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Previous article Next article Non-Parametric Estimation of a Multivariate Probability DensityV. A. EpanechnikovV. A. Epanechnikovhttps://doi.org/10.1137/1114019PDFBibTexSections ToolsAdd to favoritesExport CitationTrack CitationsEmail SectionsAbout[1] Emanuel Parzen, On estimation of a probability density function and mode, Ann. Math. Statist., 33 (1962), 1065–1076 MR0143282 0116.11302 CrossrefGoogle Scholar[2] Murray Rosenblatt, Remarks on some nonparametric estimates of a density function, Ann. Math. Statist., 27 (1956), 832–837 MR0079873 0073.14602 CrossrefGoogle Scholar[3] G. M. Manija, Remarks on non-parametric estimates of a two-dimensional density function, Soobšč. Akad. Nauk Gruzin. SSR, 27 (1961), 385–390 MR0143303 Google Scholar[4] E. A. Nadaraya, Estimation of a bivariate probability density, Soobshch. Akad. Nauk Gruz. SSR, 36 (1964), 267–268 Google Scholar[5] R. E. Bellman, , I. Glicksberg and , O. A. Gross, Some aspects of the mathematical theory of control processes, Rand Corporation, Santa Monica, Calif., Rep. No. R-313, 1958rm xix+244 MR0094281 0086.11703 Google Scholar Previous article Next article FiguresRelatedReferencesCited byDetails Kernel-based learning of birth process from evolving spatiotemporal RFS data stream in SMC CPHD filter for multi-target trackingSignal Processing, Vol. 203 Cross Ref Assessing spatial connectivity effects on daily streamflow forecasting using Bayesian-based graph neural networkScience of The Total Environment, Vol. 855 Cross Ref Joint Source-Channel Decoding of Polar Codes for HEVC-Based Video StreamingACM Transactions on Multimedia Computing, Communications, and Applications, Vol. 18, No. 4 Cross Ref A novel structure adaptive new information priority discrete grey prediction model and its application in renewable energy generation forecastingApplied Energy, Vol. 325 Cross Ref A novel structure adaptive fractional discrete grey forecasting model and its application in China’s crude oil production predictionExpert Systems with Applications, Vol. 207 Cross Ref Age-varying effects of repeated emergency department presentations for children in Canada6 May 2022 | Journal of Health Services Research & Policy, Vol. 27, No. 4 Cross Ref Probabilistic adaptive power pinch analysis for islanded hybrid energy storage systemsJournal of Energy Storage, Vol. 54 Cross Ref Should I stay or should I fly? 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Previous article Next article On the Construction and Comparison of Difference SchemesGilbert StrangGilbert Stranghttps://doi.org/10.1137/0705041PDFBibTexSections ToolsAdd to favoritesExport CitationTrack CitationsEmail SectionsAbout[1] J. Barkley Rosser, A Runge-Kutta for all seasons, SIAM Rev., 9 (1967), 417–452 10.1137/1009069 MR0219242 0243.65041 LinkISIGoogle Scholar[2] Robert D. Richtmyer and , K. W. Morton, Difference methods for initial-value problems, Second edition. Interscience Tracts in Pure and Applied Mathematics, No. 4, Interscience Publishers John Wiley & Sons, Inc., New York-London-Sydney, 1967xiv+405 MR0220455 0155.47502 Google Scholar[3] Peter D. Lax and , Burton Wendroff, Difference schemes for hyperbolic equations with high order of accuracy, Comm. Pure Appl. Math., 17 (1964), 381–398 MR0170484 0233.65050 CrossrefISIGoogle Scholar[4] Samuel Z. 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Previous article Next article Approximate Integration of Stochastic Differential EquationsG. N. Mil'shtejnG. N. Mil'shtejnhttps://doi.org/10.1137/1119062PDFBibTexSections ToolsAdd to favoritesExport CitationTrack CitationsEmail SectionsAbout[1] I. I. Gikhman and , A. V. Skorokhod, Introduction to the Theory of Random Processes, Izd-vo "Nauka", Moscow, 1965, (In Russian.) Google Scholar[2] I. I. Gikhman and , A. V. Skorokhod, Stochastic Differential Equations, Springer, New York, 1972 0242.60003 CrossrefGoogle Scholar[3] R. Z. Khas'minskii, Stability of Systems of Differential Equations under Random Perturbations of their Parameters, Izd-vo "Nauka", Moscow, 1969, (In Russian.) Google Scholar[4] E. Hills and , R. Phillips, Functional Analysis and Semigroups, American Mathematical Society, Providence, RI., 1957 0078.10004 Google Scholar[5] R. L. Stratonovich, Conditional Markov processes and their application to the theory of optimal control, Translated from the Russian by R. N. and N. 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Giant Cell Lesions exhibit variable aggressive clinical behavior. Understanding the molecular mechanisms of these lesions can facilitate a more personalized and effective therapeutic approach. The acetylation of Histone H3 at Lysine 9 (H3K9ac) and the expression of Inhibitor of Growth Protein 5 (ING5) were evaluated in 19 cases of Peripheral Giant Cell Granuloma (PGCG), 19 cases of non-aggressive Central Giant Cell Granuloma (CGCG), 19 cases of aggressive CGCG, and 19 cases of Giant Cell Tumor of Bone (GCTB), totaling 76 cases of Giant Cell Lesions. H3K9 hyperacetylation was found in aggressive Giant Cell Lesions compared to non-aggressive lesions (p&#x2009;<&#x2009;0.05). Aggressive Giant Cell Lesions also show higher ING5 expression in multinucleated giant cells and cannibalistic multinucleated giant cells compared to non-aggressive lesions (p&#x2009;<&#x2009;0.05). There was no difference in the levels of H3K9ac and ING5 between aggressive Central Giant Cell Granuloma and Giant Cell Tumor of Bone (p&#x2009;>&#x2009;0.05). H3K9ac and ING5 were associated with aggressive characteristics in the CGCG (p&#x2009;<&#x2009;0.05). H3K9 hyperacetylation highlights the significance of this epigenetic event in the aggressiveness of Giant Cell Lesions and may indicate their potential for aggressive behavior, thereby providing information to improve treatment strategies, particularly for Central Giant Cell Granuloma. Understanding the CGCG's clinical behavior is essential for determining the therapeutic modality and avoiding long-term post-treatment sequelae.

