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Background: Inhibition of indolamine-2,3-dioxygenase 1 (IDO1) has been proposed as a promising strategy for cancer immunotherapy; however, it has failed in clinical trials. Macrophages in the tumor microenvironment (TME) contribute to immune escape and serve as potential therapeutic targets. This study investigated the expression pattern of IDO1 in TME and its impact on prognosis and therapeutic response of patients with esophageal squamous cell carcinoma (ESCC). Methods: RNA sequencing data from 95 patients with ESCC from The Cancer Genome Atlas (TCGA) database were used to explore the prognostic value of IDO1. Bioinformatics tools were used to estimate scores for stromal and immune cells in tumour tissues, abundance of eight immune cell types in TME, and sensitivity of chemotherapeutic drugs and immune checkpoint (IC) blockage. The results were validated using digitalized immunohistochemistry and multiplexed immunofluorescence in ESCC tissue samples obtained from our clinical center. Results: TCGA and validation data suggested that high expression of IDO1 was associated with poor patient survival, and IDO1 was an independent prognostic factor. IDO1 expression positively correlated with macrophages in TME and PDCD1 within diverse IC genes. Single-cell RNA sequencing data analysis and multiplexed immunofluorescence verified the coexpression of IDO1 and PD-1 in tumor-associated macrophages (TAMs). Patients with high IDO1 expression showed increased sensitivity to various chemotherapeutic drugs, while were more likely to resist IC blockage. Conclusion: This study identifies IDO1 as an independent prognostic indicator of OS in patients with ESCC, reveals a compelling connection of IDO1, PD-1, and TAMs, and explores the sensitivity of patients with high IDO1 expression to chemotherapeutic drugs and their resistance to IC blockade. These findings open new avenues for potential targets in ESCC immunotherapy.
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Ischemic stroke (IS) is the predominant form of stroke pathology, and its clinical management remains constrained by therapeutic time frame. The gut microbiota (GM), comprising a multitude of bacterial and archaeal cells, surpasses the human cell count by approximately tenfold and significantly contributes to the human organism's growth, development, and overall well-being. The microbiota-gut-brain axis (MGBA) in recent years has established a strong association between gut microbes and the brain, demonstrating their intricate involvement in the progression of IS. The regulation of IS by the GM, encompassing changes in composition, abundance, and distribution, is multifaceted, involving neurological, endocrine, immunological, and metabolic mechanisms. This comprehensive understanding offers novel insights into the therapeutic approaches for IS. The objective of this paper is to examine the mechanisms of interaction between the GM and IS in recent years, assess the therapeutic effects of the GM on IS through various interventions, such as dietary modifications, probiotics, fecal microbiota transplantation, and antibiotics, and offer insights into the potential clinical application of the GM in stroke treatment.
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Background: Epilepsy is a chronic neurological disorder characterized by recurrent seizures that significantly impact patients' quality of life. Identifying predictors is crucial for early intervention. Objective: Electroencephalography (EEG) microstates effectively describe the resting state activity of the human brain using multichannel EEG. This study aims to develop a comprehensive prediction model that integrates clinical features with EEG microstates to predict drug-refractory epilepsy (DRE). Design: Retrospective study. Methods: This study encompassed 226 patients with epilepsy treated at the epilepsy center of a tertiary hospital between October 2020 and May 2023. Patients were categorized into DRE and non-DRE groups. All patients were randomly divided into training and testing sets. Lasso regression combined with Stepglm [both] algorithms was used to screen independent risk factors for DRE. These risk factors were used to construct models to predict the DRE. Three models were constructed: a clinical feature model, an EEG microstate model, and a comprehensive prediction model (combining clinical-EEG microstates). A series of evaluation methods was used to validate the accuracy and reliability of the prediction models. Finally, these models were visualized for display. Results: In the training and testing sets, the comprehensive prediction model achieved the highest area under the curve values, registering 0.99 and 0.969, respectively. It was significantly superior to other models in terms of the C-index, with scores of 0.990 and 0.969, respectively. Additionally, the model recorded the lowest Brier scores of 0.034 and 0.071, respectively, and the calibration curve demonstrated good consistency between the predicted probabilities and observed outcomes. Decision curve analysis revealed that the model provided significant clinical net benefit across the threshold range, underscoring its strong clinical applicability. We visualized the comprehensive prediction model by developing a nomogram and established a user-friendly website to enable easy application of this model (https://fydxh.shinyapps.io/CE_model_of_DRE/). Conclusion: A comprehensive prediction model for DRE was developed, showing excellent discrimination and calibration in both the training and testing sets. This model provided an intuitive approach for assessing the risk of developing DRE in patients with epilepsy.
