Search Results (776)

Land surface temperature (LST) is a key variable in the physics of land surface processes on both regional and global scales. This paper addresses the all-sky (clear-sky and cloudy-sky) LSTs retrieval from the data acquired by the Medium-Resolution Spectral Imager II on Fengyun 3D (FY-3D) satellite. First, an improved split-window algorithm to retrieve clear-sky LSTs is developed using numerical radiative transfer modeling experiments. Then, clear-sky LSTs are retrieved from MERSI-II/FY-3D data in January and July 2022 over an Asian area (70°E~130°E, 10°N~50°N), and cross-validated against MODIS/Aqua LST/emissivity (LST/E) Daily version 6 (MYD11C1 V6) product. Next, a hybrid method combining the eXtreme Gradient Boosting (XGBoost) model and the surface energy balance theory is developed to estimate cloudy-sky LSTs. After that, cloudy-sky LSTs are estimated from the MERSI-II data and validated with the China Meteorological Administration Land Data Assimilation System Version 2 (CLDAS V2) dataset. Against the MYD11C1 LSTs, the root mean square error (RMSE), bias and coefficient of determination (R²) of the retrieved clear-sky LSTs are 1.15 K, 0.01 ± 1.14 K, and 0.99, respectively. Against the CLDAS LSTs, the RMSE, bias and R² of the estimated hypothetical clear-sky LSTs are 4.05 K, 0.75 ± 3.98 K and 0.91, respectively, while they are 3.69 K, 0.36 ± 3.67 K, and 0.92 for the retrieved cloudy-sky LSTs, respectively, which indicates that the retrieval accuracy of cloudy-sky LSTs is improved after the cloud radiation effect correction. The all-sky LSTs retrieved in this study are accurate and consistent with the results in previous studies. Full article

Waldenström macroglobulinemia is a rare lymphoplasmacytic malignancy characterized by bone marrow infiltration and monoclonal immunoglobulin M production. Despite its indolent clinical course, the disease exhibits considerable biological complexity driven by recurrent genetic alterations, dysregulated signaling pathways, and a supportive bone marrow microenvironment. The identification of MYD88 and CXCR4 mutations has significantly advanced understanding of disease pathogenesis, clonal evolution, and treatment response. Additional insights from cytogenetic, epigenetic, and microRNA studies have further refined the molecular landscape of this disorder. These advances have translated into improved therapeutic strategies, particularly with the introduction of Bruton’s tyrosine kinase inhibitors, although treatment resistance remains a clinical challenge. Other targeted approaches, including BCL2 and proteasome inhibition, offer additional options for personalized therapy. Ongoing integration of molecular and microenvironmental data is expected to enhance risk stratification and support the development of more effective, tailored treatment strategies. Full article

