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Background Prolonged inactivity has been found to be a major contributor to poor bone health. However, limited research has examined the specific relationship between pelvic bone mineral density (BMD) and sedentary time. The study aims to clarify the association between sedentary time and pelvic BMD in adult Americans. Methods Data from the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2018 were examined in this cross-sectional investigation. Participants who had comprehensive information on their pelvic BMD and amount of sedentary time were included. We used multivariable linear regression to assess the association between sedentary time and pelvic BMD, and logistic regression to estimate the odds of low BMD across sedentary levels. Potential effect modification and contributing factors were explored using interaction tests and prespecified subgroup analyses. All analyses accounted for the complex NHANES sampling design with survey weights, strata, and primary sampling units. Results The analysis includes 15,328 individuals. Longer sedentary time was associated with lower pelvic BMD. In the fully adjusted model, the ≥ 8 h/day group had lower pelvic BMD compared with the < 4 h/day reference group (β = -0.018, 95% CI: -0.031, -0.006; P  < 0.01). Subgroup and interaction analyses suggested effect modification by body mass index and glucocorticoid use (P for interaction = 0.047 and 0.003, respectively). Conclusion Longer sedentary time is associated with lower pelvic BMD. This finding underscores the importance of controlling sedentary behavior to stop the decline of bone health. Nevertheless, large prospective studies are required to confirm the results.

The onset of osteoarthritis (OA) involves the interplay of mechanical stress, inflammatory responses, and metabolic disorders. Pro-inflammatory cytokines, including IL-1β, TNF-α, and IL-6, drive cartilage degradation, synovitis, and subchondral bone remodeling through activation of NF-κB and MAPK signaling pathways. Recent studies have identified disulfidptosis, a novel form of programmed cell death, and suggest its potential involvement in OA pathogenesis. This death modality is triggered by abnormal intracellular accumulation of disulfide bonds, dependent on high SLC7A11 expression and NADPH depletion, leading to cytoskeletal protein cross-linking and cellular collapse. In the OA microenvironment, chondrocytes and synovial cells are hypothesized to exhibit increased susceptibility to disulfidptosis owing to metabolic imbalance, impaired glucose uptake, and oxidative stress. This process may not only cause direct loss of cellular function but also potentially amplify inflammatory responses through the release of damage-associated molecular patterns (DAMPs) and senescence-associated secretory phenotype (SASP) factors, thereby theoretically contributing to a vicious cycle of inflammation and M1 macrophage polarization that exacerbates cartilage destruction. Potential therapeutic strategies targeting this pathway include: phytochemicals (eg, curcumin, resveratrol) that modulate redox balance; traditional Chinese medicines (eg, Duhuo Jisheng Decoction) with multi-target anti-inflammatory properties; specific inhibitors such as SLC7A11 antagonists or G6PD activators; hydrogel-based drug delivery systems for localized sustained release; and bone transport technology that activates Piezo1 mechanoreceptors to enhance antioxidant defense. While these approaches represent promising investigational directions, direct evidence validating their efficacy against disulfidptosis in OA remains limited. Future studies must clarify the functional significance of disulfidptosis in OA and rigorously evaluate targeted therapies in preclinical models before clinical translation can be considered.

Background Lung cancer is the most prevalent tumor and frequently present with distant metastases, with the bone being one of the most common affected sites. However, bone metastases leading to complete resorption of the hip joint and pelvis are extremely rare. This case aimed to report an extensive destruction of the hip and pelvis in metastatic lung adenocarcinoma, and conduct a literature review to explore the factors influencing the diagnosis and treatment decisions of bone metastasis. Case presentation A 56-year-old woman presented with progressive pain in her left hip joint and pelvis accompanied by impaired mobility for over one year. X-ray and computed tomography (CT) scan of left hip joint and pelvis showed extensive bone metastasis. A chest X-ray displayed disorganized lung texture in both lungs and multiple bilateral lung nodules of variable sizes. Surgical biopsy of the left iliac bone and histology examination indicated bone metastasis originating from lung adenocarcinoma, which was confirmed using immunohistochemical analysis. Due to multiple extensive metastases throughout the body, the patient was treated conservatively. Targeted therapy with almonertinib mesilate was administered; however, and the patient eventually passed away one week later. Conclusion Early detection of bone metastasis and identification of the original tumor are crucial, especially when the symptoms are subtle or nonspecific. Delayed diagnosis can lead to extensive skeletal destruction, loss of function, and poor prognosis. A comprehensive diagnostic approach integrating thorough physical examination, advanced imaging modalities, and pathological analysis is essential for timely and accurate diagnosis. An optimal management requires a personalized, multidisciplinary treatment strategy that considers the patient’s overall condition, the molecular profile of the primary tumor, and the anatomical complexity of the metastatic site.

