Search Results (735)

Grafting is the primary vegetative propagation technique for ornamental crabapple, and rootstock–scion compatibility critically determines graft healing efficiency and seedling quality. Selecting suitable rootstocks is essential for the popularization of new crabapple cultivars, yet the healing performance of the newly bred cultivar Malus ‘Huabiao’ grafted onto different local Malus rootstocks remains unclear. This study evaluated graft compatibility for M. ‘Huabiao’ grafted onto three rootstocks (M. hupehensis, M. robusta, and M. baccata) through histological observation and dynamic detection of soluble sugar, soluble protein, and tannin during graft healing. The results indicated that M. ‘Huabiao’/M. hupehensis and M. ‘Huabiao’/M. robusta achieved higher survival rates (80.0% and 83.3%, respectively) and complete vascular reconstruction within 28 days, whereas the M. ‘Huabiao’/M. baccata combination exhibited a lower survival rate (63.0%) and obvious healing lag. All combinations showed consistent physiological variation trends, while the M. baccata group maintained higher soluble sugar content, greater protein fluctuations, and significantly elevated tannin levels (p < 0.05). Physiological substance accumulation was closely correlated with healing performance, with higher soluble sugar and protein levels associated with better wound recovery, and excessive tannin accumulation correlated with retarded tissue regeneration capacity. Distinct healing asynchrony was observed among combinations, with incomplete vascular connection detected in the M. baccata group at day 28. This study confirms that M. hupehensis and M. robusta are superior compatible rootstocks for M. ‘Huabiao’, and the dynamic levels of the three physiological indices can serve as potential indicators for evaluating crabapple graft compatibility. Full article

Gut microbial metabolism links intestinal ecology with systemic physiology and neural pathology, but its effects vary across disease stage, tissue compartment, and host background. This review uses Alzheimer’s disease (AD) as the principal model and compares selected features with Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS). Across the AD continuum, fermentation-related changes appear in prodromal cohorts, whereas broader alterations in amino acid products, host–microbial co-metabolites, bile acids, and lipids accompany mild cognitive impairment and dementia. These group-level patterns do not constitute a fixed patient trajectory. Microbial production, intestinal absorption, hepatic conversion, renal clearance, barrier integrity, and tissue-specific receptors jointly determine biological exposure. Experimental studies connect short-chain fatty acids and indole derivatives with epithelial and neuroimmune homeostasis, while imidazole propionate, trimethylamine N-oxide, selected kynurenine products, and remodeled bile acid pools engage vascular, inflammatory, amyloid, or tau-related pathways. Cerebral pathology can also remodel the intestinal ecosystem, creating reciprocal feedback. Apolipoprotein E4 modifies lipid handling, vascular permeability, and immune responses, helping to explain why comparable metabolic profiles may carry different consequences among individuals. Translation therefore requires more than a change in community composition. Trials must verify microbial function, metabolite target engagement, AD biomarker response, and clinical benefit in appropriately stratified participants. Shared pathways in PD and ALS provide comparison points, but disease-specific cells, proteinopathies, and treatment exposures constrain direct transfer of AD-derived targets. Full article

Background: PRKD1-related congenital heart defects and ectodermal dysplasia syndrome (CHDED) is a rare multisystem developmental disorder caused by heterozygous gain-of-function variants in PRKD1. Reported phenotypes include congenital heart defects, ectodermal abnormalities, limb anomalies, and neurodevelopmental impairment, while vascular manifestations remain poorly characterized. We report an adult patient with a de novo PRKD1 variant and bilateral carotid artery dissections. Methods: Clinical, cardiovascular, neurological, and genetic evaluations were performed, including SNP-microarray and trio whole-exome sequencing with additional analysis of genes associated with heritable thoracic aortic and connective tissue disorders. Results: The patient was diagnosed at 35 years of age with a de novo PRKD1 c.1808G>A p.(Arg603His) variant. He had childhood-onset congenital heart disease, ectodermal and skeletal abnormalities, hearing impairment, infertility, and learning difficulties. In adulthood, he developed bilateral carotid artery dissections and mild aortic dilatation. No additional pathogenic or likely pathogenic variants were identified in the evaluated connective tissue and heritable aortic disease genes. The PRKD1 variant was absent or extremely rare in population databases and had supporting functional evidence for a gain-of-function effect. Conclusions: This case raises the possibility of a previously unrecognized vascular manifestation of PRKD1-related CHDED. Although a biological association is plausible, causality cannot be established from a single case. Further clinical and functional studies are needed to determine whether vascular fragility is a recurrent feature of PRKD1-related disease. This case also highlights the importance of considering rare genetic syndromes in patients with unexplained arteriopathy and congenital heart disease. Full article

