Search Results (5,813)

Background/Objectives: Non-alcoholic fatty liver disease (NAFLD) is a prevalent metabolic disorder for which there are limited pharmacotherapies. Sodium rutin (NaR), a soluble flavonoid derivative, has shown beneficial metabolic effects, but its role in NAFLD remains unclear. This study investigates whether NaR ameliorates high-fat diet (HFD)-induced NAFLD and insulin resistance through promoting hepatic lipophagy. Methods: Male mice aged 8 weeks old were fed a HFD for 12 weeks with/without NaR supplementation. Body weight was measured every week. After 12 weeks of treatment, GTT and ITT were performed to assess insulin resistance. Then, the tissues were collected and hepatic histology, serum biochemistry, and markers of autophagy and senescence were assessed. Results: NaR treatment significantly attenuated HFD-induced weight gain, reduced visceral fat and liver weights, and ameliorated hepatic steatosis and vacuolization. NaR improved serum lipid profiles; lowered alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase levels; and reduced hepatic cellular senescence. NaR enhanced hepatic autophagy, evidenced by decreased p62 levels, increased LC3-II/LC3-I ratio, and enhanced colocalization of lipid droplets with LC3 and LAMP1 in vivo and in vitro. These changes were accompanied by improved glucose tolerance and insulin sensitivity. Conclusions: NaR effectively alleviates HFD-induced NAFLD and insulin resistance by activating hepatic lipophagy. These findings support NaR as a promising multi-targeted therapeutic candidate for NAFLD. Full article

Background and Aim: Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by immune dysregulation. Environmental factors, including infectious agents, have been proposed to influence disease activity in inflammatory bowel disease. Although Borrelia burgdorferi has been shown to exert complex immunomodulatory effects on host immune responses, its seroprevalence and potential association with disease activity in patients with ulcerative colitis have not been systematically investigated. This study aimed to evaluate the seroprevalence of Borrelia burgdorferi IgG antibodies in patients with ulcerative colitis and to assess the relationship between seropositivity and laboratory markers of disease activity. Methods: In this retrospective observational study, 100 patients with ulcerative colitis (59 males, 41 females; mean age 48.5 ± 17 years) who underwent Borrelia burgdorferi IgG serological testing due to musculoskeletal or neurological symptoms suggestive of possible Lyme disease between October 2020 and October 2024 were included. Demographic characteristics, hematological and biochemical parameters, and inflammatory markers were compared between seropositive and seronegative groups. Due to the retrospective design, validated clinical disease activity indices were not consistently available; therefore, disease activity was indirectly assessed using laboratory inflammatory markers. Results: Among patients with ulcerative colitis, 22% were seropositive for Borrelia burgdorferi IgG. Seropositive patients had significantly lower uric acid, alkaline phosphatase, and C-reactive protein levels compared to seronegative patients (p = 0.001, p = 0.023, and p = 0.020, respectively). Free T4 levels were significantly higher in the seropositive group (p = 0.049). In terms of erythrocyte indices, mean corpuscular volume and mean corpuscular hemoglobin were significantly higher, while RDW-CV values were significantly lower in seropositive patients (all p < 0.05). Conclusion:Borrelia burgdorferi IgG seropositivity in patients with ulcerative colitis was associated with lower laboratory markers of systemic inflammation and a more stable hematological profile. Although causality cannot be established, these findings may suggest a potential association between prior Borrelia exposure and a distinct inflammatory phenotype in UC; however, this relationship should be interpreted with caution. Further prospective and mechanistic studies are warranted to clarify the potential immunological interactions between environmental microbial exposure and inflammatory bowel disease activity. Full article

