BACKGROUND:Idiopathic membranous nephropathy (IMN) is a major cause of nephrotic syndrome and end-stage renal disease, but the gold-standard diagnostic method is invasive. This study aims to develop a non-invasive diagnostic model for IMN, focus on the diagnostic value of anti-phospholipase A2 receptor antibody (anti-PLA2R-Ab). PATIENTS AND METHODS:In this single-center retrospective study,we included 9524 patients with chronic kidney disease patients who received renal biopsies, extracted 139 clinicopathological data from their records, and divided them into two groups based on pathological results.Renal biopsy cases were collected to form an independent external validation cohort.Seven machine learning methods were used to develop and verify models, and anti-PLA2R-Ab data were used to optimize and evaluate these models. Seventy percent of the patients were used for training, and the other 30% for verification. The area under the receiver operating characteristic curve, F1-score, accuracy, and confusion matrix were used to evaluate the diagnostic performance of the models. RESULTS:We analyzed 8840 patients and 10 indicators, excluding anti-PLA2R-Ab, to develop and validate diagnostic models, and then analyzed 2457 patients and 6 indicators, including anti-PLA2R-Ab, to develop and validate optimized models. With or without anti-PLA2R-Ab, the CatBoost model provided more accurate diagnosis of IMN (internal vs. external verification AUC:0.921 vs.0.901 and 0.950 vs.0.904, respectively) than anti-PLA2R-Ab alone (AUC: 0.867). CONCLUSION:The CatBoost model was an accurate and non-invasive method that provided better diagnosis of IMN than anti-PLA2R-Ab in Chinese patients. This model is especially when anti-PLA2R-Ab testing and kidney biopsy are difficult or impossible.

Abstract Objectives To validate blood oxygen level-dependent MRI (BOLD-MRI) for non-invasive discrimination of diabetic nephropathy (DN) vs non-diabetic renal disease (NDRD) and prediction of end-stage renal disease (ESRD) in diabetic kidney disease (DKD). Materials and methods A prospective cohort of 133 biopsy-proven DKD patients underwent BOLD-MRI. The semi-automated 12-layer concentric-objects method was used to analyze BOLD-MRI variables. Prognostic markers for ESRD were identified using univariate and multivariate Cox regression. Feature importance was used to select key diagnostic variables and establish logistic regression and machine-learning differential diagnosis models. Results Among 133 patients (44 DN, 55 NDRD, 34 combined), 20 (15.5%) progressed to ESRD over a mean of 21.8 months. Higher renal medullary R2* (MR2*) (> 24 1/s) reduced ESRD risk by 52% (HR, 0.48) in DKD. Prognostic models integrating pathological grouping, hemoglobin levels, and cysC levels achieved a c-index of 0.90. For the DN and combined groups, MR2*, glomerular grading, interstitial lesions, interstitial fibrosis, and tubular atrophy were predictive of ESRD, with a c-index of 0.91. For differential diagnosis, the random forest (RF) model achieved an AUC of 0.901, with diabetic retinopathy, diabetes duration, albumin, blood urea nitrogen, MR2*, hypertension, and glycosylated hemoglobin as the most contributing factors. For the combined group classified as DN, the AUC of the RF model was 0.791; when classified as NDRD, the AUC was 0.856. Conclusion MR2* shows potential value as a non-invasive diagnostic and prognostic tool in the assessment of DKD. However, BOLD-MRI remains a promising yet exploratory technique that requires external validation and interventional studies before clinical implementation. Critical relevance statement Blood oxygen level-dependent-MRI-derived renal medullary R2* robustly predicts ESRD risk and distinguishes DN without biopsy, offering an immediately translatable, non-invasive biomarker for the precision management of DKD in routine nephrology practice. Trial registration ClinicalTrials.gov, NCT03865914. Key Points Blood oxygen level-dependent-MRI medullary R2*(MR2*) > 24 s− 1 halves DKD ESRD risk (HR 0.48). MR2* integrated with clinical variables drives c-index to 0.90 for ESRD prognosis. RF leveraging MR2* and clinical traits attains an AUC of 0.901 for diagnosing DN. Graphical Abstract

