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The demographic traits of an organism are key components of its fitness and life history theory aims at identifying the environmental drivers underlying the evolution of life history strategies. For fishes, the equilibrium species, those investing into larval survival (large eggs, parental care) rather than into absolute fecundity, are hypothesized to have evolved in stable and predictable environments with high biotic pressure. Human induced nutrient enrichment in many lakes around the world makes them increasingly subjected to perturbations such as anoxia and toxic algal blooms. We hypothesized that eutrophication results in lakes becoming more unstable, unpredictable and less resource-limited, in turn less favorable to equilibrium species. Another hypothesis states that lacustrine environment stability increases with ecosystem size. This study presents the first attempt to compare the two hypotheses in a group of 26 lakes. We found that the population abundance of equilibrium species was negatively related to increasing eutrophication. Long-lived and highly fecund periodic species responded more positively to eutrophication than short lived opportunistic species, with no parental care. This result could be demonstrated by seasonality in primary productivity which favors periodic species, disconnection from the river which prevents good colonist (i.e., opportunistic) species to (re)-establish after perturbation events, and predation by periodic species on opportunistic species. In contrast, we found no support for the ecosystem size hypothesis. Overall, we showed that human driven eutrophication affected species according to their life history strategies, reinforcing the usefulness of life history theory as a framework for assessing fish community response to a large array of human perturbations. More generally, our study emphasizes the importance of species traits to assess, explain, and predict community responses to human and natural perturbations.
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Eutrofização , Peixes , Lagos , Animais , Características de História de Vida , Ecossistema , Monitoramento Ambiental/métodosRESUMO
Microglia activation-induced neuroinflammation is a risk factor for cognitive dysfunction in the hippocampus during the early stages of neurodegenerative diseases. Exercise is an intrinsic remedy that plays a crucial role in enhancing the survival of neurons and reducing neuroinflammation in the brain. Among these theories, alterations in intracellular signaling pathways associated with neuronal growth and inflammation have been emphasized. Based on these observations and recent evidence demonstrating the beneficial effects of exercise on suppressing brain inflammation in the elderly, we examined cellular signaling pathways in the hippocampal formation of D-galactose-induced accelerated aging mice that underwent 8 weeks of treadmill exercise. To accomplish this, we utilized immunohistochemistry and Western blotting to detect the expression of hippocampal proteins, and qPCR to detect the expression of mRNA. We found that aerobic exercise significantly promoted the survival of hippocampal neurons, inhibited microglia activation, and decreased the expression of inflammatory cytokines TNF-α, IL-1α, IL-1ß, and chemokines CXCL-1, CXCR-2 in D-galactose model mice. Furthermore, exercise contributed to decreasing the microglia activation marker Iba1-positive cell count and average optical density and increasing the number of NeuN-immunopositive cells. Exercise also reduced RIPK1 and MAP3K5 expression in the hippocampus. Surprisingly, aerobic exercise significantly decreased the expression ratios of p-p65/p65, p-IκBα/IκBα, and p-JNK/JNK. Therefore, we hypothesized that exercise has an anti-inflammatory effect on the hippocampus of mice in the D-galactose-induced aging model. This effect may be attributed to the ability of aerobic exercise to down-regulate the RIPK1-mediated NF-κB and JNK pathways.
