Interlayer Engineering and Prelithiation: Empowering Si Anodes for Low-Pressure-Operating All-Solid-State Batteries.

Silicon (Si) anodes, free from the dendritic growth concerns found in lithium (Li) metal anodes, offer a promising alternative for high-energy all-solid-state batteries (ASSBs). However, most advancements in Si anodes have been achieved under impractical high operating pressures, which can mask detrimental electrochemo-mechanical issues. Herein, we effectively address the challenges related to the low-pressure operation of Si anodes in ASSBs by introducing an silver (Ag) interlayer between the solid electrolyte layer (Li6PS5Cl) and anode and prelithiating the anodes. The Si composite electrodes, consisting of Si/polyvinylidene fluoride/carbon nanotubes, are optimized for suitable mechanical properties and electrical connectivity. Although the impact of the Ag interlayer is insignificant at an exceedingly high operating pressure of 70 MPa, it substantially enhances the interfacial contacts under a practical low operating pressure of 15 MPa. Thus, Ag-coated Si anodes outperform bare Si anodes (discharge capacity: 2430 vs 1560 mA h g-1). The robust interfacial contact is attributed to the deformable, adhesive properties and protective role of the in situ lithiated Ag interlayer, as evidenced by comprehensive ex situ analyses. Operando electrochemical pressiometry is used effectively to probe the strong interface for Ag-coated Si anodes. Furthermore, prelithiation through the thermal evaporation deposition of Li metal significantly improves the cycling performance.

Orphan nuclear receptor ERR-γ regulates hepatic FGF23 production in acute kidney injury.

Fibroblast growth factor 23 (FGF23), a hormone generally derived from bone, is important in phosphate and vitamin D homeostasis. In acute kidney injury (AKI) patients, high-circulating FGF23 levels are associated with disease progression and mortality. However, the organ and cell type of FGF23 production in AKI and the molecular mechanism of its excessive production are still unidentified. For insight, we investigated folic acid (FA)-induced AKI in mice. Interestingly, simultaneous with FGF23, orphan nuclear receptor ERR-γ expression is increased in the liver of FA-treated mice, and ectopic overexpression of ERR-γ was sufficient to induce hepatic FGF23 production. In patients and in mice, AKI is accompanied by up-regulated systemic IL-6, which was previously identified as an upstream regulator of ERR-γ expression in the liver. Administration of IL-6 neutralizing antibody to FA-treated mice or of recombinant IL-6 to healthy mice confirms IL-6 as an upstream regulator of hepatic ERR-γ-mediated FGF23 production. A significant (P < 0.001) interconnection between high IL-6 and FGF23 levels as a predictor of AKI in patients that underwent cardiac surgery was also found, suggesting the clinical relevance of the finding. Finally, liver-specific depletion of ERR-γ or treatment with an inverse ERR-γ agonist decreased hepatic FGF23 expression and plasma FGF23 levels in mice with FA-induced AKI. Thus, inverse agonist of ERR-γ may represent a therapeutic strategy to reduce adverse plasma FGF23 levels in AKI.

Circular RNA Tmcc1 improves astrocytic glutamate metabolism and spatial memory via NF-κB and CREB signaling in a bile duct ligation mouse model: transcriptional and cellular analyses.

BACKGROUND: Hepatic encephalopathy-induced hyperammonemia alters astrocytic glutamate metabolism in the brain, which is involved in cognitive decline. To identify specific therapeutic strategies for the treatment of hepatic encephalopathy, various molecular signaling studies, such as non-coding RNA functional study, have been conducted. However, despite several reports of circular RNAs (circRNAs) in the brain, few studies of circRNAs in hepatic encephalopathy-induced neuropathophysiological diseases have been conducted. METHODS: In this study, we performed RNA sequencing to identify whether the candidate circRNA cirTmcc1 is specifically expressed in the brain cortex in a bile duct ligation (BDL) mouse model of hepatic encephalopathy. RESULTS: Based on transcriptional and cellular analysis, we investigated the circTmcc1-dysregulation-induced changes in the expression of several genes that are associated with intracellular metabolism and astrocyte function. We found that the circTmcc1 binds with the NF-κB p65-CREB transcriptional complex and regulates the expression of the astrocyte transporter EAAT2. Furthermore, circTmcc1 contributed to the secretion of proinflammatory mediators and glutamate metabolism in astrocytes and subsequently modulated an improvement in spatial memory by mediating neuronal synaptic plasticity. CONCLUSIONS: Thus, circTmcc1 may be a promising circRNA candidate for targeted interventions to prevent and treat the neuropathophysiological complications that occur due to hepatic encephalopathy.

