Search Results (1,481)

Background: Vitamin D is involved not only in calcium–phosphate homeostasis but also in immune and endothelial regulation. Vitamin D deficiency has been suggested to worsen disease activity in systemic lupus erythematosus (SLE). Environmental and lifestyle factors, including seasonal sun exposure, smoking, diet, and supplementation, may influence vitamin D status and disease manifestations. This study aimed to evaluate the association between serum 25-hydroxyvitamin D [25(OH)D] levels, disease activity, and anti-double-stranded DNA (anti-dsDNA) antibody titers in patients with SLE, taking selected lifestyle and environmental factors into account. Methods: Serum 25(OH)D concentrations, SLE disease activity assessed by the Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) score, and anti-dsDNA antibody titers were measured in patients with SLE and healthy controls. Blood samples were collected during sunny (April–September) and non-sunny (October–March) months. Information on vitamin D supplementation, smoking status, and dietary habits was obtained using a structured questionnaire. Associations between vitamin D status, disease activity, anti-dsDNA seropositivity, season of blood collection, supplementation, smoking, and diet were analyzed statistically. Results: Patients with SLE had significantly higher mean serum 25(OH)D levels than controls, mainly due to frequent vitamin D supplementation. No significant associations were observed between serum 25(OH)D levels and SLEDAI-2K scores or anti-dsDNA antibody positivity. Seasonality, smoking status, and adherence to special diets were not significantly related to disease activity or anti-dsDNA seropositivity. Vitamin D supplementation was strongly associated with sufficient 25(OH)D levels but did not translate into reduced disease activity or lower anti-dsDNA prevalence. Conclusions: Serum 25(OH)D concentration was not associated with clinical or immunological activity of SLE in this cross-sectional study, despite effective correction of deficiency through supplementation. These findings likely reflect the heterogeneity of SLE and the limitations of single time-point assessments, although regular monitoring and individualized vitamin D supplementation may still be considered in SLE care, particularly in the context of recommended photoprotection. Full article

Carbohydrate-active enzymes (CAZymes) encoded by the human gut microbiome are central mediators of dietary glycan metabolism and host–microbe biochemical homeostasis. Among these, β-glucuronidases represent functionally pivotal hydrolases implicated in metabolism, intestinal physiology, and therapeutic modulation. The present study performs an integrative in silico structural and functional interrogation of β-glucuronidases derived from Acidobacterium capsulatum (3VNY), Bacteroides ovatus (6D8K), and Faecalibacterium prausnitzii (6ED2). An integrated computational framework encompassing physicochemical parameters profiling, hierarchical structural prediction, tertiary-structure validation, salt-bridge energetics, functional domain and motif annotation, protein–protein interaction reconstruction, ligand-binding thermodynamics via molecular docking, and residue-resolved non-covalent interaction network mapping using the Protein Contacts Atlas (PCA) was employed. Physicochemical analyses indicated that all enzymes are thermostable, intracellular, and hydrophilic, while secondary-structure organization revealed a functional balance between helix-mediated rigidity and coil-driven flexibility. Structural validation metrics identified 6ED2 as the most conformationally stable architecture, whereas 6D8K displayed enhanced functional complexity, including enriched motif composition, membrane-associated features, and superior ligand-binding affinity. Docking simulations highlighted castanospermine and calcium saccharate as the most favorable interacting ligands across enzyme variants. Importantly, PCA-based interaction analysis revealed distinct ligand-centered atomic contact networks, with immediate contact counts of 57 (3VNY), 32 (6D8K), and 41 (6ED2), providing residue-level insight into stabilization mechanisms and interaction topology beyond conventional docking metrics. Collectively, these findings establish a multidimensional computational framework linking structural stability, functional diversification, ligand recognition, and atomic interaction networks in gut microbial β-glucuronidases, thereby supporting future biochemical validation, microbiome-targeted therapeutics, and biotechnological or cosmeceutical applications. Full article

