RESUMEN
Extensive studies demonstrate the importance of the STING1 (also known as STING) protein as a signaling hub that coordinates immune and autophagic responses to ectopic DNA in the cytoplasm. Here, we report a nuclear function of STING1 in driving the activation of the transcription factor aryl hydrocarbon receptor (AHR) to control gut microbiota composition and homeostasis. This function was independent of DNA sensing and autophagy and showed competitive inhibition with cytoplasmic cyclic guanosine monophosphate (GMP)-AMP synthase (CGAS)-STING1 signaling. Structurally, the cyclic dinucleotide binding domain of STING1 interacted with the AHR N-terminal domain. Proteomic analyses revealed that STING1-mediated transcriptional activation of AHR required additional nuclear partners, including positive and negative regulatory proteins. Although AHR ligands could rescue colitis pathology and dysbiosis in wild-type mice, this protection was abrogated by mutational inactivation of STING1. These findings establish a key framework for understanding the nuclear molecular crosstalk between the microbiota and the immune system.
Asunto(s)
Proteómica , Receptores de Hidrocarburo de Aril , Animales , Ratones , ADN , Homeostasis , Intestinos , Receptores de Hidrocarburo de Aril/genética , Receptores de Hidrocarburo de Aril/metabolismoRESUMEN
Heparin, a mammalian polysaccharide, is a widely used anticoagulant medicine to treat thrombotic disorders. It is also known to improve outcomes in sepsis, a leading cause of mortality resulted from infection-induced immune dysfunction. Whereas it is relatively clear how heparin exerts its anticoagulant effect, the immunomodulatory mechanisms enabled by heparin remain enigmatic. Here, we show that heparin prevented caspase-11-dependent immune responses and lethality in sepsis independent of its anticoagulant properties. Heparin or a chemically modified form of heparin without anticoagulant function inhibited the alarmin HMGB1-lipopolysaccharide (LPS) interaction and prevented the macrophage glycocalyx degradation by heparanase. These events blocked the cytosolic delivery of LPS in macrophages and the activation of caspase-11, a cytosolic LPS receptor that mediates lethality in sepsis. Survival was higher in septic patients treated with heparin than those without heparin treatment. The identification of this previously unrecognized heparin function establishes a link between innate immune responses and coagulation.
Asunto(s)
Anticoagulantes/uso terapéutico , Caspasas/metabolismo , Heparina/uso terapéutico , Macrófagos/inmunología , Sepsis/tratamiento farmacológico , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Animales , Caspasas/genética , Línea Celular , Femenino , Glucuronidasa/genética , Glucuronidasa/metabolismo , Glicocálix/metabolismo , Proteína HMGB1/metabolismo , Humanos , Inmunomodulación , Lipopolisacáridos/metabolismo , Masculino , Ratones , Ratones Noqueados , Persona de Mediana Edad , Sepsis/mortalidad , Análisis de Supervivencia , Adulto JovenRESUMEN
Well-balanced and timed metabolism is essential for making a high-quality egg. However, the metabolic framework that supports oocyte development remains poorly understood. Here, we obtained the temporal metabolome profiles of mouse oocytes during in vivo maturation by isolating large number of cells at key stages. In parallel, quantitative proteomic analyses were conducted to bolster the metabolomic data, synergistically depicting the global metabolic patterns in oocytes. In particular, we discovered the metabolic features during meiotic maturation, such as the fall in polyunsaturated fatty acids (PUFAs) level and the active serine-glycine-one-carbon (SGOC) pathway. Using functional approaches, we further identified the key targets mediating the action of PUFA arachidonic acid (ARA) on meiotic maturation and demonstrated the control of epigenetic marks in maturing oocytes by SGOC network. Our data serve as a broad resource on the dynamics occurring in metabolome and proteome during oocyte maturation.