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The establishment of epiblast-derived pluripotent stem cells (PSCs) from cattle, which are important domestic animals that provide humans with milk and meat while also serving as bioreactors for producing valuable proteins, poses a challenge due to the unclear molecular signaling required for embryonic epiblast development and maintenance of PSC self-renewal. Here, we selected six key stages of bovine embryo development (E5, E6, E7, E10, E12, and E14) to track changes in pluripotency and the dependence on signaling pathways via modified single-cell transcription sequencing technology. The remarkable similarity of the gene expression patterns between cattle and pigs during embryonic lineage development contributed to the successful establishment of bovine epiblast stem cells (bEpiSCs) using 3i/LAF (WNTi, GSK3ßi, SRCi, LIF, Activin A, and FGF2) culture system. The generated bEpiSCs exhibited consistent expression patterns of formative epiblast pluripotency genes and maintained clonal morphology, normal karyotypes, and proliferative capacity for more than 112 passages. Moreover, these cells exhibited high-efficiency teratoma formation as well as the ability to differentiate into various cell lineages. The potential of bEpiSCs for myogenic differentiation, primordial germ cell like cells (PGCLCs) induction, and as donor cells for cell nuclear transfer was also assessed, indicating their promise in advancing cell-cultured meat production, gene editing, and animal breeding.
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Diferenciação Celular , Linhagem da Célula , Camadas Germinativas , Células-Tronco Pluripotentes , Animais , Bovinos , Diferenciação Celular/genética , Células-Tronco Pluripotentes/citologia , Células-Tronco Pluripotentes/metabolismo , Camadas Germinativas/metabolismo , Camadas Germinativas/citologia , Linhagem da Célula/genética , Células-Tronco Embrionárias/citologia , Células-Tronco Embrionárias/metabolismo , Desenvolvimento Embrionário/genética , Linhagem Celular , Embrião de Mamíferos/citologia , Embrião de Mamíferos/metabolismo , Técnicas de Cultura de Células/métodosRESUMO
Manipulating the properties of 2D materials through meticulously engineered artificial heterojunctions holds great promise for novel device applications. However, existing research on the crucial charge-transfer interactions and energy profile regulation is predominantly focused on 2D van der Waals structures formed via weak van der Waals forces, limiting regulatory efficiency at high costs. Herein, a refined atomic-molecular heterojunction strategy featuring strong covalent bonds between organic molecule and 2D violet phosphorus (VP) atomic crystal is developed, which enables enhanced charge-transfer dynamics and customizable band structure regulation at the molecular level. Both experimentally and theoretically, it is demonstrated that grafting efficiency, charge redistribution, and energy gap regulation critically depend on organic electronegativity, providing a low-cost yet high-efficiency regulatory effect on a large scale. As a proof of concept, the novel VP-molecular heterojunctions exhibit optimized performance in diverse application domains, presenting a general platform for future high-performance device applications.
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Constructing photonic crystals with core-shell structured nanoparticles is an important means for applications such as secure communication, anti-counterfeiting marking, and structural color camouflage. Nonetheless, the precise synthesis technology for core-shell structured nanoparticles at the hundred-nanometer scale faces significant challenges. This paper proposes a controlled synthesis method for core-shell structured nanoparticles using a template method. By using 100 nm diameter silica nanospheres as templates and coating them with a ferroferric oxide shell layer, SiO2@Fe3O4 core-shell structured nanoparticles with regular morphology and good uniformity can be obtained. The study experimentally investigated the effects of feed amount, modifiers, temperature, and feed order on the coating effect, systematically optimizing the preparation process. Centrifugal driving technology was used to achieve structural colors in the visible wavelength range. Additionally, the method successfully created well-defined and uniform core-shell structured nanoparticles using 200 nm diameter silica nanospheres as templates, demonstrating that this controllable synthesis method can effectively produce core-shell structured nanoparticles over a wide range of particle sizes. The template method proposed in this paper can significantly improve morphological regularity and size uniformity while effectively reducing the preparation cost of core-shell structured nanoparticles.