Background: Vitamin D deficiency rickets is a metabolic bone disorder caused by impaired calcium and phosphate homeostasis resulting from insufficient vitamin D. In children, severe vitamin D deficiency can disturb the mineralization of growing bones and teeth. Although the skeletal manifestations are well recognized, reports describing generalized developmental enamel defects affecting nearly all permanent teeth remain limited. Methods: A 6-year-9-month-old Japanese boy with a history of vitamin D deficiency rickets diagnosed at 2 years 5 months of age was referred to our department for evaluation of generalized discoloration and morphological abnormalities affecting multiple permanent teeth. Clinical, radiographic, and medical findings were reviewed. Results: Laboratory examination at diagnosis revealed severe vitamin D deficiency with elevated intact parathyroid hormone levels. Possible contributing factors included exclusive breastfeeding, delayed weaning, avoidance of fish and dairy products, and limited outdoor activity. Following oral alfacalcidol supplementation, skeletal and biochemical findings gradually normalized. However, clinical examination revealed generalized enamel hypoplasia affecting the permanent incisors and first molars, characterized by yellow-brown discoloration, rough enamel surfaces, morphological irregularities, and attrition, whereas the primary dentition showed no obvious abnormalities. Panoramic radiography demonstrated generalized crown malformation involving both erupted and unerupted permanent teeth, particularly the permanent incisors, first molars, and canines, while premolars and second molars were relatively unaffected. Based on the developmental timing of the affected teeth and the patient’s medical history, the enamel defects were considered to be associated with systemic mineralization disturbance during early childhood. Restorative treatment, including composite resin restorations and stainless steel crowns, was performed to improve aesthetics and occlusal function. Preventive surgical exposure followed by composite resin restoration was also performed for the permanent canines at the onset of eruption. Conclusions: Severe vitamin D deficiency during critical stages of tooth development may be associated with irreversible developmental enamel defects in the permanent dentition, even after apparent systemic recovery from rickets. Early dental assessment, long-term dental follow-up, and multidisciplinary management should be considered in children with a history of nutritional rickets. Full article

Muscle wasting associated with gastric cancer represents a complex, multifactorial systems disorder involving inflammatory, anabolic, mechanosensory, calcium-regulatory, mitochondrial, and proteostatic disruption. This review synthesizes current evidence regarding the cellular and physiological mechanisms involved in skeletal muscle dysfunction in gastric cancer and provides a unifying framework centered on loss of signaling coherence. Specifically, it examines IL-6/STAT3 and NF-κB inflammatory signaling, the myostatin–activin–ACVR2B–SMAD pathway, PI3K/Akt/mTOR signaling, mechanotransduction, excitation–metabolism coupling, calcium homeostasis, mitochondrial function, and proteostasis. Although individual components of these pathways have been implicated in muscle wasting associated with chronic disease, current evidence suggests that they interact through positive feedback loops. Inflammation, anabolic resistance, impaired force-to-signal conversion, mitochondrial stress, altered intracellular calcium homeostasis, and disrupted protein quality control may reinforce one another, contributing to metabolic, structural, and transcriptional instability. Within this context, muscle wasting reflects not only loss of muscle mass or strength, but also loss of functional integrity resulting from disrupted integration of mechanical, metabolic, inflammatory, and anabolic signals. Given the systemic nature of these effects, this review proposes kinesitherapy as a potentially useful nonpharmacological adjunctive strategy that may modulate inflammation, restore responsiveness to mechanical stimuli, support calcium homeostasis and mitochondrial function, improve anabolic sensitivity, and maintain protein quality control. Overall, this review presents a systems-biology model of gastric cancer-associated muscle wasting and supports further investigation of exercise-based therapies for this condition. Full article