Asunto(s)
Meiosis/fisiología , Oocitos/metabolismo , Animales , Epigénesis Genética/genética , Ácidos Grasos Insaturados/metabolismo , Femenino , Metaboloma/fisiología , Ratones , Ratones Endogámicos C57BL , Oogénesis/genética , Oogénesis/fisiología , Proteoma/metabolismo , ProteómicaRESUMEN
Caspase-11, a cytosolic endotoxin (lipopolysaccharide: LPS) receptor, mediates pyroptosis, a lytic form of cell death. Caspase-11-dependent pyroptosis mediates lethality in endotoxemia, but it is unclear how LPS is delivered into the cytosol for the activation of caspase-11. Here we discovered that hepatocyte-released high mobility group box 1 (HMGB1) was required for caspase-11-dependent pyroptosis and lethality in endotoxemia and bacterial sepsis. Mechanistically, hepatocyte-released HMGB1 bound LPS and targeted its internalization into the lysosomes of macrophages and endothelial cells via the receptor for advanced glycation end-products (RAGE). Subsequently, HMGB1 permeabilized the phospholipid bilayer in the acidic environment of lysosomes. This resulted in LPS leakage into the cytosol and caspase-11 activation. Depletion of hepatocyte HMGB1, inhibition of hepatocyte HMGB1 release, neutralizing extracellular HMGB1, or RAGE deficiency prevented caspase-11-dependent pyroptosis and death in endotoxemia and bacterial sepsis. These findings indicate that HMGB1 interacts with LPS to mediate caspase-11-dependent pyroptosis in lethal sepsis.
Asunto(s)
Caspasas/inmunología , Endotoxinas/inmunología , Proteína HMGB1/inmunología , Piroptosis/inmunología , Sepsis/inmunología , Animales , Caspasas/genética , Caspasas/metabolismo , Células Cultivadas , Células Endoteliales/inmunología , Células Endoteliales/metabolismo , Endotoxinas/metabolismo , Células HEK293 , Proteína HMGB1/genética , Proteína HMGB1/metabolismo , Humanos , Lipopolisacáridos/inmunología , Lipopolisacáridos/metabolismo , Macrófagos/inmunología , Macrófagos/metabolismo , Masculino , Ratones Endogámicos C57BL , Ratones Noqueados , Receptor para Productos Finales de Glicación Avanzada/inmunología , Receptor para Productos Finales de Glicación Avanzada/metabolismo , Sepsis/genética , Sepsis/metabolismo , Células THP-1RESUMEN
Apoptosis, as type I cell death, is an active death process strictly controlled by multiple genes, and plays a significant role in regulating various activities. Mounting research indicates that the unique modality of cell apoptosis is directly or indirectly related to different diseases including cancer, autoimmune diseases, viral diseases, neurodegenerative diseases, etc. However, the underlying mechanisms of cell apoptosis are complicated and not fully clarified yet, possibly due to the lack of effective chemical tools for the nondestructive and real-time visualization of apoptosis in complex biological systems. In the past 15 years, various small-molecule fluorescent probes (SMFPs) for imaging apoptosis in vitro and in vivo have attracted broad interest in related disease diagnostics and therapeutics. In this review, we aim to highlight the recent developments of SMFPs based on enzyme activity, plasma membranes, reactive oxygen species, reactive sulfur species, microenvironments and others during cell apoptosis. In particular, we generalize the mechanisms commonly used to design SMFPs for studying apoptosis. In addition, we discuss the limitations of reported probes, and emphasize the potential challenges and prospects in the future. We believe that this review will provide a comprehensive summary and challenging direction for the development of SMFPs in apoptosis related fields.
Asunto(s)
Apoptosis , Colorantes Fluorescentes , Colorantes Fluorescentes/química , Humanos , Animales , Especies Reactivas de Oxígeno/metabolismo , Especies Reactivas de Oxígeno/análisis , Bibliotecas de Moléculas Pequeñas/química , Imagen ÓpticaRESUMEN
BACKGROUND: Choline acetyltransferase (ChAT) is required for the biosynthesis of acetylcholine, the molecular mediator that inhibits cytokine production in the cholinergic anti-inflammatory pathway of the vagus nerve inflammatory reflex. Abundant work has established the biology of cytoplasmic ChAT in neurons, but much less is known about the potential presence and function of ChAT in the extracellular milieu. OBJECTIVES: We evaluated the hypothesis that extracellular ChAT activity responds to inflammation and serves to inhibit cytokine release and attenuate inflammation. METHODS: After developing novel methods for quantification of ChAT activity in plasma, we determined whether ChAT activity changes in response to inflammatory challenges. RESULTS: Active ChAT circulates within the plasma compartment of mice and responds to immunological perturbations. Following the administration of bacterial endotoxin, plasma ChAT activity increases for 12-48 h, a time period that coincides with declining tumor necrosis factor (TNF) levels. Further, a direct activation of the cholinergic anti-inflammatory pathway by vagus nerve stimulation significantly increases plasma ChAT activity, whereas the administration of bioactive recombinant ChAT (r-ChAT) inhibits endotoxin-stimulated TNF production and anti-ChAT antibodies exacerbate endotoxin-induced TNF levels, results of which suggest that ChAT activity regulates endogenous TNF production. Administration of r-ChAT significantly attenuates pro-inflammatory cytokine production and disease activity in the dextran sodium sulfate preclinical model of inflammatory bowel disease. Finally, plasma ChAT levels are also elevated in humans with sepsis, with the highest levels observed in a patient who succumbed to infection. CONCLUSION: As a group, these results support further investigation of ChAT as a counter-regulator of inflammation and potential therapeutic agent.