Background: Diabetic retinopathy (DR) and Parkinson’s disease (PD) are prevalent, progressive disorders that cause irreversible visual impairment and motor dysfunction, respectively. Increasing evidence suggests that retinal alterations may precede and predict neurodegeneration in PD, indicating potential shared pathogenic mechanisms. This study aimed to delineate the molecular and cellular connections between DR and PD, with a particular focus on their convergent neuroimmune and vascular pathways. Methods: We integrated single-cell RNA sequencing (scRNA-seq) datasets derived from proliferative DR (PDR) retinal fibrovascular membranes and PD brain tissues. Cell-type-associated transcriptional features were identified within each dataset, and corresponding cell populations were compared to identify candidate overlapping molecular features. CellChat was used to infer potential ligand–receptor interactions between cell populations. Gene set enrichment analysis (GSEA) and gene set variation analysis (GSVA) were performed to explore associated biological pathways and transcriptional programs. Results: A2M, NRP1, and ETS2 were identified as candidate shared transcriptional features in corresponding microglial and endothelial cell populations across the PDR and PD datasets. CellChat analysis predicted an ITGB2–ICAM1 (integrin beta-2-Intercellular Adhesion Molecule 1) ligand–receptor interaction in both datasets, although the predicted sender–receiver relationships differed according to tissue context. GSEA and GSVA identified overlapping inflammatory, apoptotic, hypoxia-related, and epithelial–mesenchymal transition-associated transcriptional programs across the analyzed datasets. These findings suggest potentially convergent immune–vascular and inflammatory features between PDR and PD. Conclusions: This exploratory single-cell analysis identified candidate cell-type-associated transcriptional features and potential cell–cell communication patterns shared between PDR and PD. The predicted ITGB2–ICAM1 interaction provides a hypothesis for further investigation of immune–vascular communication. Full article

Background: Sickle cell disease (SCD) is a systemic disorder marked by chronic pain and neurocognitive deficits, yet the molecular drivers of these neurocognitive features remain poorly defined. Platelets, central to inflammation and vascular homeostasis, may reflect broad pathophysiologic processes in SCD. Methods: We performed high-resolution mass spectrometry on ultra-purified platelets from 16 adults with SCD and moderate to severe pain (self-reported ≥ 3/10 in the past year), identifying 4196 proteins, of which 1046 were significant (FDR < 0.05). Unsupervised clustering was used to stratify individuals into high- and low-pain phenotypes. Results: Contrary to expectations, canonical pain pathways were not enriched. Instead, significant alterations were observed in neurodegeneration, mitochondrial metabolism, ATP regulation, mitophagy, and tRNA aminoacylation pathways between high- and low-pain phenotypes. High-pain individuals exhibited elevated levels of proteins involved in proteostasis and neurodegenerative disease processes, whereas low-pain individuals showed increased expression of proteins linked to mitochondrial integrity, neuroprotection, and reduced oxidative stress. Protein-protein interaction networks revealed tightly connected clusters within neurodegenerative and central nervous system-related pathways. Disease association analysis ranked neurodegenerative and mitochondrial pathways above traditional hematologic and nociceptive mechanisms. Conclusions: These findings suggest that platelet proteomics may serve as a peripheral window into PNS or CNS vulnerability and cognitive risk in SCD. The enrichment of tRNA aminoacylation and mitochondrial regulation pathways underscores the metabolic complexity of SCD and highlights novel targets for biomarker development and therapeutic intervention. Full article

Aortopathies in autoimmune rheumatic diseases (ARD) include a spectrum of aortic pathologies—including aortitis, aneurysms, dissections, and insufficiency—primarily caused by systemic inflammation. This comprehensive review investigates the clinical manifestations, pathophysiology, diagnostic modalities, and management strategies across various rheumatic diseases associated with aortopathies such as large vessel vasculitis (e.g., Takayasu arteritis, giant cell arteritis), connective tissue diseases (e.g., systemic lupus erythematosus, rheumatoid arthritis, ankylosing spondylitis, systemic sclerosis) and less common conditions (e.g., relapsing polychondritis, Cogan’s syndrome, Behçet’s disease, IgG4-related disease). Disease-specific pathophysiologic mechanisms of aortic wall inflammation and remodeling, including granulomatous and lymphoplasmacytic patterns and mixed inflammatory infiltrates, are described. Diagnostic imaging modalities—such as CTA, MRI, and PET/CT—are evaluated for their roles in detecting active inflammation, assessing structural complications, and guiding clinical decision-making. Histopathological findings provide insight into disease-specific vascular changes. Management strategies focus on the use of glucocorticoids, disease-modifying antirheumatic drugs (DMARDs), and biologics, including IL-6 and TNF-α inhibitors, with an emphasis on patient-centered approaches, multidisciplinary care, and timely surgical intervention for complications. Evidence gaps include optimal screening intervals and the role of novel biomarkers in risk stratification and in monitoring disease progression, highlighting the need for early recognition, frequent monitoring, and aggressive management of aortic involvement in rheumatic diseases to prevent life-threatening complications. Full article

