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BackgroundThis study aimed to compare the efficacy of the Neonatal Sequential Organ Failure Assessment (nSOFA) and the Respiratory Severity Score (RSS) in predicting Bronchopulmonary Dysplasia (BPD).MethodsWe conducted a retrospective study that included preterm infants who required invasive mechanical ventilation (IMV) within 24 hours of birth. The accuracy of each scoring system was assessed and compared using the area under the curve (AUC) derived from receiver operating characteristic (ROC) analysis. Additionally, Spearman’s correlation was used to evaluate the association between RSS and nSOFA, and logistic regression models were constructed to adjust for potential confounders.ResultsA total of 85 preterm infants were analysed, of whom 53 (62.4%) were diagnosed with BPD. Both nSOFA and RSS demonstrated strong predictive abilities for BPD, with AUCs of 0.82 and 0.81, respectively. Logistic regression analysis indicated that the relationship between the two scoring systems and BPD remained stable. However, nSOFA exhibited better predictive accuracy than RSS (0.75 vs 0.69). A significant positive correlation was observed between nSOFA and RSS (r=0.707, p<0.001).ConclusionsIn preterm infants requiring IMV, both nSOFA and RSS are effective predictors of BPD, with nSOFA showing superior accuracy.

Machine learning (ML) and deep learning (DL) show promise for fall risk prediction, but prior reviews focused mainly on real-time fall detection, in-hospital falls, or conventional statistical models. The performance of ML-DL-based models for predicting future falls in community-dwelling older adults remains unclear. This study aimed to review ML-DL studies for predicting future falls among community-dwelling older adults and meta-analyze discrimination where feasible. Six databases were searched from inception to September 23, 2024, with updates on August 31, 2025, and February 28, 2026. We included longitudinal studies developing or validating ML-DL models to predict future falls in community-dwelling adults aged ≥60 years and excluded real-time detection, simulated or no fall, and inpatient studies. Risk of bias was assessed using the Prediction Model Risk of Bias Assessment Tool (PROBAST). Areas under the curve (AUCs) were meta-analyzed using Hartung-Knapp-Sidik-Jonkman random-effects models with 95% CIs. Heterogeneity, 95% prediction intervals (PIs), sensitivity analyses, and subgroup analyses were conducted. After screening 10,253 records, 28 (0.3%) studies were included; 18 (64.3%) focused on general older adults. Prediction horizons ranged from 3 months to 7 years, and fall incidence ranged from 1.6% to 46.6%. Twenty-three (82.1%) studies applied ML, and 5 (17.9%) studies used DL. Input modalities included text (n=18, 64.3%), sensor (n=5, 17.9%), image (n=1, 3.6%), and multimodal data (n=4, 14.3%). Common predictors included age, sex, fall history, depression, and basic daily activities. Only one model underwent external validation. Calibration reporting was sparse. All models were rated at high risk of bias. Ten models were meta-analyzed, yielding a pooled AUC of 0.79 (95% CI 0.69-0.87) with extreme heterogeneity (τ2=0.64; τ=0.80; I2=99.8%; Q=4128.99). The confidence-distribution bootstrap PI was 0.20 to 0.99, indicating substantial uncertainty in expected performance across new populations. Subgroup analyses indicated moderation by sample size and population type, with higher discrimination in specific populations than in general samples; however, the specific population subgroup included only 2 studies. Although all participants were community dwelling, some cohorts were recruited through clinically enriched pathways rather than general community sampling. ML-DL models show potential for identifying community-dwelling older adults at elevated future fall risk; however, wide PIs, limited external validation, and high risk of bias suggest real-world performance may be optimistic. The pooled AUC should be interpreted as a summary of reported discrimination under study-specific conditions, predominantly from internally validated, high-risk-of-bias models, rather than as a robust estimate of transportable real-world performance. This review extends prior reviews by focusing on community-dwelling settings and by integrating PROBAST, Hartung-Knapp-Sidik-Jonkman meta-analysis, PIs, and modality-specific synthesis to evaluate both discrimination and uncertainty. Findings support the use of ML-DL models for proactive fall prevention while emphasizing the need for validation and context-specific implementation.

