Background: The effects of depression on liver function remain unclear. This study aims to assess the impact of depression on liver function based on the NHANES 2017-2020 data analysis and two-sample Mendelian randomization analysis. And employ mediation analysis to evaluate the mediating roles of BMI, alcohol consumption and prescription drug use. Methods: Using the NHANES 2017-2020 data, linear regression and logistic regression were employed to identify the association between depression and liver function based on different variable types. Then, restricted cubic spline analysis (RCS) was used to determine whether there was a non-linear association. Subsequently, mediation analysis was conducted to clarify the mediating roles of BMI, alcohol consumption, and the application of prescription drugs in this association. Finally, Mendelian randomization (MR) analysis was used to evaluate the causal relationship of this association. Results: Depression was associated with increased ALP and GGT levels, and decreased TBIL levels, with a significant non-linear relationship. Further, body mass index (BMI), alcohol consumption, and prescription drug use mediated the relationship between depression and liver function. Lastly, two-sample MR analysis provides preliminary support for a potential causal effect of depression on liver indicators: it suggests depression may contribute to increase ALP (odds ratio [OR] = 1.044, 95% confidence interval [CI]: 1.001-1.088, p = 0.047) and GGT (OR = 1.074, 95%CI: 1.030-1.120, p < 0.001), and reduce TBIL (OR = 0.930, 95%CI: 0.902-0.958, p < 0.001). Limitations: Cross-sectional NHANES may introduce reverse causality bias; Participant exclusion and unmeasured confounders could distort association estimates; The definition of some mixed factors is not detailed enough; MR's European ancestry data limits generalizability. Conclusion: Depression was positively correlated with ALP and GGT levels, and negatively correlated with TBIL levels, with a causal link. Factors such as BMI, alcohol consumption, and prescription drug use serve as mediators of this relationship. These findings highlighted the significant effects of depression on liver function. Future studies should validate our findings in multi-ethnic cohorts and explore the direct mechanism of depression-induced TBIL reduction.

Background:Primary angiitis of the central nervous system (PACNS) is a rare disease characterized by severe central nervous system (CNS) vascular inflammation. Serum aromatic amino acids have been reported to associate with inflammation. However, the aromatic amino acids in PACNS are poorly understood. Methods:We obtained serum samples from 18 PACNS patients, 35 healthy control, and 17 other neurological diseases patients without inflammation. Serum concentrations of aromatic amino acids were assayed by a liquid chromatograph mass spectrometer (LC-MS). Inflammatory cytokine levels, including interleukin (IL)-1β, IL-6, IL-8, complement 3 (C3), C4, and tumor necrosis factor-α (TNF-α) were also collected. Results:Of aromatic amino acids, tyrosine, and phenylalanine but not tryptophan in serum were significantly elevated in PACNS patients. Notably, phenylalanine levels were positively correlated with C3, C4, and IL-8. Receiver operating characteristic (ROC) curve evidence tyrosine and phenylalanine are capable of discriminating between PACNS, HC, and OND. Conclusions:Our exploratory data suggest that elevated serum phenylalanine and tyrosine may be associated with PACNS-related inflammation. Whether these metabolites can serve as differential-diagnostic biomarkers requires validation in larger, multicentre cohorts.

Despite extensive research, the systemic biological mechanisms underlying exercise-induced physiological adaptations remain incompletely understood. While animal models (e.g., rodents, non-human primates) have been instrumental in elucidating exercise-mediated benefits in aging and disease, interspecies differences in genomics, epigenetics, and metabolic regulation limit their translational relevance. The advent of induced pluripotent stem cell (iPSC)-derived 3D organoids revolutionizes exercise biology research by enabling human-specific modeling of tissue architecture and donor genomic/epigenetic profiles. This review highlights three transformative strategies: (1) Athlete-derived organoids preserving exercise-induced epigenetic memory to study muscle/neural adaptations; (2) Engineered systems integrating optogenetics and microfluidics to simulate mechanical forces (e.g., muscle contraction) and systemic signals (e.g., cytokines); (3) multi-omics mapping revealing exercise-responsive pathways like mitochondrial biogenesis. Collectively, these patient-specific models bridge pathophysiology with high-throughput screening, advancing precision medicine—from personalized training regimens to therapies counteracting sedentary-related diseases.