COVID-19 remains a relevant area of biomedical investigation because its pathogenesis involves complex virus–host interactions. This study aimed to explore, through purely in silico and hypothesis-generating insights, the predicted molecular associations between benzyl isothiocyanate (BITC) from Salvadora persica and COVID-19-associated host-response pathways. BITC-associated targets were collected from compound-target databases, while COVID-19-associated targets were obtained from disease-gene databases and transcriptomic datasets. Overlapping targets were analyzed using protein–protein interaction network construction, hub-gene prioritization, Gene Ontology and KEGG enrichment analyses, and molecular docking. A total of 271 unique BITC-associated targets and 1890 COVID-19-associated targets were identified, with 36 candidate targets overlapping. PPI analysis generated a connected network of 24 nodes and 39 edges. Hub-gene analysis prioritized ACE, JUN, MAOA, CDK1, MAOB, HCK, CCNA2, ACHE, GADD45A, and ADRA2A. Enrichment analysis indicated associations with inflammatory response, vascular regulation, calcium homeostasis, monoamine oxidase activity, NF-κB signaling, serotonergic synapse, and tryptophan metabolism. Validated active-site docking of six targets yielded comparative Vina scores ranging from −5.380 to −6.437 kcal/mol. These preliminary findings provide theoretical target–pathway associations supporting further investigation of BITC as a potential immunomodulatory candidate within COVID-19-related host-response pathways. Full article

Coronary heart disease (CHD) is a leading cause of morbidity and mortality, driven by metabolic remodeling, vascular inflammation, and perivascular adipose tissue (PVAT) dysfunction. We integrated bulk transcriptomic datasets to develop a machine learning-based diagnostic model, evaluated 113 algorithms, and identified a seven-gene signature (PYGL, PTGS2, PFKFB3, MMP9, CYP1B1, CXCR1, ABCB1) with robust predictive performance. Single-cell RNA sequencing (scRNA-seq) of coronary PVAT revealed substantial cellular heterogeneity and prioritized PFKFB3 as a hub linking glycolytic activity to nuclear factor kappa B (NF-κB) regulon activity. Macrophage-centered communication via secreted phosphoprotein 1 (SPP1), migration inhibitory factor (MIF), and other pathways was enhanced in disease conditions. Virtual knockout of PFKFB3 induced transcriptional changes enriched in immune activation, phagocytosis, and oxidative stress, while molecular dynamics (MD) simulations suggested that salidroside can adopt a stable binding pose within the PFKFB3 pocket, providing structural plausibility for their interaction. Together, these analyses provide a multi-layered framework connecting glycolytic remodeling, inflammatory transcriptional activity, and intercellular signaling in CHD. The findings support PFKFB3 as a potential biomarker and mechanistic hub and suggest that salidroside may modulate its activity. This study offers an integrative computational foundation for future experimental validation and mechanistic exploration of PVAT dysfunction in CHD. Full article