Asunto(s)
Acetilcolina , Colina O-Acetiltransferasa , Humanos , Colina O-Acetiltransferasa/metabolismo , Inflamación , Factor de Necrosis Tumoral alfa/metabolismo , Citocinas , EndotoxinasRESUMEN
Lithium-sulfur (Li-S) batteries are considered the most promising energy storage battery due to their low cost and high theoretical energy density. However, the low utilization rate of sulfur and slow redox kinetics have seriously limited the development of Li-S batteries. Herein, the electronic state modulation of metal selenides induced by the bi-metallic coupling strategy is reported to enhance the redox reaction kinetics and sulfur utilization, thereby improving the electrochemical performance of Li-S batteries. Theoretical calculations reveal that the electronic structure can be modulated by Ni-Co coupling, thus lowering the conversion barrier of lithium polysulfides (LiPSs) and Li+, and the synergistic interaction between NiCoSe nanoparticles and nitrogen-doped porous carbon (NPC) is facilitating to enhance electron transport and ion transfer kinetics of the NiCoSe@NPC-S electrodes. As a result, the assembled Li-S batteries based on NiCoSe@NPC-S exhibit high capacities (1020 mAh g-1 at 1 C) and stable cycle performance (80.37% capacity retention after 500 cycles). The special structural design and bimetallic coupling strategy promote the batteries working even under lean electrolyte (7.2 µL mg-1) with a high sulfur loading (6.5 mg cm-2). The proposed bimetallic coupling strategy modulating electronic construction with N-doping porous carbon has jointly contributed the good redox reaction kinetics and high sulfur utilization.
RESUMEN
The vagus nerve circuit, operating through the alpha-7 nicotinic acetylcholine receptor (α7 nAChR), regulates the inflammatory response by influencing immune cells. However, the role of vagal-α7 nAChR signaling in influenza virus infection is unclear. In particular, does vagal-α7 nAChR signaling impact the infection of alveolar epithelial cells (AECs), the primary target cells of influenza virus? Here, we demonstrated a distinct role of α7 nAChR in type II AECs compared to its role in immune cells during influenza infection. We found that deletion of Chrna7 (encoding gene of α7 nAChR) in type II AECs or disruption of vagal circuits reduced lung influenza infection and protected mice from influenza-induced lung injury. We further unveiled that activation of α7 nAChR enhanced influenza infection through PTP1B-NEDD4L-ASK1-p38MAPK pathway. Mechanistically, activation of α7 nAChR signaling decreased p38MAPK phosphorylation during infection, facilitating the nuclear export of influenza viral ribonucleoproteins and thereby promoting infection. Taken together, our findings reveal a mechanism mediated by vagal-α7 nAChR signaling that promotes influenza viral infection and exacerbates disease severity. Targeting vagal-α7 nAChR signaling may offer novel strategies for combating influenza virus infections.