We sought to characterize the genomic landscape of gastroesophageal adenocarcinoma (GEA) using next-generation sequencing (NGS) of circulating cell-free DNA (cfDNA), compare the genomic profile to tissue NGS, and determine the association of circulating tumor DNA (ctDNA) detection with clinical outcomes. In this prospective biospecimen-collection study (2017-2022), cfDNA was analyzed using a clinically validated 129-gene tumor-informed NGS assay Memorial Sloan Kettering-Analysis of Circulating cfDNA to Evaluate Somatic Status (MSK-ACCESS); tissue-NGS was performed using Memorial Sloan Kettering-Integrated Mutation Profiling of Actionable Cancer Targets. In total, 169 patients with GEA underwent baseline molecular profiling of cfDNA; 93 had localized disease, 55 had untreated metastatic disease, and 21 had progressive metastatic disease. The frequency of the most common alterations was similar between platforms, although copy-number alterations were detected less frequently in plasma than in tissue (10% v 40%; P < .001). Matched-tumor NGS was conducted in 154 patients (91%). Baseline ctDNA detection and on-treatment clearance were associated with improved overall survival and recurrence-free survival in patients with localized disease and progression-free survival in patients with metastatic disease. Baseline ctDNA detection was a stronger predictor of overall survival than American Joint Committee on Cancer (AJCC) clinical stage and positively predicted lymph node metastasis in 87% of cases. Trends in variant allele fractions correlated with pathologic responses to neoadjuvant therapy more closely than fluorodeoxyglucose-positron emission tomography standard uptake values. Persistence or resurgence of ctDNA was associated with worse survival and forecasted recurrent disease a median of 7 months sooner than imaging. cfDNA analysis using MSK-ACCESS in patients with GEA is a valuable adjunctive clinical tool that enhances molecular profiling, prognostication, treatment response assessment, and detection of recurrent disease in conjunction with tissue NGS, imaging, and AJCC clinical staging criteria.

Programmed death-ligand 1 (PD-L1) expression is routinely used to guide immune checkpoint inhibitor (ICI) therapy in advanced non-small cell lung cancer (NSCLC), yet clinical benefit remains heterogeneous even among PD-L1-high tumors. Liquid biopsy based on cell-free DNA (cfDNA) enables minimally invasive, real-time monitoring of tumor evolution. We report four cases of metastatic lung adenocarcinoma treated with atezolizumab, integrating longitudinal whole-exome sequencing (WES) of cfDNA with radiological assessment. Four patients with PD-L1-positive (&#x2265;60%) metastatic NSCLC received atezolizumab monotherapy. Serial cfDNA samples (1-3 per patient) were analyzed by high-depth WES. Distinct molecular trajectories paralleled divergent clinical outcomes. One patient achieved a complete molecular response, characterized by progressive clearance of KRAS, ATM, and NF1 mutant clones, which was concordant with radiological remission. A second patient showed an initial molecular response, followed by clonal rebound of TP53, NF1, and NOTCH2 mutant populations and the emergence of PTEN and KIF1A variants, suggesting clinical progression. Two patients exhibited primary resistance despite high PD-L1 expression, with persistent or expanding clones and early subclonal diversification; in one case, new EGFR and BRAF alterations emerged under treatment pressure. Notably, switching to platinum-based chemotherapy in a non-responder induced a measurable molecular response, highlighting discordance between PD-L1 status and immunotherapy efficacy. Longitudinal cfDNA WES captured dynamic clonal remodeling under immunotherapy and anticipated radiological outcomes. These findings underscore the clinical necessity of integrating dynamic molecular monitoring by liquid biopsy to overcome the limitations of static PD-L1 assessment, refine therapeutic stratification, and identify early resistance mechanisms in advanced NSCLC.