Continuous cropping obstacles in watermelon are closely linked to rhizosphere microbial imbalance, posing a major threat to the sustainability of the industry in Xinjiang. Exogenous additives are widely used to regulate soil health, yet comprehensive comparisons of their mechanisms and effects remain limited. In this study, a field experiment was conducted under continuous watermelon cropping conditions in Xinjiang to evaluate the impact of eight treatments, including chemical fertilizer (NPK) alone and its combination with organic fertilizer (NPKM), glucose (NPKG), oxalic acid (NPKOA), amino acids (NPKGA), citric acid (NPKCA), and acetic acid (NPKAA), with unfertilized soil as the control (CK). Treatment effects were assessed through soil physicochemical analysis, fruit quality evaluation, and high-throughput sequencing (16S rRNA and ITS). Among all treatments, NPKM showed the greatest improvement in soil fertility, increasing soil organic matter by 13.91%, total nitrogen by 23.08%, and single fruit weight by 35.75% compared to CK. NPKGA also enhanced fruit weight (+33.06% vs. CK) and increased catalase activity, while oxalic acid exhibited the strongest activation of alkaline phosphatase. Microbiome analysis revealed that NPKM and NPKAA significantly reshaped both bacterial and fungal community structures. NPKM enriched beneficial taxa such as unclassified Chitinophagaceae and Lophotrichus, whereas NPKCA enriched the biocontrol bacterium Pseudomonas chlororaphis. Soil organic matter and total nitrogen were identified as key environmental drivers, showing significant positive correlations with core bacterial genera (Dokdonella) and negative correlations with the pathogenic fungus Alternaria. Collectively, this study elucidates the distinct mechanisms of various additives by linking treatment-specific microbial shifts to key soil factors and crop performance, providing a theoretical and technical framework for mitigating watermelon continuous cropping obstacles through rhizosphere environmental regulation. Full article

Cyprinid herpesvirus 3 (CyHV-3) is a pathogen that causes high mortality in common carp (Cyprinus carpio) and koi. Common carp breeding lines with different genetic backgrounds exhibit different resistance levels to viral pathogens. This study aimed to determine the differences in CyHV-3 disease resistance performance between the hybrid offspring (Y × M and M × Y) of the mirror carp ‘Longke 11’ (resistant to CyHV-3) and Yellow River carp, as well as the self-crossed offspring (M and Y). The M, Y × M, M × Y and Y groups were infected with CyHV-3 by immersion. The order of mortality and the duration of death for the four groups of carp were as follows: Y group > Y × M group > M × Y group > M group. Throughout the entire infection stage, the mRNA expression levels of the viral factors thymidine kinase (TK) and open reading frame 72 (ORF72) in the four groups of carp tended to first increase but then decrease. The viral factor expression evaluated on days 30 and 31 post-infection (p.i.), which was the peak of infection mortality, was the highest in the Y group and the lowest in the M group, and compared with the Y × M group, the M × Y group had considerably lower viral gene expression (p < 0.05). The immune-related enzyme activity and content levels of the four carp groups matched the patterns of viral gene expression. On day 29 p.i., a time point with high mortality, the levels of alkaline phosphatase (AKP), glutathione peroxidase (GSH-Px) and total antioxidant capacity (T-AOC) were significantly the lowest in the Y group and significantly the highest in the M group, while the Y × M group showed a significant decrease compared to the M × Y group (p < 0.05). Quantitative real-time (q-PCR) analysis revealed that interleukin-21 receptor (IL21R), interferon regulatory factor 9 (IRF9), interferon type I (IFN-I), interleukin-6 (IL-6) and microtubule-associated protein light chain 3 (LC3), exhibited an initial increase followed by a decrease among the four experimental groups of common carp. In the peak mortality period of carp in the four groups (30 days post-infection), the expression levels of IL21R, IRF9, LC3, and IFN-I were significantly the highest in the M group and significantly the lowest in the Y group, with the mRNA expression of these genes in the M × Y group being significantly higher than that in the Y × M group (p < 0.05). In contrast, IL-6 expression levels exhibited the opposite trend. In this study, the M group exhibited the greatest resistance to CyHV-3, followed by the M × Y group, whose resistance was greater than that of the Y × M group, with the Y group showing the lowest disease resistance. Our findings demonstrate that hybridization modulates resistance to CyHV-3. Furthermore, we identified conserved immune signatures common to both susceptible and resistant carp, including the activation of nonspecific immunity and the upregulation of immune-associated genes. Full article