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Eosinophils are essential innate immune cells in allergic responses. Accumulating evidence indicates that eosinophils also participate in the pathogenesis of cardiovascular diseases (CVDs). In clinical studies, high blood eosinophil counts and eosinophil cationic protein levels have been associated with an increased risk of CVD, including myocardial infarction (MI), cardiac hypertrophy, atrial fibrillation, abdominal aortic aneurysm (AAA) and atherosclerosis. However, low blood eosinophil counts have also been reported to be a risk factor for MI, heart failure, aortic dissection, AAA, deep vein thrombosis, pulmonary embolism and ischaemic stroke. Although these conflicting clinical observations remain unexplained, CVD status, timing of eosinophil data collection, and tissue eosinophil phenotypic and functional heterogeneities might account for these discrepancies. Preclinical studies suggest that eosinophils have protective actions in MI, cardiac hypertrophy, heart failure and AAA. By contrast, cationic proteins and platelet-activating factor from eosinophils have been shown to promote vascular smooth muscle cell proliferation, vascular calcification, thrombomodulin inactivation and platelet activation and aggregation, thereby exacerbating atherosclerosis, atrial fibrillation, thrombosis and associated complications. Therefore, eosinophils seem to promote calcification and thrombosis in chronic CVD but are protective in acute cardiovascular settings. In this Review, we summarize the available clinical and preclinical data on the different roles of eosinophils in CVD.
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The piezoelectric effect refers to a physical phenomenon where piezoelectric materials generate an electric field when subjected to mechanical stress or undergo mechanical deformation when subjected to an external electric field. This principle underlies the operation of piezoelectric sensors. Piezoelectric sensors have garnered significant attention due to their excellent self-powering capability, rapid response speed, and high sensitivity. With the rapid development of sensor techniques achieving high precision, increased mechanical flexibility, and miniaturization, a range of flexible electronic products have emerged. As the core constituents of piezoelectric sensors, flexible piezoelectric composite materials are commonly used due to their unique advantages, including high conformability, sensitivity, and compatibility. They have found applications in diverse domains such as underwater detection, electronic skin sensing, wearable sensors, targeted therapy, and ultrasound diagnostics for deep tissue. The advent of flexible piezoelectric composite materials has revolutionized the design concepts and application scenarios of traditional piezoelectric materials, playing a crucial role in the development of next-generation flexible electronic products. This paper reviews the research progress on flexible piezoelectric composite materials, covering their types and typical fabrication techniques, as well as their applications across various fields. Finally, a summary and outlook on the existing issues and future development of these composite materials are provided.
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The temperature-dependent thermal conductivity of violet phosphorus on a perforated SiO2/Si substrate has been investigated via optothermal Raman spectroscopy. The obtained temperature coefficients of the Tg mode and Ptub mode of the violet phosphorus sample are -0.01268 and -0.01789 cm-1 K-1, respectively. On the basis of the temperature coefficients and power coefficients, the thermal conductivity of the violet phosphorus has been calculated to be 44.642 ± 4.995 W/mK at room temperature, which is higher than that of other two-dimensional materials such as black phosphorus and MoS2 due to the effect of boundary scattering and the phonon mean free path. Additionally, the thermal conductivity of violet phosphorus decreases as a power exponential function of the temperature, which is primarily associated with the phonon mean free path and phonon group velocity. This work provides a scientific foundation for thermal management and heat dissipation in designing micro-nano devices with violet phosphorus.
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Biobased therapy represents a promising strategy for myocardial repair. However, the limitations of using live cells, including the risk of immunogenicity of allogeneic cells and inconsistent therapeutic efficacy of autologous cells together with low stability, result in an unsatisfactory clinical outcomes. Therefore, cell-free strategies for cardiac tissue repair have been proposed as alternative strategies. Cell-free strategies, primarily based on the paracrine effects of cellular therapy, have demonstrated their potential to inhibit apoptosis, reduce inflammation, and promote on-site cell migration and proliferation, as well as angiogenesis, after an infarction and have been explored preclinically and clinically. Among various cell-free modalities, bioderived nanoparticles, including adeno-associated virus (AAV), extracellular vesicles, cell membrane-coated nanoparticles, and exosome-mimetic nanovesicles, have emerged as promising strategies due to their improved biological function and therapeutic effect. The main focus of this review is the development of existing cellular nanoparticles and their fundamental working mechanisms, as well as the challenges and opportunities. The key processes and requirements for cardiac tissue repair are summarized first. Various cellular nanoparticle modalities are further highlighted, together with their advantages and limitations. Finally, we discuss various delivery approaches that offer potential pathways for researchers and clinicians to translate cell-free strategies for cardiac tissue repair into clinical practice.