Omics' technologies have enabled clinicians to gain previously unprecedented insights into the molecular complexity and clinical heterogeneity of triple-negative breast cancer (TNBC). Increasingly it is being realized that TNBC does not respond well to current targeted therapies. This study aims to explore the antiproliferative effects and cancer regulatory mechanisms which underlie the drug resistance and aggressiveness of TNBC cells. Cryptocaryone (CPC) derived from Cryptocarya concinna demonstrated antiproliferative responses to TNBC cells (HCC1937 and MDA-MB-231), while normal breast cells (H184B5F5/M10) exhibited low cytotoxicity. In an in vivo assessment, CPC effectively reduced tumor growth in the MDA-MB-231 xenografted mouse model without significantly affecting body weight. Mechanistically, CPC triggered apoptosis, as indicated by an increase in sub-G1 and annexin V, as well as activated caspase 3 and 8. CPC also induced substantial oxidative stress by generating reactive oxygen species, mitochondrial superoxide, and membrane depolarization. CPC also induced oxidative DNA damage, as evidenced by the presence of &#x3b3;H2AX and 8-hydroxy-2-deoxyguanosine, in TNBC cells. All these CPC-induced changes were more pronounced in TNBC cells than normal cells. JNK and p38 MAPK inhibitors attenuate CPC-induced antiproliferation in TNBC cells. CPC upregulates phosphorylated JNK and p38 in TNBC cells. N-acetylcysteine pretreatment confirmed that oxidative stress plays a vital role in enhancing the antiproliferation, apoptosis, and DNA damage in TNBC cells. Moreover, the CPC-upregulated apoptosis and caspase 3/8 activations in TNBC cells were inhibited by JNK and p38 inhibitors. The impact of ERK activation on antiproliferation and apoptosis was evident in MDA-MB-231 cells, but not in HCC1937 cells. In conclusion, CPC demonstrated antiproliferative effects on TNBC cells through apoptosis and DNA damage induced by oxidative stress and MAPK activation, while showing drug safety in normal cells and breast cancer mouse model.

The polarization of naive CD4+ T cells into Th2 cells is initiated in lymphoid organs and completed as the cells become tissue resident, where they express ST2, the receptor for the alarmin interleukin (IL)-33, which may be a key signal for tissue integration. Cellular metabolic requirements associated with this transition remain poorly understood. To address this, we compared the response of lymphoid tissue (LT) Th2 cells from helminth parasite-infected mice to stimulation by IL-33 versus through the T cell receptor via anti-CD3/CD28. We found that IL-33, but not anti-CD3/CD28, induced the development of tissue-resident like Th2 cells expressing ST2. This was associated with IL-33 induced changes in arginine metabolism linked to mTORC1 activation and polyamine synthesis, which were required for the development of tissue-resident like Th2 cells. Furthermore, IL-33 induced transcriptional changes in genes involved in chemotaxis and cell adhesion that may be critical for tissue integration. Our findings provide insights into adaptations of Th2 cells responding to tissue-integration cues and more broadly support the view that IL-33 promotes the expression of the transcriptional program associated with tissue residency of GATA3-expressing cells in adipose and possibly other tissues.