Effects of SKCPT on Osteoarthritis in Beagle Meniscectomy and Cranial Cruciate Ligament Transection Models.

Osteoarthritis (OA) affects >500 million people globally, and this number is expected to increase. OA management primarily focuses on symptom alleviation, using non-steroidal anti-inflammatory drugs, including Celecoxib. However, such medication has serious side effects, emphasizing the need for disease-specific treatment. The meniscectomy and cranial cruciate ligament transection (CCLx)-treated beagle dog was used to investigate the efficacy of a modified-release formulation of SKI306X (SKCPT) from Clematis mandshurica, Prunella vulgaris, and Trichosanthes kirilowii in managing arthritis. SKCPT's anti-inflammatory and analgesic properties have been assessed via stifle circumference, gait, incapacitance, histopathology, and ELISA tests. The different SKCPT concentrations and formulations also affected the outcome. SKCPT improved the gait, histopathological, and ELISA OA assessment parameters compared to the control group. Pro-inflammatory cytokines and matrix metalloproteinases were significantly lower in the SKCPT-treated groups than in the control group. This study found that SKCPT reduces arthritic lesions and improves abnormal gait. The 300 mg modified-release formulation was more efficacious than others, suggesting a promising approach for managing OA symptoms and addressing disease pathogenesis. A high active ingredient level and a release pattern make this formulation effective for twice-daily arthritis treatment.

Transcriptome Profile in the Mouse Brain of Hepatic Encephalopathy and Alzheimer's Disease.

Hepatic encephalopathy (HE) is a chronic metabolic disease accompanied by neuropathological and neuropsychiatric features, including memory deficits, psychomotor dysfunction, depression, and anxiety. Alzheimer's disease (AD), the most common neurodegenerative disease, is characterized by tau hyperphosphorylation, excessive amyloid beta (Aß) accumulation, the formation of fibrillary tangles, hippocampus atrophy, and neuroinflammation. Recent studies have suggested a positive correlation between HE and AD. Some studies reported that an impaired cholesterol pathway, abnormal bile acid secretion, excessive ammonia level, impaired Aß clearance, astrocytic dysfunction, and abnormal γ-aminobutyric acid GABAergic neuronal signaling in HE may also be involved in AD pathology. However, the mechanisms and related genes involved in AD-like pathology in the HE brain are unclear. Thus, we compared the cortical transcriptome profile between an HE mouse model, bile duct ligation (BDL), and an AD mouse model, the 5×FAD. Our study showed that the expression of many genes implicated in HE is associated with neuronal dysfunction in AD mice. We found changes in various protein-coding RNAs, implicated in synapses, neurogenesis, neuron projection, neuron differentiation, and neurite outgrowth, and non-coding RNAs possibly associated with neuropathology. Our data provide an important resource for further studies to elucidate AD-like pathophysiology in HE patients.

An Inverse Agonist GSK5182 Increases Protein Stability of the Orphan Nuclear Receptor ERRγ via Inhibition of Ubiquitination.

The orphan nuclear receptor, estrogen-related receptor γ (ERRγ) is a constitutively active transcription factor involved in mitochondrial metabolism and energy homeostasis. GSK5182, a specific inverse agonist of ERRγ that inhibits transcriptional activity, induces a conformational change in ERRγ, resulting in a loss of coactivator binding. However, the molecular mechanism underlying the stabilization of the ERRγ protein by its inverse agonist remains largely unknown. In this study, we found that GSK5182 inhibited ubiquitination of ERRγ, thereby stabilizing the ERRγ protein, using cell-based assays and confocal image analysis. Y326 of ERRγ was essential for stabilization by GSK5182, as ligand-induced stabilization of ERRγ was not observed with the ERRγ-Y326A mutant. GSK5182 suppressed ubiquitination of ERRγ by the E3 ligase Parkin and subsequent degradation. The inhibitory activity of GSK5182 was strong even when the ERRγ protein level was elevated, as ERRγ bound to GSK5182 recruited a corepressor, small heterodimer partner-interacting leucine zipper (SMILE), through the activation function 2 (AF-2) domain, without alteration of the nuclear localization or DNA-binding ability of ERRγ. In addition, the AF-2 domain of ERRγ was critical for the regulation of protein stability. Mutants in the AF-2 domain were present at higher levels than the wild type in the absence of GSK5182. Furthermore, the ERRγ-L449A/L451A mutant was no longer susceptible to GSK5182. Thus, the AF-2 domain of ERRγ is responsible for the regulation of transcriptional activity and protein stability by GSK5182. These findings suggest that GSK5182 regulates ERRγ by a unique molecular mechanism, increasing the inactive form of ERRγ via inhibition of ubiquitination.