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Cardiopatias , Nanopartículas , Animais , Humanos , Nanopartículas/química , Cardiopatias/terapiaRESUMO
Renal dysfunction (RD) often characterizes the worse course of patients with advanced heart failure (AHF). Many prognosis assessments are hindered by researcher biases, redundant predictors, and lack of clinical applicability. In this study, we enroll 1736 AHF/RD patients, including data from Henan Province Clinical Research Center for Cardiovascular Diseases (which encompasses 11 hospital subcenters), and Beth Israel Deaconess Medical Center. We developed an AI hybrid modeling framework, assembling 12 learners with different feature selection paradigms to expand modeling schemes. The optimized strategy is identified from 132 potential schemes to establish an explainable survival assessment system: AIHFLevel. The conditional inference survival tree determines a probability threshold for prognostic stratification. The evaluation confirmed the system's robustness in discrimination, calibration, generalization, and clinical implications. AIHFLevel outperforms existing models, clinical features, and biomarkers. We also launch an open and user-friendly website www.hf-ai-survival.com , empowering healthcare professionals with enhanced tools for continuous risk monitoring and precise risk profiling.
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Insuficiência Cardíaca , Humanos , Insuficiência Cardíaca/mortalidade , Insuficiência Cardíaca/fisiopatologia , Masculino , Feminino , Idoso , Prognóstico , Pessoa de Meia-Idade , Inteligência Artificial , Medição de Risco/métodos , Análise de Sobrevida , Insuficiência Renal/mortalidade , Insuficiência Renal/fisiopatologia , Insuficiência Renal/diagnóstico , BiomarcadoresRESUMO
Herbal medicines (HMs) have long played a pivotal role in preventing and treating various human diseases and have been studied widely. However, the complexities present in HM metabolites and their unclear mechanisms of action have posed significant challenges in the modernization of traditional Chinese medicine (TCM). Over the past two decades, mass spectrometry imaging (MSI) has garnered increasing attention as a robust analytical technique that enables the simultaneous execution of qualitative, quantitative, and localization analyses without complex sample pretreatment. With advances in technical solutions, MSI has been extensively applied in the field of HMs. MSI, a label-free ion imaging technique can comprehensively map the spatial distribution of HM metabolites in plant native tissues, thereby facilitating the effective quality control of HMs. Furthermore, the spatial dimension information of small molecule endogenous metabolites within animal tissues provided by MSI can also serve as a supplement to uncover pharmacological and toxicological mechanisms of HMs. In the review, we provide an overview of the three most common MSI techniques. In addition, representative applications in HM are highlighted. Finally, we discuss the current challenges and propose several potential solutions. We hope that the summary of recent findings will contribute to the application of MSI in exploring metabolites and mechanisms of action of HMs.
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Syntaxin 17 (STX17) has been identified as a crucial factor in mediating the fusion of autophagosomes and lysosomes. However, its specific involvement in the context of atherosclerosis (AS) remains unclear. This study sought to elucidate the role and mechanistic contributions of STX17 in the initiation and progression of AS. Utilizing both in vivo and in vitro AS model systems, we employed ApoE knockout (KO) mice subjected to a high-fat diet and human umbilical vein endothelial cells (HUVECs) treated with oxidized low-density lipoprotein (ox-LDL) to assess STX17 expression. To investigate underlying mechanisms, we employed shRNA-STX17 lentivirus to knock down STX17 expression, followed by evaluating autophagy and inflammation in HUVECs. In both in vivo and in vitro AS models, STX17 expression was significantly upregulated. Knockdown of STX17 exacerbated HUVEC damage, both with and without ox-LDL treatment. Additionally, we observed that STX17 knockdown impaired autophagosome degradation, impeded autophagy flux and also resulted in the accumulation of dysfunctional lysosomes in HUVECs. Moreover, STX17 knockdown intensified the inflammatory response following ox-LDL treatment in HUVECs. Further mechanistic exploration revealed an association between STX17 and STING; reducing STX17 expression increased STING levels. Further knockdown of STING enhanced autophagy flux. In summary, our findings suggest that STX17 knockdown worsens AS by impeding autophagy flux and amplifying the inflammatory response. Additionally, the interaction between STX17 and STING may play a crucial role in STX17-mediated autophagy.