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Envelhecimento , Galactose , Hipocampo , Microglia , NF-kappa B , Condicionamento Físico Animal , Proteína Serina-Treonina Quinases de Interação com Receptores , Animais , Microglia/metabolismo , Hipocampo/metabolismo , Condicionamento Físico Animal/fisiologia , NF-kappa B/metabolismo , Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo , Masculino , Camundongos , Envelhecimento/metabolismo , Envelhecimento/fisiologia , Doenças Neuroinflamatórias/metabolismo , Camundongos Endogâmicos C57BL , Transdução de Sinais/fisiologia , Citocinas/metabolismo , Modelos Animais de Doenças , Neurônios/metabolismo , Sistema de Sinalização das MAP Quinases/fisiologiaRESUMO
Topological materials carrying topological surface states (TSSs) have extraordinary carrier mobility and robustness, which provide a new platform for searching for efficient hydrogen evolution reaction (HER) electrocatalysts. However, the majority of these TSSs originate from the sp band of topological quantum catalysts rather than the d band. Here, based on the density functional theory calculation, it is reported a topological semimetal Pd3Sn carrying TSSs mainly derived from d orbital and proposed that optimizing surface state electrons of Pd3Sn by introduction heteroatoms (Ni) can promote hybridization between hydrogen atoms and electrons, thereby reducing the Gibbs free energy (ΔGH) of adsorbed hydrogen and improving its HER performance. Moreover, this is well verified by electrocatalytic experiment results, the Ni-doped Pd3Sn (Ni0.1Pd2.9Sn) show much lower overpotential (-29 mV vs RHE) and Tafel slope (17 mV dec-1) than Pd3Sn (-39 mV vs RHE, 25 mV dec-1) at a current density of 10 mA cm-2. Significantly, the Ni0.1Pd2.9Sn nanoparticles exhibit excellent stability for HER. The electrocatalytic activity of Ni0.1Pd2.9Sn nanoparticles is superior to that of commercial Pt. This work provides an accurate guide for manipulating surface state electrons to improve the HER performance of catalysts.
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Introduction: Prostate Cancer (PCa) remains a significant concern in male cancer-related mortality. Tumour development is intricately regulated by the complex interactions between tumour cells and their microenvironment, making it essential to determine which is/are key factor(s) that influence the progression of PCa within the tumour microenvironment. Materials and methods: The current study utilised histopathology and immunohistochemistry to determine the expression of IL-38 in PCa and analysed the correlation between the expression level of IL-38 within PCa and clinical pathological characteristics. Results: There was a significant increase in IL-38 expression in PCa tissues compared to adjacent non-PCa tissues (P < 0.0001). In addition, IL-38 expression was significantly higher in tumour cells with a high proliferation index compared to those with a low value-added index. ROC curve analysis demonstrated that IL-38 has high specificity and sensitivity for the diagnosis of PCa (AUC=0.76). Moreover, we Probed the cellular source of IL-38 in prostate cancer tissue by immunofluorescence double staining. Additionally, within PCa, the expression of IL-38 was inversely correlated with the expression levels of CD8 and PD-1. Survival analysis revealed a significantly lower overall survival rate for PCa patients with high IL-38 expression (P=0.0069), and when IL-38 was co-expressed with CD8, the survival rate of the IL-38high/CD8low group was decreased significantly. Multivariate analysis indicated that the expression level of IL-38 and TNM staging were independent predictors of survival in PCa patients. Conclusion: These findings suggest that IL-38 plays a crucial role in the development of PCa, and the exploration of the correlation between IL-38 and various immune factors in the tumour microenvironment further reveals its mechanism of action, making it a potential target for immunotherapy in PCa.
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Interleucinas , Neoplasias da Próstata , Idoso , Humanos , Masculino , Pessoa de Meia-Idade , Biomarcadores Tumorais , Interleucinas/metabolismo , Prognóstico , Receptor de Morte Celular Programada 1/metabolismo , Receptor de Morte Celular Programada 1/genética , Neoplasias da Próstata/patologia , Neoplasias da Próstata/imunologia , Neoplasias da Próstata/mortalidade , Neoplasias da Próstata/metabolismo , Microambiente Tumoral/imunologiaRESUMO
Background: The progress in Colorectal cancer (CRC) screening and management has resulted in an unprecedented caseload for histopathological diagnosis. While artificial intelligence (AI) presents a potential solution, the predominant emphasis on slide-level aggregation performance without thorough verification of cancer in each location, impedes both explainability and transparency. Effectively addressing these challenges is crucial to ensuring the reliability and efficacy of AI in histology applications. Method: In this study, we created an innovative AI algorithm using transfer learning from a polyp segmentation model in endoscopy. The algorithm precisely localized CRC targets within 0.25 mm² grids from whole slide imaging (WSI). We assessed the CRC detection capabilities at this fine granularity and examined the influence of AI on the diagnostic behavior of pathologists. The evaluation utilized an extensive dataset comprising 858 consecutive patient cases with 1418 WSIs obtained from an external center. Results: Our results underscore a notable sensitivity of 90.25% and specificity of 96.60% at the grid level, accompanied by a commendable area under the curve (AUC) of 0.962. This translates to an impressive 99.39% sensitivity at the slide level, coupled with a negative likelihood ratio of <0.01, signifying the dependability of the AI system to preclude diagnostic considerations. The positive likelihood ratio of 26.54, surpassing 10 at the grid level, underscores the imperative for meticulous scrutiny of any AI-generated highlights. Consequently, all four participating pathologists demonstrated statistically significant diagnostic improvements with AI assistance. Conclusion: Our transfer learning approach has successfully yielded an algorithm that can be validated for CRC histological localizations in whole slide imaging. The outcome advocates for the integration of the AI system into histopathological diagnosis, serving either as a diagnostic exclusion application or a computer-aided detection (CADe) tool. This integration has the potential to alleviate the workload of pathologists and ultimately benefit patients.