Although transplantation of induced oligodendrocyte progenitor cells (iOPCs) is a promising strategy for white matter injury, the therapeutic efficacy of in vitro-generated iOPCs remains limited due to insufficient differentiation potential. Here, we aimed to identify key transcription factors and small-molecule drugs to optimize iOPC quality. Through transcriptome sequencing and bioinformatics analysis, we identified the transcription factor SOX10, which is differentially expressed between endogenous fetal OPCs and exogenous iOPCs. We established lentivirus-mediated SOX10 overexpression in neural stem cells (NSCs) before iOPC induction and performed cellular assays and multi-omics analysis. Early SOX10 overexpression reduced cell migration but promoted maturation into oligodendrocytes and suppressed astrocyte differentiation. Multi-omics analyses revealed that SOX10 overexpression is associated with the extensive redistribution of SOX10 chromatin binding and enrichment of regulatory programs linked to oligodendroglial differentiation, including the activation of the key signaling downstream transcription factors JUN/FOS. Moreover, TSA, Dabrafenib, and Fedratinib effectively upregulated SOX10 and improved iOPC differentiation. This study identifies SOX10 as a core upstream regulator governing the fate of iOPCs, providing a potential strategy for optimizing iOPC induction for future investigation of white matter injury therapy.

OBJECTIVE:To clarify the distribution of Traditional Chinese Medicine (TCM) symptoms, syndrome elements and complications in chronic kidney disease stage 5 (CKD5) patients with type 2 diabetes mellitus (T2DM), and to analyze the correlation factors between dialysis and non-dialysis patients, so as to provide reference for clinical syndrome differentiation and treatment. METHODS:The general information, laboratory indicators, and TCM syndrome factors of CKD5 patients with T2DM were obtained upon admission. The participants were divided into non-dialysis and dialysis groups according to the treatment methods used. Multivariate logistic regression was used for analysis. The probability of planned dialysis in CKD5 patients with T2DM was calculated by combining multiple TCM syndrome factors, and a receiver operating characteristic curve was drawn. RESULTS:Approximately 77.2% of the study participants were men, with a median age of 59 years. A total of 277 and 95 patients comprised the non-dialysis and dialysis groups, respectively. The median duration of dialysis was 49.6 d. The dialysis group had a significantly higher serum creatinine level; a significantly lower estimated glomerular filtration rate, serum uric acid level, and 24-h urinary protein level; and a significantly lower proportion of patients with atherosclerosis (P < 0.01). The frequencies of Water stagnation pattern, Damp retention pattern, Heart deficiency pattern, and Lung deficiency pattern in the dialysis group were significantly higher (P < 0.01，P < 0.05), while the frequencies of Phlegm turbidity pattern and Kidney deficiency pattern were significantly lower (P < 0.01). Male sex [odds ratio (OR) = 1.780], Heart deficiency pattern (OR = 3.714), Yindeficiency pattern (OR = 2.262), and Water stagnation pattern (OR = 1.984) were factors related to planned dialysis in CKD5 patients with T2DM. The area under the receiver operating characteristic curve for planned dialysis in CKD5 patients with T2DM was 73.8% [95% confidence interval (0.680, 0.797), P < 0.001]. CONCLUSIONS:Male sex, Heart deficiency pattern, Yindeficiency pattern, and Water stagnation pattern were correlated with planned dialysis in CKD5 patients with T2DM. Kidney deficiency pattern and Phlegm turbidity pattern were correlated with CKD5 patients with T2DM who had not yet started planned dialysis. The study of TCM syndrome elements provides therapeutic ideas for relieving the uncomfortable symptoms of CKD 5 patients with T2DM, and provides reference for clinical syndrome differentiation and treatment.