Background/Objectives: As important post-transcriptional and epigenetic regulators of gene expression, miRNAs play a pivotal role in modulating host–virus interactions. While prior reviews have addressed either direct miRNA–HIV genome interactions or miRNA-mediated immune modulation in isolation, the integrated dual functionality of these molecules has not been systematically characterized. This review aimed to comprehensively explore how miRNAs that target the HIV-1 genome simultaneously modulate key innate and adaptive host immune signaling pathways. The conceptual novelty of this study is determined not by the identification of previously unknown miRNA-target gene pairs, but by the systemic integration of two regulatory levels (direct inhibition of the viral genome and modulation of the host cell immune signaling pathways) within a unified analytical framework. Such an integrated approach reveals a proviral regulatory network that remains non-obvious when each of these levels is examined separately. Methods: A narrative review was conducted using PubMed, Scopus, Web of Science, and Google Scholar (all years through 2025). In Stage 1, publications reporting experimentally confirmed interactions between host miRNAs and the HIV-1 genome were identified, yielding a curated set of 15 miRNAs. In Stage 2, target genes for each miRNA were retrieved from miRTarBase, TarBase (experimentally validated) and TargetScan 8.0 (in silico predicted). In Stage 3, target genes were manually mapped to key immune signaling pathways (TLR, NF-κB, JAK-STAT). In Stage 4, targeted literature searches were performed for each miRNA–target gene pair to identify direct experimental evidence of interaction. All stages were performed by two independent researchers, with discrepancies resolved by a third. Results: Fifteen host miRNAs with experimentally confirmed binding to the HIV-1 genome were identified, targeting viral genes including nef, pol, vpr, gag, env, vif, and the 3′-UTR. Thirteen of these miRNAs were found to regulate components of major immune pathways. miR-92a-3p, miR-29a/b-3p, miR-150-5p, and miR-125b-5p emerged as the most pleiotropic regulators, simultaneously suppressing TLR signaling (TLR3, TLR7, TLR8, MyD88, TRAF3/6, IRAK1/4), NF-κB components (REL, RELA, NFKB1), JAK-STAT effectors (STAT1–3, STAT5A/B, JAK2), and negative regulators of cytokine signaling (SOCS and PIAS family proteins). miR-133b and miR-196b-5p were found to selectively regulate SOCS/PIAS proteins without involvement in other analyzed pathways, suggesting potential for selective therapeutic targeting. Conclusions: The analyzed miRNAs exhibit functional dualism, acting as direct post-transcriptional suppressors of the HIV-1 genome while simultaneously functioning as epigenetic modulators of host immune signaling. These two modes of action are not independent but together form a conceptual framework of a self-reinforcing proviral regulatory network that, based on the synthesis of published evidence, is proposed to promote viral latency and immune evasion. The identified miRNAs represent promising, albeit complex, targets for novel therapeutic strategies aimed at eliminating latent HIV reservoirs. Full article

In ulcerative colitis (UC), the therapeutic efficacy of nanoparticle (NP)-based drug delivery systems is limited by premature drug release, uptake or degradation of NPs during their passage through the harsh gastrointestinal tract (GIT) environment, poor colon targeting, and rapid NP clearance caused by diarrhea symptoms. This study focused on designing an advanced spatiotemporally controlled nanohybrid hydrogel drug delivery system to overcome these challenges. We developed a pH- and temperature-responsive polysaccharide-based hydrogel composed of chitosan (CS), β-glycerol phosphate disodium salt pentahydrate (GP), hydroxypropyl cellulose (HPC), and collagen type I (Col I), designated as CS/HHPC/Col I-GP. The hydrogel exhibited a dense and uniform porous reticular structure, with an average pore diameter of 127.45 ± 2.22 μm. The equilibrium swelling ratio of the CS/HHPC/Col I-GP was determined to be 32.10 ± 1.11 g/g, indicating excellent swelling capacity and sustained structural stability over 6 h—making it suitable for sustained drug release in the intestinal tract. Then, the prepared curcumin nanoparticles (CurNPs) were encapsulated into the CS/HHPC/Col I-GP hydrogel to form the CS/HHPC/Col I-GP-CurNPs composite. The polysaccharide-based hydrogel shell of the formulation withstood harsh gastrointestinal conditions, enabled targeted adhesion to the colon, and was specifically degraded by colonic enzymes. The CurNPs released in the colon benefit from their negatively charged characteristics, enabling accumulation at the positively charged inflamed sites and achieving sustained Cur release. The results of the gastrointestinal digestion simulation experiment showed that the cumulative release of CS/HHPC/Col I-GP-CurNPs was only 12.33 ± 2.17% in simulated gastric fluid (SGF) and reached 96.91 ± 1.98% in simulated colonic fluid (SCF) after 60 h. Cell and animal experimental data confirmed that the formulation significantly alleviated colitis symptoms by modulating the repolarization of pro-inflammatory M1 macrophages to anti-inflammatory M2 phenotypes and deactivating the TLR4/MyD88/NF-κB pathway. Furthermore, the integrity of the intestinal mucosal barrier and the gut microbiota were enhanced. This study provides a promising strategy for the oral drug treatment of UC. Full article