Microinjury can trigger in situ tissue repair. Bone transport consists of continuous microinjuries/microfracture and induces bone formation and angiogenesis. Tibial cortex transverse transport (TTT) was found to promote angiogenesis at the foot and the healing of diabetic foot ulcers (DFUs). However, the underlying mechanism remains largely unknown. We divided 72 Sprague-Dawley rats with DFUs into the control, sham, and TTT groups. Wound measurement and histology were performed to evaluate the wound healing processes. Enzyme-linked immunosorbent assay, flow cytometry, immunohistochemistry, and Western Blot were used to assess angiogenesis and the activity of endothelial progenitor cells (EPCs) and the Ras/Raf/MEK/ERK signaling pathway. We found accelerated wound healing, improved epidermal continuity, and increased dermal thickness in the TTT group than the control and the sham groups. Higher levels of serum TGF-β1, PDGF-BB, and VEGF were detected in the TTT group. These changes were in parallel with the expression of TGF-β1, PDGF-BB, and VEGF in the foot wounds and the frequency of EPCs in both bone marrow and peripheral circulation, which implied that the secreted TGF-β1, PDGF-BB, and VEGF promote proliferation and migration of EPCs to the foot wounds. The expression of CD31 cells, SMA-α cells, and the Ras/Raf/MEK/ERK pathway was higher in the TTT group than in the control and sham groups. The findings showed that TTT enhanced the production of growth factors that in turn activated EPC proliferation and migration through the Ras/Raf/MEK/ERK pathway, ultimately contributing to angiogenesis and DFU healing. Based on these findings, we proposed a theory that remote continuous microinjuries can trigger the repair of target tissues (ie, microinjury-induced remote repair, MIRR). Future studies are needed to validate this theory.

Rheumatoid arthritis (RA) affects millions of people worldwide and causes chronic joint pain with incompletely understood pathogenesis and challenging management. Myosin light chain 1 (MYL1) a muscle regulatory protein, has an unknown role in RA pathogenesis. We analyzed transcriptomic data from RA patients and healthy controls in the Gene Expression Omnibus (GEO). Using least absolute shrinkage and selection operator (LASSO) regression and random forest, we identified differentially expressed genes (DEGs). Diagnostic performance was assessed using receiver operating characteristic (ROC) curves and area under the curve (AUC). To explore potential mechanisms, we conducted functional enrichment and immune-infiltration analyses. We further validated MYL1 expression in a rat RA model using qRT-PCR and Western blotting. We found MYL1 significantly downregulated in RA with high diagnostic value (AUC > 0.8). Enrichment analyses revealed its involvement in muscle structure development, immune regulation, and calcium signaling pathways. CIBERSORT analysis indicated associations with immune cell infiltration, particularly regulatory T cells, activated natural killer (NK) cells, and M1 macrophages. The rat model confirmed reduced MYL1 expression at both mRNA (p < 0.001) and protein (p = 0.009) levels, consistent with human data. MYL1 is consistently downregulated in RA and may serve as a potential diagnostic biomarker. The results indicate that MYL1 may be involved in the pathological process of RA through calcium signaling, muscle function, and immune cell regulation. However, further clinical and mechanistic studies are warranted.