Heterogeneity is widely recognised across different cell types. Human oligodendrocyte progenitor cells (hOPCs), essential for myelination, exhibit considerable heterogeneity, which has not been fully characterised. In the current study, by examining the transcriptome of hOPCs at the single-cell level, three distinct subclusters were identified: PRE-OPCs, OPCs, and PRE-OLs. Single-cell RNA-sequencing and RNA-Scope detected high platelet-derived growth factor receptor alpha (PDGFRA) expression. PDGFR-α+ hOPCs exhibited greater myelination, migration, and proliferation capabilities compared to both unsorted hOPCs and PDGFR-α- hOPCs. These enhanced functions may be associated with the activation of the PI3K-AKT-mTOR and TGF-β signalling pathways, which support oligodendrocyte differentiation. hOPCs were induced by hNSCs, their characteristics were identified. RNA-Scope and single-cell RNA Seq sequencing showed PDGFRA were highly expressed at mRNA and protein level. hOPCs were sorted by MACS using PDGFR-α beads. The myelination, migration, and proliferation abilities of PDGFR-α+ hOPCs were higher than that of un-sorting hOPCs and PDGFR-α- hOPCs, possibly being associated with the activation of PI3K-AKT-mTOR and TGF-β signalling pathways, which support oligodendrocyte differentiation (Partly created with Scientific Image and Illustration Software BioRender).

ObjectiveTo assess the screening status of high-risk individuals for chronic kidney disease （CKD） in a community in Chengdu and to identify the main factors associated with incident CKD， thereby providing evidence for community-based CKD prevention and control strategies.MethodsClinical data were collected from high-risk individuals for CKD who visited the Chengdu Wuhou South Railway Station Community Health Service Center between April 17， 2014， and April 16， 2023. CKD was diagnosed based on the criterion of two consecutive abnormal findings of the same kidney damage marker persisting for at least 3 months. A Cox proportional hazards regression model was used to analyze risk factors for newly diagnosed CKD. Kaplan-Meier survival curves were applied to evaluate the effect of different numbers of risk factors on patient CKD-free survival time.ResultsA total of 7，599 high-risk individuals were included， among whom 33.12% underwent combined screening for estimated glomerular filtration rate （eGFR） and urinary microalbuminuria （MAlb）. During follow-up， 357 cases of CKD were diagnosed， with an overall annual incidence rate of 4684.83 per 100，000. Cox regression analysis showed that hypertension （HR=1.85， 95%CI： 1.28-2.69）， diabetes mellitus （HR=4.16， 95%CI： 3.02-5.74）， and obesity （HR=2.03， 95%CI： 1.62-2.54） were independent risk factors for CKD. Kaplan-Meier survival analysis showed that individuals with two or more high-risk factors had a significantly lower CKD-free survival rate （P<0.001）.ConclusionA substantial number of individuals in the community are at potential risk for CKD. Diabetes mellitus， hypertension， and obesity are the main contributing factors. The implementation rate of combined eGFR and urine MAlb screening remains low and should be further promoted. The number of individual risk factors is significantly negatively correlated with CKD-free survival time.

Objective Based on self-determination theory (SDT) and adopting a dual perspective of both patients and caregivers, this study explores the authentic experiences, behavioral challenges, and influencing factors associated with rehabilitation exercises for patients with diabetic foot. Methods This study is a phenomenological study. Using purposive sampling, we selected diabetic foot patients and caregivers who were hospitalized at our institution between May 2025 and March 2026 for semi-structured interviews. Results Guided by SDT, the interview data were analyzed, synthesized, and distilled from the perspective of the fulfillment and frustration of three basic psychological needs: autonomy, competence, and relatedness. The patient interview recordings yielded a total of 3 themes, including: frustration of the need for autonomy—lack of supervision and behavioral extinction; frustration of the need for competence—fear of restraint and erosion of confidence; and frustration of the need for relatedness—isolation and lack of support, and role compression; The caregiver interview recordings were integrated and synthesized into 3 themes, including: The Struggle for Autonomy—exhaustion of motivation and helplessness in caregiving; The Struggle for Competence—blind spots in guidance and caregiving anxiety; and The Struggle for Belonging—gaps in guidance and fighting alone. Conclusion A patient’s rehabilitation exercises are influenced by numerous factors. Healthcare professionals should analyze the factors that facilitate and hinder the implementation of rehabilitation exercises from both perspectives, providing a theoretical basis and practical guidance for developing targeted, individualized rehabilitation intervention plans and care support strategies, with the ultimate goal of improving patient outcomes and enhancing quality of life.

