcome [8][9][10] . However, in clinical work we found that there are some other types of AC-LAO, such as unilateral and/or bilateral MCA combining unilateral and/or bilateral ICA. Whether different infarction subtypes are related with different types of occlusions or whether the prognosis worsens with the degree of artery occlusion have not been studied in depth u...
Background: Transcriptomics, such as that of non-coding RNA (ncRNA), which include microRNA (miRNA), circular RNA, and the transfer RNA (tRNA)-derived fragments (tiRNA and tRF) in Alzheimer's disease (AD) have attracted much attention recently. The tiRNA and tRFs are produced when the tRNA splits at specific sites. The expression change and related function of tiRNA and tRFs in AD has not been fully investigated.Methods: In our study, APP/PS1 transgenic mice (AD mice model) and healthy control mice were used to discover the differentially expressed tiRNA and tRFs with high-throughput sequencing. Among the differentially expressed tiRNA and tRFs, we chose two tRFs (tRF-Thr-CGT-003 and tRF-Leu-CAA-004) and predicted the target messenger RNAs (mRNAs) with miRanda and Target Scan. The target mRNAs of tRF-related function and pathways were analyzed, then we performed quantitative reverse transcription polymerase chain reaction (RT-qPCR) and western blot to validate the related target mRNAs and pathways.Results: A total of 27 significantly different tiRNA and tRFs were detected between wild type (WT) and APP/PS1 groups, including 14 up-regulated and 13 down-regulated. Through analyzing the target mRNAs of all differentially expressed tiRNA and tRFs with GO enrichment, we found the target mRNAs could take part in the learning and memory biological process, synapse organization, cognition biological process, synaptic transmission, amyloid-β (Aβ) metabolic process, and so on. We then chose three differentially expressed tRFs for further qPCR validation and passed two tRFs: tRF-Thr-CGT-003 and tRF-Leu-CAA-004, that were found to regulate the calcium regulation-related proteins (the voltage-gated calcium channel γ2 subunit and the RYR1 endoplasmic reticulum calcium released protein) and the retinol metabolism-related proteins (retinoic acid metabolic enzymes CYP2S1, CYP2C68, CYP2S1). Conclusions:The APP expression and presenilin mutation in APP/PS1 mice could cause tiRNA and tRFs expression change. Among the differentially expressed tiRNA and tRFs, we found some tRFs took part in the voltage-gated calcium channel γ2 subunit expression and regulation, influencing the neuron calcium homeostasis. Moreover, we also found the tRFs may participate in the regulation of retinol metabolism. Our findings suggest that the dysregulated tiRNA and tRFs may be beneficially exploited as potential diagnostic biomarkers and/or therapeutic targets of AD.
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