Background/Objectives: Feeding with a ketogenic diet (KD), nutritionally devoid of carbohydrates, may be metabolically beneficial. The administration of a KD to mice after previous feeding with a high-fat, high-carbohydrate diet (HFD) induced weight loss, ketonemia, and glycemic normalization. Here, to compare organ-specific responses to KD, we analyzed lipogenic and gluconeogenic enzymes and genes in the liver and kidney of mice submitted to KD versus (i) HFD or (ii) a saccharose-enriched diet. Methods: Liver and kidney were from (i) mice fed a HFD followed by an 8-week switch to a chow diet (CD), KD continuation of HFD, and (ii) mice submitted to CD, KD, or a saccharose-enriched diet for 1 week. Protein expression levels were determined by Western blotting, and gene expression by qPCR. Hepatic lipid accumulation was visualized by red oil-O. Results: Switch to a KD led to a simultaneous decrease in lipogenic FASN (Fatty Acid Synthase), ACC (Acetyl-CoenzymeA Carboxylase), and its phosphorylated form (pACC-Ser79) in the liver and kidney. In parallel, we observed increased activating phosphorylation of AMPK, the kinase responsible for ACC phosphorylation. In the liver, but not in the kidney, the gluconeogenic rate-limiting enzyme G6Pase (Glucose 6-phosphatase) was repressed under a KD. The switch to a CD significantly reduced hepatic fat accumulation, while a switch to a KD did not allow a significant reversal of hepatic fat accumulation, suggesting resilience to hepatic fat loss under KD. Comparison of a KD versus saccharose-supplemented diet showed an opposite expression pattern of lipogenic enzymes. Conclusions: Administration of KD after previous HFD induced convergent repression of lipogenic enzymes in the liver and kidney, and specific repression of G6Pase in the liver, suggesting a role for kidney gluconeogenesis during KD. KD versus saccharose-supplemented diet had opposite effects on lipogenesis and glycemic control, but both induced loss of lean body mass. Full article

Tropical grasses are increasingly present in farming systems in Brazil. However, a national-scale assessment of this practice’s impact on soil health (SH) and soybean yield has been lacking. In this study, we conducted a meta-analysis of 55 studies published until February 2026, comprising field trials run in 33 locations in Brazil, aiming to assess the effects of deep-rooted tropical grasses as preceding crops on biological indicators of SH and soybean yield. Results showed that grasses (Urochloa spp. and Megathyrsus maximus) promote soybean yield by 15%, representing an average increase of 515 kg ha⁻¹ and an additional revenue of US$198 ha⁻¹. The analysis of forage grass species used, management system (single or intercropped), soybean cultivar (growth habit, life cycle, genetic modification), and edaphoclimatic controlling factors revealed positive effects of tropical grasses on soybean yield under all the study conditions and yield ranges. SH indicators also showed sizeable increment, notably the activity of arylsulfatase (+35%) and β-glucosidase (+31%), followed by acid phosphatase activity (+20%), microbial biomass carbon (+24%), and organic carbon (+11%). The results confirmed the beneficial effects of deep-rooted tropical grasses, highlighting their contribution to sustainable intensification in tropical farming systems due to their ability to enhance SH. This, in turn, leads to increased soybean yield under most agronomic and environmental conditions. Full article

The majority of terrestrial plant species establish below-ground interconnections via arbuscular mycorrhizal (AM) mycelium, thereby forming extensive common mycorrhizal networks (CMNs). CMNs serve as critical infrastructure for nutrient acquisition, mediating soil nutrient capture and distribution. In nitrogen-fixing plants, phosphorus (P) transport is particularly dependent on functional CMNs. The rapid expansion in graphene oxide (GO) production and its broad application have raised significant ecological concerns, particularly regarding its potential impacts on terrestrial ecosystems. Despite these concerns, the impact of GO on P transport dynamics within legume–arbuscular mycorrhizal fungi (AMF) symbioses remains critically scarce. This study established a symbiotic system using the model nitrogen-fixing legume Medicago sativa L. and AMF. This experimental system enabled a comprehensive assessment of GO effects on rhizosphere P mobilization, plant P acquisition, CMNs architecture, fungal community composition, and expression of key P transporter genes. Our results demonstrated that high GO concentrations significantly altered rhizosphere properties, increasing pH while reducing organic acid content and alkaline phosphatase activity. Furthermore, GO exposure significantly inhibited root growth, mycorrhizal colonization rates, and plant P acquisition efficiency. Additionally, GO exposure altered AMF community composition, reduced rhizosphere microbial diversity, and suppressed P metabolism gene expression. Specifically, 0.6% GO induced significant downregulation of MsCS and GigmPT by 83.5% and 62.3%, respectively. This indicates that GO impairs plant P uptake by disrupting the core pathway involving GigmPT and MsCS, triggering P stress in M. sativa. Collectively, these findings provide compelling evidence that GO exposure disrupts legume–AMF symbiotic integrity, ultimately impairing P transport efficiency. Full article