PURPOSE:This study aimed to identify the distinct latent profiles of exercise fear trajectories and to explore the factors influencing membership in these profiles among patients with DFU. METHODS:A multicenter, cross-sectional study was conducted from March 2025 to August 2025. Using convenience sampling method, 179 patients with DFU were recruited from five tertiary hospitals in China. Participants completed a battery of questionnaires, including a General Information Form, the Tampa Scale for Kinesiophobia, the Exercise Self-Efficacy Scale, the Mini-Nutritional Assessment, and the Activity of Daily Living Scale. Latent profile analysis was employed to identify distinct subgroups of exercise-related fear. Univariate analysis and multivariate logistic regression were used to determine factors influencing profile membership. RESULTS:The response rate was 98.90%. Latent profile analysis revealed three distinct classes of exercise fear: "low fear-functional adaptation" (n = 40,22.30%), "moderate fear-cautious engagement" (n = 58,32.40%), and "high fear-exercise avoidance" (n = 81,45.30%). Multivariate logistic regression identified that poorer nutritional status、self-paid medical expenses、advanced age、comorbid chronic conditions、higher Wagner grade、and a greater number of DFU-related hospitalizations in the preceding year were significant factors associated with an increased likelihood of belonging to the more severe fear profiles (all P < .05). CONCLUSION:The exercise-related fear trajectory in DFU patients exhibits significant heterogeneity, categorized into three distinct profiles. Healthcare providers should routinely assess patients for kinesiophobia and identify patients' specific profile. Tailored interventions, including nutritional support, psychological counseling for those with financial or comorbidity burdens, and graded exposure exercise protocols for high-fear levels, are recommended to mitigate fear and promote safe physical activity participation.

Hypoxic preconditioning is commonly used to improve the therapeutic efficacy of neural stem cells (NSCs) transplantation; however, the mechanisms by which hypoxia regulates intercellular communication in NSCs remain incompletely understood. As connexin 43 (Cx43) is a key component of gap junctional intercellular communication (GJIC), we investigated whether hypoxic preconditioning modulates Cx43 expression and function in NSCs and whether this pathway contributes to NSCs-mediated angiogenesis in a rat model of cerebral palsy (CP). In vitro, NSCs exposed to 1

ETHNOPHARMACOLOGICAL RELEVANCE:Formononetin (FMN) is a natural isoflavone found in several medicinal plants. Its effects on diabetic retinal and renal microvascular injury and EGR1/VEGF-related endothelial responses remain incompletely defined. AIM OF THE STUDY:To assess whether FMN attenuates early diabetes-associated retinal and renal injury and whether EGR1 is involved. MATERIALS AND METHODS:Alloxan-induced diabetic rabbits received FMN orally at 25 mg/kg/day from Week 4 to Week 16 after pretreatment renal and OCT/OCTA assessment. Renal function, histopathology, retinal flat mounts, longitudinal OCTA, and tissue EGR1/VEGF expression were examined. High-glucose-treated retinal, renal microvascular, and umbilical vein endothelial cells were used for functional assays. EGR1 overexpression, VEGFA promoter reporter assays, SPR, docking, and molecular dynamics simulations were also performed. RESULTS:FMN lowered serum creatinine, blood urea nitrogen, and urinary albumin-to-creatinine ratio, and reduced renal histopathological injury. It also attenuated retinal capillary loss, retinal thinning, and OCTA abnormalities despite persistent hyperglycemia. Retinal and renal tissues from FMN-treated rabbits showed lower EGR1 and VEGF expression. In endothelial cells, FMN reduced EGR1 and VEGF expression, abnormal tube formation, permeability, invasion, ROS, and inflammatory mediator release, while increasing NO-related signals. EGR1 overexpression weakened several effects and increased VEGFA promoter activity through the predicted EGR1-binding sequence. SPR detected FMN-EGR1 binding with a K_D of 3.245 μM. Computational analyses provided structural context. CONCLUSIONS:FMN attenuated early diabetes-associated retinal and renal injury and was linked to EGR1/VEGF-related endothelial responses. The data support EGR1 involvement but do not establish it as the sole target or mediator of FMN.