Heritable thoracic aortic diseases (HTADs) comprise a genetically heterogeneous group of disorders predisposing patients to thoracic aortic aneurysm and dissection, yet current medical therapies remain limited to slowing disease progression rather than preventing aortic wall failure. Although pathogenic variants affect diverse genes encoding extracellular matrix (ECM) components, smooth muscle contractile proteins, and signaling molecules, these defects converge on disruption of the mechanobiological systems that maintain aortic wall integrity. The thoracic aorta functions as a mechanically integrated tissue in which endothelial cells, vascular smooth muscle cells, fibroblasts, immune cells and ECM continuously sense and respond to pulsatile biomechanical forces. Genetic perturbations affecting ECM architecture, contractile force generation, or growth factor signaling alter force transmission across this multicellular network, leading to maladaptive mechanotransduction, cellular phenotypic modulation, and progressive aneurysm formation. Using Marfan syndrome as a paradigmatic ECM-driven aortic disease, this review synthesizes current understanding of how altered biomechanics, biochemical signaling and immune responses reshape intercellular communication and activate disease-associated signaling pathways, including dysregulated TGF-β, nitric oxide, angiotensin receptor, calcium-dependent, and metabolic signaling. We highlight how single-cell transcriptomic analyses have elaborated changes in different cell-level functions including, ECM degradation, iron homeostasis, circadian/stress responses. Changes in iron metabolism in different cell types in the aorta suggest possible coordinated metabolic changes in aneurysm progression. These mechanistic insights enable the identification of cell-type–specific pathogenic programs and therapeutic discovery through systems-level approaches. We highlight the translational opportunities and challenges emerging from mouse models and human studies, emphasizing that therapeutic efficacy depends not only on pathway selection but also on disease stage, cellular context, and timing of intervention. Together, these findings support a model in which HTAD progression reflects dynamic, multicellular failure of mechanobiological homeostasis and provide a framework for the development of more precise, mechanism-based therapies. Full article

Cracking is a major cause of concrete deterioration because it allows water and aggressive ions to penetrate the material and accelerate structural damage. Microbially induced calcite precipitation (MICP) has emerged as a promising strategy for crack repair because selected bacteria can precipitate calcium carbonate and thereby seal damaged regions. In this study, we characterized strain ITBMC36, a calcite-precipitating bacterium isolated from a limestone-rich environment in Vietnam, and evaluated its potential for MICP-based crack repair. Strain ITBMC36 produced 26.73 ± 0.81 g/L of mineral precipitate in B4 medium. Mineral characterization showed that the precipitate consisted mainly of calcite, with minor amounts of vaterite and aragonite. Enzymatic assays showed urease activity of 35.71 ± 1.24 U/mL and carbonic anhydrase activity of 162.71 ± 1.00 U/mL. Hybrid genome sequencing generated a complete circular chromosome of 4,410,549 bp, and genome-based taxonomic analysis identified the isolate as Bacillus paralicheniformis. Genome mining revealed traits relevant to MICP and survival in cementitious environments, including a complete urea uptake and urease system, five putative carbonic anhydrase genes, exopolysaccharide and biofilm-associated loci, and multiple genes involved in stress response, pH homeostasis, and sporulation. In mortar specimens containing artificial microcracks (0.5 ± 0.1 mm), ITBMC36 promoted progressive crack closure, with visible mineral deposition by day 7 and near-complete sealing by day 35. Together, these results identify B. paralicheniformis ITBMC36 as a promising, locally sourced bacterium for MICP-based crack repair and provide a high-quality genome resource for future optimization of bio-based cementitious materials. Full article