Asunto(s)
Pulmón , Infecciones por Orthomyxoviridae , Transducción de Señal , Nervio Vago , Receptor Nicotínico de Acetilcolina alfa 7 , Animales , Receptor Nicotínico de Acetilcolina alfa 7/metabolismo , Receptor Nicotínico de Acetilcolina alfa 7/genética , Nervio Vago/metabolismo , Ratones , Infecciones por Orthomyxoviridae/virología , Pulmón/virología , Pulmón/patología , Ratones Endogámicos C57BL , Células Epiteliales Alveolares/virología , Células Epiteliales Alveolares/metabolismo , Humanos , Ratones NoqueadosRESUMEN
Sepsis and septic shock driven by microbial infections are still among the most challenging health problems, causing 11 million deaths worldwide every year. How does the host's response to pathogen infections effectively restore homeostasis instead of precipitating pathogenic and potentially fatal feedforward reactions? Recently, there have been significant new advances in our understanding of the interface between mammalian immunity and coagulation ('immunocoagulation') and its impact on sepsis. In particular, the release and activation of F3 (the main initiator of coagulation) from and on myeloid or epithelial cells is facilitated by activating inflammasomes and consequent gasdermin D (GSDMD)-mediated pyroptosis, coupled to signaling via high mobility group box 1 (HMGB1), stimulator of interferon response CGAMP interactor 1 (STING1), or sequestosome 1 (SQSTM1). Pharmacological modulation of the immunocoagulation pathways emerge as novel and potential therapeutic strategies for sepsis.
Asunto(s)
Sepsis , Choque Séptico , Animales , Caspasas Iniciadoras/metabolismo , Péptidos y Proteínas de Señalización Intracelular , Proteínas de Unión a Fosfato , PiroptosisRESUMEN
Nitrous acid (HONO) is an important source of hydroxyl radicals (OH) in the atmosphere. Precise determination of the absolute ultraviolet (UV) absorption cross section of gaseous HONO lays the basis for the accurate measurement of its concentration by optical methods and the estimation of HONO loss rate through photolysis. In this study, we performed a series of laboratory and field intercomparison experiments for HONO measurement between striping coil-liquid waveguide capillary cell (SC-LWCC) photometry and incoherent broadband cavity-enhanced absorption spectroscopy (IBBCEAS). Specified HONO concentrations prepared by an ultrapure standard HONO source were utilized for laboratory intercomparisons. Results show a consistent â¼22% negative bias in measurements of the IBBCEAS compared with a SC-LWCC photometer. It is confirmed that the discrepancies occurring between these techniques are associated with the overestimation of the absolute UV absorption cross sections through careful analysis of possible uncertainties. We quantified the absorption cross section of gaseous HONO (360-390 nm) utilizing a custom-built IBBCEAS instrument, and the results were found to be 22-34% lower than the previously published absorption cross sections widely used in HONO concentration retrieval and atmospheric chemical transport models (CTMs). This suggests that the HONO concentrations retrieved by optical methods based on absolute absorption cross sections may have been underestimated by over 20%. Plus, the daytime loss rate and unidentified sources of HONO may also have evidently been overestimated in pre-existing studies. In summary, our findings underscore the significance of revisiting the absolute absorption cross section of HONO and the re-evaluation of the previously reported HONO budgets.
Asunto(s)
Contaminantes Atmosféricos , Ácido Nitroso , Ácido Nitroso/análisis , Gases/análisis , Contaminantes Atmosféricos/análisis , Análisis Espectral , FotólisisRESUMEN
Inflammation, the body's primary defensive response system to injury and infection, is triggered by molecular signatures of microbes and tissue injury. These molecules also stimulate specialized sensory neurons, termed nociceptors. Activation of nociceptors mediates inflammation through antidromic release of neuropeptides into infected or injured tissue, producing neurogenic inflammation. Because HMGB1 is an important inflammatory mediator that is synthesized by neurons, we reasoned nociceptor release of HMGB1 might be a component of the neuroinflammatory response. In support of this possibility, we show here that transgenic nociceptors expressing channelrhodopsin-2 (ChR2) directly release HMGB1 in response to light stimulation. Additionally, HMGB1 expression in neurons was silenced by crossing synapsin-Cre (Syn-Cre) mice with floxed HMGB1 mice (HMGB1f/f). When these mice undergo sciatic nerve injury to activate neurogenic inflammation, they are protected from the development of cutaneous inflammation and allodynia as compared to wild-type controls. Syn-Cre/HMGB1fl/fl mice subjected to experimental collagen antibody-induced arthritis, a disease model in which nociceptor-dependent inflammation plays a significant pathological role, are protected from the development of allodynia and joint inflammation. Thus, nociceptor HMGB1 is required to mediate pain and inflammation during sciatic nerve injury and collagen antibody-induced arthritis.