Orphan nuclear receptor ERRγ regulates hepatic TGF-ß2 expression and fibrogenic response in CCl4-induced acute liver injury.

Acute liver injury results from the complex interactions of various pathological processes. The TGF-ß superfamily plays a crucial role in orchestrating fibrogenic response. In contrast to TGF-ß1, a role of TGF-ß2 in hepatic fibrogenic response has not been fully investigated. In this study, we showed that TGF-ß2 gene expression and secretion are induced in the liver of CCl4 (1 ml/kg)-treated WT mice. Studies with hepatocyte specific ERRγ knockout mice or treatment with an ERRγ-specific inverse agonist, GSK5182 (40 mg/kg), indicated that CCl4-induced hepatic TGF-ß2 production is ERRγ dependent. Moreover, IL6 was found as upstream signal to induce hepatic ERRγ and TGF-ß2 gene expression in CCl4-mediated acute toxicity model. Over-expression of ERRγ was sufficient to induce hepatic TGF-ß2 expression, whereas ERRγ depletion markedly reduces IL6-induced TGF-ß2 gene expression and secretion in vitro and in vivo. Promoter assays showed that ERRγ directly binds to an ERR response element in the TGF-ß2 promoter to induce TGF-ß2 transcription. Finally, GSK5182 diminished CCl4-induced fibrogenic response through inhibition of ERRγ-mediated TGF-ß2 production. Taken together, these results firstly demonstrate that ERRγ can regulate the TGF-ß2-mediated fibrogenic response in a mouse model of CC14-induced acute liver injury.

Tailoring Solution-Processable Li Argyrodites Li6+xP1-xMxS5I (M = Ge, Sn) and Their Microstructural Evolution Revealed by Cryo-TEM for All-Solid-State Batteries.

Owing to their high Li+ conductivities, mechanical sinterability, and solution processability, sulfide Li argyrodites have attracted much attention as enablers in the development of high-performance all-solid-state batteries with practicability. However, solution-processable Li argyrodites have been developed only for a composition of Li6PS5X (X = Cl, Br, I) with insufficiently high Li+ conductivities (∼10-4 S cm-1). Herein, we report the highest Li+ conductivity of 0.54 mS cm-1 at 30 °C (Li6.5P0.5Ge0.5S5I) for solution-processable iodine-based Li argyrodites. A comparative investigation of three iodine-based argyrodites of unsubstituted and Ge- and Sn-substituted solution-processed Li6PS5I with varied heat-treatment temperature elucidates the effect of microstructural evolution on Li+ conductivity. Notably, local nanostructures consisting of argyrodite nanocrystallites in solution-processed Li6.5P0.5Ge0.5S5I have been directly captured by cryogenic transmission electron microscopy, which is a first for sulfide solid electrolyte materials. Specifically, the promising electrochemical performances of all-solid-state batteries at 30 °C employing LiCoO2 electrodes tailored by the infiltration of Li6.5P0.5Ge0.5S5I-ethanol solutions are successfully demonstrated.

Orphan Nuclear Receptor ERRγ Is a Transcriptional Regulator of CB1 Receptor-Mediated TFR2 Gene Expression in Hepatocytes.