The metabolic enzyme lactate dehydrogenase C4 (LDHC4) is aberrantly expressed in cancers and linked to poor prognosis. However, its role in lung adenocarcinoma (LUAD) and the molecular mechanisms beyond glycolysis remain unclear. This study investigates whether LDHC4 promotes LUAD by modulating protein lactylation, a lactate-derived post-translational modification, focusing on the tumor suppressor retinoblastoma protein (RB1). LDHC4 expression and its correlation with clinicopathological features and survival were analyzed using public databases (UALCAN, Kaplan-Meier Plotter, LOGpc) and validated in a cohort of 90 paired LUAD tissues via immunohistochemistry. The functional impact of LDHC4 on proliferation, migration, and invasion was assessed in A549 and PC-9 cells using gain- and loss-of-function models. The global lactylation profile was analyzed using DIA-based lactylation proteomics on the Astral platform. The interaction between RB1 and E2F1 (E2F transcription factor 1) was examined through molecular dynamics simulations, co-immunoprecipitation (Co-IP), and immunofluorescence. The functional consequences of site-specific RB1 lactylation at lysine 900 (RB1-K900lac) were determined using RB1-K900R mutant constructs and cell cycle analysis. LDHC4 was significantly overexpressed in LUAD tissues, correlating with poor patient survival, and was an independent prognostic risk factor. In vitro, LDHC4 promoted LUAD cell proliferation, migration, and invasion, and its tumor-promoting role was corroborated in an LUAD xenograft model, in which derived tumors exhibited increased volume and weight compared with mock-transfected controls. Mechanistically, LDHC4 overexpression elevated global protein lactylation levels and specifically increased lactylation of RB1. Bioinformatics and molecular dynamics simulations identified K900 as a key conserved residue for RB1-E2F1 binding; its lactylation destabilized the complex by increasing structural fluctuation and weakening intermolecular interactions. Cellular experiments confirmed that the lactylation-resistant RB1-K900R mutant bound E2F1 more strongly than wild-type RB1. Functionally, cells expressing RB1-K900R exhibited suppressed malignant phenotypes and G1/S cell cycle arrest, accompanied by downregulation of CDKs/cyclins and upregulation of P21. This study uncovers a novel LDHC4-driven oncogenic axis in LUAD. LDHC4 facilitates RB1 lactylation at the K900 residue, which disrupts the RB1-E2F1 tumor-suppressive complex, leading to cell cycle dysregulation and tumor progression. These findings may position the "LDHC4-RB1 lactylation" axis as a promising therapeutic target for LUAD.

Carbohydrate Response Element Binding Protein (ChREBP) is a transcription factor known to regulate glucose metabolism and other metabolic processes in various tissues, but its role in lung adenocarcinoma (LUAD) remains poorly understood. In this study, we investigated ChREBP expression and its role in regulating gene expression in LUAD cell lines. Using RT-qPCR, we assessed the expression of ChREBP-&#x3b1; and ChREBP-&#x3b2; isoforms in NCI-H1975, NCI-H1650, and NCI-H2228 LUAD cell lines. The NCI-H1975 cells exhibited the highest levels of both ChREBP isoforms, with a particularly pronounced expression of ChREBP-&#x3b2;. To explore the regulatory role of ChREBP, we generated NCI-H1975 cells with inducible expression of a dominant-negative mutant of human ChREBP (dnChREBP). Overexpression of dnChREBP led to a significant reduction in colony formation and impaired cell migration. Transcriptome analysis revealed 57 upregulated genes and 593 downregulated genes in dnChREBP-expressing cells compared to control cells. Functional annotation and gene set enrichment analysis revealed that the enriched genes were associated with cancer-related processes, including cell proliferation and epithelial-to-mesenchymal transition (EMT). Gene network analysis highlighted 17 downregulated hub genes, with 8 of these genes being associated with EMT. Interestingly, ChREBP and its transcriptionally regulated genes, including 4 top downregulated genes, 5 top upregulated genes, and 5 hub genes identified in NCI-H1975 cells overexpressing dnChREBP, showed significant prognostic value, as their expression levels correlated with overall survival in LUAD patients. Our findings suggest that ChREBP regulates distinct transcriptional programs in LUAD cells and ChREBP and its regulatory network may play a potential role in LUAD progression and patient outcomes.