BackgroundHepatitis B virus (HBV)-related liver cirrhosis (HBV-LC) is a significant global health issue, affecting gut microbiota (GM) composition and metabolic processes. This study aimed to explore the associations between intestinal microbiota, metabolic profiles, and disease progression in patients with HBV-LC.MethodsFecal samples were collected prospectively from 40 healthy controls (HC) and 83 HBV-LC patients between December 2022 and August 2023. Gut microbiota alterations at various stages of liver function were analyzed using 16S rRNA gene sequencing. Untargeted metabolomics was employed to identify potential biomarkers and metabolic pathways associated with early cirrhosis. Additionally, correlations between bacterial genera, inflammatory markers, and metabolites were investigated.ResultsHBV-LC patients demonstrated a significant reduction in bacterial diversity and relative abundance compared to the HC group. Genera such as Alistipes and Lachnospira were notably depleted, while Fusobacterium and Enterococcus were enriched in patients with Model for End-Stage Liver Disease (MELD) scores ≥ 21 or Child-Turcotte-Pugh C grade. Correlation analyses revealed strong associations between intestinal flora, clinical indicators of disease severity, and inflammatory factors. Metabolic analysis showed decreased levels of tocopherol and 21-hydroxypregnenolone, which were strongly linked to the reduced abundance of Alistipes and Lachnospira. Biosynthesis of unsaturated fatty acids and linoleic acid metabolism emerged as critical enrichment pathways.ConclusionsHBV-LC patients displayed significant alterations in gut microbiota and fecal metabolites, which correlated closely with disease severity and inflammatory status. These findings provide new insights into cirrhosis pathogenesis and suggest potential biomarkers for early diagnosis and disease monitoring.

BACKGROUND:Hepatitis B virus-induced acute-on-chronic liver failure (HBV-ACLF) has extremely high mortality rates and is closely linked to inflammatory responses. Early interventions in high-risk patients can significantly improve survival rates. METHODS:In this prospective cohort study, we used the Olink proximity extension assay to compare 96 inflammation-related proteins in survivors and non-survivors of ACLF. Functional enrichment analysis of differentially expressed proteins (DEPs) was performed using KEGG to analyse their biological characteristics and correlation with disease severity. The key proteins identified in the discovery cohort (n = 32) were quantified by enzyme-linked immunosorbent assay in the modelling cohort (n = 100) to develop a machine-learning model, which was then validated in an independent cohort (n = 52). RESULT:The analysis revealed that the expression of 26 proteins was significantly elevated in non-survivors, mainly enriched in the cytokine-cytokine receptor interaction pathway. Three key proteins were highly correlated with mortality: IL-6, MMP10, and CX3CL1. The machine learning model based on these proteins accurately predicted the 90-day mortality (AUC = 0.98). Modelling and validation in both cohorts confirmed that these three indicators effectively identified high-risk patients with ACLF. CONCLUSION:IL-6, MMP10, and CX3CL1 can be used as effective biomarkers for predicting the 90-day mortality in patients with HBV-ACLF. The progression of liver failure seems to be closely related to the abnormal activation of the cytokine-cytokine receptor interaction pathway. These findings provide new directions for the study of ACLF pathogenesis and identifying potential drug targets, which are conducive to early clinical decision-making.