Objective: The present study investigates the effect of 1,8-cineole on improving lipid metabolism disorder by regulating oxidative stress and inflammation via the TLR4/MyD88/NF-κB pathway. 1,8-Cineole is a monoterpene compound widely found in the essential oils of many plants and has been reported to possess anti-inflammatory and antioxidant activities. However, its role in regulating lipid metabolism disorders remains unclear. This study aimed to investigate the effects of 1,8-cineole on lipid metabolism and explore the potential mechanisms related to oxidative stress and inflammation. Methods: Cell viability was assessed by MTT assay to determine the optimal PA concentration for inducing lipid accumulation and the non-cytotoxic range of 1,8-cineole in HepG2 and AML-12 cells. Lipid droplets were visualized by Oil Red O staining, while triglyceride (TG) and total cholesterol (TC) levels were quantified using enzymatic kits. Oxidative stress markers (ROS by DCFH-DA fluorescence; MDA by TBA method; CAT activity by ammonium molybdate method) and inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-18 by ELISA) were measured. Western blotting analyzed key proteins in the TLR4/MyD88/NF-κB pathway (TLR4, MyD88, p-P65, p-IκBα). Pathway-specific inhibitors were employed for mechanistic validation. Results: 1,8-Cineole (up to 1000 μg/mL) showed no cytotoxicity. It significantly attenuated PA-induced lipid droplet accumulation, reduced TG and TC levels (p < 0.05), and ameliorated oxidative stress by decreasing ROS and MDA while enhancing CAT activity in AML-12 cells (p < 0.01). Furthermore, 1,8-cineole suppressed pro-inflammatory cytokine release (TNF-α, IL-6, and IL-1β; p < 0.01), whereas no significant effect was observed on IL-18 levels. Downregulated TLR4/MyD88/NF-κB pathway activation. Inhibition of TLR4 or NF-κB mirrored these protective effects. Conclusions: 1,8-Cineole alleviates PA-induced lipid metabolism disorders, oxidative stress, and inflammation in hepatocytes, likely through suppression of the TLR4/MyD88/NF-κB signaling pathway. Full article

Cryptocaryon irritans, a ciliated protozoan parasite, is the causative agent of marine white spot disease and results in significant economic losses in mariculture. In this study, golden pompano (Trachinotus ovatus) were challenged with C. irritans at different infection doses (2000, 4000, and 8000 theronts per fish) for 48 h to evaluate histopathological, oxidative stress, immune, and intestinal microbiota responses. Histopathological analysis revealed pronounced tissue damage in the gills, skin, intestine, and liver, with severity positively correlated with infection intensity. Typical lesions included intestinal mucosal damage, hepatic vacuolation, gill epithelial hyperplasia, and skin epidermal thickening. Hepatic malondialdehyde (MDA) levels increased significantly with infection intensity, while superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) showed non-linear activation patterns. Catalase (CAT), alkaline phosphatase (AKP), and acid phosphatase (ACP) activities were consistently suppressed. Immune-related gene expression exhibited tissue-specific regulation, with myd88 downregulated in gills but upregulated in skin, while pro-inflammatory cytokines (il-1β and il-8) and il-10 were significantly elevated. Infection also altered intestinal microbiota composition, reducing beneficial bacteria (e.g., Photobacterium) and increasing opportunistic pathogens such as Vibrio. These findings provide insights into host–parasite–microbiota interactions in T. ovatus and improve our understanding of the physiological and immune responses of fish to C. irritans infection. Full article

