Solvent-Mediated, Reversible Ternary Graphite Intercalation Compounds for Extreme-Condition Li-Ion Batteries.

Traditional Li-ion intercalation chemistry into graphite anodes exclusively utilizes the cointercalation-free or cointercalation mechanism. The latter mechanism is based on ternary graphite intercalation compounds (t-GICs), where glyme solvents were explored and proved to deliver unsatisfactory cyclability in LIBs. Herein, we report a novel intercalation mechanism, that is, in situ synthesis of t-GIC in the tetrahydrofuran (THF) electrolyte via a spontaneous, controllable reaction between binary-GIC (b-GIC) and free THF molecules during initial graphite lithiation. The spontaneous transformation from b-GIC to t-GIC, which is different from conventional cointercalation chemistry, is characterized and quantified via operando synchrotron X-ray and electrochemical analyses. The resulting t-GIC chemistry obviates the necessity for complete Li-ion desolvation, facilitating rapid kinetics and synchronous charge/discharge of graphite particles, even under high current densities. Consequently, the graphite anode demonstrates unprecedented fast charging (1 min), dendrite-free low-temperature performance, and ultralong lifetimes exceeding 10 000 cycles. Full cells coupled with a layered cathode display remarkable cycling stability upon a 15 min charging and excellent rate capability even at -40 °C. Furthermore, our chemical strategies are shown to extend beyond Li-ion batteries to encompass Na-ion and K-ion batteries, underscoring their broad applicability. Our work contributes to the advancement of graphite intercalation chemistry and presents a low-cost, adaptable approach for achieving fast-charging and low-temperature batteries.

The regulatory process and practical significance of non-coding RNA in the dissemination of prostate cancer to the skeletal system.

Prostate cancer is a major contributor to male cancer-related mortality globally. It has a particular affinity for the skeletal system with metastasis to bones seriously impacting prognosis. The identification of prostate cancer biomarkers can significantly enhance diagnosis and patient monitoring. Research has found that cancer and metastases exhibit abnormal expression of numerous non-coding RNA. Some of these RNA facilitate prostate cancer bone metastasis by activating downstream signaling pathways, while others inhibit this process. Elucidating the functional processes of non-coding RNA in prostate cancer bone metastasis will likely lead to innovative treatment strategies for this malignant condition. In this review, the mechanistic role of the various RNA in prostate cancer is examined. Our goal is to provide a new avenue of approach to the diagnosis and treatment of bone metastasis in this cancer.

Integrating transcriptomics and metabolomics to elucidate the mechanism by which taurine protects against DOX-induced depression.

Doxorubicin (DOX) is an effective anticancer drug with potent antitumour activity. However, the application of DOX is limited by its adverse reactions, such as depression. Taurine can alleviate depression induced by multiple factors. However, it is still unclear whether and how taurine improves DOX-induced depression. To address this question, the aim of this study was to explore the potential mechanism by which taurine protects against DOX-induced depression. Mice were randomly divided into three groups (n = 8): (1) the control group, (2) the DOX group, and (3) the DOX + taurine group. The open field test (OFT), elevated plus maze test, and forced swim test (FST) were first performed to assess the effects of DOX and taurine on the behaviour of mice. Next, a combined transcriptomic and metabolomic analysis was performed to analyse the possible antidepressive effect of taurine. Taurine pretreatment increased the total distance travelled and speed of mice in the OFT, increased the number of entries into the open arm and the time spent in the open arm, and reduced the immobility time in the FST. In addition, 179 differential genes and 51 differentially abundant metabolites were detected in the DOX + taurine group compared to the DOX group. Furthermore, differential genes and differentially abundant metabolites were found to be jointly involved in 21 pathways, which may be closely related to the antidepressant effect of taurine. Taurine alleviated DOX-induced depressive behaviour. The various pathways identified in this study, such as the serotonergic synapse and the inflammatory mediator regulation of TRP channels, may be key regulatory pathways related to depression and antidepressant effects.