Menopause represents a major neuroendocrine transition characterized by substantial hormonal, metabolic, vascular, and inflammatory changes that may increase vulnerability to cognitive decline and neurodegenerative disease. Declining estrogen levels during the menopausal transition influence multiple neural processes, including synaptic plasticity, cerebral glucose metabolism, mitochondrial function, neuroinflammatory signaling, and cerebrovascular regulation. Women account for nearly two-thirds of individuals diagnosed with Alzheimer’s disease, and mounting evidence suggests that menopause may represent a period of heightened neurological vulnerability. Physical exercise has emerged as one of the most promising non-pharmacological strategies for preserving cognitive health and reducing neurodegeneration risk in aging women. Current evidence demonstrates that exercise interventions after menopause are associated with improvements in executive function, memory performance, attention, and global cognition. These benefits appear to result from converging biological mechanisms that include enhanced neurotrophic signaling, increased brain-derived neurotrophic factor (BDNF) expression, improved cerebrovascular function, reduced systemic inflammation, improved insulin sensitivity, enhanced metabolic regulation, and preservation of structural brain integrity. Neuroimaging studies further demonstrate exercise-associated increases in hippocampal volume, cortical thickness, functional connectivity, and cerebral blood flow. Different exercise modalities appear to produce distinct but complementary neurological benefits. Aerobic exercise is strongly associated with improved cerebrovascular function and hippocampal integrity, resistance training demonstrates favorable effects on executive function and white matter preservation, and multimodal interventions combining aerobic, resistance, balance, and cognitively engaging activities appear to produce the broadest cognitive benefits. Emerging evidence further suggests that the timing of exercise initiation relative to menopause may influence outcomes, with earlier interventions potentially conferring greater neuroprotection. This review synthesizes current evidence regarding the effects of exercise on cognitive function in postmenopausal women, with emphasis on biological mechanisms, neuroimaging findings, exercise modality, timing considerations, and implications for neurodegeneration prevention. Understanding these relationships provides a scientific rationale for positioning exercise as a foundational strategy for preserving cognitive health and reducing neurodegenerative disease burden in postmenopausal women. Full article

Agronomic modulation of secondary metabolism may influence not only crop resilience but also the biological activity of fruit-derived phytochemicals. In this study, we evaluated the impact of exogenous methyl jasmonate (MeJA) application under contrasting water regimes on the selected phenolic compounds and vascular bioactivity of Vaccinium corymbosum L. cv. Legacy. Antioxidant capacity was assessed by FRAP and DPPH assays, phytochemical composition was characterized by HPLC-DAD, and antiplatelet activity was evaluated through inhibition of TRAP-6–induced P-selectin (CD62P) expression in human platelets. Selected phenolic constituents were further examined using molecular docking and molecular dynamics simulations against a platelet receptor model. Although MeJA treatment altered the abundance of selected phenolic compounds identified by HPLC-DAD, total antioxidant capacity remained largely unchanged. Blueberry extracts significantly inhibited platelet activation in a concentration-dependent manner without cytotoxic effects, and antiplatelet potency was not strictly related to global antioxidant indices. Computational analyses revealed stable ligand–receptor interactions and favorable binding free energies for selected phenolics, providing a structural explanation for receptor-level modulation. These findings suggest that elicitor-driven responses in blueberries can influence platelet functional responses and highlight the importance of qualitative phytochemical composition in determining vascular bioactivity. This multiscale approach connects plant stress physiology, natural product chemistry, and human platelet biology, underscoring the translational relevance of agronomic strategies for nutraceutical functionality. Full article

Connecting the intestinal vasculature with the pre-existing systemic circulatory system is vital for nutrient absorption and blood transport for detoxification in the liver. However, the cellular processes underlying this connection remain unclear. Using genetically modified zebrafish models and in vivo imaging, we visualized that the supra-intestinal artery (SIA) connected to the pre-existing dorsal aorta (DA) in two distinct regions, the anterior and posterior. We found that endothelial cells migrated out of the DA and formed the anterior SIA-DA junction, whereas endothelial cells sprouted from SIA and connected to the DA in the posterior region. Pharmacological and genetic analyses revealed that activin receptor-like kinase 1 (ALK1) signaling was required for the SIA-DA connections. The present study provides new insights into the cellular phenomena and regulatory mechanisms of intestinal vascular development. Full article

Vessel segmentation is a fundamental task in medical image analysis and plays an important role in disease diagnosis and treatment assessment. However, existing segmentation methods often show limited adaptability to feature extraction from single-channel X-ray coronary angiograms, which restricts their performance in segmenting small vessels and low-contrast vascular regions. To address these limitations, this study proposes a Channel-Attention U-Net, termed CA-UNet, which integrates residual connections and a channel attention mechanism. Based on the conventional encoder–decoder architecture of U-Net, the proposed method introduces a residual-enhanced double-convolution block to alleviate gradient vanishing in deeper networks. In addition, a dual-pooling channel attention module is incorporated to enhance the selection of discriminative vascular features. Furthermore, the data loading, normalization, and augmentation strategies are optimized to improve the adaptability of the network to single-channel PGM grayscale images. Under three-fold out-of-fold evaluation, CA-UNet achieved the highest mean Dice coefficient (0.7450) and IoU (0.5972) among the evaluated models, while maintaining real-time-rate inference at 41.7 frames per second. These results indicate that CA-UNet provides an effective balance of segmentation accuracy, stability, and computational efficiency for vessel segmentation. Full article