BackgroundThe systemic inflammation index (SII), neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR) and platelet-to-lymphocyte ratio (PLR) are inflammatory markers in peripheral blood, which have been proven to be associated with some central nervous system diseases. We aimed to evaluate the association of SII, NLR MLR and PLR with the severity of autoimmune encephalitis (AE) and to compare the predictive value of those biomarkers in the early identification of ICU admission.MethodsThis retrospective study was conducted in three medical centers in China. We included 176 patients diagnosed with AE and 200 age and gender-matched healthy controls and correlated their demographic and clinical data. The SII, NLR, MLR and PLR levels were calculated from the blood routine tests. The severity of the patients was evaluated by the Clinical Assessment Scale for Autoimmune Encephalitis (CASE) and the modified Rankin Scale (mRS) at admission, and the patients were divided into two groups according to the ICU admission.ResultsThe SII, NLR, MLR and PLR were significantly higher in AE patients than that in HCs (<0.001 for all). The SII and NLR were positively correlated with the CASE score (r = 0.243, p = 0.001; r = 0.237, p = 0.002) and the mRS score (r = 0.185, p = 0.014; r = 0.185, p = 0.014) in AE patients. The MLR and PLR were only positively correlated with the CASE score (r = 0.242, p = 0.001; r = 0.158, p = 0.036). The SII and NLR of the ICU group were significantly higher than that of the non-ICU group. The result of receiver operating characteristic (ROC) analysis showed that NLR was the best predictor of ICU admission for AE patients (AUC = 0.701). NLR and MLR had similar predictive ability (AUC = 0.654; AUC = 0.608) and were superior to PLR. The optimal NLR cut-off value for the incidence of ICU was 3.906.ConclusionIncreased SII, NLR, MLR and PLR at admission are positively correlated with the CASE score of AE patients. Among the four indexes, the NLR is the best predictor of ICU admission, which may be helpful for clinicians to monitor disease progression and identify potentially severe patients of AE.

The principal aim of the present study was to develop and validate a nomogram predicting overall survival (OS) in patients with α-fetoprotein (AFP)-negative hepatocellular carcinoma (AFP-NHCC) who experience dynamic changes in AFP level after hepatectomy. A cohort of 870 patients were enrolled and randomly assigned into a training cohort (n=600) and a validation cohort (n=270) at a 7:3 ratio. The key variables contributing to the nomogram were determined through random survival forest analysis and multivariate Cox regression. The discriminative ability of the nomogram was evaluated using time-dependent receiver operating characteristic curves and the area under the curves. Furthermore, the nomogram was comprehensively assessed using the concordance index (C-index), calibration curves and clinical decision curve analysis (DCA). Kaplan-Meier (KM) curves analysis was employed to discern survival rates across diverse risk strata of patients. Ultimately, the nomogram incorporated critical factors including sex, tumor size, globulin levels, gamma-glutamyl transferase and fibrinogen levels. In the training and validation cohorts, the C-indexes were 0.72 [95% confidence interval (CI): 0.685-0.755) and 0.664 (95% CI: 0.611-0.717], respectively, attesting to its predictive validity. The nomogram demonstrated excellent calibration and DCA further confirmed its clinical usefulness. Additionally, KM curve analysis unveiled statistically significant differences in OS among three distinct risk groups. In conclusion, the present study successfully formulated a nomogram predicting 3-, 5- and 8-year OS in patients with AFP-NHCC with dynamic changes in AFP level post-local resection. This model serves as a valuable tool for clinicians to promptly identify high-risk patients, thereby facilitating timely interventions and potentially enhancing patient survival outcomes.

Objectives: Observational studies have indicated that type 1 diabetes (T1D) is prevalent in multiple sclerosis (MS), yet the causality remains unclear. The purpose of this study was to assess the causal association between MS and T1D. Methods: We employed a Mendelian randomization method using two samples to research the causal association between MS and T1D. The study primarily utilized the inverse variance weighted (IVW) method, and we use three methods (MR Egger, Weighted median, Weighted mode) for auxiliary analysis. To avoid reverse causality, we employed the Steiger Test method to further examine the screened SNPs. Furthermore, sensitivity analysis was conducted to ensure the robustness of the obtained results. Results: When MS was considered as the exposure variable and T1D as the outcome variable, the results indicated a significant positive correlation (IVW, OR=1.078, 95 % CI: 1.041-1.117; p<0.001). Conversely, when T1D is the exposure in question, the causal relationship with MS remains undetermined. These results were further validated through sensitivity analysis. Conclusions: The MR analysis results indicate that there is a causal relationship between MS and T1D. We provide compelling genetic evidence to support the causal connection between MS and an increased risk of T1D.