Skeletal muscle comprises a large, heterogeneous assortment of cell populations that interact to maintain muscle homeostasis, but little is known about the mechanism that controls myogenic development in response to artificial selection. Different pig (Sus scrofa) breeds exhibit distinct muscle phenotypes resulting from domestication and selective breeding. Using unbiased single‐cell transcriptomic sequencing analysis (scRNA‐seq), the impact of artificial selection on cell profiles is investigated in neonatal skeletal muscle of pigs. This work provides panoramic muscle‐resident cell profiles and identifies novel and breed‐specific cells, mapping them on pseudotime trajectories. Artificial selection has elicited significant changes in muscle‐resident cell profiles, while conserving signs of generational environmental challenges. These results suggest that fibro‐adipogenic progenitors serve as a cellular interaction hub and that specific transcription factors identified here may serve as candidate target regulons for the pursuit of a specific muscle phenotype. Furthermore, a cross‐species comparison of humans, mice, and pigs illustrates the conservation and divergence of mammalian muscle ontology. The findings of this study reveal shifts in cellular heterogeneity, novel cell subpopulations, and their interactions that may greatly facilitate the understanding of the mechanism underlying divergent muscle phenotypes arising from artificial selection. To date, little is known about the mechanism that controls muscle phenotype modification in response to artificial selection. Using single‐cell RNA sequencing, authors delineate panoramic muscle‐resident cell profiles with identification of novel cell subpopulations and cellular interactions in pigs (Sus scrofa) representing divergent muscle phenotypes. The findings should greatly facilitate the understanding of the mechanism of divergent muscle characteristics formation.

Though RNAi and RNA-splicing machineries are involved in regulating severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) replication, their precise roles in coronavirus disease 2019 (COVID-19) pathogenesis remain unclear. Herein, we show that decreased RNAi component (Dicer and XPO5) and splicing factor (SRSF3 and hnRNPA3) expression correlate with increased COVID-19 severity. SARS-CoV-2 N protein induces the autophagic degradation of Dicer, XPO5, SRSF3, and hnRNPA3, inhibiting miRNA biogenesis and RNA splicing and triggering DNA damage, proteotoxic stress, and pneumonia. Dicer, XPO5, SRSF3, and hnRNPA3 knockdown increases, while their overexpression decreases, N protein-induced pneumonia’s severity. Older mice show lower expression of Dicer, XPO5, SRSF3, and hnRNPA3 in their lung tissues and exhibit more severe N protein-induced pneumonia than younger mice. PJ34, a poly(ADP-ribose) polymerase inhibitor, or anastrozole, an aromatase inhibitor, ameliorates N protein- or SARS-CoV-2-induced pneumonia by restoring Dicer, XPO5, SRSF3, and hnRNPA3 expression. These findings will aid in developing improved treatments for SARS-CoV-2-associated pneumonia. Here, the authors provide evidence that SARS-CoV-2 N protein leads to autophagic degradation of Dicer, XPO5, SRSF3, and hnRNPA3, inducing DNA damage and proteotoxic stress, eventually causing pneumonia. The small-molecule drug PJ34 or anastrozole alleviates N protein-induced pneumonia.