This study aimed to evaluate the protective effects of sodium humate (HNa) alone and in combination with low-dose cefixime (CFM) in mice infected with enterotoxigenic Escherichia coli (ETEC). An ETEC infection mouse model was established to compare the effects of individual or combined interventions on physiological parameters, intestinal morphology, barrier function, levels of specific intestinal bacterial groups, cell proliferation/apoptosis, and inflammatory pathways. The results showed that the HNa + CFM combination significantly promoted body weight recovery, ameliorated damage to jejunal villus structure and ultrastructure, and increased the mRNA expression of mucins (MUC1/2/3) and tight junction proteins (ZO-1, Occludin, Claudin-1) compared to the ETEC group. Concurrently, the combined treatment significantly reduced fecal E. coli counts and increased the abundance of Lactobacillus and Bifidobacterium, promoted epithelial repair by upregulating proliferation-related genes (EGFR, PCNA, TGF-β1), and decreased the Bax/Bcl-2 ratio. Furthermore, the combined intervention significantly reduced serum LPS levels and consequently suppressed ETEC-induced activation of the TLR4/MyD88/NF-κB pathway, as evidenced by reduced protein expression of TLR4 and MyD88, decreased phosphorylation of IκBα and p65, and diminished nuclear accumulation of NF-κB p65, leading to downregulation of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and elevation of IL-10. In conclusion, the combined application of HNa and low-dose CFM showed additional protective benefits against ETEC infection. These effects were associated with multi-targeted repair of the intestinal barrier, modulation of measured bacterial levels, and suppression of excessive inflammatory responses. This strategy offers a potential approach for the clinical management of bacterial enteritis and reducing antibiotic dependence. Full article

During the early growth stage, lambs are highly susceptible to pathogenic microbial invasion due to an underdeveloped intestinal structure, unstable microbial colonization, and immature mucosal immune function, leading to diarrhea, growth retardation, and elevated mortality factors that severely constrain the production efficiency and economic viability of the sheep industry. This study aimed to compare the regulatory effects of compound yeast culture (CYC) and yeast polysaccharides (YPs) on intestinal barrier function in Mongolian male lambs and clarify their underlying molecular mechanisms. Eighteen lambs were randomly assigned to three groups (n = 6/group): control group (basal diet), CYC group (40 g/kg), and YP group (3 g/kg). After a 30-day feeding trial, intestinal histomorphology, tight junction proteins, immune signaling pathways, and gut microbiota were analyzed. The results showed that both additives improved intestinal villus morphology, and CYC markedly increased the villus height/crypt depth ratio (p < 0.05). At the mechanical barrier level, CYC upregulated the protein expression of occludin, claudin-1, and ZO-1, whereas YPs increased occludin and ZO-1 expression (p < 0.05). Immunologically, CYC inhibited intestinal inflammation via the TLR4/TRAF6/MyD88/NF-κB pathway, increasing interleukin-10 (IL-10) and secretory immunoglobulin A (sIgA) while decreasing pro-inflammatory cytokines. YPs exerted similar anti-inflammatory effects through the TLR2/MyD88 pathway. Microbial analysis indicated that both additives increased the relative abundance of beneficial bacteria including Eubacterium, Bacillus, and Succinivibrio, while reducing the potential pathogen Mogibacterium. Spearman correlation analysis revealed that Mogibacterium was positively correlated with TNF-α and negatively correlated with occludin expression. In conclusion, CYC and YPs effectively enhance intestinal mechanical, immune, and biological barriers via different TLR-mediated pathways and microbial modulation. Both natural additives have great application potential for improving lamb health, reducing antibiotic dependence, and promoting sustainable green animal husbandry. Full article

Syringa oblata Lindl. (SOL) has long been used in traditional medicine for inflammatory disorders, yet its molecular actions in reproductive tract inflammation remain poorly defined. This study investigated the phytochemical composition and anti-inflammatory mechanisms of an aqueous SOL leaf extract using murine and cellular models of endometritis. Ultra-performance liquid chromatography–tandem mass spectrometry (UPLC–MS/MS) analysis revealed major constituents including rutin, salidroside, and esculetin. In a murine model of bacterial endometritis induced by Escherichia coli and Staphylococcus aureus, SOL markedly attenuated uterine edema, epithelial disruption, leukocyte infiltration, and bacterial burden. Mechanistic analyses demonstrated that SOL suppressed the Toll-like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88) axis and decreased the uterine expression of interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α). In lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages, SOL and its principal monomers significantly reduced nitric oxide (NO) and reactive oxygen species (ROS) production both in the presence and absence of the TLR4 inhibitor TAK-242, suggesting additional modulation of redox-responsive pathways beyond canonical TLR4 signaling. Moreover, SOL selectively decreased the M1 macrophage marker CD86 in uterine tissue without altering CD163, consistent with partial inhibition of pro-inflammatory macrophage polarization. Collectively, these findings indicate that SOL exerts potent antimicrobial, anti-inflammatory, and antioxidative effects through coordinated regulation of innate immune signaling and macrophage activation, supporting its potential as a natural therapeutic candidate for inflammation-associated reproductive disorders. Full article