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Aterosclerose , Autofagia , Células Endoteliais da Veia Umbilical Humana , Inflamação , Lipoproteínas LDL , Proteínas Qa-SNARE , Autofagia/genética , Animais , Humanos , Aterosclerose/metabolismo , Aterosclerose/genética , Aterosclerose/patologia , Células Endoteliais da Veia Umbilical Humana/metabolismo , Inflamação/metabolismo , Inflamação/patologia , Inflamação/genética , Proteínas Qa-SNARE/metabolismo , Proteínas Qa-SNARE/genética , Camundongos , Lipoproteínas LDL/metabolismo , Técnicas de Silenciamento de Genes , Lisossomos/metabolismo , Camundongos Knockout , Masculino , Camundongos Endogâmicos C57BL , Modelos Animais de Doenças , Dieta Hiperlipídica/efeitos adversos , Apolipoproteínas E/genética , Apolipoproteínas E/metabolismo , Apolipoproteínas E/deficiênciaRESUMO
Urine metabolomics based on ultra-performance liquid chromatography-quadrupole time-of-flight tandem mass spectrometry(UHPLC-Q-TOF-MS) was utilized to investigate the metabolic regulation mechanism of Tingli Dazao Xiefei Decoction(TLDZ) in rats with allergic asthma. SD male rats were divided into a normal group, a model group, a dexamethasone group, and a TLDZ group. The allergic asthma model was established by intraperitoneal injection of ovalbumin(OVA) to induce allergy, combined with atomization excitation. Urine metabolites from all rats were collected by UHPLC-Q-TOF-MS. The metabolic profiles of rats in each group were built by principal component analysis(PCA). Besides, the differential metabolites between the model group and the TLDZ group were selected by orthogonal partial least squares discriminant analysis(OPLS-DA), t-test(P<0.05), and variable importance in the projection(VIP) values of more than 3. The differential metabolites were identified through HMDB, METLIN, and other online databa-ses. Heat maps and clustering analysis for relative quantitative information of biomarkers in each group were drawn by MeV 4.8.0 software. Finally, MetaboAnalyst, MBRole, and KEGG databases were used to enrich related metabolic pathways and construct metabolic networks. The result demonstrated that TLDZ could effectively regulate the disordered urine metabolic profiles of asthmatic rats. Combined with multivariate statistical analysis and online databases, a total of 45 differential metabolites with significant changes(P<0.05) between the model group and the TLDZ group were screened out. Metabolic pathways including histidine metabolism, tryptophan metabolism, and arginine and proline metabolism were enriched. TLDZ could improve asthma by regulating related metabolic pathways and interfering with pathological processes such as immune homeostasis airway inflammation. The study investigates the molecular mechanism of anti-asthma of TLDZ from the perspective of urine metabolomics, and combined with previous pharmacological studies, it provides a scientific basis for the clinical development and application of TLDZ in the treatment of asthma.
