Search Results (8,931)

Phyllosphere microorganisms interact with host plants to regulate growth, promote nutrient uptake and enhance stress tolerance with host specificity, while arbuscular mycorrhizal fungi facilitate plant nutrient absorption and stress adaptation. Current poplar microbial studies mostly focus on hermaphroditic species, with limited research on dioecious poplars. This study selected four poplar species commonly hybridized with Populuscathayana and Populus deltoides in the Xinmin area of Liaoning Province as research subjects: two female plants, DM-9-18 and DX-08-01, and two male plants, 2111 and Qingshan poplar. We performed MiSeq high-throughput sequencing targeting bacterial 16S rRNA, fungal ITS, and arbuscular mycorrhizal fungal (AMF) marker genes from poplar phyllosphere, coupled with chemical quantification of leaf, root and rhizosphere soil, to disentangle clone- and sex-associated divergence in microbial assemblages and their core environmental drivers. No significant gender differences were observed in leaf and rhizosphere nutrient levels and microbial α diversity, whereas male poplars had higher rhizosphere soil nutrients. Male and female poplars genotypes harbored distinct microbial ASVs. The dominant phyllosphere microbes and arbuscular mycorrhizal fungi exhibited gender-specific abundance variations, and nutrient content was the key factor shaping microbial communities. This study clarifies microbial community differences among the four selected hybrid poplar clones. While the experimental design confounds sex with host genotype, the observed patterns provide insights into potential sex-related variations. Our results advance the mechanistic understanding of how dioecious poplar genotype and sexual phenotype jointly filter leaf and root-associated microbial symbionts, with applied implications for hybrid poplar breeding and shelterbelt microbial regulation. Full article

Geometric misalignment degrades industrial cone-beam computed tomography (CBCT), particularly when a dedicated calibration phantom cannot be deployed during object acquisition. This study presents a three-stage, scan-specific geometric refinement framework that searches a bounded five-coordinate correction space around a nominal geometry. Coarse candidates are screened using the normalized residual between a geometry-corrected center-of-mass trajectory and its best-fitting low-order periodic model. Translation- and rotation-dominant coordinates are then refined within system-specific physical bounds, and an energy-normalized nuclear-norm score of corrected row-wise sinograms is used for local correlation refinement. The periodic and low-rank terms are treated as object-dependent surrogate objectives rather than as standalone guarantees of physical parameter identifiability. An exact-ASTRA implementation check using a Shepp–Logan volume verified the detector-plane reindexing convention: applying the injected correction reduced valid-mask projection discrepancy to 35.2%, 13.7%, and 8.66% of the uncorrected values for small, medium, and large perturbations, respectively, with round-trip resampling NRMSE of 0.022–0.023 and a mean valid fraction of 98.4%. Three industrial datasets acquired with horizontal gantry CT, temperature-stage in situ CT, and vertical micro-CT provided comparative reconstruction evidence. In addition, a controlled reduced-resolution industrial object reprojection benchmark was used for direct comparison with MI-PSO, PR, and a stability-regularized implementation of the public epipolar-consistency formulation (Open-ECC-R). Over 20 fixed-ROI axial slices, Open-ECC-R increased the mean SSIM from 0.6852 ± 0.0454 for the uncalibrated reconstruction to 0.8450 ± 0.0155 and reduced the NRMSE from 0.5180 ± 0.0526 to 0.1671 ± 0.0125. The proposed method achieved the highest mean SSIM of 0.9933 ± 0.0002 and the lowest NRMSE of 0.0321 ± 0.0009. For the Bluetooth earphone dataset, local sagittal and axial MTF₅₀ estimates increased from 0.84 to 0.94 lp/mm and from 0.45 to 1.05 lp/mm, respectively. These results support scan-specific image-quality refinement around a nominal geometry while avoiding unsupported claims of absolute parameter recovery. Full article