Human spaceflight in microgravity induces profound physiological adaptations, yet its effects on the sensory system remain comparatively underexplored. While musculoskeletal and cardiovascular changes are well documented, sensory alterations pose equally important challenges to astronaut safety, performance, and post-mission recovery. Calcium ions (Ca²⁺), as universal intracellular messengers, play central roles in sensory transduction, neurotransmitter release, and adaptive signaling across all sensory modalities. Emerging evidence suggests that microgravity may influence Ca²⁺ homeostasis and Ca²⁺-dependent cellular processes, potentially affecting the functional integrity of sensory pathways. In this review, we synthesize current findings on the impact of microgravity on Ca²⁺-dependent processes in the five classical senses. Evidence from spaceflight studies, ground-based analogs, and related physiological models suggests possible alterations in taste receptor signaling, Ca²⁺-binding protein expression, mechanotransduction pathways, and vestibular function. However, direct evidence for microgravity-induced disruption of Ca²⁺ signaling remains limited for several sensory modalities. Collectively, these changes are associated with altered taste and smell perception, visual disturbances, reduced tactile sensitivity, and vestibular imbalance. By integrating both direct evidence and mechanistic hypotheses across sensory systems, this review highlights Ca²⁺ signaling as a potential unifying mechanism underlying sensory adaptation to microgravity. We further identify key knowledge gaps and discuss potential directions for developing targeted countermeasures aimed at preserving sensory function during long-duration missions. Beyond spaceflight, these insights contribute to a broader understanding of Ca²⁺-mediated sensory physiology under extreme environmental conditions. Full article

Pomegranate (Punica granatum), a shrub belonging to the Lythraceae family, has long been recognized for its diverse pharmacological benefits, including potential roles in managing inflammation and diabetes. The present study explored the insulin-secretory and β-cell proliferative properties of the ethanol extract of P. granatum fruit peel (EEPG) and assessed its influence on glucose regulation in high-fat-fed diet-induced obese mice (HFDi-OM) through in vivo and in silico studies. In vitro, EEPG was found to activate cAMP-dependent pathways and regulate K_ATP channels, thereby enhancing glucose-stimulated insulin secretion from BRIN-BD11 β-cells, with partial reliance on extracellular calcium. EEPG promoted β-cell proliferation, as indicated by an increase in Ki-67 positive cells, and displayed inhibitory effects on glucose diffusion and starch hydrolysis, suggesting a capacity to delay carbohydrate digestion and absorption. Furthermore, EEPG demonstrated antioxidant activity by neutralizing free radicals. In an acute test, EEPG (at doses of 150 and 250 mg/5 mL/kg) improved oral glucose tolerance and elevated plasma insulin levels. Long-term oral treatment for 21 days to HFDi-OM led to a significant reduction in fasting blood glucose, body weight, and food and fluid intake. It also enhanced gastrointestinal motility and improved lipid profiles by increasing HDL and lowering total cholesterol, LDL, and triglycerides. The therapeutic properties of EEPG are likely attributed to its rich bioactive components, including flavonoids (quercetin, kaempferol, catechin, and epicatechin) and phenolic acids (ellagic acid), which exhibited strong multi-target binding affinities in in silico molecular docking studies toward SUR1, PDE4, PI3K, and α-amylase, thereby supporting enhanced insulin secretion, β-cell function and glucose homeostasis. Full article

Ryanodine receptor-like (RyR-like) is a key endoplasmic reticulum (ER) Ca²⁺ release channel governing intracellular Ca²⁺ homeostasis and cellular stress responses in invertebrates. However, its function in bivalves under high-temperature stress remains unclear. In the present study, one RyR-like was identified from Yesso scallop Patinopecten yessoensis (PyRyR-like). Its function in regulating intracellular Ca²⁺, IRE1α-mediated unfolded protein response (UPR) and apoptosis in the mantle after high-temperature (25 °C) treatment was investigated using molecular cloning, qRT-PCR, Western blot, pull-down assay, cellular calcium imaging, TUNEL and histology assays; High temperature treatment significantly increased intracellular Ca²⁺ content at 1 and 6 h (p < 0.05), but decreased it at 3, 12 and 24 h (p < 0.05); meanwhile, the cAMP level, PyPKA activity, mRNA expression level of PyRyR-like, and protein expression levels of PyFKBP12 and PyGRP78 were significantly increased at different times. However, high temperature did not affect the expression level of PyNVL and PyXBP1(S). The SPRY and RYR domains of PyRyR-like separately interacted with PyFKBP12 and PyPKA. Moreover, RyR antagonist Dantrolene reversed high-temperature-induced alterations in Ca concentration, PKA activity, and core UPR- and apoptosis-related molecules, and suppressed Caspase-3 activity. These findings suggest that PyRyR-like plays an important role in the high-temperature response of scallops by regulating intracellular Ca²⁺ homeostasis and mediating UPR activation and apoptosis, providing new insight into the molecular mechanism underlying scallop adaptation to high temperature. Full article