Self-terminating, heterogeneous solid-electrolyte interphase enables reversible Li-ether cointercalation in graphite anodes.

Ether solvents are suitable for formulating solid-electrolyte interphase (SEI)-less ion-solvent cointercalation electrolytes in graphite for Na-ion and K-ion batteries. However, ether-based electrolytes have been historically perceived to cause exfoliation of graphite and cell failure in Li-ion batteries. In this study, we develop strategies to achieve reversible Li-solvent cointercalation in graphite through combining appropriate Li salts and ether solvents. Specifically, we design 1M LiBF4 1,2-dimethoxyethane (G1), which enables natural graphite to deliver ~91% initial Coulombic efficiency and >88% capacity retention after 400 cycles. We captured the spatial distribution of LiF at various length scales and quantified its heterogeneity. The electrolyte shows self-terminated reactivity on graphite edge planes and results in a grainy, fluorinated pseudo-SEI. The molecular origin of the pseudo-SEI is elucidated by ab initio molecular dynamics (AIMD) simulations. The operando synchrotron analyses further demonstrate the reversible and monotonous phase transformation of cointercalated graphite. Our findings demonstrate the feasibility of Li cointercalation chemistry in graphite for extreme-condition batteries. The work also paves the foundation for understanding and modulating the interphase generated by ether electrolytes in a broad range of electrodes and batteries.

Enteromorpha Prolifera Polysaccharide-Derived Injectable Hydrogel for Fast Intraoperative Hemostasis and Accelerated Postsurgical Wound Healing Following Tumor Resection.

Intraoperative bleeding and delayed postsurgical wound healing caused by persistent inflammation can increase the risk of tumor recurrence after surgical resection. To address these issues, Enteromorpha prolifera polysaccharide (PEP) with intrinsic potentials for hemostasis and wound healing, is chemically modified into aldehyde-PEP and hydrazine-PEP. Thereby, an injectable double-network hydrogel (OPAB) is developed via forming dual dynamic bonding of acylhydrazone bonds between the decorated aldehyde and hydrazine groups and hydrogen bonds between hydroxyl groups between boric acid and PEP skeletons. The OPAB exhibits controllable shape-adaptive gelation (35.0 s), suitable mechanical properties, nonstimulating self-healing (60 s), good wet tissue adhesion (30.9 kPa), and pH-responsive biodegradability. For in vivo models, owing to these properties, OPAB can achieve rapid hemostasis within 30 s for the liver hemorrhage, and readily loading of curcumin nanoparticles to remarkably accelerate surgical wound closure by alleviating inflammation, re-epithelialization, granulation tissue formation, and collagen deposition. Overall, this multifunctional injectable hydrogel is a promising material that facilitates simultaneous intraoperative hemorrhage and postsurgical wound repair, holding significant potential in the clinical managements of bleeding and surgical wounds for tumor resection.

Asynchronous domain dynamics and equilibration in layered oxide battery cathode.

To improve lithium-ion battery technology, it is essential to probe and comprehend the microscopic dynamic processes that occur in a real-world composite electrode under operating conditions. The primary and secondary particles are the structural building blocks of battery cathode electrodes. Their dynamic inconsistency has profound but not well-understood impacts. In this research, we combine operando coherent multi-crystal diffraction and optical microscopy to examine the chemical dynamics in local domains of layered oxide cathode. Our results not only pinpoint the asynchronicity of the lithium (de)intercalation at the sub-particle level, but also reveal sophisticated diffusion kinetics and reaction patterns, involving various localized processes, e.g., chemical onset, reaction front propagation, domains equilibration, particle deformation and motion. These observations shed new lights onto the activation and degradation mechanisms of state-of-the-art battery cathode materials.

Correlating Rate-Dependent Transition Metal Dissolution between Structure Degradation in Li-Rich Layered Oxides.