The high heterogeneity of lung adenocarcinoma (LUAD) is largely due to its complex tumor immune microenvironment (TIME). Cancer-associated fibroblasts (CAFs) are a core matrix component of TIME. However, their functional heterogeneity and the specific molecular mechanisms driving tumor progression have not been fully elucidated. In addition, the role of nuclear receptor NR2F2 in tumor development is still controversial. This study integrated scRNA-seq data from the GEO database with RNA-seq data from TCGA and GEO and then performed multiple levels of validation through in vitro experiments. We adopted a systematic computational biology strategy and analyzed the cellular composition, interaction networks and functional states of cancer-associated fibroblasts (CAFs) in lung adenocarcinoma using Seurat, CellChat, and AUCell. According to the marker genes of key CAF subgroup, prognostic risk models were constructed through LASSO-Cox regression and validated in an independent cohort (GSE72094). Afterwards, we carried out in vitro experiments and validated the biological role of NR2F2 through a coculture system. Functional validation was conducted through siRNA knockdown, plasmid overexpression, CCK-8 assay, EdU labeling, and Transwell experiments. We noticed the CAF - 2 subgroup, characterized by the highest level of TGF - &#x3b2; signaling activation, sends various signals to different cell types. We constructed and verified a consistent prognostic signature made of 16 genes using the LASSO-Cox method. This model can effectively assess the risk of LUAD patients. The prognosis in high-risk group is worse. And we also do some analysis to find out that risk score is highly associated with immunosuppressive TME and high expressions of PD - L1. We have found in our further study that the expression of NR2F2 in CAF is associated with the promoting of matrix remodeling and metabolic reprogramming. From the coculture system and in vitro functional experiments, overexpression of NR2F2 in CAFs enhanced tumor cell proliferation and invasion, whereas knockdown of NR2F2 attenuated these malignant phenotypes. Using single-cell RNA sequencing data, we identified a CAF subgroup with the most active TGF-&#x3b2; signaling. Based on the marker genes of the subgroup, we constructed and validated an effective prognostic model, then we further screened and confirmed NR2F2 as a major pro-tumorigenic regulator from this feature gene set through single cell and transcriptome data as well as in&#xa0;vitro experiments. NR2F2 promotes malignant remodeling of TIME by synergistically enhancing TGF-&#x3b2; signaling and EMT processes. Our study provides not only a solid theoretical foundation but also a therapeutic target to explore new therapeutic options targeting the CAFs-TGF-&#x3b2;-EMT axis.

The rising incidence and mortality of lung adenocarcinoma (LUAD) present a significant public health challenge. Histidine, an essential amino acid, plays a pivotal role in metabolic processes, yet its specific contribution to LUAD pathogenesis remains to be elucidated. This study obtained bulk and single-cell RNA sequencing (scRNA-seq) data for LUAD from UCSC Xena and Code Ocean platforms, respectively. By integrating differential expression analysis, univariate/multivariate Cox analysis, and LASSO regression analysis, prognostic genes for LUAD were identified, and a prognostic risk model was constructed. Algorithms including ESTIMATE, ssGSEA, and CIBERSORT were employed to investigate immune heterogeneity across different groups. Furthermore, molecular subtypes of LUAD were identified through consensus clustering. This study, through the integration of bulk and scRNA-seq data, identified epithelial cells as the key effector cell population in LUAD, which can be further subdivided into four functionally heterogeneous subpopulations. Seven histidine metabolism-related epithelial cell-specific genes with prognostic significance in LUAD were identified (WIF1, GATA2, CD69, ID1, C4BPA, WFDC2, and CCL20), enabling the construction of a robust prognostic risk model. Immune infiltration analysis revealed that low-risk patients exhibited more robust immune infiltration and activity. Furthermore, cross-cancer exploratory evidence suggested potential sensitivity to CTLA-4 and PD-L1 inhibitors in this group. Furthermore, consensus clustering analysis successfully partitioned LUAD into two molecular subtypes exhibiting immune heterogeneity. The prognostic model constructed based on epithelial cell-specific genes associated with histidine metabolism effectively distinguishes LUAD patients and their immune characteristics, revealing epithelial cells as a key cell population regulating LUAD histidine metabolism. This study identified seven epithelial cell-specific genes associated with histidine metabolism (WIF1, GATA2, CD69, ID1, C4BPA, WFDC2, and CCL20) related to the prognosis of LUAD, and based on this, a robust prognostic risk model for LUAD was constructed.Based on seven epithelial cell-specific genes associated with histidine metabolism, this study successfully classified LUAD into two different molecular subtypes, and significant immune heterogeneity was exhibited among the subtypes.Epithelial cells are the key effector cell population in LUAD and can be further divided into four subpopulations with distinct functions.

In head and neck squamous cell carcinoma (HNSCC), immunotherapy response rates remain modest, with difficulty predicting responders. Previous studies characterizing immunotherapy-associated cellular changes in HNSCC focus on immune cells, providing limited insight into malignant cell responses. Here, we perform single-cell RNA sequencing (RNA-seq) on 16 HNSCC patients pre- and post-neoadjuvant pembrolizumab treatment. We identify an interferon (IFN)/major histocompatibility complex class II (MHC-II) expression program in malignant cells, characterized by MHC-II and IFN-response genes, which is associated with response to pembrolizumab. We validate malignant cell MHC-II expression at the protein level via multiplexed immunofluorescence. In a murine HNSCC model, IFN-&#x3b3;-induced malignant cell MHC-II expression marks immunotherapy-sensitive tumors with favorable immune microenvironments. Finally, we confirm that pre-treatment malignant-IFN/MHC-II is a marker of response through deconvolution of bulk RNA-seq data from an independent cohort. Beyond identifying the malignant IFN/MHC-II program as a potential biomarker for immunotherapy response in HNSCC, our work elucidates the important role of malignant cells in immunotherapy.

Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease, is one of the most prevalent liver diseases globally, contributing to both economic and health-related challenges. We aimed to evaluate the global, regional, and national burden of MASLD from 1990 to 2023, quantify the contribution of identified modifiable risk factors, and project future prevalence up to the year 2050. Estimates of MASLD prevalence and disability-adjusted life-years (DALYs) were produced by age, sex, region, Socio-demographic Index (SDI), and Healthcare Access and Quality (HAQ) index across 204 countries and territories from 1990 to 2023 as part of the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2023. The MASLD burden attributable to three risk factors (smoking, high BMI, and high fasting plasma glucose) was assessed as part of the GBD comparative risk assessment. As a secondary analysis, we used these estimates to forecast MASLD prevalence up to 2050 using fasting plasma glucose and mean BMI as predictors. Furthermore, to examine the relative contributions of population ageing, population growth, and changes in MASLD prevalence rate to the forecasted changes in case counts from 2023 to 2050, we conducted a decomposition analysis. In 2023, approximately 1&#xb7;3 billion (95% uncertainty interval [UI] 1&#xb7;2 to 1&#xb7;4) individuals were estimated to be living with MASLD (ie, 16&#xb7;1% of the global population), with an age-standardised prevalence rate of 14&#x2009;429&#xb7;3 (95% UI 13&#x2009;268&#xb7;3 to 15&#x2009;990&#xb7;6) per 100&#x2009;000 population, representing a percentage increase of 142&#xb7;7% (95% UI 139&#xb7;2 to 146&#xb7;7) in crude numbers from 1990 (0&#xb7;5 billion [0&#xb7;5 to 0&#xb7;6]) and of 28&#xb7;6% (27&#xb7;8 to 29&#xb7;5) in the rate (11&#x2009;217&#xb7;2 [10&#x2009;276&#xb7;8 to 12&#x2009;467&#xb7;0] per 100&#x2009;000 in 1990). An estimated 3&#xb7;6 million (2&#xb7;8 to 4&#xb7;5) total DALYs were attributable to MASLD worldwide in 2023, corresponding to an age-standardised DALY rate of 39&#xb7;6 (31&#xb7;2 to 49&#xb7;9) per 100&#x2009;000 population. Despite a 116&#xb7;3% (93&#xb7;3 to 139&#xb7;4) increase in crude DALYs (from 1&#xb7;7 million [1&#xb7;3 to 2&#xb7;1] in 1990), its age-standardised estimate remained consistent (1&#xb7;8% [-8&#xb7;6 to 12&#xb7;8]) from 1990 (38&#xb7;9 [30&#xb7;1 to 49&#xb7;8] per 100&#x2009;000) to 2023. There was substantial variation in age-standardised estimates across regions. North Africa and the Middle East had the highest prevalence rate (29&#x2009;246&#xb7;1 [26&#x2009;848&#xb7;3 to 32&#x2009;048&#xb7;7] per 100&#x2009;000) and Andean Latin America showed the highest DALY rate (152&#xb7;3 [114&#xb7;1 to 194&#xb7;7] per 100&#x2009;000). By contrast, the high-income Asia Pacific region had the lowest prevalence rate (8653&#xb7;5 [7923&#xb7;7 to 9592&#xb7;8] per 100&#x2009;000) and east Asia had the lowest DALY rate (16&#xb7;3 [13&#xb7;5 to 19&#xb7;9] per 100&#x2009;000) among all GBD regions. North Africa and the Middle East showed disproportionately higher prevalence rates relative to other regions with similar SDIs. Lower SDIs and HAQs were associated with higher age-standardised DALY rates. The age-standardised prevalence rate was consistently higher in males (15&#x2009;616&#xb7;4 [14&#x2009;349&#xb7;2 to 17&#x2009;263&#xb7;3] per 100&#x2009;000 people in 2023) than in females (13&#x2009;245&#xb7;2 [12&#x2009;132&#xb7;0 to 14&#x2009;692&#xb7;6] per 100&#x2009;000 people), and peaked at age 80-84 years in both sexes. The number of MASLD prevalent cases was the highest in younger adults, peaking at age 35-39 years for males and age 55-59 years for females. Among the risk factors for MASLD, high fasting plasma glucose presented the largest contribution to the age-standardised DALY rate of total MASLD in 2023 (2&#xb7;2 [95% UI 1&#xb7;6 to 3&#xb7;1] per 100&#x2009;000 people), followed by high BMI (1&#xb7;4 [0&#xb7;6 to 2&#xb7;4] per 100&#x2009;000 people) and smoking (1&#xb7;0 [0&#xb7;3 to 1&#xb7;8] per 100&#x2009;000 people). Our forecasting model estimates that 1&#xb7;8 billion (95% UI 1&#xb7;6 to 2&#xb7;0) individuals are likely to have MASLD by 2050, representing a 42&#xb7;0% increase from 2023. The age-standardised prevalence rate is expected to increase to 15&#x2009;774&#xb7;9 (95% UI 14&#x2009;613&#xb7;9 to 17&#x2009;336&#xb7;2) per 100&#x2009;000 people in 2050, representing an average annual percentage change of 0&#xb7;3% (95% UI 0&#xb7;3-0&#xb7;3). According to our decomposition analysis, this change will be primarily due to population growth, particularly in sub-Saharan Africa and North Africa and Middle East, and less by population ageing or epidemiological change. With a global prevalence of 16&#xb7;1% and approximately 1&#xb7;3 billion people already living with MASLD in 2023, the condition has and will continue to have substantial health and economic impacts worldwide. An inverse association between the HAQ Index and age-standardised DALY rates suggests that countries with lower health-care access and quality might be less well positioned to manage the growing MASLD burden, underscoring the need for strengthened health-system capacity in these settings. Gates Foundation.

