Search Results (23,021)

Extremely low-frequency (ELF, 3–30 Hz) signals are effective for cross-medium transmission, yet conventional implementations are hindered by their large size and low efficiency. To address these limitations, a compact electromechanical–magnetic antenna (EMA) was developed and experimentally validated for ELF magnetic communication. The basic unit of the antenna, a single-EMA, consists of a stacked magnetostrictive composite beam, piezoelectric ceramic plates, and tip-mounted permanent magnets. The total envelope volume of a single EMA is only 3.3 cm³ with a maximum length of 12 cm, representing a substantial reduction compared with conventional ELF antennas. Building on this compact architecture, two EMAs were operated in parallel to form a parallel-EMA system, which significantly enhanced magnetic radiation through constructive magnetic coupling. Moreover, the optimal separation distance between the two EMAs was identified, ensuring efficient cooperative radiation. When driven at 50.2 mW, the parallel-EMA configuration generated a magnetic flux density of 114 pT at a transmission distance of 20 m in seawater. This performance demonstrates nearly a twofold improvement over a single-EMA unit, validating the scalability of parallel operation for stronger magnetic radiation. The compact form factor of the single EMA combined with the enhanced radiation performance of the parallel-EMA system enables portable ELF magnetic communication across diverse cross-medium scenarios, including air-to-sea and underground-to-air links. Full article

Focal cortical dysplasia (FCD) is a major cause of drug-resistant epilepsy, yet its molecular basis remains poorly understood. Numerous studies have analyzed RNA, protein, and microRNA alterations, but results are often inconsistent across subtypes and methodologies. To address this gap, we conducted a systematic review integrating transcriptomic, proteomic, and microRNA data from 117 human studies of FCD subtypes I–III. Differentially expressed factors were extracted, categorized by subtype, and analyzed using pathway enrichment and network approaches. Our integrative analysis revealed convergent dysregulation of neuroinflammatory, synaptic, cytoskeletal, and metabolic pathways across FCD subtypes. Consistently altered genes, including IL1B, TLR4, BDNF, HMGCR, and ROCK2, together with dysregulated microRNAs such as hsa-miR-21-5p, hsa-miR-155-5p, and hsa-miR-132-3p, were linked to PI3K–Akt–mTOR, Toll-like receptor, and GABAergic signaling, emphasizing shared pathogenic mechanisms. Importantly, we identified overlapping transcript–protein patterns and subtype-specific molecular profiles that may refine diagnosis and inform therapeutic strategies. This review provides the first cross-omics molecular framework of FCD, demonstrating how convergent pathways unify heterogeneous findings and offering a roadmap for biomarker discovery and targeted interventions. Full article

SHORT INTERNODE (SHI)-Related Sequence (SRS) transcription factors play crucial roles in plant growth, development, and stress responses and have been extensively studied in various plant species. However, the molecular functions and regulatory mechanisms of SRS genes in the economically important tropical fruit crop pitaya (Hylocereus undatus) remain poorly understood. This study identified 9 HuSRS genes in pitaya via bioinformatics analysis, with subcellular localization predicting nuclear distributions for all. Gene structure analysis showed 1–4 exons, and conserved motifs (RING-type zinc finger and IXGH domains) were shared across subclasses. Phylogenetic analysis classified the HuSRS genes into three subfamilies. Subfamily I (HuSRS1–HuSRS4) is closely related to poplar and tomato homologs and subfamily III (HuSRS6–HuSRS8) contains a recently duplicated paralogous pair (HuSRS7/HuSRS8) and shows affinity to rice SRS genes. Protein structure prediction revealed dominance of random coils, α-helices, and extended strands, with spatial similarity correlating to subfamily classification. Interaction networks showed HuSRS1, HuSRS2, HuSRS7 and HuSRS8 interact with functional proteins in transcription and hormone signaling. Promoter analysis identified abundant light/hormone/stress-responsive elements, with HuSRS5 harboring the most motifs. Transcriptome and qPCR analyses revealed spatiotemporal expression patterns: HuSRS4, HuSRS5, and HuSRS7 exhibited significantly higher expression levels in callus (WG), which may be associated with dedifferentiation capacity. In seedlings, HuSRS9 exhibited extremely high transcriptional accumulation in stem segments, while HuSRS1, HuSRS5, HuSRS7 and HuSRS8 were highly active in cotyledons. This study systematically analyzed the characteristics of the SRS gene family in pitaya, revealing its evolutionary conservation and spatio-temporal expression differences. The research results have laid a foundation for in-depth exploration of the function of the SRS gene in the tissue culture and molecular breeding of pitaya. Full article