Background/Objectives: Hypocalcemia is a major transition-cow disorder in dairy cattle, with clinical and subclinical forms differing in detectability, severity, timing, and herd-level consequences. This systematic review integrates evidence on calcium (Ca) homeostasis, classification of clinical hypocalcemia (CHC) and subclinical hypocalcemia (SCH), diagnostic interpretation, risk factors, systemic effects, and preventive and therapeutic strategies in dairy cows. Methods: Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 statement, PubMed, ScienceDirect, SpringerLink, and CAB Abstracts were searched in February 2026 for 1994–2025 publications, and 23 reports were included in a qualitative synthesis; meta-analysis was not performed because of methodological and outcome heterogeneity. Results: The evidence indicates that hypocalcemia should be interpreted as a failure of homeorhetic adaptation to abrupt mammary Ca export rather than as a simple mineral deficiency. The parathyroid hormone–vitamin D axis, skeletal Ca mobilization, renal Ca conservation, intestinal Ca absorption, magnesium (Mg) status, dietary cation–anion difference (DCAD), dry matter intake, parity, and acid–base balance jointly determine whether blood Ca is maintained during early lactation. Total calcium (tCa) thresholds are useful decision aids for herd-level monitoring, but their interpretation depends on sampling time, parity, persistence pattern, clinical signs, and the relationship between tCa and ionized calcium (iCa). Subclinical hypocalcemia is most relevant when it is delayed, persistent, or occurs in high-risk cows because reduced Ca availability can impair smooth muscle function, feed intake, immune competence, uterine health, and metabolic resilience. Management should therefore combine prepartum ration control, Mg adequacy, DCAD and urine pH monitoring, selective Ca testing in high-risk cows, targeted oral Ca supplementation for standing cows, and intravenous Ca treatment for recumbent CHC cases. Conclusions: The evidence supports a risk-based, context-aware strategy rather than universal threshold-driven treatment. Full article

Porcine reproductive and respiratory syndrome virus (PRRSV) is a major cause of disease in swine production, resulting in a high economic impact that has been exacerbated by the recent North American outbreaks of highly virulent PRRSV-2 strain (L1C.5). However, there is limited knowledge about how underlying systemic infections, particularly with this emergent PRRSV strain, affect calcium regulation and bone in pigs fed varying levels of vitamin D. To address this, the goal of this study was to determine the effect of different dietary vitamin D levels and PRRSV infection on calcium regulation and phenotypic changes in bone. Three-week-old pigs (n = 42) were assigned to four treatment groups: marginal dietary vitamin D3 (200 IU/kg) + PRRSV (n = 12), industry standard dietary vitamin D3 (1500 IU/kg) + PRRSV (n = 12), industry standard dietary vitamin D3 (1500 IU/kg) supplemented with 25-hydroxy-vitamin D3 (25-OH D3) (2000 IU/kg) + PRRSV (n = 12), or marginal dietary vitamin D3 without PRRSV inoculation (200 IU/kg) (control, n = 6). Following 26 days of dietary acclimation, assigned treatment groups were inoculated with a PRRSV-2 L1C.5 isolate. Blood samples were collected to evaluate the ionized calcium, 25-OH D3, calcium, phosphorus, and parathyroid hormone levels. The 2nd and 10th ribs were collected at 14 days post challenge for bone ash and density analysis, as well as examination of microscopic changes and scoring of the physis. High mortality was noted in all pigs infected with the virus, regardless of the vitamin D diet. Additionally, a significant depletion of serum calcium was observed at 7 DPC in infected animals, suggesting a high calcium demand at early stages of PRRSV infection. No significant differences in serum calcium, phosphorus, or ionized calcium concentrations were observed between dietary groups during the first 14 days of PRRSV-2 L1C infection. In pigs that succumbed to PRRSV at the early stage of infection, microscopic lesions of multifocal myelonecrosis were noted. This study provides the first report of microscopic changes of bone marrow necrosis and inflammation associated with PRRSV infection and demonstrates calcium dysregulation at the early stage of infection by this highly virulent PRRSV strain. Full article