Asunto(s)
Proteína HMGB1/metabolismo , Neuronas/fisiología , Nociceptores/metabolismo , Animales , Anticuerpos/inmunología , Artritis/inducido químicamente , Células Cultivadas , Colágeno/inmunología , Citocinas/genética , Citocinas/metabolismo , Femenino , Ganglios Espinales/citología , Regulación de la Expresión Génica , Proteína HMGB1/genética , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Transgénicos , Optogenética , Ratas , Ratas Sprague-Dawley , Ratas Wistar , Neuropatía Ciática/metabolismoRESUMEN
Cancer is a highly heterogeneous disease that poses a serious threat to human health worldwide. Despite significant advances in the diagnosis and treatment of cancer, the prognosis and survival rate of cancer remain poor due to late diagnosis, drug resistance, and adverse reactions. Therefore, it is very necessary to study the development mechanism of cancer and formulate effective therapeutic interventions. As widely available bioactive substances, natural products have shown obvious anticancer potential, especially by targeting abnormal epigenetic changes. The main active part of garlic is organic sulfur compounds, of which diallyl trisulfide (DATS) content is the highest, accounting for more than 40% of the total composition. The garlic-derived compounds have been recognized as an antioxidant for cancer prevention and treatment. However, the molecular mechanism of the antitumor effect of garlic-derived compounds remains unclear. Recent studies have identified garlic-derived compound DATS that plays critical roles in enhancing CpG demethylation or promoting histone acetylation as an epigenetic inhibitor. Here, we review the therapeutic progress of garlic-derived compounds against cancer through epigenetic pathways.
Asunto(s)
Compuestos Alílicos , Productos Biológicos , Ajo , Neoplasias , Humanos , Antioxidantes/farmacología , Apoptosis , Sulfuros/farmacología , Neoplasias/tratamiento farmacológico , Compuestos Alílicos/farmacología , Productos Biológicos/farmacologíaRESUMEN
In this research, the authors studied the synthesis of a silicon-based quaternary ammonium material based on the coupling agent chloromethyl trimethoxysilane (KH-150) as well as its adsorption and separation properties for Th(IV). Using FTIR and NMR methods, the silicon-based materials before and after grafting were characterized to determine the spatial structure of functional groups in the silicon-based quaternary ammonium material SG-CTSQ. Based on this, the functional group grafting amount (0.537 mmol·g-1) and quaternization rate (83.6%) of the material were accurately calculated using TGA weight loss and XPS. In the adsorption experiment, the four materials with different grafting amounts showed different degrees of variation in their adsorption of Th(IV) with changes in HNO3 concentration and NO3- concentration but all exhibited a tendency toward anion exchange. The thermodynamic and kinetic experimental results demonstrated that materials with low grafting amounts (SG-CTSQ1 and SG-CTSQ2) tended to physical adsorption of Th(IV), while the other two tended toward chemical adsorption. The adsorption mechanism experiment further proved that the functional groups achieve the adsorption of Th(IV) through an anion-exchange reaction. Chromatographic column separation experiments showed that SG-CTSQ has a good performance in U-Th separation, with a decontamination factor for uranium in Th(IV) of up to 385.1, and a uranium removal rate that can reach 99.75%.
RESUMEN
The United Nations proposed the Sustainable Development Goals with the aim to make human settlements in cities resilient and sustainable. The excessive discharge of urban waste including sludge and garden waste can pollute groundwater and lead to the emission of greenhouse gases (e.g., CH4). The proper recycling of urban waste is essential for responsible consumption and production, reducing environmental pollution and addressing climate change issues. This study aimed to prepare biochar with high adsorption amounts of iodine using urban sludge and peach wood from garden waste. The study was conducted to examine the variations in the mass ratio between urban sludge and peach wood (2/1, 1/1, and 1/2) as well as pyrolysis temperatures (300 °C, 500 °C, and 700 °C) on the carbon yield and adsorption capacities of biochar. Scanning electron microscopy, Brunauer-Emmett-Teller analysis, Fourier transform infrared spectrometry, powder X-ray diffraction, and elemental analysis were used to characterize the biochar produced at different pyrolysis temperatures and mass ratios. The results indicate that the carbon yield of biochar was found to be the highest (>60%) at a pyrolysis temperature of 300 °C across different pyrolysis temperatures. The absorbed amounts of iodine in the aqueous solution ranged from 86 to 223 mg g-1 at a mass ratio of 1:1 between urban sludge and peach wood, which were comparably higher than those observed in other mass ratios. This study advances water treatment by offering a cost-effective method by using biochar derived from the processing of urban sludge and garden waste.