Type 2 diabetes is a major global health burden, causing approximately 2 million deaths annually. Recent studies have revealed a strong positive correlation between elevated triglyceride levels and plasma glucose, as well as increased prevalence, incidence, and mortality of type 2 diabetes, suggesting a potential causal link. This review explores the metabolic interconversion between triglycerides and glucose, emphasizing how excess carbohydrate intake leads to ectopic triglyceride accumulation, which in turn enhances hepatic gluconeogenesis. It highlights key signaling pathways through which ectopic triglyceride deposition drives insulin resistance, hyperinsulinemia, β-cell dysfunction and apoptosis, and increased glucose production—central mechanisms in diabetes pathogenesis. Evidence from clinical interventions, such as the reversal of type 2 diabetes through bariatric surgery and dietary energy restriction, supports the hypothesis that ectopic triglyceride accumulation is a driving factor. Furthermore, this review explains why omega-3 fatty acids and niacin, in contrast to fibrates, do not protect against type 2 diabetes, despite lowering triglycerides. Overall, this review emphasizes the contribution of ectopic triglyceride accumulation—driven by obesity, hypertriglyceridemia, excessive consumption of carbohydrates and fats, and physical inactivity—to the onset and progression of type 2 diabetes, offering valuable insights into potential therapeutic strategies. Full article

Background: Periodontitis is a chronic disease triggered by disturbed oral microbiota. We have previously reported that hepatocyte growth factor (HGF) could mitigate early-stage experimental periodontitis but exacerbate the condition in its late stage. Here, we investigated the impact of HGF on the periodontal microbiome during periodontitis progression. Methods: We established ligation-induced periodontitis in wild-type (WT) mice and HGF high-expression transgenic (HGF-Tg) mice. We quantified the levels of IL-6 and TNF-α in periodontal tissues, as well as the serum concentrations of CTXI and PINP. Ligatures were collected on days 0, 7, and 28 after ligation for 16S rRNA sequencing and microbial analysis. Results: HGF significantly altered the diversity of ligatures during periodontitis. Interestingly, specific microbial genera, such as Lactobacillus, exhibited opposing trends between the two disease stages of HGF-Tg mice, aligning with the different effects of HGF on periodontitis progression. We also identified some taxa, such as Sphingomonas, associated with IL-6, TNF-α, CTXI, and PINP. The predicted inflammatory pathways (e.g., IL-17 signaling pathways) were enriched in HGF-Tg mice on day 28 but decreased on day 7. Conclusions: HGF exerted different influences on the microbiota of ligatures during early and late stages of periodontitis, which may account for the divergent effects of HGF on periodontitis progression. Full article

Ginsenosides, the primary bioactive components of Panax ginseng, have demonstrated significant immunomodulatory potential. While major ginsenosides have been extensively studied, rare ginsenosides produced through deglycosylation, heating, and steaming show enhanced biological activities with improved bioavailability. This review aimed to comprehensively analyze the immunomodulatory mechanisms, structure-activity relationships (SARs), therapeutic applications, and clinical translation strategies of five emerging rare ginsenosides: F1, Rg5, Rk1, Rh1, and Rg2. We conducted a comprehensive literature review examining the production methods, immunological effects, molecular mechanisms, pharmacokinetics, safety profiles, and clinical applications of these five compounds. Analysis focused on chemical structures, immune cell modulation, signaling pathways, disease model efficacy, and bioavailability enhancement strategies. Ginsenoside F1 uniquely demonstrated immunostimulatory effects, enhancing natural killer (NK) cell cytotoxicity and macrophage phagocytosis through mitogen-activated protein kinase (MAPK)/nuclear factor-κB (NF-κB) activation. Conversely, Rg5, Rk1, Rh1, and Rg2 exhibited anti-inflammatory properties via distinct mechanisms: Rg5 through Toll-like receptor 4 (TLR4)/NF-κB inhibition, Rk1 via triple pathway modulation (NF-κB, p38 MAPK, signal transducer and activator of transcription (STAT)), Rh1 by selective p38 MAPK and STAT1 inhibition, and Rg2 through modulation of both central nervous system (neuroinflammation) and peripheral organ systems. Structure-activity analysis revealed that sugar moiety positions critically determine immunological outcomes. Crucially, advanced delivery systems including nanostructured lipid carriers, self-microemulsifying systems, and specialized liposomes have overcome the major translational barrier of poor bioavailability, achieving up to 2.6-fold improvements and enabling clinical development. Safety assessments demonstrated favorable tolerability profiles across preclinical and clinical studies. These five rare ginsenosides represent promising immunomodulatory agents with distinct therapeutic applications. F1’s unique immunostimulatory properties position it for cancer immunotherapy, while the complementary anti-inflammatory mechanisms of Rg5, Rk1, Rh1, and Rg2 offer opportunities for precision medicine in inflammatory diseases. Advanced formulation technologies and optimized production methods now enable their significant clinical translation potential, providing promising therapeutic options for immune-related disorders pending further development. Full article