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Asma , Medicamentos de Ervas Chinesas , Metabolômica , Ratos Sprague-Dawley , Animais , Asma/tratamento farmacológico , Asma/urina , Asma/metabolismo , Medicamentos de Ervas Chinesas/farmacologia , Medicamentos de Ervas Chinesas/administração & dosagem , Masculino , Ratos , Cromatografia Líquida de Alta Pressão , Humanos , Urina/química , Espectrometria de Massas em TandemRESUMO
BACKGROUND: There is evidence indicating that both lipoprotein(a) [Lp(a)] and fibrinogen (FIB) are associated with mortality, However, the impact of their combination on mortality has not been determined. Thus, the aim of this study was to examine the association between the combination of Lp(a) and FIB with all-cause and cause-specific mortality. METHODS: This prospective cohort study enrolled 4,730 participants from the third National Health and Nutrition Examination Survey. The exposure variables included Lp(a), FIB and their combination, while the outcome variables consisted of all-cause, cardiovascular disease (CVD) and cancer-related mortality. Multivariate COX regression, subgroup analysis, sensitivity analysis and restricted cubic spline (RCS) were used to investigate the association between Lp(a), FIB and their combination with all-cause, CVD and cancer-related mortality. RESULTS: Over a median follow-up period of 235 months, 2,668 individuals died, including 1,051 deaths attributed to CVD and 549 deaths due to cancer. Multivariate Cox regression analyses revealed independent associations between both Lp(a) and FIB with all-cause, CVD, and cancer-related mortality. Compared to participants in the 1st to 50th percentiles of both Lp(a) and FIB, those in the 90th to 100th percentiles exhibited multivariable adjusted HRs of 1.813 (95% CI: 1.419-2.317, P < 0.001), 2.147 (95% CI: 1.483-3.109, P < 0.001) and 2.355 (95% CI: 1.396, 3.973, P = 0.001) for all-cause, CVD and cancer-related mortality, respectively. Subgroup and sensitivity analyses did not substantially attenuate the association between the combination of high Lp(a) and high FIB with the risk of all-cause and CVD-related mortality. Additionally, the RCS analysis showed that the relationship between Lp(a) and the risk of all-cause and cancer-related mortality, as well as the relationship between FIB and the risk of cancer-related mortality, were linear (P for nonlinearity > 0.05). Conversely, the relationship between Lp(a) and the risk of CVD-related mortality, as well as the relationship between FIB and the risk of all-cause and CVD-related mortality, were nonlinear (P for nonlinearity < 0.05). CONCLUSIONS: High levels of Lp(a) and FIB together conferred a greater risk of mortality from all-cause, CVD and cancer.
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Doenças Cardiovasculares , Causas de Morte , Fibrinogênio , Lipoproteína(a) , Neoplasias , Inquéritos Nutricionais , Humanos , Neoplasias/mortalidade , Lipoproteína(a)/sangue , Doenças Cardiovasculares/mortalidade , Masculino , Feminino , Pessoa de Meia-Idade , Estudos Prospectivos , Fibrinogênio/análise , Adulto , Estados Unidos/epidemiologia , Idoso , Fatores de RiscoRESUMO
Ferroptosis is a form of cell death that is triggered by the presence of ferrous ions and is characterized by lipid peroxidation induced by these ions. The mechanism exhibits distinct morphological characteristics compared to apoptosis, autophagy, and necrosis. A notable aspect of ferroptosis is its ability to inhibit uncontrolled tumor replication and immortalization, especially in malignant, drug-resistant, and metastatic tumors. Additionally, immunotherapy, a novel therapeutic approach for tumors, has been found to have a reciprocal regulatory relationship with ferroptosis in the context of anti-tumor therapy. A comprehensive analysis of ferroptosis and immunotherapy in tumor therapy is presented in this paper, highlighting the potential for mutual adjuvant effects. Specifically, we discuss the mechanisms underlying ferroptosis and immunotherapy, emphasizing their ability to improve the tumor immune microenvironment and enhance immunotherapeutic effects. Furthermore, we investigate how immunotherapeutic factors may increase the sensitivity of tumor cells to ferroptosis. We aim to provide a prospective view of the promising value of combined ferroptosis and immunotherapy in anticancer therapy by elucidating the mutual regulatory network between each.