Orphan nuclear receptor estrogen-related receptor γ (ERRγ) is an important transcription factor modulating gene transcription involved in endocrine control of liver metabolism. Transferrin receptor 2 (TFR2), a carrier protein for transferrin, is involved in hepatic iron overload in alcoholic liver disease (ALD). However, TFR2 gene transcriptional regulation in hepatocytes remains largely unknown. In this study, we described a detailed molecular mechanism of hepatic TFR2 gene expression involving ERRγ in response to an endocannabinoid 2-arachidonoylglycerol (2-AG). Treatment with 2-AG and arachidonyl-2'-chloroethylamide, a selective cannabinoid receptor type 1 (CB1) receptor agonist, increased ERRγ and TFR2 expression in hepatocytes. Overexpression of ERRγ was sufficient to induce TFR2 expression in both human and mouse hepatocytes. In addition, ERRγ knockdown significantly decreased 2-AG or alcohol-mediated TFR2 gene expression in cultured hepatocytes and mouse livers. Finally, deletion and mutation analysis of the TFR2 gene promoter demonstrated that ERRγ directly modulated TFR2 gene transcription via binding to an ERR-response element. This was further confirmed by chromatin immunoprecipitation assay. Taken together, these results reveal a previously unrecognized role of ERRγ in the transcriptional regulation of TFR2 gene expression in response to alcohol.

Repetitive hyperbaric oxygen therapy for paroxysmal sympathetic hyperactivity after acute carbon monoxide poisoning.

Delayed neuropsychological sequelae (DNS) are relatively common complications of acute carbon monoxide (CO) poisoning, and usually develop within several days to weeks after the initial clinical recovery from acute CO poisoning. DNS can consist of various symptoms such as memory loss, confusion, ataxia, seizures, urinary incontinence, fecal incontinence, emotional lability, disorientation, hallucinations, mutism, cortical blindness, psychosis, parkinsonism, gait disturbances, rigidity, bradykinesia, and other motor disturbances. Paroxysmal sympathetic hyperactivity (PSH) is a potentially life-threatening disease secondary to acute acquired brain injury. It is characterized by episodic and simultaneous paroxysmal increases in sympathetic and motor activities, not rare in patients with a severe traumatic brain injury. The term PSH is clinically more accurate than the previously used ones describing such conditions as non-stimulated tachycardia, hypertension, tachypnea, hyperthermia, external posturing, diaphoresis, and paroxysmal autonomic instability with dystonia. Development of PSH typically prolongs the length of hospital stay and potentially leads to a secondary brain injury or even death. To date, the occurrence of PSH in the DNS after acute CO poisoning has not been reported in the literature. Potential mechanisms underlying the development of DNS in the deep white matter of the brain are immune-related inflammation and vasodilatation. Repetitive hyperbaric oxygen therapy, combined with methylprednisolone administration, may inhibit DNS progression by inducing cerebral oxygenation, inhibiting inflammation, and reducing cerebral edema. Herein, we report three cases in which the patients recovered from the PSH as DNS after CO poisoning after receiving repetitive hyperbaric oxygen therapy.

An inverse agonist of estrogen-related receptor γ regulates 2-arachidonoylglycerol synthesis by modulating diacylglycerol lipase expression in alcohol-intoxicated mice.

Chronic alcohol feeding increases the levels of 2-arachidonoylglycerol (2-AG) in the liver, which activates hepatic cannabinoid receptor type 1 (CB1R), leading to oxidative liver injury. 2-AG biosynthesis is catalyzed by diacylglycerol lipase (DAGL). However, the mechanisms regulating hepatic DAGL gene expression and 2-AG production are largely unknown. In this study, we show that CB1R-induced estrogen-related receptor γ (ERRγ) controls hepatic DAGL gene expression and 2-AG levels. Arachidonyl-2'-chloroethylamide (ACEA), a synthetic CB1R agonist, significantly upregulated ERRγ, DAGLα, and DAGLß, and increased 2-AG levels in the liver (10 mg/kg) and hepatocytes (10 µM) of wild-type (WT) mice. ERRγ overexpression upregulated DAGLα and DAGLß expressions and increased 2-AG levels, whereas ERRγ knockdown abolished ACEA-induced DAGLα, DAGLß, and 2-AG in vitro and in vivo. Promoter assays showed that ERRγ positively regulated DAGLα and DAGLß transcription by binding to the ERR response element in the DAGLα and DAGLß promoters. Chronic alcohol feeding (27.5% of total calories) induced hepatic steatosis and upregulated ERRγ, leading to increased DAGLα, DAGLß, or 2-AG in WT mice, whereas these alcohol-induced effects did not occur in hepatocyte-specific CB1R knockout mice or in those treated with the ERRγ inverse agonist GSK5182 (40 mg/kg in mice and 10 µM in vitro). Taken together, these results indicate that suppression of alcohol-induced DAGLα and DAGLß gene expressions and 2-AG levels by an ERRγ-specific inverse agonist may be a novel and attractive therapeutic approach for the treatment of alcoholic liver disease.