Insects periodically undergo molting to replace their old epidermis for growth and morphological adaptation. Muscleblind-like (MBNL) is a multifunctional protein involved in miRNA processing. To explore the role of miRNA processing in insect molting, we characterized BmMBNL in Bombyx mori. BmMBNL exhibited spatiotemporal expression across tissues and developmental stages, with the highest levels in the epidermis and upregulation during molting. CRISPR/Cas9-mediated knockout of BmMBNL (BmMBNL-KO) caused molting defects at the 3rd and 4th instar larvae, resulting in reduced size and eventual lethality. Moreover, BmMBNL-KO individuals showed a thinner chitin layer between the new and old epidermises. RT-PCR and transcriptome analyses revealed upregulation of miR-1, miR-71, miR-263, miR-8-5p, and miR-2a-3p, which suppressed chitinase expression, ultimately leading to molting failure. This study provides novel insights into the potential correlation between BmMBNL, miRNA abundance and insect molting in Bombyx mori. Full article

Moyamoya disease (MMD) is a progressive cerebrovascular disorder characterized by intracranial arterial stenosis and abnormal collateral vessel formation. The molecular mechanisms by which extracellular vesicle (EV)-derived microRNAs contribute to endothelial dysfunction remain poorly understood. We investigated whether circulating extracellular vesicle-derived microRNAs (EV-miRNAs) contribute to endothelial dysfunction and serve as functional mediators of MMD pathogenesis. Plasma EV-miRNA profiles were compared among patients with MMD, intracranial atherosclerosis (ICAS), and healthy controls, and differentially expressed EV-miRNAs were validated in an independent cohort. Functional studies were performed in human umbilical vein endothelial cells and patient-derived induced pluripotent stem cell-derived endothelial cells. Three EV-miRNAs were significantly upregulated in MMD, among which miR-558 showed the strongest diagnostic performance. miR-558 overexpression impaired endothelial tube formation and proliferation, whereas its inhibition enhanced angiogenic activity. Mechanistically, HMGB2 was identified as a direct target of miR-558, and miR-558 overexpression reduced HMGB2 protein expression. Patient-derived endothelial cells recapitulated increased miR-558 expression, reduced HMGB2 levels, and impaired angiogenic capacity. These findings identify circulating EV-miR-558 a potential biomarker and show that miR-558 suppresses HMGB2 and impairs endothelial angiogenesis in adult MMD, suggesting that the EV-miR-558/HMGB2 pathway represents a potential mechanism underlying endothelial dysfunction and therapeutic target for MMD. Full article

Endometriosis is a chronic, oestrogen-responsive inflammatory disease characterised by endometrial-like tissue outside the uterine cavity. Because retrograde menstruation is common, lesion establishment probably requires cellular competence and a permissive ectopic microenvironment. This hypothesis-driven narrative review evaluates fascin (FSCN1) as a candidate cytoskeletal effector and considers antecedent eutopic priming versus induction after ectopic adhesion. Functional evidence was integrated with a targeted public-data screen. Donor-level reanalysis of GSE179640 found no conclusive overall eutopic case–control difference and predominantly non-epithelial expression. Exploratory analysis of GSE203191 suggested higher FSCN1 expression within a HSPA6+ stromal subcluster in diagnosed cases, without a comparable epithelial signal or detectable increase in subcluster abundance. This small post hoc analysis remains hypothesis-generating. FSCN1 was absent from the published HECA stromal/macrophage differential-expression lists and was not prioritised by the 2023 endometriosis GWAS. The current evidence therefore argues against uniform epithelial or whole-eutopic overexpression but permits a lineage-restricted stromal state. Fascin participates in autophagy- and miR-145-sensitive invasion networks, although these pathways are pleiotropic. Validation requires cycle- and lineage-resolved tissue mapping, compositional controls, matched lesions, and direct FSCN1 perturbation. Fascin should currently be regarded as a candidate multi-marker component and preclinical target, not a validated biomarker or systemic therapeutic target. Full article