Land surface temperature (LST) is a core physical parameter that characterizes land surface processes and surface-atmosphere energy exchange. As the demand for high-accuracy LST products intensifies across diverse research domains—including climate science, hydrology, and ecosystem modeling—the systematic quantification of pixel-level retrieval uncertainties has become essential for generating long-term, consistent Climate Data Records (CDRs). However, existing studies predominantly emphasize algorithmic development or localized validation, with limited attention to systematic cross-site and long-term uncertainty assessments. This gap impedes a comprehensive understanding of the compositional structure and spatiotemporal variability of LST retrieval uncertainties under heterogeneous surface and atmospheric conditions. In this study, based on the improved generalized split-window (GSW) algorithm and error propagation theory, the total uncertainty (U_total) and its four primary components—algorithm uncertainty (U_a), land surface emissivity uncertainty (U_e), noise equivalent delta temperature uncertainty (U_n), and atmospheric water vapor uncertainty (U_w)—at the pixel level over long time series and across multiple sites are quantified. Our analysis spans a 21-year period (2003–2023) and encompasses multiple geographically distributed sites, utilizing high-quality Moderate Resolution Imaging Spectroradiometer (MODIS) thermal infrared data—specifically MYD11_L2 and MOD11_L2 products—collocated at the locations of 15 globally distributed ground-based reference sites. These sites are used to represent diverse climatic regimes and land-cover conditions, rather than to provide point-scale “true” LST values for residual-based validation. Results show that the interquartile range (IQR) of U_total is consistently concentrated between 1.0 and 1.2 K, demonstrating long-term stability. Systematic differences in U_total are identified across sensor platforms and diurnal cycles: U_total for Aqua/MYD data (1.13–1.25 K) is marginally higher than that for Terra/MOD data (1.05–1.17 K); similarly, daytime U_total (1.08–1.23 K) is generally slightly elevated relative to nighttime U_total (1.05–1.18 K). The contributions of individual uncertainty components to U_total exhibit substantial variation, with mean relative contributions of 81.97%, 11.32%, 4.46%, and 2.25% for U_e, U_a, U_n, and U_w, respectively. The dominant drivers of U_total differ markedly across climatic regions: in arid regions, U_total is predominantly governed by U_e, termed “emissivity-dominated,” accounting for over 85% of the total; conversely, humid tropical regions exhibit a “surface-atmosphere co-influenced” regime, characterized by a reduced contribution from U_e and correspondingly enhanced contributions from U_a and U_w. Furthermore, U_total decreases with increasing total column water vapor (TCWV) (Pearson correlation coefficient r = −0.498; linear slope k = −0.0425 K/(g/cm²)), and increases with increasing viewing zenith angle (VZA) (r = 0.208; k = 0.0022 K/degree). While U_a, U_n, and U_w all increase with TCWV, U_e decreases. Full article

Laryngeal cancer is a relatively uncommon malignancy with predisposing genetic factors that remain unclear. Single-nucleotide polymorphisms (SNPs) in genes involved in innate immune signaling may contribute to the development and progression of laryngeal carcinoma. This study aimed to evaluate the association of TLR4 (rs7037225, rs11536889, rs7037117) and MYD88 (rs7744, rs6853) polymorphisms with the risk of laryngeal squamous cell carcinoma (LSCC), as well as its clinical and pathological characteristics and survival. A retrospective case–control study involving 172 LSCC patients and 220 healthy controls was conducted. Genotyping was performed using real-time PCR from venous blood samples. MYD88 rs7744 was significantly associated with tumor size and lymph node involvement. Survival analysis showed a significant association between rs7744 and recurrence-free survival (RFS), with the AG and GG genotypes linked to poorer outcomes. Conversely, carriers of the TLR4 rs7037225 CT genotype showed significantly improved RFS, with p ranging from 0.024 to 0.037 across models. Considering the significant roles of TLR4 and MYD88 in Toll-like receptor signaling, these findings may reflect the involvement of innate immune pathways in LSCC progression. In summary, MYD88 rs7744 was associated with clinicopathological features and RFS, while TLR4 rs7037225 appeared to have a potential protective effect on survival. Full article