Asunto(s)
Carbón Orgánico , Yodo , Pirólisis , Aguas del Alcantarillado , Carbón Orgánico/química , Yodo/química , Aguas del Alcantarillado/química , Adsorción , Temperatura , Jardines , Espectroscopía Infrarroja por Transformada de Fourier , CiudadesRESUMEN
A 15-year-old female with Hodgkin's lymphoma underwent ovarian tissue cryopreservation for preserving fertility in Reproductive Department of Sir Run Run Shaw Hospital, Zhejiang University School of Medical after receiving one course of chemotherapy. During the ovarian tissue cryopreservation, one Mâ ¡mature oocyte and three germinal vesicle oocytes were found. The three immature oocytes underwent in vitro maturation but failed. Ultimately, one mature oocyte and 12 ovarian cortex slices were cryopreserved using vitrification. This case indicates that for patients with established gonadal axis feedback, ovarian tissue cryopreservation may not be the only method for fertility preservation. It is advisable to consider ovarian stimulation and oocyte retrieval for oocyte cryopreservation. Alternatively, for individuals in the ovulation phase of their menstrual cycle, attempting oocyte retrieval before ovarian tissue cryopreservation to obtain mature oocytes from the natural cycle, followed by oocyte cryopreservation, may enhance the likelihood of successful fertility preservation.
Asunto(s)
Criopreservación , Preservación de la Fertilidad , Oocitos , Ovario , Femenino , Criopreservación/métodos , Humanos , Oocitos/citología , Preservación de la Fertilidad/métodos , Adolescente , Enfermedad de HodgkinRESUMEN
The appearance of disordered lithium dendrites and fragile solid electrolyte interfaces (SEI) significantly hinder the serviceability of lithium metal batteries. Herein, guided by theoretical predictions, a multi-component covalent triazine framework with partially electronegative channels (4C-TA0.5TF0.5-CTF) is incorporated as a protective layer to modulate the interface stability of the lithium metal batteries. Notably, the 4C-TA0.5TF0.5-CTF with optimized electronic structure at the molecular level by fine-tuning the local acceptor-donor functionalities not only enhances the intermolecular interaction thereby providing larger dipole moment and improved crystallinity and mechanical stress, but also facilitates the beneficial effect of lithiophilic sites (C-F bonds, triazine cores, C=N linkages and aromatic rings) to further regulate the migration of Li+ and achieve a uniform lithium deposition behavior as determined by various in-depth in/ex situ characterizations. Due to the synergistic effect of multi-component organic functionalities, the 4C-TA0.5TF0.5-CTF modified full cells perform significantly better than the common two/three-component 2C-TA-CTF and 3C-TF-CTF electrodes, delivering an excellent capacity of 116.3â mAh g-1 (capacity retention ratio: 86.8 %) after 1000â cycles at 5â C and improved rate capability. This work lays a platform for the prospective molecular design of improved organic framework relative artificial SEI for highly stable lithium metal batteries.
RESUMEN
Fatal issues in lithium metal anodes (LMA), such as detrimental lithium dendrites growth and fragile solid-electrolyte interphase (SEI) during the Li plating/stripping process, often hinder the practical application of Li metal batteries (LMBs). Herein, cobalt-coordinated sp-carbon-conjugated organic polymer (Co-spc-COP) is constructed as the protective layer for regulating the interface stability of LMA. The unique synergistic beneficial effect of organic functional groups (C≡C linkage, C=N units and aromatic rings) and Co sites not only regulate the Li+ coordination environment and rearrange Li+ concentration to facilitate its transport by optimizing the electronic density, enhancing the compatibility with electrolyte interface and supplying "external magnetic driving strategy", but also strengthens the interfacial stiffness with high Young's modulus to better withstand the mechanical stress. These beneficial effects and relative underlying working mode and mechanism of uniform Li plating and rapid Li+ migration on the Co-spc-COP are also revealed by various in situ/ex situ experimental technologies and theory calculation. The Co-spc-COP-based cell delivers an extraordinary lifespan of 6600â h and ultrahigh capacity retention of 78.3 % (111.9â mAh g-1) after 1000â cycles at 1â C. This demonstrated synergistic strategy in Co-coordinated organic polymer may gain new insights to regulate the uniform and non-dendritic deposition/dissolution behaviors for highly stable LMBs.