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Ferroptose , Imunoterapia , Neoplasias , Microambiente Tumoral , Ferroptose/efeitos dos fármacos , Ferroptose/genética , Humanos , Neoplasias/imunologia , Neoplasias/terapia , Neoplasias/patologia , Neoplasias/tratamento farmacológico , Microambiente Tumoral/imunologia , Microambiente Tumoral/efeitos dos fármacos , Animais , Peroxidação de Lipídeos/efeitos dos fármacosRESUMO
OBJECTIVE: The study aimed to investigate the effects of castration on performance, carcass characteristics, and meat quality in sheep, as well as explore the expression of key genes related to metabolic pathways and muscle growth following castration. METHODS: A meta-analysis approach was utilized to analyze data from multiple studies to compare the performance, carcass characteristics, and meat quality of castrated sheep (wethers) with intact rams. Additionally, protein-protein interaction (PPI) networks, differential gene expression (DEG) interactions, Gene Ontology (GO) terms, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were examined to identify molecular mechanisms associated with fat metabolism and muscle development in sheep tails. RESULTS: The analysis revealed that castrated sheep (wethers) exhibited improved average daily gain, increased tenderness, lower backfat thickness, and a tendency for greater loin muscle area compared to intact rams. This suggests that castration promotes faster growth and results in leaner carcasses with potentially higher muscle content. Furthermore, the identification of downregulated DEGs like ACLY, SLC27A2, and COL1A1 and upregulated DEGs such as HOXA9, PGM2L1, and ABAT provides insights into the molecular mechanisms underlying fat deposition and muscle development in sheep. CONCLUSIONS: The findings support the practice of castration in sheep production as it enhances growth performance, leads to leaner carcasses with higher muscle content, and improves meat tenderness. The identified changes in gene expression offer valuable insights for further research into understanding the impact of castration on muscle development and fat metabolism in sheep. This meta-analysis contributes to the knowledge of molecular mechanisms involved in fat deposition in sheep, opening avenues for future investigations in livestock fat metabolism research.
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We demonstrate that layered violet phosphorus, an emerging 2D semiconductor, undergoes strong anisotropic third-harmonic generation (THG). Polarization dependence of in-plane THG presents a cruciate-flower-shaped curve. Through theoretical modeling of the in-plane THG response, done by considering crystalline symmetry of violet phosphorus, we successfully quantify four non-zero third-order nonlinear optical susceptibility tensor elements. From control experiments, the magnitude of third-order nonlinear optical susceptibility |χ3| is calculated to be about 4.0 × 10-19 m2 V-2, which is comparable to those of conventional 2D layered semiconductors. These results indicate that the layered violet phosphorus can serve as an ideal building block for nonlinear optical applications.
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Creatures in nature make extensive use of structural color adaptive camouflage to survive. Cholesteric liquid crystals, with nanostructures similar to those of natural organisms, can be combined with actuators to produce bright structural colors in response to a wide range of stimuli. Structural colors modulated by nano-helical structures can continuously and selectively reflect specific wavelengths of light, breaking the limit of colors recognizable by the human eye. In this review, the current state of research on cholesteric liquid crystal photonic actuators and their technological applications is presented. First, the basic concepts of cholesteric liquid crystals and their nanostructural modulation are outlined. Then, the cholesteric liquid crystal photonic actuators responding to different stimuli (mechanical, thermal, electrical, light, humidity, magnetic, pneumatic) are presented. This review describes the practical applications of cholesteric liquid crystal photonic actuators and summarizes the prospects for the development of these advanced structures as well as the challenges and their promising applications.
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Background: While clinical research has indicated a potential link between Helicobacter pylori infection and the onset of glaucoma, the causality of this association remains uncertain due to the susceptibility of observational studies to confounding factors and reverse causation. Methods: A comprehensive two-sample bidirectional Mendelian randomization (MR) analysis was conducted to assess the causal connection between H. pylori infection and glaucoma. Glaucoma was categorized into primary open-angle glaucoma (POAG), normal tension glaucoma (NTG), and pseudo-exfoliation glaucoma (PEG). Various methods, including inverse variance weighted, MR-Egger regression, weighted median, and mode-based estimator, were employed for effect estimation and pleiotropy testing. To enhance result robustness, a sensitivity analysis was performed by excluding proxy single nucleotide polymorphisms. Results: Genetic predisposition for H. pylori infection has no causal effect on glaucoma: (OR 1.00; 95% CI 0.95-1.06, p = 0.980), (OR 0.97; 95% CI 0.86-1.09, p = 0.550), and (OR 0.99; 95% CI 0.90-1.08, p = 0.766) with POAG, NTG, and PEG, respectively. An inverse MR showed no causal effect of POAG, NTG, and PEG on H. pylori infection (OR 1.01; 95% CI 0.97-1.05, p = 0.693), (OR 1.00; 95% CI 0.98-1.03, p = 0.804), and (OR 0.99; 95% CI 0.96-1.01, p = 0.363), respectively. Heterogeneity (p > 0.05) and pleiotropy (p > 0.05) analysis confirmed the robustness of MR results. Conclusion: These results indicated that there was no genetic evidence for a causal link between H. pylori and glaucoma, suggesting that the eradication or prevention of H. pylori infection might not benefit glaucoma and vice versa.