Acute heart failure (AHF) and cardiogenic shock (CS) remain major causes of cardiovascular morbidity, mortality, and healthcare utilization worldwide. Although inotropic agents are central to the management of low-output states, their clinical utility is fundamentally constrained by mechanisms that increase myocardial oxygen consumption, disrupt calcium homeostasis, and promote arrhythmogenesis, without improving long-term outcomes. These limitations reflect not only pharmacological shortcomings, but a broader conceptual reliance on amplification of intracellular calcium flux as the primary means of augmenting contractility. While effective in increasing cardiac output, this strategy imposes substantial energetic and electrophysiological costs and fails to address key abnormalities of the failing myocardium, including impaired calcium recirculation and diastolic dysfunction. Istaroxime is a first-in-class agent that combines Na⁺/K⁺-ATPase inhibition with enhancement of sarcoplasmic reticulum Ca²⁺-ATPase (sarcoplasmic reticulum Ca²⁺-ATPase isoform 2a (SERCA2a)) function, thereby modulating both calcium availability and reuptake. This dual mechanism promotes a more coordinated pattern of excitation–contraction coupling, integrating systolic augmentation with improved diastolic relaxation. Early clinical studies demonstrate a distinct hemodynamic profile characterized by increased stroke volume, preservation of heart rate, and stabilization or elevation of arterial pressure. These properties suggest a potential role for istaroxime in specific hemodynamic phenotypes, particularly hypotensive AHF and early cardiogenic shock, where conventional inotropes are limited by tachycardia or vasodilatory effects. However, current evidence is limited to phase II studies focused on hemodynamic endpoints, and the impact of istaroxime on survival, organ function, and disease progression remains unknown. Istaroxime represents a mechanistically distinct approach to inotropic therapy, shifting the paradigm from calcium amplification toward partial restoration of calcium cycling. Its clinical relevance will depend on whether this strategy can translate into improved patient outcomes—an objective that has thus far eluded the entire class of inotropic agents. Full article