•Sarcopenia is a disease characterized by the progressive loss of muscle strength and function associated with aging.•Geriatric Nutritional Risk Index (GNRI) is a measure of nutritional status and can be used as a predictor for people with some chronic diseases.•GNRI is a reliable predictor of sarcopenia and has a nonlinear negative correlation with sarcopenia.•Some populations including high school graduates and above, non-Hispanic white, married or living with a partner, and nondiabetic are more sensitive to GNRI, which reduces the incidence of sarcopenia in individuals. Nutrition is closely related to the occurrence of sarcopenia. Evidence shows that sarcopenia has a serious impact on population health and the social economy. Geriatric Nutritional Risk Index (GNRI) is a useful prognostic predictor for several chronic diseases. Our original intention was to investigate whether GNRI correlates with sarcopenia. We included 4,709 adults aged 45 years and older from the National Health and Nutrition Examination Survey from 2009 to 2018 in this cross-sectional study. According to the level of GNRI, they were categorized into High-GNRI and Low-GNRI groups, while sarcopenia was assessed using skeletal muscle index. Multivariate logistic regression was employed to investigate the independent relevance between the GNRI and the prevalence of sarcopenia. We examined the linear or nonlinear relevance between GNRI and sarcopenia using the Restricted Cubic Spline (RCS) curve, and the threshold effect was analyzed. We explored whether some specific populations are more susceptible to GNRI affecting the occurrence of sarcopenia through subgroup analysis. The incidence of sarcopenia was substantially reduced in the High-GNRI group (17.7% vs. 13.2%; p = 0.013). We found that GNRI is an essential predictor of sarcopenia (OR: 0.57; 95%CI: 0.41–0.79; p = 0.001). The occurrence of sarcopenia was reduced by increasing GNRI. Subgroup analysis showed that some specific populations were more susceptible to GNRI, which reduced the incidence of sarcopenia in individuals. These populations included high school graduates and above (p = 0.006), non-Hispanic white (p = 0.045), married or living with a partner (p = 0.03), and non-diabetic (p = 0.021). The RCS curve showed a non-linear inverse relevance between GNRI and sarcopenia (non-linear p = 0.033), with a threshold identified at GNRI = 91.935. GNRI is a reliable predictor of sarcopenia in Americans aged 45 and older, with a nonlinear inverse relationship identified at a threshold GNRI of 91.935.

Purpose: Rheumatoid arthritis (RA) affects millions of people worldwide and causes chronic joint pain with incompletely understood pathogenesis and challenging management. Myosin light chain 1 (MYL1) a muscle regulatory protein, has an unknown role in RA pathogenesis. Methods: We analyzed transcriptomic data from RA patients and healthy controls in the Gene Expression Omnibus (GEO). Using least absolute shrinkage and selection operator (LASSO) regression and random forest, we identified differentially expressed genes (DEGs). Diagnostic performance was assessed using receiver operating characteristic (ROC) curves and area under the curve (AUC). To explore potential mechanisms, we conducted functional enrichment and immune-infiltration analyses. We further validated MYL1 expression in a rat RA model using qRT-PCR and Western blotting. Results: We found MYL1 significantly downregulated in RA with high diagnostic value (AUC > 0.8). Enrichment analyses revealed its involvement in muscle structure development, immune regulation, and calcium signaling pathways. CIBERSORT analysis indicated associations with immune cell infiltration, particularly regulatory T cells, activated natural killer (NK) cells, and M1 macrophages. The rat model confirmed reduced MYL1 expression at both mRNA (p < 0.001) and protein (p = 0.009) levels, consistent with human data. Conclusion: MYL1 is consistently downregulated in RA and may serve as a potential diagnostic biomarker. The results indicate that MYL1 may be involved in the pathological process of RA through calcium signaling, muscle function, and immune cell regulation. However, further clinical and mechanistic studies are warranted. Keywords: rheumatoid arthritis, myosin light chain 1, machine learning algorithm, immune cells

