Objectives: Osteoporosis is a silent disease with low screening rates in many developing countries. This study aimed to evaluate the feasibility of using an artificial intelligence (AI)-based system to screen osteoporosis from pelvic and hip radiographs in Vietnam. Methods: We conducted a cross-sectional study at a tertiary medical center in Central Vietnam in 2023. A total of 2000 consecutive pelvic and hip radiographs from patients aged ≥ 40 years were collected. After excluding poorquality images, 1987 radiographs were analyzed using an AI-based software designed to estimate bone mineral density (BMD) from plain radiographs and derive T-scores. Osteoporosis was defined as a T-score ≤ − 2.5. Patient characteristics, radiographic findings, and risk factors for osteoporosis were analyzed. Results: Among 1987 patients (mean age 66.4 ± 15.1 years; 41.3% men), osteoporosis was identified in 872 patients (43.9%). The prevalence increased with age and was higher in women than in men (58.7% vs 22.8%, P < 0.001). Osteoporosis was associated with femoral neck (OR = 3.8, 95% CI: 2.7–5.2) and intertrochanteric fractures (OR = 7.0, 95% CI: 4.5–11.0). Patients with lower T-scores had a higher risk of hip fractures, especially those with T-scores ≤ − 3.0 (OR = 11.5, 95% CI: 5.5–24.5). Conclusions AI-based analysis of pelvic and hip radiographs is a feasible and effective tool for osteoporosis screening in Vietnam. The prevalence of osteoporosis in this hospital-based setting was high, particularly among elderly women.AI-assisted screening may offer an accessible strategy for early detection of osteoporosis in resource-limited settings.

Background: While advanced age is a known risk factor for postoperative complications following hip arthroplasty, its role as an independent predictor versus a surrogate for comorbidity remains unclear, particularly in developing countries. This study aimed to investigate the independent impact of age on postoperative outcomes and explore the mediating role of key comorbidities in a resource-limited setting. Methods: We retrospectively reviewed 769 adult patients undergoing hip arthroplasty at a Vietnamese tertiary hospital (2021–2024), categorized into three groups: younger adults (18–64 years), older adults (65–79 years), and oldest old (≥80 years). The primary outcome was a composite of major postoperative complications. Multivariable logistic regression and structural equation modeling were used to identify independent predictors and assess mediation effects. Results: Among 769 patients, 363 were younger (47.2%), 241 older adults (31.3%), and 165 oldest old (21.5%). Complication rates increased significantly with age (18.7%, 36.9%, and 60.0%, respectively; p<0.001). However, multivariable adjustment showed that age was not an independent predictor. Instead, heart failure (adjusted odds ratio [aOR]=5.49, 95% confidence interval [CI] 2.19–13.74) and preoperative anemia (aOR=1.77, 95% CI 1.21– 2.59) were identified as independent risk factors. Mediation analysis revealed that the effect of age on complications was significantly mediated through preoperative anemia. Conclusion Increased postoperative risk in older adults is driven by comorbidity burden rather than chronological age. Preoperative anemia and heart failure are critical, independent predictors, with anemia acting as a key mediator for the effects of age. Individualized correction of modifiable comorbidities may be more beneficial than using age alone to assess surgical risk.

Autophagy is a conserved catabolic process that degrades proteins and damaged organelles to maintain cellular homeostasis, and its role in cancer depends on stage and context. Farnesyl-diphosphate farnesyltransferase 1 (FDFT1) is an essential enzyme in the sterol branch of the mevalonate pathway, but its functions in hepatocellular carcinoma (HCC) and in the regulation of autophagy remain poorly understood. In this study, we show that FDFT1 acts as a negative regulator of autophagy in HCC cells. Loss of FDFT1 led to increased autophagosome formation and fusion with lysosomes, whereas its overexpression suppressed both basal and induced autophagy. These changes were associated with AMPK–ULK1 signaling, suggesting that FDFT1 influences a central pathway controlling autophagy. Our findings connect cholesterol metabolism with autophagy regulation and tumor growth, highlighting FDFT1 as a potential prognostic marker and therapeutic target in liver cancer.

Background: Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, largely because of challenges in early diagnosis and the limited sensitivity of conventional biomarkers. Therefore, reliable molecular tools for early detection, prognostic stratification, and individualized treatment predictions are urgently required. Methods: This retrospective study analyzed publicly available gene expression datasets. Candidate biomarkers were identified from the GSE14520 cohort using a multistep screening workflow that integrated differential expression analysis, diagnostic performance, and prognostic relevance. A 10-gene diagnostic model was constructed using least absolute shrinkage and selection operator logistic regression and subsequently validated across multiple independent cohorts. Survival outcomes were evaluated using the Kaplan-Meier analysis and treatment responses to sorafenib and transarterial chemoembolization (TACE) were assessed using receiver operating characteristic analysis. Results: A 10-gene signature (TOP2A, CDK1, CYP3A4, MASP2, EPHX2, HAO1, RACGAP1, GLYAT, ADH1B, and CYP4A11) was established. The model demonstrated robust internal performance and consistent accuracy across external validation cohorts (area under the curve [AUC], >0.9). This signature effectively identified early-stage HCC and distinguished malignancy from cirrhosis. High-risk scores were significantly associated with poor overall survival and recurrence-free survival (p<0.05). Furthermore, the model could predict treatment sensitivity, with higher risk scores associated with better outcomes for sorafenib (AUC, 0.791), whereas lower risk scores correlated with an improved response to TACE (AUC, 0.768). Conclusion Our gene expression-based machine learning model provides a robust tool for HCC diagnosis, prognosis, and treatment response prediction, with potential as a supportive system for personalized clinical decision-making.