Background: Mature microRNAs (miRNAs) have been implicated in inflammation and fibrosis and are associated with the pathogenesis of renal dysfunction. miRNAs are single-stranded RNAs approximately 22 nucleotides in length that can posttranscriptionally modify mRNA by base-pairing with its complementary sequences leading to the silencing of mRNA. Methods: We assessed circulating levels of miRNAs in the blood of dogs that were clinically diagnosed as having chronic kidney disease (CKD) post-mortem, after the dogs had lived their full lives. Gene expression was measured using a Canine miRNA PCR array from blood samples that were collected at the natural end-of-life necropsy from dogs with CKD (2–17 yr) and control dogs (5–13.5 yr). Results: End-of-life pathology reports indicated interstitial inflammation, fibrosis, and thickening of the Bowman’s capsule. Histopathological analysis of H&E-stained renal sections taken from end-of-life samples showed a significantly higher number of healthy glomeruli as assessed morphologically in controls compared with CKD. There was a significant decline in the levels of miRNAs cfa-let-7a, cfa-let-7c, cfa-let-7f, and cfa-let-7g in dogs with CKD compared with controls. In addition, there was also a ≥1.5-fold reduction in levels of cfa-miR-93, cfa-miR-122, cfa-miR-200a, and cfa-miR-204 in CKD compared with controls (all ns). These microRNAs may have potential anti-fibrogenesis effect and are also down-regulated in rodent models and in in vitro mechanistic models of renal fibrosis, leading to increased fibrosis. There was also a down-regulation of cfa-miR-16 (−2.76 fold, ns), which is consistent with its reported role in attenuating kidney injury independent of fibrosis. Conclusions: Down-regulation of these miRNAs may be indicative of a reduction in their role in attenuating renal function, leading to impaired kidney function and possibly fibrogenesis. Importantly, the circulating miRNAs may serve as non-invasive biomarkers for impaired renal function in CKD. Nutritional interventions that upregulate selected miRNAs may serve as important targets for slowing the progression of CKD. Full article

Background: Frontotemporal dementia (FTD) is a neurodegenerative disease that shares numerous clinical features with other forms of dementia. In this context, non-coding RNAs, specifically microRNAs (miRNAs), represent a promising tool for differential diagnosis. Since these miRNAs can be isolated from circulating extracellular vesicles (EVs) in peripheral blood, they provide a direct insight into FTD-specific molecular processes. Consequently, while EV-contained miRNAs hold potential as disease-specific biomarkers, investigating their relative target genes can help elucidate their precise functional roles. Aim: This work aimed to identify a specific miRNA signature to better characterize FTD pathology. Methods: Building on a previous Next-Generation Sequencing (NGS) analysis, three candidate miRNAs were selected for validation in both EVs and peripheral blood mononuclear cells (PBMCs) of FTD patients. Subsequently, the predicted target genes of two of these miRNAs were validated in PBMCs to assess their expression levels. Results: Our findings revealed that miR-365a-3p and miR-212 were significantly down-regulated in FTD. Conclusions: Together with their target genes, these miRNAs are involved in cell cycle and apoptotic pathways, suggesting a potential role in the pathological mechanisms of the disease. Full article

Background: The Investigator Quantiplex Pro RGQ Kit (Qiagen, Hilden, Germany) enables rapid quantification of total human and male DNA on the Rotor-Gene Q platform while simultaneously assessing PCR inhibition, DNA degradation, and mixed DNA profiles. This study evaluated whether reducing the recommended qPCR reaction volume by half affects analytical performance, with the aim of improving throughput and reducing reagent costs in forensic laboratories. Methods: Control DNA (50 ng/µL) and DNA extracted from 20 simulated forensic samples representing common forensic evidence (including bloodstains, semen stains, saliva samples, vaginal swabs, touch DNA, hair roots, and mixed biological traces deposited on different substrates) were analyzed using standard and half-volume qPCR reactions with identical reagent proportions. Quantification and quality indices—including inhibition (IC), degradation (DI), and mixture (MI)—were evaluated using Q-Rex software. Ct values, ΔCt, and standard deviations were compared between protocols using paired statistical analysis, with significance set at p < 0.05. Results: Standard curves generated under both reaction conditions showed efficient amplification, with R² values > 0.998 and slopes within recommended ranges. Control samples demonstrated strong agreement between expected and measured DNA concentrations for both protocols. Although forensic samples displayed variable DNA quantity and quality, highly concordant results were obtained between standard and reduced volumes. Mean Ct values showed minimal ΔCt variation and low dispersion across all sample types. IC, DI, and MI indices were also consistent, indicating reliable detection of inhibition, degradation, and mixed DNA profiles under reduced-volume conditions. Conclusions: Half-volume qPCR reactions using the Investigator Quantiplex Pro RGQ Kit maintained accurate, precise, and reproducible DNA quantification and quality assessment. Reduced-volume protocols may therefore provide a cost-effective strategy to increase throughput and improve workflow efficiency in forensic laboratories without compromising analytical robustness. Full article