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INTRODUCTION: Osteoarthritis (OA) is a progressive disease that poses a significant threat to human health, particularly in aging individuals: Although sympathetic activation has been implicated in bone metabolism, its role in the development of OA related to aging remains poorly understood. Therefore, this study aimed to investigate how sympathetic regulation impacts aging-related OA through experiments conducted both in vivo and in vitro. METHODS: To analyze the effect of sympathetic regulation on aging-related OA, we conducted experiments using various mouse models. These models included a natural aging model, a medial meniscus instability model, and a load-induced model, which were used to examine the involvement of sympathetic nerves. In order to evaluate the expression levels of ß1-adrenergic receptor (Adrß1) and sirtuin-6 (Sirt6) in chondrocytes of naturally aging OA mouse models, we performed assessments. Additionally, we investigated the influence of ß1-adrenergic receptor knockout or treatment with a ß1-adrenergic receptor blocker on the progression of OA in aging mice and detected exosome release and detected downstream signaling expression by inhibiting exosome release. Furthermore, we explored the impact of sympathetic depletion through tyrosine hydroxylase (TH) on OA progression in aging mice. Moreover, we studied the effects of norepinephrine(NE)-induced activation of the ß1-adrenergic receptor signaling pathway on the release of exosomes and miR-125 from chondrocytes, subsequently affecting osteoblast differentiation in subchondral bone. RESULTS: Our findings demonstrated a significant increase in sympathetic activity, such as NE levels, in various mouse models of OA including natural aging, medial meniscus instability, and load-induced models. Notably, we observed alterations in the expression levels of ß1-adrenergic receptor and Sirt6 in chondrocytes in OA mouse models associated with natural aging, leading to an improvement in the progression of OA. Critically, we found that the knockout of ß1-adrenergic receptor or treatment with a ß1-adrenergic receptor blocker attenuated OA progression in aging mice and the degraded cartilage explants produced more exosome than the nondegraded ones, Moreover, sympathetic depletion through TH was shown to ameliorate OA progression in aging mice. Additionally, we discovered that NE-induced activation of the ß1-adrenergic receptor signaling pathway facilitated the release of exosomes and miR-125 from chondrocytes, promoting osteoblast differentiation in subchondral bone. CONCLUSION: In conclusion, our study highlights the role of sympathetic innervation in facilitating the transfer of exosomal miR-125 from osteoarthritic chondrocytes, ultimately disrupting subchondral bone homeostasis and exacerbating cartilage damage in aging mice. These findings provide valuable insights into the potential contribution of sympathetic regulation to the pathogenesis of aging-related OA.
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Introduction: Wound healing poses a clinical challenge in diabetes mellitus (DM) due to compromised host immunity. CD64, an IgG-binding Fcgr1 receptor, acts as a pro-inflammatory mediator. While its presence has been identified in various inflammatory diseases, its specific role in wound healing, especially in DM, remains unclear. Objectives: We aimed to investigate the involvement of CD64 in diabetic wound healing using a DM animal model with CD64 KO mice. Methods: First, we compared CD64 expression in chronic skin ulcers from human DM and non-DM skin. Then, we monitored wound healing in a DM mouse model over 10 days, with or without CD64 KO, using macroscopic and microscopic observations, as well as immunohistochemistry. Results: CD64 expression was significantly upregulated (1.25-fold) in chronic ulcerative skin from DM patients compared to non-DM individuals. Clinical observations were consistent with animal model findings, showing a significant delay in wound healing, particularly by day 7, in CD64 KO mice compared to WT mice. Additionally, infiltrating CD163+ M2 macrophages in the wounds of DM mice decreased significantly compared to non-DM mice over time. Delayed wound healing in DM CD64 KO mice correlated with the presence of inflammatory mediators. Conclusion: CD64 seems to play a crucial role in wound healing, especially in DM conditions, where it is associated with CD163+ M2 macrophage infiltration. These data suggest that CD64 relies on host immunity during the wound healing process. Such data may provide useful information for both basic scientists and clinicians to deal with diabetic chronic wound healing.