Systemic inflammation plays a crucial role in the pathogenesis and prognosis of diabetes and cardiovascular diseases. System inflammation response index (SIRI), is an emerging biomarker designed to assess the extent of systemic inflammation. We aimed to delineate the prognostic significance of SIRI in patients with both AF and type 2 diabetes mellitus (T2DM). Utilizing the Medical Information Mart for Intensive Care IV (MIMIC-IV) (v2.2) repository, subjects divided into three groups based on the SIRI index. The primary endpoint of our study was all-cause mortality during hospitalization, with one-year mortality serving as the secondary endpoint. A cohort of 2054 AF and T2DM patients participated. COX regression analysis revealed elevated SIRI levels as an independent risk factor for both in-hospital and 1-year mortality. 192 patients died during hospitalization, and 265 died during the follow-up of 1 year. When treating the SIRI as a continuous variable, a higher SIRI was significantly associated with increased all-cause mortality both in-hospital [hazard ratio (HR) 1.015, 95%CI 1.010–1.020, P  = 0.015] and 1-year (HR 1. 016, 95%CI 1.008–1.015, P  = 0.012). Additionally, compared to patients with the lowest tertiles of SIRI, those with the highest tertiles of SIRI possessed significantly higher all-cause mortality both in-hospital and 1-year after multivariable adjustment, and this relationship remained pronounced in AF and T2DM patients [in-hospital mortality (HR: 1.863, 95% CI 1.189–2.918, P  = 0.007); one-year mortality (HR: 2.143, 95% CI 1.621–2.831, P  < 0.001)]. Our RCS analyses indicated a pronounced linear association between SIRI and mortality in T2DM (p-value for non-linear < 0.001). In AF patients with T2DM, high SIRI is an independent predictor of poor survival and may be helpful for patient’s risk stratification.

In this study, a Mn-modified Pt-based catalyst loaded on nitrogen-doped Ketjen black (Mn-Pt/NKB) is prepared using a simple ethylene glycol reduction method. The size of Pt nanoparticles (NPs) is effectively controlled by doping with Mn and N. With the smallest average particle size of 1.7 nm, Mn-Pt/NKB demonstrates half-wave potentials of 0.890 and 0.688 V in the alkaline and neutral electrolytes, respectively, which are superior to those of commercial platinum on activated carbon (Pt/C). When applied as an air cathode in aluminum-air battery, it exhibits ultra-high power densities of 190 (alkaline) and 26.2 mW·cm −2 (neutral). Moreover, the voltage remains stable after 5 h of discharge. The practical application performance of the Mn-Pt/NKB catalyst in an aluminum-air battery is better than that of commercial Pt/C. Furthermore, the oxygen reduction reaction (ORR) mechanism on surfaces with different particle sizes is analyzed using density functional theory. Oxygen cracking is the major pathway on the surface of the small particles with lower energy consumption of 0.5 eV, while water molecule cleavage is the major pathway on the surface of the large particles with higher energy consumption of 0.97 eV. The lower energy consumption of the oxygen cracking pathway further confirms the ORR mechanism for higher activity on small-sized surfaces. This study provides a direction for the rational design of Pt-based catalysts for ORR and sheds light on the commercial development of aluminum-air batteries.

Background The triglyceride–glucose (TyG) index has demonstrated correlations with adverse clinical outcomes in patients with ischaemic stroke, coronary heart disease and cardiac failure. However, its association with overall mortality in individuals concurrently experiencing heart failure (HF) and chronic kidney disease (CKD) remains inadequately explored. Methods Utilizing the Medical Information Mart for Intensive Care IV (Version 2.2) repository, subjects underwent quartile stratification based on the TyG index. The primary endpoint was all‐cause mortality during hospitalization. Cox proportional hazard models were employed to examine the correlation between TyG and all‐cause mortality in HF patients with CKD. Evaluation involved Kaplan–Meier (KM) analysis and restricted cubic splines (RCSs) to compare mortality rates during hospitalization and 1 year after admission across cohorts with varying TyG index levels. Results A cohort of 1537 HF and CKD patients participated. Cox regression analysis revealed elevated TyG levels as an independent risk factor for both in‐hospital and 1 year mortality. RCS analysis indicated a rising, non‐linear association between TyG levels and all‐cause mortality (P value for non‐linear <0.001). KM survival curves demonstrated a statistically significant reduction in survival rates within the high TyG index group compared with the low one (log‐rank P < 0.001). Conclusions The TyG index exhibited substantial independent prognostic value for elevated in‐hospital and 1 year all‐cause mortality among the cohort with HF and CKD. These findings suggest that assessing the TyG index could play a crucial role in developing novel therapeutic strategies to improve outcomes for this high‐risk demographic.