BACKGROUND:Although gut microbiota has been implicated in various liver disorders, its relationship with cirrhotic portal hypertension (CPH) remains unclear. AIMS:To investigate the structural and functional alterations of gut microbiota in patients with CPH and the potential role of these alterations in the progression of CPH. METHODS:We collected faecal samples from 35 patients with CPH and 71 patients without CPH (controls) to conduct microbiome and metabolomic analyses. Gut microbes, faecal metabolites and their functional pathways associated with CPH were identified using multiple bioinformatics approaches. To understand the role of gut microbiota in the pathogenesis of CPH, we carried out faecal microbiota transplantation, CPH-characteristic bacterial transplantation and antibacterial experiments in mice. RESULTS:Microbial diversity was diminished, and gut microbial structures were altered in patients with CPH compared to the controls, primarily manifested as increased abundance of lipopolysaccharide-producing bacteria and decreased abundance of anti-inflammatory bacteria. This dysbiosis of gut microbiota was accompanied by changes in the faecal metabolome, particularly in arginine biosynthesis and nitric oxide production. Transplantation of gut microbiota from CPH patients, as well as the transplantation of CPH-associated bacteria Veillonella nakazawae, was found to exacerbate CPH progression in mice. Antibiotic treatment significantly alleviated the CPH progression induced by N-dimethylnitrosamine in mice. CONCLUSIONS:Our study reveals that gut microbiota dysbiosis is implicated in CPH progression, potentially providing new avenues for microbiome-based treatment for CPH.

BACKGROUND:Autoimmune liver diseases, including primary biliary cholangitis (PBC), autoimmune hepatitis (AIH), and their overlap syndrome (OS), involve immune-mediated liver injury, with OS occurring in 1.2%-25% of PBC patients. OS carries a higher risk of cirrhosis, hepatocellular carcinoma, and reduced survival. While its pathogenesis remains unclear, gut microbiota dysbiosis and serum metabolite alterations may play key roles. This study uses 16S rRNA sequencing and liquid chromatography-mass spectrometry (LC-MS) metabolomics to compare gut microbiota and serum metabolites among PBC, AIH, and OS patients, and explores their associations with liver function. AIM:To differentiate OS from PBC and AIH based on gut microbiota, serum metabolites, and liver function. METHODS:Gut microbiota profiles were analyzed using 16S rRNA sequencing, while untargeted serum metabolomics was conducted via LC-MS. Comparative analyses were performed to identify differences in microbial composition and serum metabolite levels among PBC, AIH, and OS groups. Correlation analyses and network visualization techniques were applied to elucidate the interactions among liver function parameters, gut microbiota, and serum metabolites in OS patients. RESULTS:Compared to patients with PBC or AIH, OS patients demonstrated significantly reduced microbial diversity and richness. Notable taxonomic shifts included decreased abundances of Firmicutes, Bacteroidetes, and Actinobacteria, alongside increased levels of Proteobacteria and Verrucomicrobia. Distinct serum metabolites, such as pentadecanoic acid and aminoimidazole carboxamide ribonucleotide, were identified in OS patients. Correlation analysis revealed that aspartate aminotransferase (AST) levels were negatively associated with the bacterial genus Fusicatenibacter and the metabolite L-Tyrosine. A microbial-metabolite network diagram further confirmed a strong association between Fusicatenibacter and L-Tyrosine in OS patients. CONCLUSION:OS patients show decreased gut microbiota diversity and unique serum metabolites. Multi-omics linked AST, Fusicatenibacter, and L-Tyrosine, revealing OS mechanisms and diagnostic potential.