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Diabetes Mellitus Experimental , Úlcera Cutânea , Cicatrização , Animais , Camundongos , Diabetes Mellitus Experimental/metabolismo , Modelos Animais de Doenças , Macrófagos/metabolismo , Pele/metabolismo , Cicatrização/genéticaRESUMO
Introduction: Colorectal cancer (CRC) presents a substantial challenge characterized by unacceptably high mortality and morbidity, primarily attributed to delayed diagnosis and reliance on palliative care. The immune response of the host plays a pivotal role in carcinogenesis, with IL-38 emerging as a potential protective factor in CRC. However, the precise involvement of IL-38 among various leucocytes, its interactions with PD-1/PD-L1, and its impact on metastasis require further elucidation. Results: Our investigation revealed a significant correlation between IL-38 expression and metastasis, particularly concerning survival and interactions among diverse leucocytes within draining lymph nodes. In the mesentery lymph nodes, we observed an inverse correlation between IL-38 expression and stages of lymph node invasions (TNM), invasion depth, distance, and differentiation. This aligns with an overall survival advantage associated with higher IL-38 expression in CRC patients' nodes compared to lower levels, as well as elevated IL-38 expression on CD4+ or CD8+ cells. Notably, a distinct subset of patients characterized by IL-38high/PD-1low expression exhibited superior survival outcomes compared to other combinations. Discussion: Our findings demonstrate that IL-38 expression in colorectal regional nodes from CRC patients is inversely correlated with PD-1/PD-L1 but positively correlated with infiltrating CD4+ or CD8+ lymphocytes. The combined assessment of IL-38 and PD-1 expression in colorectal regional nodes emerges as a promising biomarker for predicting the prognosis of CRC.
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Antígeno B7-H1 , Neoplasias Colorretais , Humanos , Antígeno B7-H1/metabolismo , Receptor de Morte Celular Programada 1/metabolismo , Antígeno CTLA-4/metabolismo , Relevância Clínica , Fatores de Transcrição Forkhead/metabolismo , Linfonodos , Interleucinas/metabolismoRESUMO
Synthetic lethality is a phenomenon wherein the simultaneous deficiency of two or more genes results in cell death, while the deficiency of any individual gene does not lead to cell death. In recent years, synthetic lethality has emerged as a significant topic in the field of targeted cancer therapy, with certain drugs based on this concept exhibiting promising outcomes in clinical trials. Nevertheless, the presence of tumor heterogeneity and the intricate DNA repair mechanisms pose challenges to the effective implementation of synthetic lethality. This review aims to explore the concepts, development, and ethical quandaries surrounding synthetic lethality. Additionally, it will provide an in-depth analysis of the clinical application and underlying mechanism of synthetic lethality.