Stroke Incidence in Survivors of Carbon Monoxide Poisoning in South Korea: A Population-Based Longitudinal Study.

BACKGROUND Carbon monoxide (CO) poisoning is a suspected risk factor for stroke. However, the association between stroke occurrence and carbon monoxide poisoning remains unclear. This nationwide study in Korea analyzed the incidence of stroke in survivors of CO poisoning. MATERIAL AND METHODS In this nationwide, population-based longitudinal study, the database of the Health Insurance Review and Assessment Service was searched to identify patients diagnosed with CO poisoning from 2012 to 2018. Their incidence of ischemic and hemorrhagic strokes, the patterns of stroke incidences, the annual incidence rates in sequential time, the standardized incidence ratio (SIR), and the effects of hyperbaric oxygen therapy (HBOT) were analyzed. RESULTS Of the 29 301 patients diagnosed with CO poisoning during the study period, 984 (3.36%) were diagnosed with stroke after CO poisoning, with approximately 50% occurring within 1 year after CO poisoning. The overall SIR for stroke was 19.49 (95% confidence interval [CI], 17.92-21.12) during the first year, decreasing to 5.64 (95% CI, 4.75-6.66) during the second year. Overall stroke hazard ratio (HR) in the patients admitted to the ICU for CO poisoning was 2.28 (95% CI, 1.19-2.27), compared with 2.35 (95% CI, 1.94-2.84) for ischemic stroke and 1.76 (95% CI, 1.11-2.78) for hemorrhagic stroke. Cumulative HRs did not differ between patients who were and were not treated with HBOT for stroke. CONCLUSIONS CO poisoning is a high-risk factor for the development of stroke, evidenced by high incidences of stroke after CO poisoning. Practical strategies for preventing stroke after CO poisoning are needed, because stroke after CO poisoning affects adults of almost all ages, significantly increasing their socioeconomic burden.

Orphan Nuclear Receptor ERRγ Is a Novel Transcriptional Regulator of IL-6 Mediated Hepatic BMP6 Gene Expression in Mice.

Bone morphogenetic protein 6 (BMP6) is a multifunctional growth factor involved in organ development and homeostasis. BMP6 controls expression of the liver hormone, hepcidin, and thereby plays a crucial role in regulating iron homeostasis. BMP6 gene transcriptional regulation in liver is largely unknown, but would be of great help to externally modulate iron load in pathologic conditions. Here, we describe a detailed molecular mechanism of hepatic BMP6 gene expression by an orphan nuclear receptor, estrogen-related receptor γ (ERRγ), in response to the pro-inflammatory cytokine interleukin 6 (IL-6). Recombinant IL-6 treatment increases hepatic ERRγ and BMP6 expression. Overexpression of ERRγ is sufficient to increase BMP6 gene expression in hepatocytes, suggesting that IL-6 is upstream of ERRγ. In line, knock-down of ERRγ in cell lines or a hepatocyte specific knock-out of ERRγ in mice significantly decreases IL-6 mediated BMP6 expression. Promoter studies show that ERRγ directly binds to the ERR response element (ERRE) in the mouse BMP6 gene promoter and positively regulates BMP6 gene transcription in IL-6 treatment conditions, which is further confirmed by ERRE mutated mBMP6-luciferase reporter assays. Finally, an inverse agonist of ERRγ, GSK5182, markedly inhibits IL-6 induced hepatic BMP6 expression in vitro and in vivo. Taken together, these results reveal a novel molecular mechanism on ERRγ mediated transcriptional regulation of hepatic BMP6 gene expression in response to IL-6.

The SMILE transcriptional corepressor inhibits cAMP response element-binding protein (CREB)-mediated transactivation of gluconeogenic genes.