The prevalence and impact on physical function of osteosarcopenia in the Chinese population remain unclear. The purpose of this study was to assess the prevalence of osteosarcopenia and its association with physical function in the elderly population of China. A total of 519 participants (327 males, 192 females; mean age: 67.2 years) elderly people were recruited. Physical performance was evaluated using the Timed Up and Go test and the Short Physical Performance Battery (SPPB). Osteoporosis was diagnosed based on the 1994 WHO criteria, while sarcopenia was defined according to the AWGS guidelines. Osteosarcopenia was diagnosed when both sarcopenia and osteoporosis were present. Among the participants, osteosarcopenia was identified in 27 (5.20

Background:Autoimmune diseases comprise a spectrum of illnesses stemming from a common etiology: the loss of self-tolerance. The organ crucial for the establishment and maintenance of central and peripheral tolerance, namely the thymus, has rarely been explored across these diseases. Methods:In a multicentre radiological case-control study, we characterized the thymus in 16 prevalent autoimmune diseases using chest computed tomography (CT) images from patients and age- and sex-1:1 matched healthy controls. Participants underwent a routine CT examination, and baseline information on demographic, clinical, and potential risk factors was gathered at the time of enrollment. A semi-automatic algorithm was developed and employed for the analysis of thymic radiological characteristics, encompassing structural features and density. Thymic fatty replacement was evaluated using a four-point visual scoring scale (0-3). This study is registered with the Chinese Clinical Trial Registry (ChiCTR2300078417). Findings:After matching, 2441 participants in each group were included in case-control study. As individuals age, the thymus undergoes involution, leading to marked changes in thymic features over time, yet the degree of thymic feature alterations varies among groups. Compared to healthy controls, multiple characteristics of the thymus were distinct in the autoimmune disease patients, featuring higher trapezoidal proportions (68.21% vs 46.29%; p < 0.0001), larger bilobed size, and reduced density (-9.50; 95% CI, -10.95 to -8.04; p < 0.0001). In addition, the autoimmune disease patients displayed a greater proportion of fatty replacement (score 0, score 1, and score 2, 94.23% vs 87.83%, p < 0.0001). This consistent trend of thymic characteristic alternations, was observed across the 16 diseases (albeit varying in degree) and in newly diagnosed as early-stage patients. Notably, the subgroup for female patients of childbearing age (≤49 years) exhibited an especially prominent difference in thymic density (-16.23; 95% CI, -19.19 to -13.26; p < 0.0001 in all comparisons) and in the proportion of fatty replacement (85.37% vs 71.68%; p < 0.0001). Interpretation:Radiological assessments reveal a consistent pattern of exacerbated age-dependent thymic involution across 16 autoimmune diseases, suggesting a common underlying mechanism in the development of these diseases. This mechanism may involve the compromise of self-tolerance due to thymic involution. Funding:The National Key R&D Program of China, the National Science Foundation of China, and the Tianjin Key Medical Discipline (Specialty) Construction Project.

Cerebral small vessel disease (CSVD) leads to an extensive white matter damage associated with cognitive decline, yet the underlying damaging mechanisms remain incompletely understood. Here we established a positive correlation between plasma levels of serine proteinase elastase ELANE and periventricular white matter hyperintensity (PV-WMH) in a cohort of CSVD patients. In a CSVD murine model induced by bilateral carotid artery stenosis (BCAS), upregulated ELANE was detected both in microglia and peripheral blood neutrophils. Genetic ELANE deficiency significantly alleviated oligodendrocyte loss, thereby reducing white matter lesions (WMLs) as well as ameliorating sensorimotor and cognitive impairments in BCAS mice. In vitro studies demonstrated that ELANE triggered time-dependent and dose-dependent oligodendrocyte lineage cell death. Bone marrow transplantation showed that ELANE from microglia and peripheral blood both contributed to WML development and BCAS-induced neurological deficits. Mechanistically, ELANE, accumulated by oligodendrocytes, cleaved the phosphodiesterase domain of 2,3-cyclic nucleotide 3-phosphodiesterase (CNPase). Pharmacological inhibition of ELANE with Sivelestat reduced oligodendrocyte loss and WMLs leading to the restoration of white matter integrity and neurological improvements in BCAS mice. In post-mortem brain specimens of CSVD patients ELANE accumulated within WMLs being predominantly localized in microglia (and hence defined as microglial ELANE) rather than in the brain-infiltrating neutrophils. We therefore posit microglial ELANE as an instigator of whiter matter injury in CSVD and suggest its potential therapeutic relevance. ### Competing Interest Statement The authors have declared no competing interest.