Under the combined effects of climate change, overexploitation, and intense grazing, temperate steppe in northern China is experiencing increasing deterioration, which is typified by a shift from structural degradation to functional disruption. Accurately tracking steppe degradation using remote sensing technology has emerged as a crucial scientific concern. Prior research failed to integrate ecosystem structure and function and lacked reference baselines, relying only on individual indicators to quantify degradation. To resolve these gaps, this study established a novel degradation evaluation index system integrating ecosystem structure and function, incorporating vegetation community distribution and proportions of degradation-indicator species to define reference states and quantify degradation severity. Analyzed spatiotemporal evolution and drivers across the temperate typical steppe (2013–2022). Key findings reveal (1) non-degraded and slightly degraded areas dominated (75.57% mean coverage), showing an overall fluctuating improvement trend; (2) minimal transitions between degradation levels, with stable conditions prevailing (59.52% unchanged area), indicating progressive degradation reversal; and (3) natural factors predominated as degradation drivers. The integrated structural–functional framework enables more sensitive detection of early degradation signals, thereby informing more effective steppe restoration management. Full article

As the world’s first geosynchronous (GEO) orbit synthetic aperture radar (SAR) satellite, LuTan-4 was successfully launched on 13 August 2023. It was developed by the China Academy of Space Technology, with which the authors are affiliated. This study presents a comprehensive review of the recent advancements in GEO SAR technology. The review first begins by summarizing key considerations in GEO SAR system design, including orbital parameters and synthetic aperture time, transmit power and antenna aperture, two-dimensional beam-steering, imaging parameters and non-ideal factors. In terms of GEO SAR signal processing, the article focuses on two fundamental models, i.e., the high-order slant-range model and the coupled space-variant signal model. It also introduces the current GEO SAR imaging algorithms. Furthermore, the study presents an analysis between GEO SAR and low-Earth orbit SAR systems, highlighting the superior capability of GEO SAR for large-scale surface dynamic processes. Finally, the paper outlines the future development directions and potential applications of GEO SAR technology. Full article

L-fucose is a monosaccharide derived from brown algae and has potential applications as a functional food ingredient. Previous studies have reported that L-fucose reduces lipid accumulation in murine adipose tissue. Adipose tissue not only regulates energy metabolism but also functions as an endocrine organ involved in inflammation through the production and secretion of various adipokines. L-fucose is expected to exert anti-inflammatory effects and modulate adipokine secretion in adipocytes. In the present study, we investigated the anti-inflammatory effects of L-fucose in adipocytes. L-fucose significantly suppressed the expression of pro-inflammatory mediators and reduced the production of reactive oxygen species induced by inflammatory stimulation with a combination of lipopolysaccharide (LPS), tumor necrosis factor-⍺ (TNF-⍺), and interferon-γ (IFN-γ). These effects are likely mediated through the inhibition of key signaling pathways, including mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) pathways. Additionally, we found that L-fucose promoted the multimerization and secretion of high molecular weight (HMW) adiponectin, even under inflammatory conditions. Our results suggest that although L-fucose downregulates adiponectin expression, it contributes to the formation and/or stabilization of HMW adiponectin, which is functionally more relevant in anti-inflammatory and metabolic regulation. L-fucose thus holds promise as a functional food ingredient for mitigating inflammation in adipocytes. Full article