Under fasting conditions, activation of several hepatic genes sets the stage for gluconeogenesis in the liver. cAMP response element-binding protein (CREB), CREB-regulated transcription coactivator 2 (CRTC2), and peroxisome proliferator-activated receptor γ coactivator 1-alpha (PGC-1α) are essential for this transcriptional induction of gluconeogenic genes. PGC-1α induction is mediated by activation of a CREB/CRTC2 signaling complex, and recent findings have revealed that small heterodimer partner-interacting leucine zipper protein (SMILE), a member of the CREB/ATF family of basic region-leucine zipper (bZIP) transcription factors, is an insulin-inducible corepressor that decreases PGC-1α expression and abrogates its stimulatory effect on hepatic gluconeogenesis. However, the molecular mechanism whereby SMILE suppresses PGC-1α expression is unknown. Here, we investigated SMILE's effects on the CREB/CRTC2 signaling pathway and glucose metabolism. We found that SMILE significantly inhibits CREB/CRTC2-induced PGC-1α expression by interacting with and disrupting the CREB/CRTC2 complex. Consequently, SMILE decreased PGC-1α-induced hepatic gluconeogenic gene expression. Furthermore, SMILE inhibited CREB/CRTC2-induced phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) gene expression by directly repressing the expression of these genes and by indirectly inhibiting the expression of PGC-1α via CREB/CRTC2 repression. Indeed, enhanced gluconeogenesis and circulating blood glucose levels in mice injected with an adenovirus construct containing a constitutively active CRTC2 variant (CRTC2-S171A) were significantly reduced by WT SMILE, but not by leucine zipper-mutated SMILE. These results reveal that SMILE represses CREB/CRTC2-induced PGC-1α expression, an insight that may help inform potential therapeutic approaches targeting PGC-1α-mediated regulation of hepatic glucose metabolism.

Inverse agonist of ERRγ reduces cannabinoid receptor type 1-mediated induction of fibrinogen synthesis in mice with a high-fat diet-intoxicated liver.

Upon liver intoxication with malnutrition or high-fat diet feeding, fibrinogen is synthesized by hepatocytes and secreted into the blood in human and mouse. Its primary function is to occlude blood vessels upon damage and thereby stop excessive bleeding. High fibrinogen levels may contribute to the development of pathological thrombosis, which is one mechanism linking fatty liver disease with cardiovascular disease. Our previous results present ERRγ as key regulator of hepatocytic fibrinogen gene expression in human. In a therapeutic approach, we now tested ERRγ inverse agonist GSK5182 as regulator of fibrinogen levels in mouse hyperfibrinogenemia caused by diet-induced obesity and in mouse hepatocytes. ACEA, a CB1R agonist, up-regulated transcription of mouse fibrinogen via induction of ERRγ, whereas knockdown of ERRγ attenuated the effect of ACEA (10 µM) on fibrinogen expression in AML12 mouse hepatocytes. Deletion analyses of the mouse fibrinogen γ (FGG) gene promoter and ChIP assays revealed binding sites for ERRγ on the mouse FGG promoter. ACEA or adenovirus ERRγ injection induced FGA, FGB and FGG mRNA and protein expression in mouse liver, while ERRγ knockdown with Ad-shERRγ attenuated ACEA-mediated induction of fibrinogen gene expression. Moreover, mice maintained on a high-fat diet (HFD) expressed higher levels of fibrinogen, whereas cannabinoid receptor type 1 (CB1R)-KO mice fed an HFD had nearly normal fibrinogen levels. Finally, GSK5182 (40 mg/kg) strongly inhibits the ACEA (10 mg/kg) or HFD-mediated induction of fibrinogen level in mice. Taken together, targeting ERRγ with its inverse agonist GSK5182 represents a promising therapeutic strategy for ameliorating hyperfibrinogenemia.

Infiltration of Solution-Processable Solid Electrolytes into Conventional Li-Ion-Battery Electrodes for All-Solid-State Li-Ion Batteries.