BACKGROUND:Primary biliary cholangitis (PBC) is associated closely with the gut microbiota. This study aimed to explore the characteristics of the gut microbiota after the progress of PBC to cirrhosis. METHOD:This study focuses on utilizing the 16S rRNA gene sequencing method to screen for differences in gut microbiota in PBC patients who progress to cirrhosis. Then, we divided the data into training and verification sets and used seven different machine learning (ML) models to validate them respectively, calculating and comparing the accuracy, F1 score, precision, and recall, and screening the dominant intestinal flora affecting PBC cirrhosis. RESULT:PBC cirrhosis patients showed decreased diversity and richness of gut microbiota. Additionally, there are alterations in the composition of gut microbiota in PBC cirrhosis patients. The abundance of Faecalibacterium and Gemmiger bacteria significantly decreases, while the abundance of Veillonella and Streptococcus significantly increases. Furthermore, machine learning methods identify Streptococcus and Gemmiger as the predominant gut microbiota in PBC patients with cirrhosis, serving as non-invasive biomarkers (AUC = 0.902). CONCLUSION:Our study revealed that PBC cirrhosis patients gut microbiota composition and function have significantly changed. Streptococcus and Gemmiger may become a non-invasive biomarker for predicting the progression of PBC progress to cirrhosis.

Type 2 diabetes mellitus (T2DM) is a major risk factor of a number of neurodegenerative diseases (NDDs). Ketogenic diet (KD) has significant beneficial effects on glycemic control and may act effectively against NDDs, but the mechanism remains unclear. In this study, we aimed to investigate the potential effects of KD on gene expressions in the brains of T2DM model mice. Male db/db mice at the age of 9 weeks were fed with KD or normal diet to the age of 6 months, and the whole brains were subjected to mRNA-seq analysis for differentially expressed genes. KD significantly lowered fasting glucose and body weights in db/db mice (P<0.05), and the expression of 189 genes in the brain were significantly changed (P<0.05, |log2|>1). Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses revealed that the differentially expressed genes upon KD are involved in inflammatory responses and the functions of biosynthesis. In inflammatory responses, NF-κB signaling pathway, viral protein interaction with cytokine and cytokine receptor, and cytokine-cytokine receptor interaction pathways were enriched, and in biosynthesis pathways, genes functioning in lipid and amino acid metabolism, protein synthesis, and energy metabolism were enriched. Moreover, consistent with the gene set enrichment analysis results, proteasomal activity measured biochemically were enhanced in KD-fed T2DM mice. These data may facilitate the understanding of how KD can be protective to the brain in T2DM background. KD could be a new strategy for the prevention of NDDs in T2DM patients.

BACKGROUND Dyslipidemia and type 2 diabetes mellitus (T2DM) are chronic conditions with substantial public health implications. Effective management of lipid metabolism in patients with T2DM is critical. However, there has been insufficient attention given to the relationship between thyroid hormone sensitivity and dyslipidemia in the T2DM population, particularly concerning non-high-density lipoprotein cholesterol (non-HDL-C). AIM To clarify the association between thyroid hormone sensitivity and dyslipidemia in patients with T2DM. METHODS In this cross-sectional study, thyroid hormone sensitivity indices, the thyroid feedback quantile-based index (TFQI), the thyroid-stimulating hormone index (TSHI), the thyrotrophic T4 resistance index (TT4RI), and the free triiodothyronine (FT3)/free thyroxine (FT4) ratio were calculated. Logistic regression analysis was performed to determine the associations between those composite indices and non-HDL-C levels. Random forest variable importance and Shapley Additive Explanations (SHAP) summary plots were used to identify the strength and direction of the association between hyper-non-HDL-C and its major predictor. RESULTS Among the 994 participants, 389 (39.13%) had high non-HDL-C levels. Logistic regression analysis revealed that the risk of hyper-non-HDL-C was positively correlated with the TFQI (OR: 1.584; 95%CI: 1.088-2.304; P = 0.016), TSHI (OR: 1.238; 95%CI: 1.034-1.482; P = 0.02), and TT4RI (OR: 1.075; 95%CI: 1.006-1.149; P = 0.032) but was not significantly correlated with the FT3/FT4 ratio. The relationships between composite indices of the thyroid system and non-HDL-C levels differed according to sex. An increased risk of hyper-non-HDL-C was associated with elevated TSHI levels in men (OR: 1.331; 95%CI: 1.003-1.766; P = 0.048) but elevated TFQI levels in women (OR: 2.337; 95%CI: 1.4-3.901; P = 0.001). Among the analyzed variables, the average SHAP values were highest for TSHI, followed by TT4RI. CONCLUSION Impaired sensitivity to thyroid hormones was associated with high non-HDL-C levels in patients with T2DM.

