Search Results (3,067)

Conventional audio and video codecs are designed for human perception, often discarding subtle spectral cues that are essential for machine-based analysis. To overcome this limitation, we propose a machine-oriented compression framework that reinterprets spectrograms as visual objects and applies Feature Coding for Machines (FCM) to anomalous sound detection (ASD). In our approach, audio signals are transformed log-mel spectrograms, from which intermediate feature maps are extracted, compressed, and reconstructed through the FCM pipeline. For comparison, we implement AAC-LC (Advanced Audio Coding Low Complexity) as a representative perceptual audio codec and VVC (Versatile Video Coding) as spectrogram-based video codec. Experiments were conducted on the DCASE (Detection and Classification of Acoustic Scenes and Events) 2023 Task 2 dataset, covering four machine types (fan, valve, toycar, slider), with anomaly detection performed using the official Autoencoder baseline model released in DCASE 2024. Detection scores were computed from reconstruction error and Mahalanobis distance. The results show that the proposed FCM-based ACoM (Audio Coding for Machines) achieves comparable or superior performance to AAC at less than half the bitrate, reliably preserving critical features even under ultra-low bitrate conditions (1.3–6.3 kbps). While VVC retains competitive performance only at high bitrates, it degrades sharply at low bitrates. These findings demonstrate that feature-based compression offers a promising direction for next-generation ACoM standardization, enabling efficient and robust ASD in bandwidth-constrained industrial environments. Full article

This study reports the construction and validation of a CAFLUX (Chemically Activated Fluorescent Expression) HepG2 reporter cell line engineered to express a histone H2B–green fluorescent protein (H2B–GFP) fusion protein under the control of a dioxin-responsive cytochrome P450 1A1 (CYP1A1) promoter. A lentiviral construct containing a synthetic promoter with multiple dioxin-responsive elements (DREs) upstream of the H2B–EGFP coding sequence was cloned into the pFUGW vector, packaged in human embryonic kidney (HEK) 293FT cells, and used to transduce HepG2 hepatocellular carcinoma cells. Stable clones obtained by limiting dilution were screened for GFP expression in response to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The resulting CAFLUX HepG2 cells exhibited dose-dependent nuclear GFP fluorescence when exposed to aryl hydrocarbon receptor (AhR) agonists, with limits of detection of approximately 0.01 pM for TCDD and 0.1 pM for benzo[a]pyrene (B[a]P), a polycyclic aromatic hydrocarbon (PAH). This reporter activity correlated with endogenous CYP1A1 mRNA expression as determined by quantitative polymerase chain reaction (qPCR), confirming that GFP signals reflected native transcriptional responses. In functional assays, curcumin suppressed GFP expression in a concentration-dependent manner and induced apoptotic morphology at higher doses, while extracellular vesicles (EVs) derived from adipose-derived stem cells (ADSCs) significantly reduced both GFP fluorescence and CYP1A1 mRNA levels, suggesting an inhibitory effect on AhR-driven transcription. The CAFLUX HepG2 reporter system therefore provides a sensitive and reproducible platform for real-time, nuclear-localized monitoring of AhR-mediated gene expression. Its responsiveness to both agonists and antagonists underscores its potential utility in toxicological evaluation, drug discovery, and the investigation of EV-mediated signaling in liver cancer models. Full article

Stochastic computing (SC) has the characteristics of low complexity and is expected to solve the bottleneck problem of conventional binary computing. Stochastic normalization units are widely used in stochastic decoding and stochastic signal detection, and have achieved hardware efficiency far exceeding conventional methods. However, they also have problems such as 1-bit representation and low calculation accuracy, calculation overflow, and fluctuation in the sum of normalized probabilities, which lead to prolonged processing latency and degraded hardware efficiency. Thus, this paper proposes a novel stochastic normalization unit using multi-bit random variables. Benefiting from the high representation accuracy of multi-bit random variables, the accuracy of the proposed unit is greatly improved. Meanwhile, the proposed unit completely solves the problems of calculation overflow and fluctuation in the sum of normalized probabilities. Simulation results show that the proposed 3-bit unit achieves a fourfold improvement in convergence speed and 2 times higher hardware efficiency compared to the state-of-the-art stochastic normalization unit. Finally, we verify that the proposed 3-bit unit demonstrates a 75% improvement in hardware efficiency for stochastic sparse-code multiple-access (SCMA) detection. Full article