BACKGROUND:Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. The retinal microvasculature, as the only directly observable microvasculature, may reflect DN progression. This study aims to construct a non-invasive diagnostic and prognostic prediction model using the mixed effects of retinal vascular geometric parameters and clinical data. METHODS:We constructed a multimodal database including 397 patients with type 2 diabetes and chronic kidney disease from multiple centers in China. The primary cohort (374 patients) was recruited from the Department of Nephrology at the First Medical Center of the Chinese People's Liberation Army General Hospital in Beijing between 2017 and 2022, while an external validation cohort (23 patients) was collected from five other hospitals across China from September 2022 to March 2023. Fundus images, clinical characteristics, renal biopsy diagnoses, and follow-up data were collected. Unsupervised learning and Resnet neural networks were used to segment and calculate retinal vascular geometric parameters. Weighted quantile regression (WQS), Lasso, and COX univariable regressions were employed to assess the mixed effects of retinal vascular geometric parameters and select relevant clinical characteristics. Logistic regression and Cox regression with random forest (COX-RF) were used for model construction. RESULTS:A multimodal database of 397 patients was constructed. A diagnostic model combining retinal parameters (WQS-diagnosis) and seven clinical characteristics achieved superior performance: AUC 0.98, accuracy 0.92 on the test set, outperforming models using only clinical data (AUC 0.93) or two retinal parameters plus clinical data (AUC 0.94). On the multi-centre validation set, the model maintained accuracy 0.91 and AUC 0.95. For prognosis, a mixed-effects parameter (WQS-prognosis) was derived; the COX-RF model achieved an AUC of 0.88. CONCLUSIONS:Retinal microvasculature are effective biomarkers for DN. The proposed non-invasive model demonstrated high accuracy and generalizability, offering a valuable tool for optimising DN management.

Background Diabetes mellitus is a complex metabolic condition defined by hyperglycemia, leading to various difficulties, including diabetic nephropathy. Diabetic nephropathy is a serious condition of diabetes, defined by progressive kidney injury and dysfunction.Purpose In this study, we committed to assessing the therapeutic effects of angelicin against streptozotocin (STZ)-induced diabetic nephropathy in rats.Materials and Methods Diabetic nephropathy was induced in the experimental rats by injecting 65 mg/kg of STZ. The rats with diabetic nephropathy were subsequently administered angelicin and/or standard drug metformin for a duration of 10 weeks. Upon conclusion of the treatments, the body weight, food and water consumption, blood glucose, and kidney index in the experimental rats were assessed. The concentrations of kidney function markers, inflammatory cytokine concentrations, and oxidative stress-related marker levels were assessed. The kidneys of the experimental rats underwent histological examinations.Results The administration of angelicin significantly increased body weight and subsequently decreased glucose and kidney index in rats with STZ-induced diabetic nephropathy. In addition, angelicin treatment reduced the concentrations of renal dysfunction indicators in diabetic nephropathy rats. Angelicin significantly decreased the inflammatory response and oxidative stress by enhancing anti-oxidant levels in rats with diabetic nephropathy. The histological examination results corroborated the therapeutic efficacy of angelicin in treating diabetic nephropathy.Conclusion The current results suggest that angelicin may effectively alleviate diabetic nephropathy induced by STZ in rats. Overall, our results highlight that angelicin may be a beneficial therapeutic option for diabetic nephropathy.