The association between the geriatric nutritional risk index (GNRI) and osteosarcopenia in older adults with type 2 diabetes mellitus (T2DM) is not clear. A total of 573 individuals with T2DM were included in this cross-sectional study. Osteosarcopenia was defined as the presence of both osteoporosis and sarcopenia. Appendicular skeletal muscle mass and bone mineral density (BMD) was measured by dual energy X-ray absorptiometry to diagnose sarcopenia and osteoporosis. Multivariate analyses were used to assess the association between Geriatric Nutritional Risk Index (GNRI) and osteosarcopenia. The patients were divided into four groups: robust (n = 367), osteoporosis alone (n = 154), sarcopenia alone (n = 29), and osteosarcopenia (n = 23). The GNRI was the lowest in osteosarcopenia group and was positively correlated with skeletal muscle index (SMI) (r = 0.122, p = 0.004), grip strength (r = 0.154, p < 0.001), gait speed (r = 0.123, p = 0.004), and BMD of lumbar spine 2–4, femoral neck, and total hip (r = 0.137, p = 0.002; r = 0.096, p = 0.028; r = 0.086, p = 0.049, respectively). In the logistic regression model low GNRI was significantly associated with an increased risk of osteosarcopenia (adjusted OR, 4.164; 95

目的:探讨运动疲劳对空间认知能力的影响及海马突触可塑性调控机制.方法:采用随机数字法将雄性SD大鼠分为对照组(control)和疲劳组(fatigue),选用3级递增负荷跑台训练方案,建立慢性力竭运动疲劳模型.利用Y迷宫空间识别记忆实验评估大鼠的空间识别和记忆变化,使用Western Blot测定海马组织cAMP反应元件结合蛋白(CREB)表达及磷酸化水平,并利用在体电生理记录大鼠海马CA1区晚期时相长时程增强效应(L-LTP),随后通过免疫组织化学染色观察大鼠海马CA1区小清蛋白(PV)的表达.结果:疲劳组大鼠在新异臂的停留时间比和在各臂的总穿梭次数均明显低于对照组(P＜0.01).高频刺激后30、60、120直至180 min,疲劳组大鼠海马CA1区场兴奋性突触后电位(fEPSP)斜率较对照组大鼠均显著降低(P＜0.01).Western Blot结果表明,疲劳组大鼠海马组织磷酸化CREB(p-CREB)水平明显低于对照组(P＜0.05).免疫组织化学染色显示,疲劳组大鼠海马CA1区PV表达下调(P＜0.05).结论:运动疲劳可导致大鼠空间认知能力受损,其机制可能与海马L-LTP抑制、CREB磷酸化水平降低以及PV阳性神经元减少有关.