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Neoplasias , Mutações Sintéticas Letais , Morte Celular , Reparo do DNA , Neoplasias/tratamento farmacológico , Neoplasias/genéticaRESUMO
Adenocarcinoma of the bladder is a rare urinary bladder carcinoma with limited therapy options due to lack of molecular characterization. Here, we aimed to reveal the mutational and transcriptomic landscapes of adenocarcinoma of the bladder and assess any relationship with prognosis. Between February 2015 and June 2021, a total of 23 patients with adenocarcinoma of the bladder were enrolled. These included 16 patients with primary bladder adenocarcinomas and seven patients with urachal adenocarcinoma. Whole exome sequencing (16 patients), whole genome sequencing (16 patients), bulk RNA sequencing (RNA-seq) (19 patients), and single-cell RNA-seq (5 patients) were conducted for the specimens. Correlation analysis, survival analysis, and t-tests were also performed. Prevalent T>A substitutions were observed among somatic mutations, and major trinucleotide contexts included 5'-CTC-3' and 5'-CTG-3'. This pattern was mainly contributed by COSMIC signature 22 related to chemical carcinogen exposure (probably aristolochic acid), which has not been reported in bladder adenocarcinoma. Moreover, genes with copy number changes were also enriched in the KEGG term 'chemical carcinogenesis'. Transcriptomic analysis suggested high immune cell infiltration and luminal-like features in the majority of samples. Interestingly, a small fraction of samples with an APOBEC-derived mutational signature exhibited a higher risk of disease progression compared with samples with only a chemical carcinogen-related signature, confirming the molecular and prognostic heterogeneity of bladder adenocarcinoma. This study presents mutational and transcriptomic landscapes of bladder adenocarcinoma, and indicates that a chemical carcinogen-related mutational signature may be related to a better prognosis compared with an APOBEC signature in adenocarcinoma of the bladder. © 2024 The Pathological Society of Great Britain and Ireland.
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Adenocarcinoma , Bexiga Urinária , Humanos , Bexiga Urinária/patologia , Mutação , Adenocarcinoma/genética , Adenocarcinoma/patologia , Carcinógenos , PrognósticoRESUMO
The practical application of Li-S batteries is still severely restricted by poor cyclic performance caused by the intrinsic polysulfides shuttle effect, which is even more severe under the high-temperature condition owing to the inevitable increase of polysulfides' solubility and diffusion rate. Herein, tungsten-doped vanadium dioxide (W-VO2) micro-flowers are employed with first-order metal-insulator phase transition (MIT) property as a robust and multifunctional modification layer to hamper the shuttle effect and simultaneously improve the thermotolerance of the common separator. Tungsten doping significantly reduces the transition temperature from 68 to 35 °C of vanadium dioxide, which renders the W-VO2 easier to turn from the insulating monoclinic phase into the metallic rutile phase. The systematic experiments and theoretical analysis demonstrate that the temperature-induced in-suit MIT property endows the W-VO2 catalyst with strong chemisorption against polysulfides, low energy barrier for liquid-to-solid conversion, and outstanding diffusion kinetics of Li-ion under high temperatures. Benefiting from these advantages, the Li-S batteries with W-VO2 modified separator exhibit significantly improved rate and long-term cyclic performance under 50 °C. Remarkably, even at an elevated temperature (80 °C), they still exhibit superior electrochemical performance. This work opens a rewarding avenue to use phase-changing materials for high-temperature Li-S batteries.
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Electrochemical oxygen reduction (ORR) for the production of clean hydrogen peroxide (H2O2) is an effective alternative to industrial anthraquinone methods. The development of highly active, stable, and 2e- ORR oxygen reduction electrocatalysts while suppressing the competing 4e- ORR pathway is currently the main challenge. Herein, bimetallic doping was successfully achieved based on graphitic carbon nitride (g-C3N4) with the simultaneous introduction of K and Co, whereby 2D porous K-Co/CNNs nanosheets were obtained. The introduction of Co promoted the selectivity for H2O2, while the introduction of K not only promoted the formation of 2D nanosheets of g-C3N4, but also inhibited the ablation of H2O2 by K-Co/CNNs. Electrochemical studies showed that the selectivity of H2O2 in K-Co/CNNs under neutral electrolyte was as high as 97%. After 24 h, the H2O2 accumulation of K-Co/CNNs was as high as 31.7 g L-1. K-Co/CNNs improved the stability of H2O2 by inhibiting the ablation of H2O2, making it a good 2e- ORR catalyst and providing a new research idea for the subsequent preparation of H2O2.