Brain arteriovenous malformations (AVMs) are complex cerebrovascular lesions characterized by abnormal direct connections between arteries and veins, resulting in altered hemodynamics and an increased risk of rupture. Following PRISMA, a comprehensive review on CFD-based modelling in brain AVMs was conducted across major scientific databases, including Pub-Med/MEDLINE, Scopus, Web of Science, Google Scholar, EBSCO Academic Search and IEEE Xplore, evaluating its role in hemodynamic analysis and pre-procedural planning. Twenty-three studies met the inclusion criteria and were analyzed through both qualitative synthesis and bibliometric approaches. Bibliometric analysis revealed a growing research interest in image-based modelling, 4D flow imaging and virtual embolization after 2021. Despite recent advances in study of hemodynamics simulations, the application of computational fluid dynamics (CFD) to brain AVMs remains challenging due to their complex vascular architecture and highly heterogeneous flow patterns. Nevertheless, CFD remains an important imaging modality for characterizing the lesion and guiding pre-interventional decision making. Full article

Background and Objectives: Cardiovascular disease remains the leading cause of premature mortality worldwide. Subclinical glucose dysregulation, a contributor to accelerated vascular aging, is undetectable by conventional screening in apparently healthy individuals; even within the normal glycemic range, postprandial glucose excursions promote endothelial injury and inflammatory pathways independently of mean glucose levels. Hypothesis: Continuous glucose monitoring (CGM)-guided metabolic phenotyping, combined with personalized dietary optimization, structured fasting protocols, and selective longevity-oriented pharmacotherapy, constitutes a mechanistically coherent, hypothesis-generating preventive strategy that may attenuate cardiovascular risk and biological aging in apparently healthy non-diabetic adults, pending confirmation in prospective outcome trials. Materials and Methods: This narrative review synthesizes evidence from prospective cohort studies, randomized controlled trials, and mechanistic investigations connecting CGM-guided metabolic assessment with preventive cardiology and the emerging field of longevity medicine, focusing on glycemic variability biology, nutrient-sensing pathways, and the cardiovascular and longevity profiles of low-dose metformin and acarbose. Results: CGM-derived metrics capture inter-individual glycemic variability invisible to standard assessments and provide behavioral feedback for dietary personalization. Structured fasting and low-dose metformin converge on shared nutrient-sensing pathways implicated in both vascular aging and longevity, with CGM enabling objective confirmation of metabolic adaptation. Acarbose has shown cardiovascular and lifespan benefit signals in secondary trial analyses and preclinical longevity models, though these findings require replication and are not yet established in non-diabetic populations. Conclusions: We propose a four-phase research framework integrating CGM metabolic phenotyping, dietary optimization, fasting titration, and selective pharmacological augmentation for apparently healthy adults at cardiovascular risk. Prospective hard-endpoint trials are lacking, and this framework should be regarded as hypothesis-generating rather than an established clinical strategy, warranting rigorous outcome-based evaluation before clinical adoption. Full article

Background/Objectives: Accurate arterial tree reconstruction from computed tomography angiography (CTA) is essential for vascular diagnosis, surgical planning, and hemodynamic modelling. A persistent and underappreciated problem is vessel discontinuity: thin distal branches appear as disconnected fragments rather than continuous structures, caused by bifurcations, image noise, contrast variation, arterial plaque, motion artifacts, and partial volume effects. This scoping review aimed to systematically characterize computational approaches addressing vessel breakage in CTA segmentation and identify methodological gaps warranting further investigation. Methods: This scoping review was conducted in accordance with PRISMA-ScR guidelines. Google Scholar and PubMed were queried for studies published between March 2000 and March 2026. Eligible studies included peer-reviewed journal articles and conference proceedings presenting original methodological contributions to three-dimensional vascular segmentation from CTA. Results: Three generations of computational solutions were identified: classical geometric and geodesic methods, deep learning approaches with topology-aware training, and hybrid post-processing frameworks. Topology-sensitive metrics (clDice, Topology Sensitivity) were identified as preferred metrics to better capture clinical utility than standard voxel-based metrics such as the Dice coefficient. Conclusions: Vessel discontinuity remains a clinically relevant and challenge in vascular CTA segmentation. Hybrid post-processing frameworks combining deep learning with geodesic connectivity restoration represent the current state of the art. Standardized adoption of topology-aware evaluation metrics is recommended to better reflect clinical utility in future studies. Full article