ObjectivesTo investigate the association between body fat (BF%) and sarcopenia in older adults with type 2 diabetes mellitus (T2DM) and potential link with increased levels of inflammatory indicators and insulin resistance.MethodsA total of 543 older adults with T2DM were included in this cross-sectional study. Appendicular skeletal muscle (ASM), handgrip strength and gait speed were measured to diagnose sarcopenia according to the updated Asian Working Group for Sarcopenia (AWGS) 2019 criteria. Body composition data were tested using dual-energy X-ray absorptiometry (DEXA). Levels of serum high-sensitive C-reactive protein (hs-CRP), interleukin-6, fasting blood insulin (FINS), hemoglobin A1c (HbA1c), 25-hydroxyvitamin D3 [25(OH) D3] were also determined.ResultsThe prevalence of sarcopenia in all participants was 8.84%, of which 11.90% were male and 5.84% females. The Pearson’s correlation analysis revealed that BF% was negatively correlated with gait speed in men and women (R =-0.195, P=0.001; R = -0.136, P =0.025, respectively). After adjusting for all potential confounders, sarcopenia was positive associated with BF% (male, OR: 1.38, 95% CI: 1.15–1.65, P< 0.001; female, OR: 1.30, 95% CI: 1.07–1.56, P=0.007), and negatively associated with body mass index (BMI) (male, OR: 0.57, 95% CI: 0.44–0.73, P<0.001; female, OR: 0.48, 95% CI: 0.33–0.70, P<0.001). No significant differences were found in hs-CRP, interleukin-6, and insulin resistance between older T2DM adults with and without sarcopenia.ConclusionHigher BF% was linked to an increased risk of sarcopenia in older adults with T2DM, suggesting the importance of assessing BF% rather than BMI alone to manage sarcopenia.

Objective:Our aim was to explore the effects of the energy-limiting balance intervention on serum uric acid (SUA) and high sensitivity C-reactive protein (hs-CRP) and analyze the correlation between the two. Methods:Retrospectively chosen study patients were 98 obese individuals who received diagnoses and care in Xuanwu Hospital Capital Medical University between January 2021 and September 2022. The patients were divided into the intervention group and the control group via random number table, with 49 patients in each group. The control group received standard food interventions, while the intervention group received minimal energy balance interventions. The clinical outcomes in both groups were compared. We also compared patients' pre- and post-intervention levels of SUA, hs-CRP, and markers of glucose and lipid metabolism were assessed. Analysis was done on the relationship between markers of glucose and lipid metabolism and SUA and hs-CRP levels. Results:Patients in the intervention and control groups had respective ineffective rates of 6.12% and 20.41%, effective rates of 51.02% and 57.14%, substantial effective rates of 42.86% and 22.45% and overall effective rates of 93.88% and 79.59%. The intervention group's overall effective rate was substantially greater than the control group's rate (P < .05). After the intervention, patients in the intervention group had markedly decreased SUA and hs-CRP levels than patients in the control group (P < .05). Prior to the intervention, there was no clinically meaningful discrepancy between the two groups in terms of fasting blood glucose, insulin, glycated hemoglobin (HbA1c) or 2 hours postprandial blood glucose (P > .05). Following the intervention there was a statistically significant discrepancy between the intervention group and the control group in terms of fasting blood glucose, insulin, HbA1c and 2 hours postprandial blood glucose (P < .05). According to a Pearson correlation study, high-density lipoprotein (HDL) was negatively correlated with the SUA levels and positively correlated with fasting blood sugar, insulin, triglycerides, total cholesterol and low-density lipoprotein (LDL). Before the intervention, there was no clinically meaningful variation in the intervention or control groups in triglycerides, total cholesterol, LDL or HDL (P > .05). Following the intervention, patients in the intervention group had markedly decreased triglycerides, total cholesterol and LDL levels than patients in the control group, while their HDL levels had substantially increased compared with the control group (P < .05). Fasting blood sugar, insulin, triglycerides and LDL all had a positive correlation with their SUA levels (P < .05). The amount hs-CRP was inversely correlated with HDL (P < .05) and positively correlated with fasting blood glucose, insulin, 2h postprandial blood glucose, HbA1c, triglycerides and LDL. Conclusion:An energy-limiting balance intervention can effectively reduce SUA and hs-CRP, regulate the metabolism of glucose and lipid and were closely related.