Pyroptosis is an inflammatory programmed cell death process closely related to reactive oxygen species (ROS), in which hydrogen peroxide (H2O2) is considered to play a significant role. However, the specific stage at which H2O2 changes and whether it serves as the predominant ROS during pyroptosis remain unclear, hindering a deeper understanding of the underlying mechanism. In this study, a near-infrared fluorescence probe (DXM-CHO-B) with a high fluorescence quantum yield and large Stokes shift was obtained by molecular modification. DXM-CHO-B exhibited excellent specificity and high sensitivity to H2O2, featuring a wide linear range (50 nM-92 &#x3bc;M), a low detection limit (39 nM), and the ability to perform real-time H2O2 tracking in both cell and zebrafish models. DXM-CHO-B also maintained a high selectivity for H2O2 in cells, and the accuracy of the high selectivity was verified. Based on the excellent detection performance of DXM-CHO-B, the pyroptosis process of cells was monitored. The experimental results revealed that H2O2 was overexpressed during pyroptosis, and its amount undergoes significant changes in the early stage of pyroptosis. This conclusion was further supported by scanning electron microscopy imaging, lactate dehydrogenase release testing, and propidium iodide staining staining assays of pyroptosis cells at different time points. More importantly, further research has shown that the majority of ROS produced during pyroptosis were H2O2. These findings established H2O2 as the core mediator of pyroptosis, providing insights into its molecular mechanism and potential therapeutic strategies for enhancing tumor immunotherapy.

Current spatial T cell receptor (TCR) profiling approaches lack the resolution needed to link clonal identity, transcriptional state, and spatial positioning of individual T cells in the tumor microenvironment. Here, we introduce a spatial TCR profiling strategy that resolves individual T cell clones together with their transcriptional states at single-cell resolution and applied the method to human head and neck squamous cell carcinoma. Presumed tumor-specific T cells were broadly dispersed throughout the tumor microenvironment, and cells of the same clone occupied distinct transcriptional states in different locations: Immune-rich regions contained more plastic or progenitor cells, whereas tumor-dense regions were enriched for exhausted states. Patients exhibited notably different spatial architectures of antitumor T cell responses, revealing variation that was not captured by high-resolution, spatially agnostic methods such as spectral flow cytometry and single-cell RNA sequencing. These results provide a blueprint for dissecting antigen-specific T cell states in human tumors and reveal how T cell states are spatially coordinated with local cues across the tumor microenvironment.