Yeast β-glucan is a natural antioxidant and has been reported to improve growth performance of piglets, but its application in improving pork quality is limited. This study investigated the effects of dietary yeast β-glucan supplementation on meat quality, antioxidant capacity and gut microbiota of finishing pigs. In a 40-day experiment, ninety finishing pigs (Duroc × Landrace × Yorkshire, 70.47 ± 0.04 kg) were randomly allocated into five treatments including a basal diet supplemented with 0, 50, 100, 200 and 400 mg/kg yeast β-glucan. Results showed that yeast β-glucan significantly increased pH45 min (linear and quadratic, p < 0.01) and a*45 min (linear, p < 0.05), and reduced cooking loss (linear, p < 0.05) and drip loss (quadratic, p < 0.05) of meat in finishing pigs. Importantly, the 200 mg/kg group exhibited the highest values of pH45 min (p < 0.01) and the lowest values of drip loss (p < 0.05), accompanied by a decreased lactate content (p < 0.05) and glycolytic potential (p < 0.05). Dietary supplementation of 200 mg/kg yeast β-glucan markedly increased catalase (CAT) (p < 0.05), superoxide dismutase (SOD) (p < 0.05) and total antioxidant capacity (T-AOC) (p < 0.01) activities in skeletal muscle. Moreover, WPS-2 abundance was decreased significantly in colonic digesta by 200 mg/kg yeast β-glucan and exhibited a positive association with muscle lactate content and drip loss. Together, dietary 200 mg/kg yeast β-glucan supplementation effectively improved pH value and the water-holding capacity of fresh meat through reducing muscle postmortem glycolysis, increasing antioxidant capacity and altering the gut microbiota composition of finishing pigs.

This study is aimed at exploring the mechanism underlying the homeostasis between myogenesis and adipogenesis in skeletal muscle using a special porcine model with a distinct phenotype on muscle growth rate and intramuscular fat deposition. Differentiation potential of muscle-derived Myo-lineage cells of lean-type pigs was significantly enhanced relative to obese-type pigs, while that of their Adi-lineage cells was similar. Single-cell RNA sequencing revealed that lean-type pigs reserved a higher proportion of Myo-lineage cells in skeletal muscle relative to obese-type pigs. Besides, Myo-lineage cells of the lean-type pig settled closer to the original stage of muscle-derived progenitor cells. Proteomics analysis found that differentially expressed proteins between two sources of Myo-lineage cells are mainly involved in muscle development, cell proliferation and differentiation, ion homeostasis, apoptosis, and the MAPK signaling pathway. The regulation of intracellular ion homeostasis, Ca2+ in particular, significantly differed between two sources of Myo-lineage cells. Ca2+ concentration in both cytoplasm and endoplasmic reticulum was lower in Myo-lineage cells of lean-type pigs relative to obese-type pigs. In conclusion, a higher proportion and stronger differentiation capacity of Myo-lineage cells are the main causes for the higher capability of myogenic differentiation and lower intramuscular fat deposition. Relative low concentration of cellular Ca2+ is advantageous for Myo-lineage cells to keep a potent differentiation potential.

Background Cytosolic Ca 2+ plays vital roles in myogenesis and muscle development. As a major Ca 2+ release channel of endoplasmic reticulum (ER), ryanodine receptor 1 (RyR1) key mutations are main causes of severe congenital myopathies. The role of RyR1 in myogenic differentiation has attracted intense research interest but remains unclear. Results In the present study, both RyR1-knockdown myoblasts and CRISPR/Cas9-based RyR1-knockout myoblasts were employed to explore the role of RyR1 in myogenic differentiation, myotube formation as well as the potential mechanism of RyR1-related myopathies. We observed that RyR1 expression was dramatically increased during the late stage of myogenic differentiation, accompanied by significantly elevated cytoplasmic Ca 2+ concentration. Inhibition of RyR1 by siRNA-mediated knockdown or chemical inhibitor, dantrolene, significantly reduced cytosolic Ca 2+ and blocked multinucleated myotube formation. The elevation of cytoplasmic Ca 2+ concentration can effectively relieve myogenic differentiation stagnation by RyR1 inhibition, demonstrating that RyR1 modulates myogenic differentiation via regulation of Ca 2+ release channel. However, RyR1-knockout-induced Ca 2+ leakage led to the severe ER stress and excessive unfolded protein response, and drove myoblasts into apoptosis. Conclusions Therefore, we concluded that Ca 2+ release mediated by dramatic increase in RyR1 expression is required for the late stage of myogenic differentiation and fusion. This study contributes to a novel understanding of the role of RyR1 in myogenic differentiation and related congenital myopathies, and provides a potential target for regulation of muscle characteristics and meat quality.