Background and Objectives: This study aimed to evaluate associations between dental caries, periodontal pockets, and radiologically detected periapical lesions in relation to serum levels of Dickkopf-1 (Dkk-1) and tartrate-resistant acid phosphatase 5B (TRAP-5B) in oncologic patients with ear, nose, and throat (ENT) cancer compared with healthy controls. Materials and Methods: The study included 63 subjects divided into a study group of 33 patients diagnosed with ENT cancer and a control group of 30 healthy individuals. Blood samples were collected to assess serum Dkk-1 levels using a sandwich enzyme immunoassay and TRAP-5B levels. Radiological dental evaluation included orthopantomography (OPT) and cone beam computed tomography (CBCT) to assess the number and depth of dental caries and the presence of periapical lesions. Periodontal pockets were recorded through clinical examination. Results: Serum biomarker analysis demonstrated significant differences between groups: TRAP-5B levels were significantly higher in patients with ENT cancer, whereas Dkk-1 concentrations were significantly lower compared with healthy controls (p < 0.001). OPT revealed up to eight carious lesions in both groups. The mean number of carious lesions was higher in healthy subjects (2.97 ± 2.48) than in patients with ENT cancer (2.06 ± 2.29). CBCT evaluation revealed 0–8 carious lesions in healthy individuals and 0–6 lesions in patients with ENT cancer, with a significantly higher mean number of lesions in the control group (2.97 ± 2.48 vs. 1.85 ± 1.89). Periodontal pockets were more frequent in patients with ENT cancer (0.67 ± 1.32) than in controls (0.37 ± 0.81). OPT evaluation also showed a higher mean number of periapical lesions in patients with ENT cancer (0.82 ± 1.29) compared with controls (0.37 ± 0.67). CBCT examination demonstrated that the mean number of periapical lesions in patients with ENT cancer was more than twice that of the control group, although this difference did not reach statistical significance. Conclusions: Patients with ENT cancer exhibited significantly altered systemic bone turnover biomarker profiles, characterized by increased TRAP-5B and decreased Dkk-1 levels. Clinically, these patients also presented a higher prevalence of periodontal pockets and periapical lesions, whereas carious lesions were more frequently detected in healthy individuals. The combined radiological and biochemical findings contribute to a better understanding of oral–systemic interactions in oncologic patients and highlight the importance of comprehensive dental evaluation prior to oncologic therapy. Full article

Shear stress is a significant consideration in 3D bioprinting systems, with implications for cell viability and behaviour. This study hypothesised that relevant levels of shear stress would be generated during the process of 3D bioprinting human nasoseptal chondrocytes in a nanocellulose alginate bioink, with implications for cell viability and chondrogenic gene expression. Through a combined approach of in silico modelling and in vitro testing, we assessed chondrocyte viability and gene expression immediately within the first 72 h post-printing. Cell viability was determined using live–dead, alamarBlue and lactate dehydrogenase assays immediately and 24 h post-printing compared to cell-only and unprinted cell–biomaterial controls. Gene expression analysis of Type 2 collagen, SOX9, aggrecan and alkaline phosphatase gene expression was performed 4 h and 72 h post-printing. Computational fluid dynamics predicted a shear stress of 292 Pa and maximum fluid velocity of 19 mm/s during the bioprinting process. No statistically significant cell death or cell lysis was detected between groups immediately post-printing; however, statistically significant chondrocyte cell death was observed at 24 h in the printed group (p = 0.047). Moreover, the bioprinting process evoked a transient initial rise in both chondrogenic (SOX9, aggrecan) and osteogenic gene expression (ALP) with a marked suppression in type 2 collagen expression at 72 h (0.05, p = 0.0005), indicating biological effects evoked by shear stress during printing. This study highlights the importance of optimising the bioprinting process to facilitate low shear stress conditions for durable cartilage tissue engineering. Full article