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Objective: To compare the clinical efficacy and safety of electroacupuncture combined with extracorporeal shock wave therapy (EESWT) and extracorporeal shock wave therapy (ESWT) in the treatment of knee osteoarthritis (KOA). Methods: A total of 135 KOA patients who received EESWT treatment were selected as the EESWT group, and 135 KOA patients who received extracorporeal shock wave therapy (ESWT) were selected as the ESWT group. The clinical efficacy, inflammatory factors in joint synovial fluid and adverse events during treatment were compared before and after treatment. Results: The clinical effective rate of patients in the EESWT group (89.63 %) after treatment was significantly higher than that of the ESWT group (74.81 %) (p < 0.01). The lysholm kness (LKSS) score and range of motion (ROM) of the patients in the EESWT group after treatment were higher than those of the ESWT group, while Lequesne index score, visual analogue scale (VAS) score and Western Ontario and McMaster Universities Arthritis Index (WOMAC) were lower than those of the ESWT group (p < 0.01). Compared with ESWT group, the changes in the expression levels of nitric oxide (NO), superoxide dismutase (SOD), interleukin 1ß (IL-1ß), tumor necrosis factor-α (TNF-α), matrix metalloproteinase-3 (MMP-3), and transforming growth factor ß1 (TGF-ß1) in the synovial fluid of the EESWT group after treatment were significantly greater than those of the ESWT group (p < 0.01). No significant difference in the incidence of adverse events between the EESWT group and the ESWT group (p > 0.05). Conclusion: EESWT significantly improves pain symptoms and inflammatory factor levels in KOA patients and is an optional KOA treatment option worthy of clinical attention.
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Uncontrolled and excessive progression of liver fibrosis is thought to be the prevalent pathophysiological cause of liver cirrhosis and hepatocellular cancer, and there are currently no effective antifibrotic therapeutic options available. Intercellular communication and cellular heterogeneity in the liver are involved in the progression of liver fibrosis, but the exact nature of the cellular phenotypic changes and patterns of interregulatory remain unclear. Here, we performed single-cell RNA sequencing on nonparenchymal cells (NPCs) isolated from normal and fibrotic mouse livers. We identified eight main types of cells, including endothelial cells, hepatocytes, dendritic cells, B cells, natural killer/T (NK/T) cells, hepatic stellate cells (HSCs), cholangiocytes and macrophages, and revealed that macrophages and HSCs exhibit the most variance in transcriptional profile. Further analyses of HSCs and macrophage subpopulations and ligand-receptor interaction revealed a high heterogeneity characterization and tightly interregulated network of these two groups of cells in liver fibrosis. Finally, we uncovered a profibrotic Thbs1+ macrophage subcluster, which expands in mouse and human fibrotic livers, activating HSCs via PI3K/AKT/mTOR signaling pathway. Our findings decode unanticipated insights into the heterogeneity of HSCs and macrophages and their intercellular crosstalk at a single-cell level, and may provide potential therapeutic strategies in liver fibrosis.
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Transition metal sulfide (TMS) CoS2 is considered an ideal anode material for new-generation lithium-ion batteries (LIBs) because of its high specific capacity, high electrochemical activity, and low cost. However, CoS2 is prone to volume expansion and structural collapse when it participates in the internal conversion reaction of the battery, which limits its practical application. After analyzing the failure mechanism of CoS2 as the anode material of LIBs, the concept of nanoengineered materials is introduced here. CoS2 particles are nanosized and stabilized by constructing a composite structure on an alkali-treated two-dimensional Ti3C2 Mxene conductive network. Both experiments and theoretical calculations show that special Ti-O-Co bonds are formed at the interface of the Ti3C2/CoS2 composite through oxygen-containing functional groups. Ti-O-Co bonding with adjustable electronic characteristics can effectively promote the utilization rate of anode materials, electronic conductivity, and ionic diffusivity and thus enhance the redox reaction kinetics of the device. When the Ti3C2/CoS2 composite is used as the anode material for LIBs, it still provides a high specific capacity of 405.8 mAh g-1 after 100 cycles at 0.1 A g-1. After running for 1000 cycles at a high current of 1 A g-1, the capacity retention is still close to 100%. Also, high cycle stability under the condition of highly active material loading (10.58 mg cm-2) and low electrolyte/active material ratio (10 µL mg-1) is achieved. This work provides a new idea for the development of commercial LIBs as anode materials.