Background: Vitamin D has traditionally been recognized for its role in calcium homeostasis and skeletal health, but vitamin D receptor expression and vitamin D-metabolizing enzymes have also been identified in extra-skeletal tissues, including components of the male reproductive tract. Observational evidence has suggested associations between vitamin D status and androgen-related markers; however, whether vitamin D supplementation has a measurable effect on androgen bioavailability remains uncertain. Objective: This systematic review and meta-analysis evaluated the effects of vitamin D supplementation on total testosterone (TT) and androgen bioavailability markers in adult men, including sex hormone-binding globulin (SHBG), free androgen index (FAI), calculated free testosterone (calculated FT), and bioactive testosterone (BAT) where methodologically compatible. Methods: The review was registered in PROSPERO (CRD420261365005) and conducted according to PRISMA 2020 and Cochrane methodological guidance. Searches were conducted from database inception to April 2026 in PubMed, Web of Science, Scopus, ClinicalTrials.gov, and the WHO ICTRP. Embase was initially planned but was not searched because institutional access was unavailable; this amendment was made before screening, extraction, risk-of-bias assessment, and synthesis. Records were deduplicated in Zotero, screened in a structured matrix, and converted from report-level records into independent comparison-level datasets where appropriate. Meta-analyses used random-effects REML models with Hartung–Knapp adjustment. Results: The official search set comprised 2854 records, of which 703 duplicates were removed, leaving 2151 records for title and abstract screening. The full-text screening file was reconciled to 162 PRISMA-countable reports/records: 135 reports were assessed, 27 reports could not be assessed because the full text was unavailable or had not been obtained for review, and 27 reports/studies were retained for qualitative synthesis. Eighteen reports were considered candidate sources for quantitative synthesis and were operationalized into 21 comparison-level records. The primary TT model included 11 comparisons and showed no clear effect of vitamin D supplementation on final TT (MD 0.47 nmol/L, 95% CI −0.50 to 1.44; I² = 24.1%). No clear effects were observed for SHBG (MD 0.27 nmol/L, 95% CI −2.14 to 2.68), FAI (MD −0.37, 95% CI −4.28 to 3.55), calculated FT sensitivity evidence (MD −0.0096 nmol/L, 95% CI −0.0525 to 0.0332), or BAT exploratory evidence (MD −0.47 nmol/L, 95% CI −1.77 to 0.83). GRADE certainty was low for TT, SHBG, and FAI, and very low for calculated FT and BAT. Conclusions: Current randomized evidence does not demonstrate a statistically clear or reproducible effect of vitamin D supplementation on total testosterone or androgen bioavailability markers in adult men. GRADE certainty was low for total testosterone, SHBG, and FAI, and very low for calculated free testosterone and bioactive testosterone. Because directly measured and calculated free testosterone are not analytically equivalent, free testosterone was not pooled as a primary outcome; method-compatible calculated FT was handled as sensitivity evidence and BAT as exploratory evidence. Full article

Vitamin D has long been recognized for its role in calcium homeostasis and bone metabolism; however, it is now emerging as an important regulator of central nervous system (CNS) function. Recent evidence suggests that vitamin D signaling contributes to the pathogenesis and progression of several neurodegenerative disorders. Vitamin D exerts neuroprotective effects through multiple mechanisms, including regulation of calcium homeostasis, modulation of immune responses, reduction in oxidative stress, stimulation of neurotrophic factors, and maintenance of blood–brain barrier (BBB) integrity. Vitamin D receptors and metabolizing enzymes are widely distributed across several brain regions, highlighting their direct involvement in neuronal function. This review summarizes the biosynthesis, metabolism, and signaling pathways of vitamin D. It explores its role in neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), stroke, and traumatic brain injury (TBI). Evidence from experimental and clinical studies indicates that vitamin D deficiency is associated with an increased risk and severity of these conditions, while supplementation may provide therapeutic benefits. Full article

The YABBY family consists of plant-specific transcription factors that regulate organ polarity and reproductive development. As a member of this family, CRABS CLAW (CRC) plays crucial roles, but its molecular mechanism in oilseed rape stigma development remains unclear. In this study, we identified YABBY genes in four Brassicaceae species. The results showed that CRC proteins are highly conserved in structure, but their cis-acting elements vary among species. To explore its function, we performed transcriptome sequencing on an oilseed rape CRC-deficient mutant (sd). The transcriptome data revealed multiple changes in the sd mutant. Specifically, brassinosteroid (BR) signaling factors were downregulated. Sugar transporters and auxin-related genes showed abnormal expression. Furthermore, pro-senescence and programmed cell death (PCD) genes were upregulated, whereas the classic senescence pathway remained unchanged. Based on these findings, we propose a potential mechanism. The loss of CRC disrupts BR signaling, sugar transport, and calcium homeostasis. This disruption triggers non-classic death of stigma papilla cells, which hinders pollen tube penetration and reduces seed set. Notably, increasing environmental humidity partially rescued the seed set, likely by delaying cell death. Although these transcriptomic insights warrant further experimental validation, this study provides valuable clues and genetic resources for future research on reproductive development in oilseed rape. Full article