Background: Cardiometabolic syndromes, including diabetes, obesity, and metabolic syndrome, significantly contribute to cardiovascular fibrosis, a major driver of heart failure. Non-coding RNAs (ncRNAs)—notably microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs)—have emerged as critical epigenetic regulators of fibrotic remodeling. Recent studies indicate that widely used metabolic modulators can influence ncRNA expression, potentially impacting on cardiovascular fibrosis. This review synthesizes evidence on the interplay between metabolic therapies and ncRNA regulation, with emphasis on therapeutic and biomarker potential of miRNAs. Methods: A literature search was manually curated and conducted on PubMed for studies published mainly in the last decade and evaluating the effects of metformin, sodium-glucose cotransporter-2 (SGLT2) inhibitors, peroxisome proliferator-activated receptor gamma (PPARγ) agonists, glucagon-like peptide 1 (GLP-1) receptor agonists, and fatty acid oxidation inhibitors on ncRNA expression in the context of cardiovascular fibrosis. Data from in vitro, in vivo, and clinical studies were extracted and categorized by drug class, ncRNA target, and functional outcomes. Results: Several metabolic modulators specifically downregulate pro-fibrotic (miR-21, miR-92, H19, and metastasis associated lung adenocarcinoma transcript 1 (MALAT1)) and upregulate anti-fibrotic ncRNAs (miR-29, miR-133a, miR-711, miR-133a, miR-30a and miR-200 family). This results in global attenuation of the transforming growth factor- beta (TGF-β) signaling, which limits extracellular matrix (ECM) accumulation thus improving myocardial compliance. Across drug classes, changes in ncRNA profiles paralleled improvements in fibrosis-related endpoints. Conclusions: Metabolic modulators exert anti-fibrotic effects partly through ncRNA regulation, offering novel therapeutic strategies and potential biomarkers for cardiovascular fibrosis in cardiometabolic disease. Targeting metabolic–ncRNA crosstalk may enable more precise and synergistic interventions for preventing or reversing pathological remodeling. Full article

The parallel global increase in obesity and Alzheimer’s disease (AD) underscores an urgent public health challenge, with converging evidence indicating that metabolic dysfunction strongly contributes to neurodegeneration. Obesity is now recognized not only as a systemic metabolic condition but also as a modifiable risk factor for AD, acting through mechanisms such as chronic low-grade inflammation, insulin resistance, and adipose tissue dysfunction. Among the molecular mediators at this interface, adipokines have emerged as pivotal regulators linking metabolic imbalance to cognitive decline. Adipokines are hormone-like proteins secreted by adipose tissue, including adiponectin, leptin, and resistin, that regulate metabolism, inflammation and can influence brain function. Resistin, frequently elevated in obesity, promotes neuroinflammation, disrupts insulin signaling, and accelerates β-amyloid (Aβ) deposition and tau pathology. Conversely, adiponectin enhances insulin sensitivity, suppresses oxidative stress, and supports mitochondrial and endothelial function, thereby exerting neuroprotective actions. The imbalance between resistin and adiponectin may shift the central nervous system toward a pro-inflammatory and metabolically compromised state that predisposes to neurodegeneration. Beyond their mechanistic relevance, adipokines hold translational promise as biomarkers for early risk stratification and therapeutic monitoring. Importantly, natural compounds, including polyphenols, alkaloids, and terpenoids, have shown the capacity to modulate adipokine signaling, restore metabolic homeostasis, and attenuate AD-related pathology in preclinical models. This positions adipokines not only as pathogenic mediators but also as therapeutic targets at the intersection of diabetes, obesity, and dementia. By integrating mechanistic, clinical, and pharmacological evidence, this review emphasizes adipokine signaling as a novel axis for intervention and highlights natural compound-based strategies as emerging therapeutic approaches in obesity-associated AD. Beyond nutraceuticals, antidiabetic agents also modulate adipokines and AD-relevant pathways. GLP-1 receptor agonists, metformin, and thiazolidinediones tend to increase adiponectin and reduce inflammatory tone, while SGLT2 and DPP-4 inhibitors exert systemic anti-inflammatory and hemodynamic benefits with emerging but still limited cognitive evidence. Together, these drug classes offer mechanistically grounded strategies to target the adipokine–inflammation–metabolism axis in obesity-associated AD. Full article

The aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor, plays a crucial role in regulating immune homeostasis, inflammatory responses, and intestinal barrier function. Indole compounds and their derivatives are ligands of AHR, which can activate the AHR signal transduction pathway and show significant regulatory potential in various inflammatory and immune diseases. Cystic fibrosis (CF) is a life-threatening autosomal recessive genetic disorder. Cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction affects multiple systems throughout the body. The core of its pathological process is chronic infection, abnormal inflammation, and tissue damage caused by mucus accumulation. Exploring alternative or adjunctive therapeutic strategies targeting pathological pathways downstream of CFTR is of significant importance. The aim of the present study is to explore the multiple beneficial effects that indole compounds may exert in regulating pulmonary infection and inflammation, repairing intestinal barrier function, and regulating immune homeostasis in CF patients by activating the AHR signaling pathway. Additionally, this study discusses the risks and challenges associated with developing indole compounds as CF drugs, offering a novel research approach distinct from traditional CFTR modulators for creating new CF therapeutics. Full article