Understanding the mechanism of the rate-dependent electrochemical performance degradation in cathodes is crucial to developing fast charging/discharging cathodes for Li-ion batteries. Here, taking Li-rich layered oxide Li1.2 Ni0.13 Co0.13 Mn0.54 O2 as the model cathode, the mechanisms of performance degradation at low and high rates are comparatively investigated from two aspects, the transition metal (TM) dissolution and the structure change. Quantitative analyses combining spatial-resolved synchrotron X-ray fluorescence (XRF) imaging, synchrotron X-ray diffraction (XRD) and transmission electron microscopy (TEM) techniques reveal that low-rate cycling leads to gradient TM dissolution and severe bulk structure degradation within the individual secondary particles, and especially the latter causes lots of microcracks within secondary particles, and becomes the main reason for the fast capacity and voltage decay. In contrast, high-rate cycling leads to more TM dissolution than low-rate cycling, which concentrates at the particle surface and directly induces the more severe surface structure degradation to the electrochemically inactive rock-salt phase, eventually causing a faster capacity and voltage decay than low-rate cycling. These findings highlight the protection of the surface structure for developing fast charging/discharging cathodes for Li-ion batteries.

Proof of principle study: synchrotron X-ray fluorescence microscopy for identification of previously radioactive microparticles and elemental mapping of FFPE tissues.

Biobanks containing formalin-fixed, paraffin-embedded (FFPE) tissues from animals and human atomic-bomb survivors exposed to radioactive particulates remain a vital resource for understanding the molecular effects of radiation exposure. These samples are often decades old and prepared using harsh fixation processes which limit sample imaging options. Optical imaging of hematoxylin and eosin (H&E) stained tissues may be the only feasible processing option, however, H&E images provide no information about radioactive microparticles or radioactive history. Synchrotron X-ray fluorescence microscopy (XFM) is a robust, non-destructive, semi-quantitative technique for elemental mapping and identifying candidate chemical element biomarkers in FFPE tissues. Still, XFM has never been used to uncover distribution of formerly radioactive micro-particulates in FFPE canine specimens collected more than 30 years ago. In this work, we demonstrate the first use of low-, medium-, and high-resolution XFM to generate 2D elemental maps of ~ 35-year-old, canine FFPE lung and lymph node specimens stored in the Northwestern University Radiobiology Archive documenting distribution of formerly radioactive micro-particulates. Additionally, we use XFM to identify individual microparticles and detect daughter products of radioactive decay. The results of this proof-of-principle study support the use of XFM to map chemical element composition in historic FFPE specimens and conduct radioactive micro-particulate forensics.

Operando characterization and regulation of metal dissolution and redeposition dynamics near battery electrode surface.

Mn dissolution has been a long-standing, ubiquitous issue that negatively impacts the performance of Mn-based battery materials. Mn dissolution involves complex chemical and structural transformations at the electrode-electrolyte interface. The continuously evolving electrode-electrolyte interface has posed great challenges for characterizing the dynamic interfacial process and quantitatively establishing the correlation with battery performance. In this study, we visualize and quantify the temporally and spatially resolved Mn dissolution/redeposition (D/R) dynamics of electrochemically operating Mn-containing cathodes. The particle-level and electrode-level analyses reveal that the D/R dynamics is associated with distinct interfacial degradation mechanisms at different states of charge. Our results statistically differentiate the contributions of surface reconstruction and Jahn-Teller distortion to the Mn dissolution at different operating voltages. Introducing sulfonated polymers (Nafion) into composite electrodes can modulate the D/R dynamics by trapping the dissolved Mn species and rapidly establishing local Mn D/R equilibrium. This work represents an inaugural effort to pinpoint the chemical and structural transformations responsible for Mn dissolution via an operando synchrotron study and develops an effective method to regulate Mn interfacial dynamics for improving battery performance.

Comprehensive analysis of metabolic changes in spontaneously hypertensive rats.