Rheumatoid arthritis (RA) is a prevalent autoimmune disease characterized by chronic joint inflammation. Its pathophysiology involves complex interactions among immune cells, leading to joint damage, primarily in the synovial membrane. MicroRNAs (miRs), single-stranded non-coding RNAs, play a critical role in regulating pathways affecting RA progression, particularly in fibroblast-like synoviocytes and peripheral blood mononuclear cells. Key pathways influenced by miRs include NF-κB, apoptosis, PI3K/AKT signaling, and cytokine production. Dysregulated miRs impact cell proliferation, survival, and inflammatory responses. This review explores not only the role of miRs in RA pathogenesis, but also highlights their potential as biomarkers for early detection and severity prediction. Moreover, therapeutic approaches targeting miRs, including mimics and inhibitors, show promise in animal models, with methods like intra-articular administration being favored due to better efficacy and reduced side effects. While early studies highlight potential pathways for RA treatment, challenges remain in translating these findings into safe and effective clinical therapies. Full article

Background/Objectives: Psoriasis is currently treated with biologics targeting the IL-17A signaling, which plays a major role in immune response and keratinocyte hyperproliferation. These include inhibitors of IL-17A and/or its heterodimer with IL-17F (Secukinumab, Ixekinumab and Bimekizumab) and the receptor IL17-RA (Brodalumab). Although these drugs are safe and highly effective, there is significant variability in response among patients. This can be partly attributed to the patients’ genetic background, thus pointing to the need to identify pharmacogenetic markers for treatment response. Methods: The study involved 88 Greek patients who were treated with inhibitors of the IL-17A signaling for at least 6 months. Patients were classified as responders and non-responders according to the change in Psoriasis Area Severity Index. A total of 730,000 variants were genotyped and analyzed for association with the 3-month and 6-month responses to treatment. Results: The analysis identified 21 variants which were associated with the response, showing statistical significance after Bonferroni correction. These include variants located in protein coding genes (TP63, NRG1, SCN8A, TAF9, TMEM9, SMIM36, SYT14, BPIFC, SEZ6L2, PCARE), as well as intergenic and long non-coding RNA intronic variants. The functional significance of the variants was assessed using in silico analysis and for several variants, a link with immune processes was proposed. Notably, rs11649499 status, which was associated with complete clinical remission at 3 months, may influence key lipid mediators involved in psoriasis. Conclusions: This GWAS identified novel variants that could be utilized upon validation in larger populations as predictive markers regarding patient response to drugs targeting the IL-17A pathway. Full article

Asthma is a chronic respiratory disease affecting over 262 million people worldwide, with obesity-associated asthma emerging as a distinct endotype of increasing prevalence characterized by metabolic inflammation and airway remodeling. Unlike allergic asthma, this phenotype is driven by chronic low-grade inflammation, originating from hypertrophic and hypoxic adipose tissue. This dysregulated state leads to the activation of pro-inflammatory pathways and the secretion of cytokines, contributing to airway dysfunction and remodeling. Recent evidence highlights non-coding RNAs (ncRNAs) as key regulators of these processes. MicroRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) influence inflammation and remodeling by modulating immune cell polarization, cytokine secretion, extracellular matrix composition, and airway smooth muscle cell (ASMC) proliferation. Notably, H19, MEG3, GAS5, miR-26a-1-3p, and miR-376a-3p have been implicated in both asthma and obesity, suggesting their role in linking metabolic dysfunction with airway pathology. Moreover, ncRNAs regulate Treg/Th17 balance, fibroblast activation, and autophagy-related pathways, further influencing airway remodeling. Our in silico analysis highlighted the IGF1R signaling pathway as a key enriched mechanism, linking selected ncRNAs with metabolic dysregulation and inflammation in obesity-related asthma. This paper reviews how ncRNAs regulate inflammation and airway remodeling in obesity-associated asthma, emphasizing their potential molecular links between metabolic dysfunction and airway pathology. Full article