The red-spotted grouper nervous necrosis virus (RGNNV) exhibits high pathogenicity in larval C. sonnerati, yet the immune molecular mechanism remains unclear. Non-coding RNAs (ncRNAs) are vital in the host’s immune responses during viral infection. However, there has been no study on ncRNA research for this species to date. We systematically identified 105 DE microRNAs (miRNAs), 157 DE long non-coding RNAs (lncRNAs) and 31 DE circular RNAs between the infection group and control group. Functional enrichment analysis revealed that these differentially expressed genes were significantly enriched in pathways associated with innate immune defense, inflammatory, and cell death, such as JAK-STAT signaling pathway, NF-κB signaling pathway, apoptosis, and necroptosis. Furthermore, the lncRNA–miRNA–mRNA interaction network involving miR-93 was constructed, which may represent a promising candidate therapy target for future investigations. This study presents the first comprehensive ncRNA transcriptome dataset of C. sonnerati infected with RGNNV, identifies key antiviral defense and cell death-related genes and hub pathways, and thereby identifies miR-93-involved lncRNA–miRNA–mRNA network and key targeted genes (STAT1, TRIM25, UNC93B, IL12RB1, IRF8, CDKN1A, FCGR1A) as hub molecular regulators in immune response of this species. Full article

Background/Objectives: Loss of phosphatase and tensin homolog (PTEN) activity is a frequent feature of non-small-cell lung cancer (NSCLC), and epigenetic repression may contribute to its reduced expression. This study investigated the effects of 5-aza-2′-deoxycytidine (5-aza-dC) on PTEN, DNA methyltransferase 1 (DNMT1), PTEN promoter methylation-specific amplification patterns, and miR-148a-3p expression in NSCLC models. Methods: Publicly available cancer-genomics datasets were analyzed to compare PTEN and DNMT1 transcript abundance and to assess the association between PTEN methylation and transcript abundance in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). A549 and H460 cells were exposed to 2.5 or 5 µM 5-aza-dC for 72 h. Reverse-transcription quantitative PCR (RT-qPCR), Western blotting, methylation-specific PCR (MSP-PCR), and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays were used to evaluate RNA expression, protein abundance, methylation-specific amplification, and metabolic activity, respectively. Results: Bioinformatic analyses showed lower PTEN and higher DNMT1 expression in both NSCLC subtypes, together with inverse associations between PTEN methylation and transcript abundance. In both cell lines, 5-aza-dC reduced MTT metabolic activity and DNMT1 expression. PTEN mRNA and protein abundance increased significantly at 5 µM, whereas no significant changes were detected at 2.5 µM. MSP-PCR revealed persistent heterogeneous PTEN methylation-specific amplification patterns without clear evidence of progressive promoter demethylation. miR-148a-3p exhibited a biphasic response in A549 cells but remained unchanged in H460 cells. Conclusions: These findings support an association between 5-aza-dC exposure, increased PTEN expression, and reduced DNMT1 expression in NSCLC cells. Quantitative methylation analysis and mechanistic validation are required to clarify the contribution of miR-148a-3p to this regulatory association. Full article