Background: Nonalcoholic fatty liver disease, a progressive condition caused by the accumulation of fat in the liver, begins with simple steatosis and can potentially progress to metabolic dysfunction-associated steatohepatitis (MASH) in the presence of inflammation and fibrosis, ultimately leading to cirrhosis or hepatocellular carcinoma. Increasing evidence indicates that sodiumglucose cotransporter 2 (SGLT2) inhibitors effectively alleviate MASH in mouse models. However, there is a lack of research on the effects of enavogliflozin on liver disease. In the present study, we investigated the effects of SGLT2 inhibitors on MASH induced by a high-fat, high-cholesterol (HFHC) diet in mice. Methods: Male C57BL/6 mice were fed a normal chow diet, HFHC diet, or HFHC diet with enavogliflozin for 12 weeks. LX-2 and HepG2 cells were treated with enavogliflozin in the presence of various pathological stimuli. Results: The HFHC diet induced excessive hepatic lipid accumulation, inflammation, and severe fibrosis. Administration of enavogliflozin not only ameliorated hepatic steatosis and fibrotic conditions but also suppressed the production of inflammatory cytokines. Positive outcomes were also observed in in vitro experiments, where enavogliflozin demonstrated the ability to impede the activation of hepatic stellate cells and alleviate lipid accumulation in hepatocytes. The potential pathway through which enavogliflozin attenuated liver fibrosis development may be associated with the transforming growth factor β1/Smad signaling pathway. Conclusion Our results suggest that enavogliflozin is effective in a mouse model of MASH by attenuating hepatic steatosis, suppressing inflammation, and improving liver fibrosis.

BACKGROUND: Acellular tubular artery scaffolds offer structural support for vascular regeneration but are inherently limited by poor anticoagulant properties, which increases the risk of thrombus formation following implantation. This thrombogenicity remains a major obstacle to their clinical application, particularly in small-diameter vascular grafts. METHODS: To address this challenge, the present study investigates the use of the Layer-by-Layer (LbL) assembly technique for heparin immobilization under low-speed rotation. Utilizing a roller tube system, heparin was immobilized onto decellularized scaffolds through electrostatic interactions facilitated by a DHI-based linker. This low-speed rotation LbL approach enhanced the uniformity and stability of heparin deposition compared to traditional static methods. One, 4, 7, 10, 13 deposition cycles were performed to achieve optimal heparin loading, resulting in scaffolds capable of sustained heparin release over 28 days. RESULTS: The heparinized scaffolds exhibited an initial burst release (approximately 80%), followed by a sustained phase with 18.24% ± 0.242 remaining to support prolonged anticoagulant activity. Importantly, the modified scaffolds significantly reduced thrombus formation and exhibited minimal hemolytic activity, indicating improved hemocompatibility. In addition to their antithrombotic properties, the scaffolds also promoted endothelial cell adhesion, which is critical for restoring vascular integrity, regulating vascular tone, and maintaining long-term patency. CONCLUSION These findings highlight the efficacy of roller-assisted LbL heparinization as a practical and scalable strategy to enhance the blood compatibility of acellular vascular grafts. This method holds considerable promise for addressing thrombogenicity in vascular tissue engineering and advancing the clinical translation of bioengineered vascular constructs.

Background: Catecholamines play a crucial role in muscle biogenesis, but their persistent elevation is linked to muscle wasting, which is poorly understood. This study aimed to investigate the association between catecholamine levels and age-related muscle loss. Methods: This retrospective study evaluated the plasma levels of two catecholamines, metanephrine and normetanephrine, and the clinical characteristics of 830 patients with adrenal incidentaloma on computed tomography (CT). Cross-sectional CT data at the L3 lumbar vertebrae were used to measure muscle areas. In vitro studies on C2C12 myotubes were conducted to examine β-adrenergic receptor signaling pathways and their role in myogenesis. Results: Men had significantly higher mean metanephrine levels of 0.17 nmol/L and normetanephrine levels of 0.63 nmol/L than women (P<0.05). Total abdominal muscle area was negatively correlated with catecholamine levels in both men and women, with the strongest negative correlation between normetanephrine levels and total abdominal muscle area in men (r=–0.31, P<0.001). Similarly, the strongest negative correlation between visceral fat area and metanephrine was observed in men (r=–0.25, P=0.004). Clenbuterol, a β-adrenergic receptor agonist, inhibited myogenesis, including myotube formation by extracellular signal-regulated kinase (ERK) suppression in C2C12 myoblasts. Conversely, β-blockers increased myogenesis via increasing ERK phosphorylation in C2C12 cells. These findings suggest that β-adrenergic modulation influences skeletal muscle differentiation, with ERK phosphorylation. Conclusion Catecholamine levels are associated with age, sex, muscle mass, and fat mass. Monitoring catecholamine levels, particularly in older men and in individuals with reduced muscle mass, may help manage age-related muscle loss and lead to individualized treatment strategies.