Bacterial wilt is a highly destructive disease affecting a wide range of crops, with no effective chemical control methods currently available. Consequently, the development of microbial strategies for disease management has become increasingly important. Among these, plant immunity-intensifying microbes have demonstrated promising efficacy in controlling bacterial wilt. However, the influence of environmental factors, particularly light intensity, on the effectiveness of these microbes remains unclear. Light intensity is a critical regulator of the photosynthetic system and plant biochemical functions, including defense responses. In this study, we specifically utilized Arabidopsis plants grown under distinct light intensities to systematically examine how light conditions affect the induction of plant immune responses and the occurrence of bacterial wilt. Our findings revealed that Arabidopsis grown under high light intensity exhibited significantly stronger immune responses and reduced disease severity, compared to plants grown under low light intensity. Further, application of Bacillus amyloliquefaciens PMB05, a plant immunity-intensifying strain, resulted in more pronounced immune signaling and disease control efficacy under high light conditions. Experiments using salicylic acid (SA)-deficient mutants demonstrated that disruption of the SA pathway abolished the enhanced suppression of bacterial wilt conferred by B. amyloliquefaciens PMB05 under high light intensity, indicating that the SA pathway is indispensable for PMB05-mediated disease resistance. Moreover, the validation experiments in tomato plants supported these results, with B. amyloliquefaciens PMB05 significantly reducing bacterial wilt development under high light intensity. Collectively, our study demonstrates that growing plants under varying light intensities provides critical insights into how environmental conditions modulate the effectiveness of plant immunity-intensifying microbes, offering a potential strategy for integrated disease management in crops. Full article

Glucosylceramide (GlcCer), a central glycosphingolipid derived from ceramide, is increasingly recognized as a bioactive lipid that intersects with key metabolic, inflammatory, and oncogenic pathways. While its dysregulation has long been associated with lysosomal storage disorders such as Gaucher disease (GD), growing evidence implicates GlcCer in cancer initiation and progression, particularly within tumor-predisposing conditions. GlcCer modulates membrane microdomains, intracellular trafficking, and cell signaling, counteracting ceramide-induced apoptosis and promoting cellular survival. In cancer, aberrant upregulation of UDP-glucose ceramide glucosyltransferase (UGCG), the enzyme responsible for GlcCer synthesis, drives tumor growth, metastasis, and multidrug resistance through activation of pathways such as phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), mitogen-activated protein kinase (MAPK), canonical Wnt pathway (Wnt/β-catenin), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways. Specific GlcCer species (e.g., C16:0, C18:0, C24:1) display tissue-dependent functions, adding structural specificity to their oncogenic potential. Moreover, emerging links between GlcCer metabolism and chronic inflammation, oxidative stress, and altered glucose utilization highlight its role as a metabolic node bridging inherited metabolic disorders and malignancy. This review integrates recent advances in GlcCer biology, emphasizing its roles in tumor-predisposing diseases and exploring its potential as a biomarker and therapeutic target in oncology. Full article

Obesity, characterized by the accumulation of excess adipocytes, is a significant risk factor for type 2 diabetes and non-alcoholic fatty liver disease. Medicinal plants, including Hibiscus sabdariffa, have been traditionally employed to prevent or treat conditions such as obesity and inflammation due to their safety profile and minimal side effects during long-term use. However, the anti-obesity potential of Hibiscus syriacus, a taxonomically distinct species within the same genus, remains unexplored. In this study, we screened 181 varieties of H. syriacus buds for anti-obesity effects and identified the water extract of the ‘Pyeonghwa’ bud (HPWE) as a potent inhibitor of adipogenesis. Using 3T3-L1 murine pre-adipocyte cells, we demonstrated that HPWE significantly reduced lipid accumulation without inducing cytotoxicity. Mechanistically, HPWE downregulated the expression of key adipogenic signaling proteins and transcription factors, including peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα), which serve as molecular markers of adipogenesis. Additionally, in vivo experiments employing a high-fat-diet-induced obesity mouse model using C57BL/6 species confirmed the anti-obesity effects of HPWE. Collectively, these findings suggest that HPWE represents a promising candidate for the prevention of obesity. Full article