Objective:This study aimed to investigate the effect of dietary acid-base load on patients with chronic kidney disease (CKD) and type 2 diabetes mellitus (T2DM). Design:A total of 300 patients with CKD were enrolled and divided into three groups according to DAL tertiles. Dietary intake was assessed using a 24-h dietary recall, and diet-based acidity was assessed using net endogenous acid production (NEAP), potential renal acid load (PRAL), and dietary acid load (DAL). Multivariable logistic regression models were used to determine the association between diet-based acid load scores and CKD and T2DM. Results:Within the food category groupings, the DAL score was positively associated with poultry and eggs and negatively associated with fruits and vegetables. Regarding energy and macronutrients, the DAL score was positively correlated with the intake of protein, animal protein, monounsaturated fatty acids, saturated fatty acids, and fat, while it was negatively correlated with the intake of carbohydrates, plant protein, and dietary fiber. In terms of micronutrients, DAL scores were positively associated with phosphorus intake and negatively associated with potassium, magnesium, and copper intake. After adjusting for age, BMI, energy, and eGFR, and stratifying by sex, logistic regression analysis showed that DAL level (OR = 6.47, 95% CI 1.19-35.18, p = 0.031) was a related factor for CKD and T2DM in females. Conclusion:DAL score is a related factor for patients with T2DM and CKD.

Mounting evidence implicates transforming growth factor-β1 (TGF-β1)-mediated renal tubular cell apoptosis in the pathogenesis of diabetic nephropathy. This investigation sought to elucidate the molecular mechanisms governing the pathogenic role of TGF-β1 in diabetic nephropathy progression. In vitro, human renal fibroblasts purchased were divided into six groups after different stimuli. Western blot was used to observe the cell protein expression, and CCK-8 was used to observe cell proliferation. In the in vivo experiment, 32 SD male rats were randomly divided into Control group, Model group, Model + TGFβ1 group, and Model + TGFβ1 + Notch1-KD group, and Model group was experimentally induced by a high-fat diet (HFD)/streptozocin(STZ) regimen in type 2 diabetes mellitus ( T2DM ) mouse model. HE staining was used to observe the degree of renal tissue fibrosis, and Western blot was used to observe the protein expression in renal tissues. In the in vitro experiment, TGFβ1 induced fibrosis and fibroblast proliferation by regulating the BRD4/Notch1/YAP signaling pathway. In the in vivo experiment, it was found that diabetic nephropathy rats treated with TGFβ1 showed significantly increased renal tissue fibrosis; when Notch1 was knocked down, the renal tissue fibrosis in diabetic nephropathy rats was significantly reduced. TGFβ1 accelerates the progression of diabetic nephropathy by inducing fibrosis and fibroblast proliferation through the regulation of the BRD4/Notch1/YAP signaling pathway.

Background One type of chronic kidney disease is diabetic nephropathy. One of the main causes of end-stage renal disease and chronic kidney disease is diabetic nephropathy. The objective of this study was to assess the effects of treating diabetic nephropathy with conessine extract on male wistar rats with diabetes that had been triggered by streptozotocin. Materials and Methods Twenty-four rats were split up into four groups. The regular diet was fed to the negative control animals in the first group. After receiving a single intravenous injection of streptozotocin to cause diabetes, the remaining 18 rats were split equally into three groups: the diabetic control group was placed in group 2, the third group received oral treatment with 20 mg/ kg of conessine, and the fourth group received oral treatment with 5 mg/kg of gliclazide. Results In comparison to the negative control, the rats in the second group had higher glucose and lipid peroxide levels and lower SOD, CAT, GR, GPx, and GSH activity. Diabetes also led to an increase in immunoglobulins, interleukin-6, and carboxymethyl lysine. Potassium and sodium levels were lowered, while kidney function metrics were also raised. renal tissues also displayed significant histological alterations. Conclusion Conessine treatments, administered to the diabetic rats in the third improved all altered biochemical and pathological tests that were getting closer to the negative control.