RESUMEN
Organic compounds are regarded as important candidates for potassium-ion batteries (KIBs) due to their light elements, controllable polymerization, and tunable functional groups. However, intrinsic drawbacks largely restrict their application, including possible solubility in electrolytes, poor conductivity, and low diffusion coefficients. To address these issues, an ultrathin layered pyrazine/carbonyl-rich material (CT) is synthesized via an acid-catalyzed solvothermal reaction and homogeneously grown on carbon nanotubes (CNTs), marked as CT@CNT. Such materials have shown good features of exposing functional groups to guest ions and good electron transport paths, exhibiting high reversible capacity and remarkable rate capability over a wide temperature range. Two typical electrolytes are compared, demonstrating that the electrolyte of LX-146 is more suitable to maximize the electrochemical performances of electrodes at different temperatures. A stepwise reaction mechanism of K-chelating with CâO and CâN functional groups is proposed, verified by in/ex situ spectroscopic techniques and theoretical calculations, illustrating that pyrazines and carbonyls play the main roles in reacting with K+ cations, and CNTs promote conductivity and restrain electrode dissolution. This study provides new insights to understand the K-storage behaviors of organic compounds and their "all-temperature" application.
RESUMEN
Summertime surface ozone in China has been increasing since 2013 despite the policy-driven reduction in fuel combustion emissions of nitrogen oxides (NOx). Here we examine the role of soil reactive nitrogen (Nr, including NOx and nitrous acid (HONO)) emissions in the 2013-2019 ozone increase over the North China Plain (NCP), using GEOS-Chem chemical transport model simulations. We update soil NOx emissions and add soil HONO emissions in GEOS-Chem based on observation-constrained parametrization schemes. The model estimates significant daily maximum 8 h average (MDA8) ozone enhancement from soil Nr emissions of 8.0 ppbv over the NCP and 5.5 ppbv over China in June-July 2019. We identify a strong competing effect between combustion and soil Nr sources on ozone production in the NCP region. We find that soil Nr emissions accelerate the 2013-2019 June-July ozone increase over the NCP by 3.0 ppbv. The increase in soil Nr ozone contribution, however, is not primarily driven by weather-induced increases in soil Nr emissions, but by the concurrent decreases in fuel combustion NOx emissions, which enhance ozone production efficiency from soil by pushing ozone production toward a more NOx-sensitive regime. Our results reveal an important indirect effect from fuel combustion NOx emission reduction on ozone trends by increasing ozone production from soil Nr emissions, highlighting the necessity to consider the interaction between anthropogenic and biogenic sources in ozone mitigation in the North China Plain.
Asunto(s)
Modelos Químicos , Ozono , China , Nitrógeno , SueloRESUMEN
It was to investigate the mechanism of Maspin gene methylation induced by specific shRNA primer sequences in the proliferation of oral squamous cell carcinoma (OSCC) cells. Human OSCC HN13 cell line was selected as the study object, and the corresponding specific shRNA primer sequences were designed to construct Maspin-shRNA recombinant adenovirus using human Maspin nucleotide sequences as the target gene, and it was transfected into HN13 cells. The growth curve, Maspin expression level, migration and invasion ability, and proliferation activity of the transfected cells were analyzed. The results showed that the growth efficiency of transfected cells was significantly improved, and the OD value at 450 nm of cells in the specific sequence group (SSG) was greater than that of cells in the non-specific sequence group (nSSG). Maspin methylation was higher in the SSG than in the nSSG (P < 0.05). The number of cell migration and invasion in the SSG were higher than those in the nSSG (P < 0.05). The proliferation activity of cells in the SSG was higher than that of cells in the nSSG (P < 0.05). It showed that specific shRNA sequences induced Maspin gene methylation to inhibit Maspin expression, thereby participating in the migration and invasion motility of oral squamous carcinoma cells and improving proliferative activity.