Drought is a leading constraint on plant productivity and will intensify with climate change. Plant acclimation emerges from a multilayered regulatory system that integrates signaling, transcriptional reprogramming, RNA-based control, and chromatin dynamics. Within this hierarchy, non-coding RNAs (ncRNAs) provide a unifying regulatory layer; microRNAs (miRNAs) modulate abscisic acid and auxin circuits, oxidative stress defenses, and root architecture. This balances growth with survival under water-deficient conditions. Small interfering RNAs (siRNAs) include 24-nucleotide heterochromatic populations that operate through RNA-directed DNA methylation, which positions ncRNA control at the transcription–chromatin interface. Long non-coding RNAs (lncRNAs) act in cis and trans, interact with small RNA pathways, and can serve as chromatin-associated scaffolds. Circular RNAs (circRNAs) are increasingly being detected as responsive to drought. Functional studies in Arabidopsis and maize (e.g., ath-circ032768 and circMED16) underscore their regulatory potential. This review consolidates ncRNA biogenesis and function, catalogs drought-responsive modules across model and crop species, especially cereals, and outlines methodological priorities, such as long-read support for isoforms and back-splice junctions, stringent validation, and integrative multiomics. The evidence suggests that ncRNAs are tractable entry points for enhancing drought resilience while managing growth–stress trade-offs. 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

Background/Objectives: Miscanthus Andersson, a genus of perennial grasses that includes wild relatives of key crop species, remains poorly characterized in terms of genetic diversity and evolutionary relationships. The aim of this study was to elucidate the phylogenetic structure of Miscanthus through comparative genomic analysis of the chloroplast genomes of six Korean species. Methods: Complete chloroplast genomes were assembled and analyzed for six Miscanthus species. Informative nucleotide motifs and their associated gene locations were identified as potential markers, and their phylogenetic relationships with related crops were examined. Results: The chloroplast genomes exhibited a conserved quadripartite structure, with genome sizes and GC contents within typical ranges. Analysis of codon usage showed a preference for A/U-ending codons, consistent with patterns in other angiosperms. Simple sequence repeats and long repeats demonstrated non-random distributions, indicating their value as molecular markers for phylogenetic and population studies. Comparative analyses confirmed structural conservation across Miscanthus species, whereas variation in non-coding regions provided important phylogenetic signals. Phylogenetic reconstruction based on 21 chloroplast genomes revealed four major clades, corroborating previous findings and highlighting complex evolutionary relationships within Miscanthus, including close affinities between African and Himalayan species and the genus Saccharum L. Conclusions: This study provides complete chloroplast genomes of six Miscanthus species, contributing to enhanced understanding of the relationships within the subtribe Saccharinae. The findings support the inclusion of Miscanthus species in the Korea Crop Wild Relatives inventory and highlight their potential as a genetic resource for breeding programs aimed at enhancing crop resilience to environmental stress. Full article

Schizophrenia is a highly polygenic and clinically heterogeneous disorder. In this paper, we first review layer-specific evidence across genetics, epigenetics, transcriptomics, proteomics, and patient-derived induced pluripotent stem cell (iPSC) models, then integrate cross-layer findings. Genetics research identifies widespread risk architecture. Hundreds of loci from common, rare, and CNV analyses. Epigenetics reveals disease-associated DNA methylation and histone-mark changes. These occur at neuronally active enhancers and promoters, together with chromatin contacts that link non-coding risk to target genes. Transcriptomics show broad differential expression, isoform-level dysregulation, and disrupted co-expression modules. These alterations span synaptic signaling, mitochondrial bioenergetics, and immune programs. Proteomics demonstrates coordinated decreases in postsynaptic scaffold and mitochondrial respiratory-chain proteins in cortex, with complementary inflammatory signatures in serum/plasma. iPSC models recapitulate disease-relevant phenotypes: including fewer synaptic puncta and excitatory postsynaptic currents, electrophysiological immaturity, oxidative stress, and progenitor vulnerability. These same models show partial rescue under targeted perturbations. Integration across layers highlights convergent pathways repeatedly supported by ≥3 independent data types: synaptic signaling, immune/complement regulation, mitochondrial/energetic function, neurodevelopmental programs and cell-adhesion complexes. Within these axes, several cross-layer convergence genes/proteins (e.g., DLG4/PSD-95, C4A, RELN, NRXN1/NLGN1, OXPHOS subunits, POU3F2/BRN2, PTN) recur across cohorts and modalities. Framing results through cross-layer and shared-pathway convergence organizes heterogeneous evidence and prioritizes targets for mechanistic dissection, biomarker development, and translational follow-up. Full article