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The exploitation of high-performance supercapacitors is crucial to promote energy storage technologies. Benefiting from the three-dimensional conductive micronanostructures and high specific capacity of the PPy@CuCo2S4@NF (polypyrrole/copper cobalt sulfide/nickel foam) composite electrode, this electrode exhibits a high specific capacity of 1403.21 C g-1 at 1 A g-1 and a capacitance retention of 85.79% after 10,000 cycles at 10 A g-1. The assembled PPy@CuCo2S4@NF//AC aqueous hybrid supercapacitor (AHSC) reveals a wide operating potential window of 1.5 V and achieves a high specific capacity of 322.52 C g-1 at 1 A g-1 and a capacitance retention of 86.84% after 15,000 cycles at 10 A g-1. The AHSC also exhibits a high power density of 733.69 W kg-1 at an energy density of 67.19 W h kg-1, surpassing those of previously reported spinel-based supercapacitors. Ex situ X-ray diffraction and X-ray photoelectron spectroscopy results show that the CuCo2S4 spinel structure changes to CuS2 and CoS2 cube structures, and the oxidation states of Cu and Co increase during charging and discharging processes. Density functional theory calculations suggest a superior conductivity for CuCo2S4 compared to that for CuCo2O4, demonstrating that CuCo2S4 has superior electrochemical performance. These findings attest to the considerable potential of the spinel materials for advanced energy storage applications.
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Although spinal cord injury (SCI) represents a primary etiology of disability, currently, there are exist limited viable therapies modalities. Acquiring comprehension of the diverse pathways that drive mitochondrial aberration may facilitate the identification of noteworthy targets for ameliorating the deleterious consequences precipitated by SCI. Our objective was to determine the efficiency of exosomes produced from Schwann cells (SCDEs) in protecting against mitochondrial dysfunction. This evaluation was conducted using a rat model of compressed SCI and in vitro experiments involving rat pheochromocytoma cells (PC12) exposed to oxygen-glucose deprivation (OGD). The conducted experiments yielded evidence that SCDEs effectively mitigated oxidative stress (OS) and inflammation subsequent to SCI, while concurrently diminishing necroptosis. Subsequent in vitro inquiry assessed the impact of SCDEs on PC12, with a specific emphasis on mitochondrial functionality, necrotic cell prevalence, and mitophagy. The study findings revealed that SCDEs enhanced mitophagy in PC12 cells, leading to a decrease in the generation of reactive oxygen species (ROS) and inflammatory cytokines (CK) provoked by OGD-induced injury. This, in turn, mitigated mitochondrial dysfunction and necroptosis. Mechanistically, SCDEs facilitated cellular mitophagy through activation of the AMPK signaling pathway. In conclusion, our data strongly support the notion that SCDEs hold considerable promise as a therapeutic approach for managing SCI. Furthermore, our investigation serves to elucidate the pivotal role of AMPK-mediated mitophagy in reducing cell damage, thereby unveiling novel prospects for enhancing neuro-pathological outcomes following SCI.
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Exossomos , Traumatismos da Medula Espinal , Ratos , Animais , Mitofagia , Proteínas Quinases Ativadas por AMP/genética , Proteínas Quinases Ativadas por AMP/metabolismo , Exossomos/metabolismo , Necroptose , Transdução de Sinais , Traumatismos da Medula Espinal/genética , Traumatismos da Medula Espinal/terapia , Traumatismos da Medula Espinal/metabolismo , Mitocôndrias/metabolismo , Oxigênio/metabolismo , Células de Schwann/metabolismo , Células de Schwann/patologiaRESUMO
Efficient electrocatalysts and catalytic mechanisms remain a pressing need in Li-S electrochemistry to address lithium polysulfide (LiPS) shuttling and enhance conversion kinetics. This study presents the development of multifunctional VO2@rGO heterostructures, incorporating interfacial built-in electric field (BIEF) enhancement, as a Mott-Schottky electrocatalyst for Li-S batteries. Electrochemical experiments and theoretical analysis demonstrate that the interfacial BIEF between VO2 and rGO induces self-driven charge redistribution, resulting in accelerated charge transport rates, enhanced LiPS chemisorption, reduced energy barriers for Li2S nucleation/decomposition, and improved Li-ion diffusion behavior. The Mott-Schottky electrocatalyst, combining the strengths of VO2's anchoring ability, rGO's metallic conductivity, and BIEF's optimized charge transport, exhibits an outstanding "trapping-conversion" effect. The modified Li-S battery with a VO2@rGO-modified separator achieves a highly reversible capacity of 558.0 mAh g-1 at 2 C over 600 cycles, with an average decay rate of 0.048% per cycle. This research offers valuable insights into the design of Mott-Schottky electrocatalysts and their catalytic mechanisms, advancing high-efficiency Li-S batteries and other multielectron energy storage and conversion devices.