Familial thoracic aortic aneurysm and dissection (FTAAD), caused by the pathogenic Myh11 K1256del variant, is characterized by impaired aortic contractility; however, how reduced contractility predisposes the aorta to dissection remains incompletely understood. In this study, we performed a data-driven trans-omic upstream analysis using Genome Enhancer to identify key regulatory mechanisms in aortas from Myh11 K1256del mice under baseline conditions, without exposure to exogenous pathological stimuli. Transcriptome analysis revealed enrichment of genes related to smooth muscle contraction and regulation of myosin light chain phosphatase activity. Upstream computational analysis of regulatory regions identified nuclear factor of activated T cells 1 and lymphoid enhancer-binding factor 1 as major transcription factors, and further highlighted Rho-associated, coiled-coil-containing protein kinase 1 (ROCK1) as a predicted central regulator of the dysregulated transcriptional network. Druggability analysis suggested ROCK1 and the JunB proto-oncogene AP-1 transcription factor subunit as potential therapeutic targets. Furthermore, it predicted 51 candidate therapeutants, including atorvastatin, GSK-269962A, and atovaquone. These findings indicate that even in the absence of overt pathological stimulation, aortic tissue carrying the Myh11 K1256del variant exhibits a transcriptional program centered on ROCK signaling, which may prime the aorta for maladaptive responses to additional stress and may enhance susceptibility to dissection. This computational analysis requires experimental validation, but may provide a hypothesis-generating framework for development of preventive pharmacological interventions against FTAAD. Full article

Alcoholic liver disease (ALD), secondary to chronic alcohol abuse, encompasses a spectrum of liver disorders that progress from steatosis and hepatitis to fibrosis, cirrhosis, and acute-on-chronic liver failure. It poses a considerable global health burden due to its elevated rates of associated morbidity and mortality. The rising prevalence of ALD, coupled with the lack of approved pharmacotherapies, presents considerable unmet clinical needs. In this study, long-chain acyl-CoA synthetase 4 (ACSL4) was identified as a pathogenic driver in the context of chronic alcohol consumption. Hepatocyte Acsl4 ablation mitigated key pathological manifestations in Gao-Binge model mice, as evidenced by reduced inflammatory cell infiltration and attenuated lipid accumulation. Mechanistically, ACSL4 inhibition augmented cellular antioxidant defence through elevating gamma-glutamylcysteine (γ-GC) levels. In addition, γ-GC bound to and suppressed the expression of protein tyrosine phosphatase type IVA member 1 (PTP4A1). Both genetic silencing and pharmacological inhibition of PTP4A1 attenuated the activation of the downstream MAPK-NF-κB inflammatory cascade. Dronedarone, identified as a novel compound targeting ACSL4, demonstrated efficacy in ameliorating the progression of ALD. Overall, these findings elucidate a novel mechanism wherein ACSL4 modulates antioxidant responses via a small bioactive peptide, highlighting ACSL4 as a potential therapeutic target for ALD. Full article

Background: Gumming disease caused by Fusarium tricinctum severely threatens Zanthoxylum bungeanum production. This study investigated the antifungal potential of volatile organic compounds (VOCs) produced by an endophytic fungus, Schizophyllum commune, isolated from Z. bungeanum. Methods: A dual-culture assay evaluated VOCs inhibition against F. tricinctum. Compounds were identified using headspace solid-phase microextraction gas chromatography-mass spectrometry, and the antifungal mechanism of this component was explored. Results: VOCs from S. commune significantly inhibited mycelial growth and sporulation of the pathogen. Among 53 identified compounds, 1-octen-3-ol (mushroom alcohol) was the most abundant (35.98% relative content) and exhibited strong antifungal activity with an EC₅₀ of 0.15 µL/mL against F. tricinctum. Mechanistically, 1-octen-3-ol disrupted cell membrane integrity by increasing alkaline phosphatase and β-1,3-glucanase activities, leading to enhanced permeability and content leakage. It also induced oxidative stress by promoting reactive oxygen species accumulation via elevated NADPH oxidase and superoxide dismutase activities, while suppressing antioxidant enzymes. Conclusions: 1-octen-3-ol inhibits F. tricinctum through membrane disruption and oxidative stress, offering a promising eco-friendly strategy for controlling gumming disease. Full article