Cerebral ischemia/reperfusion (I/R) injury remains a significant contributor to adult neurological morbidity, primarily due to exacerbated neuroinflammation and cell apoptosis. These processes amplify brain damage through the release of various pro-inflammatory cytokines and pro-apoptotic mediators. Although long non-coding RNAs (lncRNAs) are increasingly recognized for their involvement in regulating diverse biological pathways, their precise role in cerebral I/R injury has not been fully elucidated. In the current study, transcriptomic profiling was conducted using a rat model of focal cerebral I/R, leading to the identification of lncRNA-1810026B05Rik—also referred to as CHASERR—as a novel lncRNA responsive to ischemic conditions. The elevated expression of this lncRNA was observed in mouse brain tissues subjected to middle cerebral artery occlusion followed by reperfusion (MCAO/R), as well as in primary cortical neurons derived from rats exposed to oxygen-glucose deprivation and subsequent reoxygenation (OGD/R). The results suggested that lncRNA-1810026B05RiK mediates the activation of the nuclear factor-kappaB (NF-κB) signaling pathway by physically binding to NF-kappa-B inhibitor alpha (IκBα) and promoting its phosphorylation, thus leading to neuroinflammation and neuronal apoptosis during cerebral ischemia/reperfusion. In addition, lncRNA-1810026B05Rik knockdown acts as an NF-κB inhibitor in the OGD/R and MCAO/R pathological processes, suggesting that lncRNA-1810026B05Rik downregulation exerts a protective effect on cerebral I/R injury. In summary, the lncRNA-1810026B05Rik has been identified as a critical regulator of neuronal apoptosis and inflammation through the activation of the NF-κB signaling cascade. This discovery uncovers a previously unrecognized role of 1810026B05Rik in the molecular mechanisms underlying ischemic stroke, offering valuable insights into disease pathology. Moreover, its involvement highlights its potential as a novel therapeutic target, paving the way for innovative treatment strategies for stroke patients. Full article

Background/Objectives: Individuals with anorexia nervosa (AN) are known to exhibit both reduced pain sensitivity—when assessed via thresholds and subjective ratings—and diminished facial expressions of emotion. Therefore, investigating the facial response to pain in this population is of particular interest. Method: Seventeen patients with AN and 18 age- and sex-matched healthy controls were assessed using a thermode to induce heat pain. Subjective pain measures included pain threshold, pain tolerance, and pain ratings of supra-threshold stimuli, rated on a numerical rating scale (NRS). Facial responses to the suprathreshold stimuli were analyzed using the Facial Action Coding System (FACS). Eating pathology was assessed using the Eating Attitudes Test (EAT-26), the Eating Disorder Inventory-2 (EDI-2) and the body mass index (BMI), while depression was measured using the Beck Depression Inventory-II (BDI-II). Results: Compared with healthy controls, AN patients showed altogether significantly reduced facial expressions of pain, with particularly pronounced reductions in Action Units AU 6_7 and AU 9_10. In contrast, subjective pain measures showed only marginal differences between groups. Importantly, the reduction in facial expression could not be accounted for by differences in pain thresholds or ratings, nor by levels of eating pathology or depression. Conclusions: Individuals with AN display a markedly reduced facial expression of pain, which was observed for the first time, consistent with similar findings regarding the facial expressions of emotions. As this reduction cannot be explained by subjective pain report, it suggests that the communication of pain is impaired on two levels in AN: both in verbal and in nonverbal signaling. This may hinder the ability of others to recognize and respond to their pain appropriately. Full article

Integrated sensing and communication (ISAC) has emerged as a transformative technology for intelligent transportation systems. Index modulation (IM), recognized for its high robustness and energy efficiency (EE), has been successfully incorporated into ISAC systems. However, most existing IM-based ISAC schemes overlook the spatial multiplexing potential of millimeter-wave channels and remain confined to single-hop vehicle-to-vehicle (V2V) setups, failing to address the challenges of energy consumption and noise accumulation in real-world multi-hop V2V networks with complex road topologies. To bridge this gap, we propose a spatial scattering modulation-based ISAC (ISAC-SSM) scheme and introduce it to multi-hop V2V networks. The proposed scheme leverages the sensed positioning information to select maximum signal-to-noise ratio relay vehicles and employs a detect-amplify-and-forward (DAF) protocol to mitigate noise propagation, while utilizing sensed angle data for Doppler compensation to enhance communication reliability. At each hop, the transmitter modulates index bits on the angular-domain spatial directions of scattering clusters, achieving higher EE. We initially derive a closed-form bit error rate expression and Chernoff upper bound for the proposed DAF ISAC-SSM under multi-hop V2V networks. Both theoretical analyses and Monte Carlo simulations have been made and demonstrate the superiority of DAF ISAC-SSM over existing alternatives in terms of EE and error performance. Specifically, in a two-hop network with 12 scattering clusters, compared with DAF ISAC-conventional spatial multiplexing, DAF ISAC-maximum beamforming, and DAF ISAC-random beamforming, the proposed DAF ISAC-SSM scheme can achieve a coding gain of 1.5 dB, 2 dB, and 4 dB, respectively. Moreover, it shows robust performance with less than a 1.5 dB error degradation under 0.018 Doppler shifts, thereby verifying its superiority in practical vehicular environments. Full article