Ulcerative colitis (UC) is a form of inflammatory bowel disease (IBD), which is marked by severe abdominal pain, weight loss, perianal bleeding, and diarrhea. This study successfully isolated and purified four low-molecular-weight fucoidan oligosaccharides through acid hydrolysis and Bio Gel P10 gel filtration. The molecular weights were 2.9 × 10⁴–1.36 × 10⁵ Da, 182–1012 Da, 161–939 Da and 161–939 Da, respectively. A mouse model of colitis was induced using Dextran Sulfate Sodium (DSS). The results indicated that fucoidan and fucoidan oligosaccharides could ameliorate murine ulcerative colitis, with the oligosaccharides (200 mg/kg/d) demonstrating superior therapeutic effects. This superiority was likely attributed to the lower molecular weight and higher content of total sugars and fucose. The primary mechanisms involved the modulation of gene and protein expression levels associated with the Toll-like receptor 4, Myeloid differentiation primary response 88, nuclear factor kappa-light-chain-enhancer of activated B cells, p65, and Inhibitor of kappa light polypeptide gene enhancer in B cells, alpha (TLR4, MYD88, NF-κB p65, and IκB-α) signaling pathways, which reduce the production of inflammatory cytokines such as tumor necrosis factor-alpha, Interleukin-1 beta and Interleukin-6 (TNF-α, IL-1β, and IL-6). Additionally, these oligosaccharides alleviated oxidative stress, enhanced the levels of intestinal barrier proteins (Claudin family member 4 and Zonula occludens protein 1), regulated the abundance and diversity of the gut microbiota, and increased the levels of short-chain fatty acids (SCFAs) in the intestine. It is worth emphasizing that this study can only demonstrate that fucoidan oligosaccharides have a mitigating effect on intestinal inflammation in mice. Further research is needed in the future to investigate the structure–activity relationship of fucoidan oligosaccharides and their impact on human intestinal microbiota, in order to further elucidate their anti-inflammatory mechanisms. Full article

Aims: Coronary heart disease (CHD) associated with rheumatoid arthritis (RA) is a primary driver of mortality in RA patients. In this study, we sought to establish a combined rat model of CHD and RA by integrating cardiac ischemia/reperfusion (I/R), high-fat diet (HFD), and intradermal administration of bovine type II collagen emulsified in complete Freund’s adjuvant. The aim of constructing this model is to investigate and analyze the pathogenesis of RA-induced CHD under the modulation of HFD and cardiac I/R exposure. Methods and Results: Sixty-four male Sprague–Dawley rats were randomly categorized into eight groups (n = 8 per group): control, I/R, HFD, collagen-induced arthritis (CIA), I/R + CIA, HFD + CIA, I/R + HFD, and I/R + HFD + CIA groups (n = 8 per group). We applied Synchrotron radiation-based X-ray micro-computed tomography (micro-CT) to observe the structural changes within the model over time. To further elucidate molecular mechanisms, transcriptome RNA-seq analysis was carried out to identify key signaling pathways, with particular emphasis on the homeostasis of Toll-like receptor 4 (TLR4)/Myd88 signaling in the ischemic myocardium. Furthermore, we conducted in vivo shRNA-mediated knockdown of polymerase I and transcription release factor (PTRF) and evaluated the co-localization of PTRF and TLR4 through immunofluorescence experiments. It is worth mentioning that our rat model of RA-induced (CHD) under a high-fat diet effectively manifested the relevant pathological features that align with the Traditional Chinese Medicine (TCM) definition of “bi” syndrome. The results indicate that the combined stimulation of HFD and CIA significantly elevated cardiac injury markers (CK-MB, LDH, CRP, and c-TNT) and was accompanied by a more severe expansion of the infarct area and increased cardiomyocyte apoptosis compared to the I/R group alone. In addition, the histopathological evaluation revealed significantly aggravated myocardial inflammation and fibrosis deposition, accompanied by extensive areas of tissue damage, further indicating a state of heightened inflammation and severe cardiac degenerative changes. Consistently, myocardial tissues from rats in the I/R + CIA + HFD group exhibited robust activation of the TLR4/MyD88 signaling pathway and a pronounced elevation in the p-JNK/JNK ratio. Moreover, pronounced co-localization between PTRF and TLR4 was evident in small vessels surrounding the infarcted myocardium. Importantly, AAV-mediated knockdown of PTRF attenuated the HFD- and CIA-induced exacerbation of myocardial injury in I/R rats. Conclusions: We successfully established a rat model of CHD with rheumatic syndrome using I/R in combination with RA and HFD. The present findings suggest that the PTRF-related TLR4/MyD88-JNK signaling pathway may act as an important regulatory mechanism underlying myocardial injury aggravated by combined HFD and CIA stimulation. Full article