OBJECTIVES: Hypertension is a chronic disease with multiple causative factors that involve metabolic disturbances and can cause various complications. However, the metabolic characteristics of hypertension at different stages are still unclear. This study aimed to explore the metabolic changes induced by hypertension at different ages. METHODS: Spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats were divided into four groups according to age: 5-week-old SHR (n = 6), 5-week-old WKY rats (n = 6), 32-week-old SHR (n = 6), and 32-week-old WKY rats (n = 6). Metabolites were analyzed in primary tissues (serum, heart, lung, kidney, brain, and brown adipose) using a non-targeted metabolomics approach. RESULTS: Thirty-five metabolites and nine related metabolic pathways were identified in 5-week-old SHR, mainly related to the metabolism of amino acids. Fifty-one metabolites and seven related metabolic pathways were identified in the 32-week-old SHR, involving glycolysis, lipid, and amino acid metabolisms. CONCLUSION: This experiment elucidates the metabolic profile of SHR at different ages and provides a basis for predicting and diagnosing hypertension. It also provides a reference for the pathogenesis of hypertension.

Suppressing Universal Cathode Crossover in High-Energy Lithium Metal Batteries via a Versatile Interlayer Design.

The universal cathode crossover such as chemical and oxygen has been significantly overlooked in lithium metal batteries using high-energy cathodes which leads to severe capacity degradation and raises serious safety concerns. Herein, a versatile and thin (≈25 µm) interlayer composed of multifunctional active sites was developed to simultaneously regulate the Li deposition process and suppress the cathode crossover. The as-induced dual-gradient solid-electrolyte interphase combined with abundant lithiophilic sites enable stable Li stripping/plating process even under high current density of 10 mA cm-2 . Moreover, X-ray photoelectron spectroscopy and synchrotron X-ray experiments revealed that N-rich framework and CoZn dual active sites can effectively mitigate the undesired cathode crossover, hence significantly minimizing Li corrosion. Therefore, assembled lithium metal cells using various high-energy cathode materials including LiNi0.7 Mn0.2 Co0.1 O2 , Li1.2 Co0.1 Mn0.55 Ni0.15 O2 , and sulfur demonstrate significantly improved cycling stability with high cathode loading.

FDX1-dependent and independent mechanisms of elesclomol-mediated intracellular copper delivery.

Recent studies have uncovered the therapeutic potential of elesclomol (ES), a copper-ionophore, for copper deficiency disorders. However, we currently do not understand the mechanism by which copper brought into cells as ES-Cu(II) is released and delivered to cuproenzymes present in different subcellular compartments. Here, we have utilized a combination of genetic, biochemical, and cell-biological approaches to demonstrate that intracellular release of copper from ES occurs inside and outside of mitochondria. The mitochondrial matrix reductase, FDX1, catalyzes the reduction of ES-Cu(II) to Cu(I), releasing it into mitochondria where it is bioavailable for the metalation of mitochondrial cuproenzyme- cytochrome c oxidase. Consistently, ES fails to rescue cytochrome c oxidase abundance and activity in copper-deficient cells lacking FDX1. In the absence of FDX1, the ES-dependent increase in cellular copper is attenuated but not abolished. Thus, ES-mediated copper delivery to nonmitochondrial cuproproteins continues even in the absence of FDX1, suggesting alternate mechanism(s) of copper release. Importantly, we demonstrate that this mechanism of copper transport by ES is distinct from other clinically used copper-transporting drugs. Our study uncovers a unique mode of intracellular copper delivery by ES and may further aid in repurposing this anticancer drug for copper deficiency disorders.

Hypoxic postconditioning restores mitophagy against transient global cerebral ischemia via Parkin-induced posttranslational modification of TBK1.