Background: Hypertrophic cardiomyopathy (HCM) is the most common monogenic cardiac disorder (prevalence 1:500), a major substrate of sudden cardiac death (SCD) in adolescents and young adults, and is modulated by regulatory mechanisms including non-coding RNAs (ncRNAs) such as microRNAs (miRNAs), long non-coding RNAS (lncRNAs) and circular RNAs (circRNAs), which act as epigenetic modulators and potential biomarkers. Methods: The study involves a PRISMA-based systematic review of 989 records from PubMed, Scopus, Embase, Web of Science and Cochrane, including 96 studies evaluating ncRNAs as diagnostic, prognostic, genotype-specific or mechanistic markers in clinically/genetically confirmed HCM. Human biomarker studies (circulating/tissue ncRNAs) were analyzed separately from experimental models (human myocardium, animal models, iPSC-derived cardiomyocytes, cardiac organoids). Results: Key findings include upregulated miR-29a, miR-21 and miR-133a in HCM plasma/tissue (correlating with hypertrophy/fibrosis), miR-499a-5p as an MYH7-specific marker, and miR-208b-3p/miR-155 associated with MYBPC3-related HCM. Pro-hypertrophic lncRNAs (e.g., NEAT1, UCA1), fibrotic lncRNAs (e.g., MIAT) and protective/mitochondrial circRNAs (e.g., circZFPM2) contribute to ceRNA networks linking hypertrophy, fibrosis, mitochondrial dysfunction and arrhythmic remodeling. Multi-ncRNA panels have shown discriminatory performance between HCM and selected phenocopies, while some signatures have been associated with atrial fibrillation and composite cardiac outcomes; however, these findings remain heterogeneous and require independent validation. Conclusions: NcRNAs are biologically relevant regulators of HCM and represent promising candidates for mechanistic investigation, biomarker development and, potentially, therapeutic targeting. Current clinical evidence remains insufficient to support their incorporation into established SCD risk prediction models or their use as standalone diagnostic tools, particularly given the heterogeneity of cohorts, sample sources and analytical approaches. Their potential forensic relevance is also exploratory: ncRNA profiling may provide an additional molecular layer for the characterization of cardiomyopathic substrates in unexplained SCD, but its specificity, post-mortem stability and incremental value over conventional autopsy, histopathology and molecular autopsy remain unestablished. Dedicated longitudinal clinical and forensic studies are required before ncRNAs can be considered for routine clinical or post-mortem application. Full article

Antarctic soils harbor highly specialized bacterial communities that perform essential functions in the functioning of polar ecosystems; however, the composition and structure of these communities remain poorly understood in many areas of Antarctica. The objective of this study was to characterize the diversity and structure of bacterial communities present in soils from four islands in the South Shetland Archipelago (Torre, Barrientos, Greenwich, and Dee) using 16S rRNA gene amplicon sequencing. Total genomic DNA was extracted from composite soil samples, followed by amplification of the 16S rRNA gene and sequencing on the Illumina MiSeq platform. Taxonomic classification allowed the sequences to be assigned from the domain level down to the species level, achieving classification rates between 98.47% and 99.39% at the domain level and between 57.39% and 65.88% at the species level. The bacterial communities were dominated by the phyla Bacillota, Pseudomonadota, Actinomycetota, and Bacteroidota, although variations in relative abundance patterns were observed among the composite samples analyzed. Alpha diversity indices revealed high taxonomic complexity, with greater species richness on Dee Island and greater evenness in Greenwich, highlighting differences in the diversity patterns observed among the composite samples analyzed. Taken together, these results expand our understanding of bacterial biodiversity in Antarctic soils and provide a baseline for future research in microbial ecology, biogeography, and the exploration of the biotechnological potential of microorganisms adapted to extreme environments. Full article

Lonicera japonica Thunb. (honeysuckle), a traditional herb with “food-medicine homology” status in Chinese medicine, is valued for its antipyretic and detoxifying properties. This review systematically summarizes its chemical composition—over 507 identified compounds, including phenylpropanoids, flavonoids, triterpenoids, saponins, and the plant-specific miR2911—as well as its multi-target pharmacological mechanisms and emerging translational applications, with particular emphasis on the gut–brain axis-mediated neuroprotective effects. Despite low oral bioavailability, honeysuckle polysaccharides and chlorogenic acid have been shown to exert significant neuroprotection in Alzheimer’s disease models by modulating gut microbiota composition, increasing short-chain fatty acid production, and restoring intestinal barrier integrity—a mechanism that challenges conventional direct-action paradigms. We also outline the applications of honeysuckle in functional foods, pharmaceuticals, animal husbandry, and cosmetics, and propose future directions including precision fermentation and mechanism-driven clinical trials. By integrating phytochemistry, pharmacology, and biotechnology, this review provides a roadmap for the evidence-based development of honeysuckle as a precise medicinal and edible resource. Full article