The normal function of skeletal muscle and adipose tissue ensures whole-body glucose homeostasis. Ca 2+ release channel inositol 1,4,5-trisphosphate receptor 1 (IP3R1) plays a vital role in regulating diet-induced obesity and disorders, but its functions in peripheral tissue regulating glucose homeostasis remain unexplored. In this study, mice with Ip3r1 specific knockout in skeletal muscle or adipocytes were used for investigating the mediatory role of IP3R1 on whole-body glucose homeostasis under normal or high-fat diet. We reported that IP3R1 expression levels were increased in the white adipose tissue and skeletal muscle of diet-induced obese mice. Ip3r1 knockout in skeletal muscle improved glucose tolerance and insulin sensitivity of mice on a normal chow diet, but worsened insulin resistance in diet-induced obese mice. These changes were associated with the reduced muscle weight and compromised Akt signaling activation. Importantly, Ip3r1 deletion in adipocytes protected mice from diet-induced obesity and glucose intolerance, mainly due to the enhanced lipolysis and AMPK signaling pathway in the visceral fat. In conclusion, our study demonstrates that IP3R1 in skeletal muscle and adipocytes exerts divergent effects on systemic glucose homeostasis, and characterizes adipocyte IP3R1 as a promising target for treating obesity and type 2 diabetes.

Respiratory syncytial virus (RSV) infects neuronal cells in the central nervous system (CNS), resulting in neurological symptoms. In the present study, we intended to explore the mechanism of RSV infection‐induced neuroinflammatory injury from the perspective of the immune response and sought to identify effective protective measures against the injury. The findings showed that toll‐like receptor 4 (TLR4) was activated after RSV infection in human neuronal SY5Y cells. Furthermore, TLR4 activation induced autophagy and apoptosis in neuronal cells, promoted the formation of the NOD‐like receptor family pyrin domain containing 3 (NLRP3) inflammasome, and increased the secretion of downstream inflammatory cytokines such as interleukin‐1β (IL‐1β), interleukin‐18 (IL‐18) and tumour necrosis factor‐α (TNF‐α). Interestingly, blockade of TLR4 or treatment with exogenous melatonin significantly suppressed TLR4 activation as well as TLR4‐mediated apoptosis, autophagy and immune responses. Therefore, we infer that melatonin may act on the TLR4 to ameliorate RSV‐induced neuronal injury, which provides a new therapeutic target for RSV infection.

DDA1 is a protein involved in protein degradation, cell cycle regulation, and DNA damage repair. Although its expression varies across tumor types, the precise role of DDA1 in gliomagenesis remains unclear. We investigated the function of DDA1 in multiple glioblastoma cell models using biochemical assays, phosphorylation analysis, subcellular localization studies, and integrated genomic and transcriptomic profiling to determine its signaling interactions and downstream effects. We identified a physical association between cytoplasmic DDA1 and Raptor, a core component of lysosome-associated mTORC1. Amino acid stimulation triggered phosphorylation of DDA1 at serine 33 promoting its nuclear translocation and involvement in DNA damage repair. Integrated transcriptomic analyses revealed that the mTORC1-DDA1 -DNA repair axis regulates the expression of a subset of metabolic genes, including ENO2, CA12, and NMRK1. Functional assays further suggested that these genes contribute to the survival capacity of glioblastoma cells, particularly under DDA1-deficient conditions. Consistently, DDA1 deficiency markedly impaired glioblastoma growth and induced compensatory upregulation of metabolic activity. Our findings identify DDA1 as a previously unrecognized phosphorylation target downstream of mTORC1 and a critical mediator of the mTORC1 driven DNA damage response. Through its involvement in DNA repair and metabolic gene regulation, DDA1 appears to support glioblastoma progression, providing mechanistic insight into mTORC1 related gliomagenesis and suggesting potential therapeutic relevance.