Bulk-type all-solid-state lithium-ion batteries (ASLBs) have the potential to be superior to conventional lithium-ion batteries (LIBs) in terms of safety and energy density. Sulfide SE materials are key to the development of bulk-type ASLBs because of their high ionic conductivity (max of ∼10-2 S cm-1) and deformability. However, the severe reactivity of sulfide materials toward common polar solvents and the particulate nature of these electrolytes pose serious complications for the wet-slurry process used to fabricate ASLB electrodes, such as the availability of solvent and polymeric binders and the formation of ionic contacts and networks. In this work, we report a new scalable fabrication protocol for ASLB electrodes using conventional composite LIB electrodes and homogeneous SE solutions (Li6PS5Cl (LPSCl) in ethanol or 0.4LiI-0.6Li4SnS4 in methanol). The liquefied LPSCl is infiltrated into the tortuous porous structures of LIB electrodes and solidified, providing intimate ionic contacts and favorable ionic percolation. The LPSCl-infiltrated LiCoO2 and graphite electrodes show high reversible capacities (141 and 364 mA h g-1) at 0.14 mA cm-2 (0.1 C) and 30 °C, which are not only superior to those for conventional dry-mixed and slurry-mixed ASLB electrodes but also comparable to those for liquid electrolyte cells. Good electrochemical performance of ASLBs employing the LPSCl-infiltrated LiCoO2 and graphite electrodes at 100 °C is also presented, highlighting the excellent thermal stability and safety of ASLBs.

Bendable and thin sulfide solid electrolyte film: a new electrolyte opportunity for free-standing and stackable high-energy all-solid-state lithium-ion batteries.

Bulk-type all-solid-state lithium batteries (ASLBs) are considered a promising candidate to outperform the conventional lithium-ion batteries. Unfortunately, the current technology level of ASLBs is in a stage of infancy in terms of cell-based (not electrode-material-based) energy densities and scalable fabrication. Here, we report on the first ever bendable and thin sulfide solid electrolyte films reinforced with a mechanically compliant poly(paraphenylene terephthalamide) nonwoven (NW) scaffold, which enables the fabrication of free-standing and stackable ASLBs with high energy density and high rate capabilities. The ASLB, using a thin (∼70 µm) NW-reinforced SE film, exhibits a 3-fold increase of the cell-energy-density compared to that of a conventional cell without the NW scaffold.

Na3 SbS4 : A Solution Processable Sodium Superionic Conductor for All-Solid-State Sodium-Ion Batteries.

All-solid-state sodium-ion batteries that operate at room temperature are attractive candidates for use in large-scale energy storage systems. However, materials innovation in solid electrolytes is imperative to fulfill multiple requirements, including high conductivity, functional synthesis protocols for achieving intimate ionic contact with active materials, and air stability. A new, highly conductive (1.1 mS cm(-1) at 25 °C, Ea =0.20 eV) and dry air stable sodium superionic conductor, tetragonal Na3 SbS4 , is described. Importantly, Na3 SbS4 can be prepared by scalable solution processes using methanol or water, and it exhibits high conductivities of 0.1-0.3 mS cm(-1) . The solution-processed, highly conductive solidified Na3 SbS4 electrolyte coated on an active material (NaCrO2 ) demonstrates dramatically improved electrochemical performance in all-solid-state batteries.

Carbon monoxide-induced cardiomyopathy.

BACKGROUND: Previous reports demonstrated mechanisms of cardiac toxicity in acute carbon monoxide (CO) poisoning. Still, none established CO-induced cardiomyopathy (CMP) as a clinical entity. The aim of this study is to investigate CO-induced CMP in patients with acute CO poisoning in terms of its epidemiology, clinical characteristics, and prognosis. METHODS AND RESULTS: A retrospective study was conducted on consecutive patients who were diagnosed with acute CO poisoning at the emergency department of Ajou University Hospital during the period of 62 month. Six hundred and twenty-six patients were diagnosed with acute CO poisoning. During the initial echocardiography, 19 patients were abnormal: (1) global hypokinesia/akinesia (n=7), (2) regional wall hypokinesia/akinesia [n=12; takotsubo type (n=6), reverse takotsubo type (n=2), non-specific type (n=4)]. The ejection fraction (EF) was 36.3±13.5% (from 15% to 55%) and less than 45% for 14 patients. In the follow-up echocardiography performed within 12 days after the initial performance, most patients were found to have cardiac wall motion abnormalities, and their EF had returned to normal (ie, EF ≥50%). CONCLUSIONS: CO-induced CMP was identified in 3.04% (n=19) of all patients (n=626). It might not be too critical in acute clinical courses of acute CO poisoning because the prognosis seems favorable. Considering the common factors between CO-induced CMP and takotsubo CMP, myocardial stunning subject to a catecholamine surge most likely plays a central role in the development of CO-induced CMP.