Perirenal adipose tissue (PRAT) has emerged as a clinically relevant endocrine organ connecting obesity to cardiovascular disease (CVD), chronic kidney disease, and certain malignancies. Its unique anatomical location, surrounding the kidneys, accounts for PRAT’s role in altering intrarenal haemodynamics and hydrostatic pressure. Accordingly, PRAT’s expansion is associated with the activation of the renin–angiotensin–aldosterone system (RAAS), further increasing blood pressure. Adipokine dysregulation, together with overexpression of miR-24-3p, miR-155, miR-146a, and miR-21 in PRAT, modulates inflammation and oxidative stress, leading to endothelial dysfunction and increased risk of atherosclerosis and hypertension in obesity. Imaging assessment of PRAT thickness through computed tomography, magnetic resonance, or ultrasound has also emerged as a complementary measure for the evaluation of CVD risk. Potential therapeutic strategies targeting PRAT include lifestyle interventions, antidiabetic agents, RAAS inhibitors, adipose tissue browning agents, NOD-like receptor protein 3 (NLRP3) inflammasome inhibitors, peroxisome proliferator-activated receptor gamma (PPARγ) agonists, and surgery. Currently, novel therapeutic interventions targeting PRAT activity in CVD, such as senotherapeutic strategies, bioengineering approaches aimed at enhancing adipose-derived mesenchymal stem cell (ADMSC) function, gut microbiota modulation, and colchicine and bone morphogenetic protein 4 (BMP4) administration, are also being explored. In light of these findings, PRAT’s clinical relevance extends beyond its energy storage role, highlighting it as a metabolically active fat depot. Its assessment and therapeutic modulation may complement existing cardiovascular prevention strategies, particularly in patients with obesity. Full article

Circulating extracellular vesicle-associated microRNAs (EV-miRNAs) are emerging as promising peripheral biomarkers in multiple sclerosis (MS). This prospective, observational pilot study was conceived as a hypothesis-generating investigation to characterize the expression profile of four candidate EV-miRNAs (miR-223-5p, miR-155-5p, miR-30a-5p, and miR-146a-5p) within an EV-enriched plasma fraction. The cohort comprised 16 patients with secondary progressive MS (SPMS) undergoing siponimod therapy, 13 age- and sex-matched healthy controls (HCs), and 7 patients with relapsing–remitting MS (RRMS) included as an exploratory comparator. Quantification was performed by quantitative real-time PCR employing the ΔΔC_t methodology, with miR-16-5p as the endogenous normalizer. Analyses were conducted cross-sectionally and longitudinally, the latter within a paired subgroup of 11 SPMS patients evaluated at baseline and after twelve months of uninterrupted treatment. Cross-sectional comparisons demonstrated a significant downregulation of EV-miR-223-5p in SPMS patients relative to HCs (fold-change [FC] = 0.26; FDR q = 0.026), whereas EV-miR-155-5p was significantly reduced in both the SPMS (FC = 0.35; FDR q = 0.033) and RRMS (FC = 0.28; FDR q = 0.046) cohorts compared with HCs. No significant intergroup differences were observed for EV-miR-30a-5p or EV-miR-146a-5p. Longitudinal assessment revealed no significant modulation of any target EV-miRNA following one year of siponimod therapy. These preliminary observations should be interpreted with caution, given the exploratory nature and modest cohort size. Importantly, the isolation of total plasma EVs does not permit resolution of the specific cellular provenance of the observed signals, nor does it capture their downstream functional consequences. Nevertheless, the selective downregulation of EV-miR-223-5p and EV-miR-155-5p may tentatively suggest candidate molecular signatures warranting further interrogation. Adequately powered studies incorporating cell-specific EV sorting and paired cerebrospinal fluid sampling will be required to substantiate these signals and clarify their potential utility in monitoring disease progression and therapeutic response in progressive MS. Full article