Hypoxic postconditioning (HPC) has been reported to enhance Parkin-catalyzed mitochondrial ubiquitination to restore mitophagy in hippocampal CA1 against transient global cerebral ischemia (tGCI). However, the molecular mechanism leading ubiquitinated mitochondria to final clearance during HPC-mediated mitophagy after tGCI is unclear. This study aims to investigate whether HPC restores mitophagy after tGCI through Parkin-induced K63-linked poly-ubiquitination (K63-Ub) to activate tumor necrosis factor associated factor family member associated nuclear factor κB activator -binding kinase 1 (TBK1) in CA1 of male rats. We found that HPC maintained TBK1 expression, promoted p62 and TBK1 phosphorylation in mitochondria, and enhanced their recruitments to mitochondria in CA1 after tGCI. However, these effects were partially abolished by TBK1 inhibitor BX795. K63-Ub of mitochondrial TBK1 was disturbed at 26 h of reperfusion after tGCI, which was reversed by HPC. The maintenance of K63-Ub of mitochondrial TBK1 induced by HPC was counteracted under Parkin knockdown with AAV-mediated Prkn small-interfering RNA, accompanied by the suppression on TBK1 activation and the reduction of mitochondrial p62 phosphorylation. This innovative study indicated that HPC maintained K63-Ub of TBK1 in a Parkin-dependent manner to promote TBK1 phosphorylation, and then phosphorylated TBK1 activated p62 to restore mitophagy, thereby alleviating neuronal damage in CA1 after tGCI.

Direct measurement of Stokes-Einstein diffusion of Cowpea mosaic virus with 19 µs-resolved XPCS.

Brownian motion of Cowpea mosaic virus (CPMV) in water was measured using small-angle X-ray photon correlation spectroscopy (SA-XPCS) at 19.2 µs time resolution. It was found that the decorrelation time τ(Q) = 1/DQ2 up to Q = 0.091 nm-1. The hydrodynamic radius RH determined from XPCS using Stokes-Einstein diffusion D = kT/(6πηRH) is 43% larger than the geometric radius R0 determined from SAXS in the 0.007 M K3PO4 buffer solution, whereas it is 80% larger for CPMV in 0.5 M NaCl and 104% larger in 0.5 M (NH4)2SO4, a possible effect of aggregation as well as slight variation of the structures of the capsid resulting from the salt-protein interactions.

Evaluation of Neurotoxicity in BALB/c Mice following Chronic Exposure to Polystyrene Microplastics.

BACKGROUND: The toxicity of microplastics (MPs) has attracted wide attention from researchers. Previous studies have indicated that MPs produce toxic effects on a variety of organs in aquatic organisms and mammals. However, the exact neurotoxicity of MPs in mammals is still unclear. OBJECTIVES: We aimed to confirm the neurotoxicity of chronic exposure to polystyrene MPs (PS-MPs) at environmental pollution concentrations. METHODS: In the present study, mice were provided drinking water containing 100µg/L and 1,000µg/L PS-MPs with diameters of 0.5, 4, and 10µm for 180 consecutive days. After the exposure period, the mice were anesthetized to gain brain tissues. The accumulation of PS-MPs in brain tissues, integrity of the blood-brain barrier, inflammation, and spine density were detected. We evaluated learning and memory ability by the Morris water maze and novel object recognition tests. RESULTS: We observed the accumulation of PS-MPs with various particle diameters (0.5, 4, and 10µm) in the brains of exposed mice. Meanwhile, exposed mice also exhibited disruption of the blood-brain barrier, higher level of dendritic spine density, and an inflammatory response in the hippocampus. In addition, exposed mice exhibited cognitive and memory deficits compared with control mice as determined using the Morris water maze and novel object recognition tests, respectively. There was a concentration-dependent trend, but no particle size-dependent differences were seen in the neurotoxicity of MPs. CONCLUSIONS: Collectively, our results suggested that PS-MPs exposure can lead to learning and memory dysfunctions and induce neurotoxic effects in mice, findings which have wide-ranging implications for the public regarding the potential risks of MPs. https://doi.org/10.1289/EHP10255.