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BACKGROUND: This study aimed to accurately evaluate the matching of proximal and distal femoral segments and fitting of the femur-femoral stem in patients with Crowe type IV developmental dysplasia of the hip (DDH) who have undergone subtrochanteric osteotomy at different locations with an implanted Wagner cone stem to improve the rate of the bone union at the osteotomy site. METHODS: Three-dimensional femur morphology of 40 patients with Crowe type IV DDH was evaluated at each cross-section to determine the femoral cortical bone area. This study focused on five osteotomy lengths (2.5, 3, 3.5, 4, and 4.5 cm). The overlapped area between the proximal and distal cortical bone segments was defined as the contact area (S, mm2), and the contact area to distal cortical bone area ratio was defined as the coincidence rate (R). Three indicators were used to evaluate the matching and fitting of the osteotomy sites with the implanted Wagner cone stems: (1) higher S and R between the proximal and distal segments; (2) the effective fixation length of the femoral stem at the distal segments being at least 1.5 cm; and (3) osteotomy did not involve the isthmus. RESULTS: In all groups, S significantly decreased in the two proximal levels above the 0.5 cm level below the lesser trochanter (LT) compared with those below this level. In comparison, at osteotomy lengths from 2.5 to 4 cm, R significantly decreased in the three proximal levels. The optimal osteotomy levels ranged from 1.5 and 2.5 cm below the LT for an appropriately sized stem. CONCLUSIONS: Subtrochanteric osteotomy at the optimal level not only ensures fitting of the femur-femoral stem but also meets the requirements of a higher S and R to ensure adequate reduction and stabilization at the osteotomy site, which may contribute to the bone union. Although the optimal osteotomy level varies with the size of the femoral stem and the length of the subtrochanteric osteotomy, the optimal osteotomy levels for an appropriately sized Wagner cone femoral stem implantation range from 1.5 to 2.5 cm below the LT.
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Artroplastia de Quadril , Displasia do Desenvolvimento do Quadril , Luxação Congênita de Quadril , Sinostose , Humanos , Artroplastia de Quadril/métodos , Luxação Congênita de Quadril/diagnóstico por imagem , Luxação Congênita de Quadril/cirurgia , Displasia do Desenvolvimento do Quadril/cirurgia , Estudos Retrospectivos , Fêmur/diagnóstico por imagem , Fêmur/cirurgia , Osteotomia/métodos , Sinostose/cirurgiaRESUMO
Polysulfide shuttle effect and sluggish sulfur reaction kinetics severely impede the cycling stability and sulfur utilization of lithium-sulfur (Li-S) batteries. Modulating d-band electronic structures of molybdenum disulfide electrocatalysts via p/n doping is promising to boost polysulfide conversion and suppress polysulfide migration in lithium-sulfur batteries. Herein, p-type V-doped MoS2 (V-MoS2 ) and n-type Mn-doped MoS2 (Mn-MoS2 ) catalysts are well-designed. Experimental results and theoretical analyses reveal that both of them significantly increase the binding energy of polysulfides on the catalysts' surface and accelerate the sluggish conversion kinetics of sulfur species. Particularly, the p-type V-MoS2 catalyst exhibits a more obvious bidirectional catalytic effect. Electronic structure analysis further demonstrates that the superior anchoring and electrocatalytic activities are originated from the upward shift of the d-band center and the optimized electronic structure induced by duplex metal coupling. As a result, the Li-S batteries with V-MoS2 modified separator exhibit a high initial capacity of 1607.2 mAh g-1 at 0.2 C and excellent rate and cycling performance. Moreover, even at a high sulfur loading of 6.84 mg cm-2 , a favorable initial areal capacity of 8.98 mAh cm-2 is achieved at 0.1 C. This work may bring widespread attention to atomic engineering in catalyst design for high-performance Li-S batteries.