Despite the growing interest in cell- and exosome-based therapies for neurological diseases including Alzheimer's disease (AD), there is still a gap in the investigation of more effective treatments in terms of efficacy, safety, and durability of effect. This study aimed to compare the therapeutic potential of astrocyte cells and their derived exosomes (AS-Exos) in restoring cognitive function in a mouse model of AD. AD model was induced by bilateral electrical lesioning of the nucleus basalis of Meynert (NBM). Astrocytes were isolated from neonatal rat brains, and AS-Exos were harvested from astrocyte-conditioned media using an AnaCell extraction kit. Seven days after lesion induction, astrocytes and AS-Exos were stereotaxically injected into the NBM. Four weeks later, behavioral assessments (passive avoidance and locomotor activity), electrophysiological recordings (EEG), and biochemical measurements of hippocampal brain-derived neurotrophic factor (BDNF) and acetylcholine (ACh) levels were performed. AS-Exos were confirmed as cup-shaped vesicles (30-150&#x202f;nm) expressing the exosomal surface markers CD9, CD63, and CD81. NBM lesions significantly reduced step-through latency (STL), hippocampal BDNF and ACh levels, and disrupted EEG oscillatory patterns. Treatment with AS-Exos markedly improved STL and produced greater increases in hippocampal BDNF and ACh levels compared with AD and AD+saline groups. EEG analysis also revealed enhanced beta, alpha, and gamma power, with the most robust normalization observed in the AS-Exos group. AS-Exos demonstrated superior biochemical and electrophysiological benefits compared with astrocyte transplantation and provided equal or greater improvement in behavioral outcomes. These findings highlight AS-Exos as a promising cell-free therapeutic strategy for alleviating cognitive deficits associated with AD.

Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease for which novel therapeutic approaches are urgently needed. Transforming Growth Factor-&#x3b2; (TGF-&#x3b2;) plays a central role in IPF pathogenesis by activating lung fibroblasts. Inhibitor of DNA binding (ID) proteins are regulated by TGF-&#x3b2;; however, their role in IPF remains poorly understood. We aimed to evaluate the regulation of ID proteins in IPF and to determine their functional role in human lung fibroblasts (HLF) in vitro and pulmonary fibrosis in vivo. ID protein expression was assessed in lungs and lung fibroblasts from mice and patients with pulmonary fibrosis. In vitro, the effects of ID1/ID3 inhibition and overexpression on HLF proliferation, migration and differentiation into myofibroblasts were evaluated. Genetic and pharmacological approaches were used in vivo to determine the role of ID1/ID3 in pulmonary fibrosis. ID1/ID3 levels were elevated in lungs and lung fibroblasts from mice and patients with pulmonary fibrosis, as well as in HLFs treated with TGF-&#x3b2;. ID1/ID3 knockdown reduced proliferation, migration and differentiation of healthy and IPF-derived HLFs. Bleomycin-exposed ID1/ID3 double KO mice exhibited improved lung function and reduced fibrosis compared with WT mice. Pharmacological inhibition of ID1/ID3 decreased HLF proliferation, migration and differentiation in vitro and attenuated pulmonary fibrosis in vivo. Lung-specific inhibition of ID1/ID3 using adeno-associated viruses expressing short hairpins targeting ID1 and ID3 also reversed pulmonary fibrosis in mice. Mechanistically, ID1/ID3 inhibition reduced fibroblast proliferation through regulation of cell cycle genes and attenuated fibroblast differentiation via the MEK/ERK pathway. Simultaneous inhibition of ID1 and ID3 attenuates pulmonary fibrosis. Targeting ID1/ID3 represents a potential novel therapeutic strategy for IPF.

Oral squamous cell carcinoma (OSCC) is marked by frequent recurrence rates and an unclear etiology, underscoring the critical need for early detection to improve therapeutic outcomes and reduce healthcare costs. MicroRNAs (miRNAs) have emerged as key regulators of oral carcinogenesis by modulating gene expression at the posttranscriptional level and influencing various aspects of cellular physiology. This study aimed to comprehensively evaluate the prognostic significance of miR-1304 and miR-4652 expression levels in patients with OSCC, and to explore their potential as predictive biomarkers for disease progression and patient survival. TargetScan was used to predict potential gene interactions of the microRNAs. Subsequently, the expression levels of C-Myc and the microRNAs miR-1304-3p and miR-4652-5p were evaluated in 30 pairs of OSCC and adjacent normal tissue samples. qRT-PCR analyses were performed to compare the expression of these molecules between tumor and normal tissues. Additionally, receiver operating characteristic (ROC) curves were generated to assess the potential diagnostic value of these microRNAs in OSCC. The expression levels of miR-1304, miR-4652, and C-Myc were significantly higher in OSCC tissues compared to their matched adjacent non-tumor tissues (p&#x2009;<&#x2009;0.0001). Notably, high C-Myc expression was significantly correlated with both tumor grade (p&#x2009;=&#x2009;0.003) and tumor stage (p&#x2009;=&#x2009;0.005). ROC curve analysis demonstrated that the areas under the curve (AUCs) for C-Myc, hsa-miR-1304, and hsa-miR-4652 were 0.99, 0.99, and 0.95, respectively (p&#x2009;<&#x2009;0.0001), indicating strong diagnostic potential. These findings suggest that the upregulation of miR-1304 and miR-4652 could be used as biomarkers in OSCC. However, more studies with large samples are necessary.