Moderate Resolution Imaging Spectroradiometer (MODIS) and Visible Infrared Imaging Radiometer Suite (VIIRS) active fire products are widely used for global fire monitoring, but single-sensor records are limited by differences in observation geometry, spatial resolution, detection sensitivity, and swath coverage. To combine the long-term continuity of Aqua MODIS with the higher sensitivity of Suomi NPP VIIRS, this study developed a correction-before-fusion framework for MYD14 and VNP14IMG and generated a daily fused fire radiative power (FRP) dataset at the native MODIS footprint scale. MYD14 and VNP14IMG observations from 2012 to 2024 were processed using duplicate-detection correction, footprint-scale near-synchronous matching, area-based VIIRS cloud correction, and anomalous-sample screening. Cloud-corrected VIIRS FRP was then used as the reference to develop an empirical viewing zenith angle (VZA)-dependent correction model for MODIS FRP. Finally, VZA-corrected MODIS FRP and cloud-corrected VIIRS FRP were integrated using a quality-prioritized fusion strategy. The correction model achieved high fitting accuracy ($R^2\ge 98.18\%$) and reduced MODIS underestimation under large-VZA conditions. Compared with the original MODIS product, the fused product increased detected fire pixels by approximately 3.82-fold, improved spatial continuity, and reduced temporal data gaps. Landsat-based validation showed improved low-intensity fire detection while maintaining low commission error. This framework provides a harmonized long-term FRP dataset for fire monitoring, emission estimation, and fire-climate studies. Full article

Background: Type 2 diabetes mellitus (T2DM) represents a pressing global health challenge, underscoring the urgency of developing effective dietary interventions derived from natural resources. Zaojiaomi polysaccharide (ZJMP) from the endosperm of Gleditsia sinensis seeds (zaojiaomi), a traditional edible product, exhibits largely underexplored potential in T2DM management. Methods: In the present study, the antidiabetic effects and underlying mechanisms of ZJMP were investigated using a rat model of T2DM induced by a high-fat diet (HFD) combined with streptozotocin (STZ). Relevant biochemical indicators were detected, and histopathological examination was performed. The expression levels of key components of the TLR4/MyD88/NF-κB signaling pathway, as well as the inflammatory cytokines IL-6 and IL-1β in renal tissues, were further analyzed. Additionally, gut microbiota composition and the levels of short-chain fatty acids were determined. Results: ZJMP treatment significantly ameliorated hyperglycemia and dyslipidemia, elevated serum insulin levels, reduced intestinal mucosal permeability, and attenuated histopathological lesions in the heart, kidney, and pancreas of T2DM rats. Meanwhile, ZJMP notably alleviated renal inflammation by suppressing the production of IL-1β and IL-6, as well as inhibiting the TLR4/MyD88/NF-κB pathway. Furthermore, ZJMP administration effectively modulated gut microbiota composition and increased fecal concentrations of acetic acid and propionic acid. Conclusions: Collectively, these findings elucidate the novel bioactivity of ZJMP and highlight its potential as a promising functional food ingredient or dietary supplement for T2DM management. Full article