Citrobacter braakii is an emerging opportunistic pathogen of escalating clinical significance in animal hosts, though its pathogenic mechanisms remain poorly characterized. This study isolated a C. braakii strain (SCGY-1L) from diseased Siniperca chuatsi and confirmed its identity through integrated morphological, physiological, and molecular analyses. Comprehensive genomic sequencing revealed a 5.75 Mb genome comprising one circular chromosome and two plasmids. A Circos plot was constructed to visualize the genomic architecture of strain SCGY-1L, revealing 5482 protein-coding genes, 25 tRNA genes, and 86 rRNA genes. Additionally, 738 virulence-associated genes and 366 antibiotic resistance determinants were annotated, elucidating multidrug-resistant phenotypes including insensitivity to erythromycin and penicillin. Pathogenicity assessment established an LD₅₀ of 1.28 × 10⁶ CFU/mL in infected hosts, with histopathological analysis showing significant hemorrhage and necrosis in target organs (liver, spleen, kidney). Host transcriptome profiling generated 41.21 Gb of high-quality clean data, identifying 2201 differentially expressed genes post-infection (1568 up-regulated; 633 down-regulated). These were significantly enriched in phagocytosis, cytokine-mediated signaling, and inflammatory regulation pathways. These molecular insights establish C. braakii’s mechanistic framework for pathogenesis and host adaptation, providing critical targets for diagnostics and therapeutics against emerging Citrobacter infections. Full article

Background: Trelegy Ellipta is a widely prescribed triple inhaler therapy for chronic obstructive pulmonary disease (COPD). Although its clinical efficacy is well established, evidence on sex-specific differences in adverse event (AE) profiles from real-world pharmacovigilance data remains limited. In addition, some AEs may reflect underlying disease characteristics rather than drug exposure, which complicates interpretation of safety signals. Objective: To explore sex-related differences in AEs associated with Trelegy Ellipta using the FDA Adverse Event Reporting System (FAERS). The study aimed to identify potential safety signals while accounting for alternative explanations, including comorbidity burden and disease-related variation. Methods: We retrospectively analyzed FAERS reports from January 2018 to April 2025, identifying 4555 AEs attributed to Trelegy Ellipta. Events were coded by System Organ Class (SOC) and stratified by patient sex. Frequencies were compared between male (n = 1621) and female (n = 2934) patients using chi-square tests, and associations were expressed as reporting odds ratios (RORs) with 95% confidence intervals (CIs). Results: Male patients more frequently reported hypertension (63.4% vs. 47.0%; p = 0.01), pneumonia (87.8% vs. 76.8%; p < 0.001), anxiety (91.0% vs. 66.9%; p < 0.001), sleep disorders (20.1% vs. 6.8%; p < 0.001), and hyperglycemia (92.7% vs. 52.1%; p < 0.001). Female patients more often reported headache (56.7% vs. 32.6%; p < 0.001), depression (33.1% vs. 9.0%; p < 0.001), and osteoporosis (41.7% vs. 2.4%; p < 0.001). Further variation was observed across neurological, musculoskeletal, and respiratory categories, suggesting a multidimensional pattern of sex differences. Conclusions: This FAERS-based analysis indicates distinct sex-specific safety signals for Trelegy Ellipta, particularly in cardiovascular, neuropsychiatric, and steroid-related domains. These findings are hypothesis-generating and highlight the importance of incorporating sex-disaggregated analyses into future pharmacovigilance and clinical studies. Full article