Origin of structural degradation in Li-rich layered oxide cathode.

Li- and Mn-rich (LMR) cathode materials that utilize both cation and anion redox can yield substantial increases in battery energy density1-3. However, although voltage decay issues cause continuous energy loss and impede commercialization, the prerequisite driving force for this phenomenon remains a mystery3-6 Here, with in situ nanoscale sensitive coherent X-ray diffraction imaging techniques, we reveal that nanostrain and lattice displacement accumulate continuously during operation of the cell. Evidence shows that this effect is the driving force for both structure degradation and oxygen loss, which trigger the well-known rapid voltage decay in LMR cathodes. By carrying out micro- to macro-length characterizations that span atomic structure, the primary particle, multiparticle and electrode levels, we demonstrate that the heterogeneous nature of LMR cathodes inevitably causes pernicious phase displacement/strain, which cannot be eliminated by conventional doping or coating methods. We therefore propose mesostructural design as a strategy to mitigate lattice displacement and inhomogeneous electrochemical/structural evolutions, thereby achieving stable voltage and capacity profiles. These findings highlight the significance of lattice strain/displacement in causing voltage decay and will inspire a wave of efforts to unlock the potential of the broad-scale commercialization of LMR cathode materials.

Impact of financial inclusion and globalization on environmental quality: evidence from G20 economies.

Sustainable development and addressing climate change are among the most pressing issues faced by countries around the world. This research investigates the dynamic associations between financial inclusion, globalization and CO2 emissions of G20 nations from 2005 to 2018, considering the effects of industrial structure, corruption, green energy utilization and economic growth as control variables. In this study, both financial inclusion and globalization index were measured using principal component analysis (PCA). This study examines long-term associations using cross-sectional augmented autoregressive distributed lag (CS-ARDL) technique that offers more accurate outcomes. In addition, the VECM Granger causality method was applied to find causal relationships between study variables. Findings show that in financial inclusion, globalization has positive significant effect on carbon emissions. Moreover, corruption and economic have positive impact on carbon emissions, and renewable energy shows negative impact on environmental quality. The findings of this research are critical for achieving sustainable development and pollution control goals. Governments need to work to bring into line the financial inclusion goals with renewable energy consumption habits and environmental strategies.

Peripheral Blood Mononuclear Cells Regulate Differentially Expressed Proteins in the Proximal Sciatic Nerve of Rats after Transection Anastomosis.

Peripheral nerve injury (PNI) is a common disease that causes the partial loss of sensory, exercise, and autonomic nervous function. In clinical practice, accurate end-to-end neurorrhaphy of the epineurium without tension is the ideal treatment when there is no nerve defect. We have confirmed that peripheral blood mononuclear cells (PBMCs) can effectively improve nerve regeneration and motor function recovery after PNI. However, the global protein profile and signaling conduction pathways regulated by PBMCs remain unclear. This study employed the transection anastomosis model to detect the walking track analysis, gastrocnemius wet weight rate, and morphological examination in order to validate the effect of PBMCs on sciatic nerve injury in rats. Results showed that PBMCs improved nerve regeneration after sciatic nerve dissociation and anastomosis in rats, which reflected in the improvement of the sciatic nerve function index, wet weight rate of gastrocnemius muscles, muscle fiber structure, and the number of axons. We then used TMT labeling quantitative proteomics to explore the underlying mechanism by which PBMCs ameliorated sciatic nerve injury. Results showed that PBMCs regulated 40 differential proteins and the regulated proteins were primarily involved in the complement and coagulation cascade pathways, the notch signaling pathway, the renin angiotensin system, DNA replication, histidine metabolism, ß-alanine metabolism, and other types of O-glycan biosynthesis. Immunohistochemical results supported our findings on the changes in expression of Kininogen 1 and Psen1, the relationships between PNI and the notch pathway and the complement and coagulation level pathways.