This study was designed to comprehensively elucidate the mechanism by which human umbilical cord-derived mesenchymal stem cell (hUC-MSC) therapy modulates epithelial cell apoptosis and preserves the integrity of the intestinal barrier. A series of meticulously planned in vivo and in vitro experiments were conducted to evaluate the effects of hUC-MSC treatment on various pathological parameters. Our in vivo findings demonstrated that hUC-MSC therapy significantly attenuated pathological damage, as evidenced by decreased tissue necrosis and inflammation. Furthermore, ultrastructural injury to the intestinal epithelium and mast cell infiltration were notably alleviated. With respect to the systemic immune response, serum levels of key immune factors, including IgG, IgE, mouse mast cell protease (mMCP-1), histamine, interleukin (IL)-6, and tumor necrosis factor (TNF)-α, were observably reduced following hUC-MSC treatment. At the molecular level, in jejunal tissue from food allergy mice treated with hUC-MSCs, the expression of IL-6 and TNF-α mRNA was downregulated, whereas the expression of , interferon (IFN)-γ, T-box transcription factor (T-bet) mRNA was upregulated. In vitro experiments using histamine-induced apoptosis in FHs 74 Int cells revealed that hUC-MSC therapy led to a marked decrease in the expression levels of pro-apoptotic proteins Bax, caspase-3, and cleaved caspase-3. Concurrently, significant upregulation of both the anti-apoptotic protein Bcl-2 and tight junction protein Zonula Occludens-1 (ZO-1) was observed. hUC-MSCs substantially improved cellular viability during histamine challenge by suppressing apoptosis (quantified by Annexin V/7-AAD staining) and reducing reactive oxygen species (ROS) generation in FHs 74 Int cells, demonstrating dual cytoprotective effects against histamine-induced toxicity. Our findings provide compelling evidence that hUC-MSCs mediate anti-apoptotic effects via modulation of the Bax/Bcl-2 pathway in histamine-stimulated intestinal mucosa during allergic responses. These results reveal novel therapeutic potential for hUC-MSCs in maintaining epithelial homeostasis and intestinal barrier function in food allergy-associated enteritis, suggesting promising clinical applications for this disorder.

This study explored the associations between triglyceride glucose (TyG), TyG with body mass index (TyG-BMI), triglyceride-to-high-density lipoprotein cholesterol (TG/HDL-C) ratio, and metabolic score for insulin resistance (METS-IR) and the effects of dietary acid-base load in patients with chronic kidney disease (CKD). Methods:A total of 288 patients with CKD were included in this study. Four non-insulin-based insulin resistance (IR) markers were used to assess IR levels in patients with CKD; dietary intake - 24-h dietary recall; and diet-based acidity - potential renal acid load (PRAL), net endogenous acid production (NEAP), and dietary acid load (DAL). Multiple linear regression analysis correlated dietary acid-base load and non-insulin-based IR markers. Results:Spearman's correlation indicated DAL was significantly associated with TyG-BMI (r = 0.251, P < 0.001) and METS-IR (r = 0.274, P < 0.001), but weakly correlated with the TG/HDL-C ratio (r = 0.14, P = 0.018). After adjusting for sex, age, energy, hypertension (HTN), diabetes, and estimated glomerular filtration rate, multiple linear regression analysis showed that DAL was associated with TyG-BMI (β = 0.336; P = 0.008) and METS-IR (β = 0.091; P = 0.007). Conclusions:