Lysosomal diseases (LDs) are a group of rare inherited disorders belonging to inborn metabolism errors. LDs are characterized by the excessive storage of undegraded substrates, most often due to the enzymatic deficiency resulting from disease-causing gene variants. LDs lead to dysregulated cellular pathways and imbalanced molecular homeostasis and can affect multiple organs and tissues. Despite being rare, LDs account for a significant incidence when considered collectively. Due to complex molecular and genetic fingerprints, considerable challenges in LD management must be overcome. Diagnosis can be significantly delayed due to the broad and nonspecific clinical manifestations and the lack of specific biomarkers. Available treatments fail to fully stop the disease progression and can alter the disease's typical phenotypes with novel manifestations. Therefore, a paradigm shift is crucial to better understand LDs and provide actionable insights. Herein, we comprehensively review the literature to demonstrate that multi-omics approaches are promising for pathophysiology elucidation, biomarker discovery, and precision therapy in LDs. We recommend adopting longitudinal study designs integrated with a multi-omics-empowered framework to facilitate mechanistic delineation, biomarker discovery, and treatment development. Relevant approaches exploring the association between LDs and common neurodegenerative disorders are also discussed, paving a potential path for improved therapeutic development and ultimately improving the patient's quality of life.

Background: Sepsis and septic shock are life-threatening global health challenges associated with high mortality rates. Early identification of high-risk patients is critical for improving outcomes. In the present study, the association between the neutrophil-to-lymphocyte-to-albumin ratio (NLAR) and mortality in septic patients was evaluated. Methods: A retrospective study was performed at a tertiary hospital in Vietnam. Patients ≥18 years of age diagnosed with sepsis or septic shock based on the Sepsis-3 criteria were included. Exclusion criteria included recent corticosteroid use within 7 days, autoimmune diseases, hematological disorders, and active cancer within 5 years. NLAR was calculated from complete blood counts and albumin levels within the first 24 hours of intensive care unit admission. Receiver operating characteristic (ROC) curves were used to determine the predictive ability of NLAR for in-hospital mortality. Results: The present study included 141 patients with a mean age of 72 years. Non-survivors were significantly older with higher rates of mechanical ventilation. NLAR was significantly elevated in non-survivors compared with survivors (0.88 [0.57–1.24] vs. 0.44 [0.28–0.77], P<0.001). In ROC analysis, the area under the curve for NLAR was 0.70 (P<0.001). Using a cutoff value of 0.56, NLAR showed a sensitivity of 77.8% and a specificity of 61.5% for predicting in-hospital mortality. Conclusions Elevated NLAR on admission was associated with a higher mortality rate in sepsis patients. NLAR could be used as an early prognostic marker for sepsis mortality.

Objectives: Vertebral fractures are associated with disability and mortality, but most vertebral fractures are asymptomatic. The present study aimed to determine the incidence of and develop a predictive nomogram for asymptomatic vertebral fractures in Vietnamese adults. Methods: This cohort study as a part of the Vietnam Osteoporosis Study involved 168 men and 287 women aged 50 years and older without a clinically diagnosed vertebral fracture. Their spine x-rays were taken at the recruitment and subsequent 2-year visit. Vertebral fractures were ascertained using the Genant’s semiquantitative method. We employed the Bayesian Model Averaging method to search for the optimal model for predicting asymptomatic vertebral fractures. A predictive nomogram was also developed to facilitate risk prediction. Results: During a median of 2.38 years of follow-up, 13 men and 16 women developed an asymptomatic vertebral fracture, yielding the overall incidence rate of 28 fractures per 1000 person-years, or 33 fractures/1000 personyears in men and 24 fractures/1000 person-years in women, respectively. Most asymptomatic vertebral fractures were moderate, almost 1.5 times more common than mild fractures. The optimal model for predicting incident asymptomatic vertebral fractures included age, male sex and lower femoral neck T-score. The area under the receiver’s operating characteristic curve was 0.91, with 95% CI ranging from 0.86 to 0.96. Conclusions Asymptomatic vertebral fractures were relatively common among adults in Vietnam. A simple model with sex, age and femoral neck T-score is helpful for selective screening of asymptomatic vertebral fractures in Vietnamese individuals.