Glucosamine (GlcN) is an essential amino monosaccharide widely used in pharmaceuticals, nutraceuticals, and cosmetics. Microbial fermentation presents a sustainable alternative to its traditional chemical production. However, in Saccharomyces cerevisiae, competitive carbon flux towards ethanol significantly limits GlcN yields. In this study, an S. cerevisiae strain for GlcN biosynthesis was engineered by integrating heterologous GlmD (glucosamine-6-phosphate deaminase) and GlmP (glucosamine-6-phosphate phosphatase) genes. To redirect carbon flux, the pyruvate decarboxylase genes pdc1, pdc5, and pdc6 were sequentially knocked out using the Clustered Regularly Interspaced Short Palindromic Repeats Cas9 (CRISPR-Cas9) approach, generating strains S. cerevisiaeGlmDP/pdc1Δ, GlmDP/pdc1Δpdc5Δ, and GlmDP/pdc1Δpdc5Δpdc6Δ. S. cerevisiae GlmDP/pdc1Δpdc5Δpdc6Δ achieved a GlcN titer of 2.20 ± 0.11 g/L, a 1.54-fold increase over the parental S. cerevisia GlmDP strain, while its ethanol yield decreased by 26%. This enhancement was achieved without significantly affecting cell growth or glucose consumption. Comparative transcriptomics between the triple-knockout and parental yeasts revealed 892 differentially expressed genes. Pathways related to glycolysis and ethanol formation were predominantly downregulated, whereas pathways potentially supporting GlcN synthesis were upregulated. The engineered strain demonstrated high genetic stability over 50 generations. Our findings demonstrate that disrupting ethanol formation is an effective strategy to enhance GlcN production in S. cerevisiae, providing valuable insights for carbon flux redistribution. Full article

Radiation-induced bone injury, characterized by oxidative stress damage and impaired osteogenesis, lacks effective treatments. Exosome-based therapies have recently emerged as a safe and effective modality for radiation damage, and their functional capacity can be further potentiated through tailored preconditioning strategies—such as nanoparticle induction or physical stimulation. This study developed a novel exosome-based therapy by preconditioning bone marrow mesenchymal stem cells (BMSCs) with Iron oxide (Fe₃O₄) magnetic nanoparticles (MNPs, 50 µg/mL) and a static magnetic field (SMF, 100 mT). Exosomes derived from these preconditioned cells (BMSC-Fe₃O₄-SMF-Exos) exhibited enhanced yield and dual functionality. In irradiated BMSCs, BMSC-Fe₃O₄-SMF-Exos significantly promoted osteogenic differentiation, restoring alkaline phosphatase activity, mineralization, and expression of RUNX2, OCN, and COL1A1. They concurrently alleviated oxidative stress by scavenging reactive oxygen species, reducing malondialdehyde, and boosting superoxide dismutase activity. Mechanistically, miR-429 was found to be highly enriched in BMSC-Fe₃O₄-SMF-Exos, which directly targeted Noggin (NOG). Our functional validation experiments also confirmed that overexpression of miR-429 could inhibit NOG, alleviate oxidative stress and rescue the osteogenic differentiation of irradiated BMSCs. In conclusion, exosomes derived from preconditioning BMSCs with Fe₃O₄ MNPs and SMF mitigate radiation-induced damage via the miR-429/NOG pathway, presenting a promising cell-free strategy for bone regeneration. Full article

Background/Objectives: Hungry bone syndrome (HBS) is a clinically significant metabolic complication following parathyroidectomy for primary hyperparathyroidism (PHPT), characterized by profound and prolonged hypocalcemia resulting from rapid skeletal remineralization. Although multiple risk factors have been proposed, published data remain inconsistent regarding the most reliable predictors. This study aimed to evaluate potential risk factors associated with the development of HBS and to clarify controversial findings reported in the literature. Methods: Patients who underwent surgery for PHPT between January 2019 and May 2025 were retrospectively analyzed. Individuals who developed HBS were compared with those who did not in terms of clinical, biochemical, and surgical parameters. Results: HBS occurred in 4.7% of patients. Those in the HBS group exhibited significantly higher preoperative serum calcium, parathyroid hormone, alkaline phosphatase (ALP), and Ca/P ratio, while phosphate, vitamin D, and T-scores were significantly lower. Postoperative day 1 calcium levels were also markedly reduced. Multivariate analysis identified increased ALP, low T-score, concomitant thyroid surgery, and decreased postoperative day 1 calcium as independent predictors. A postoperative day 1 calcium cutoff of 8.6 mg/dL demonstrated strong predictive accuracy. Conclusions: HBS is more commonly observed in patients with low bone density and high bone turnover. Patients with these risk factors should be considered high-risk and closely monitored in the early postoperative period to enable prompt intervention and prevent severe complications. Full article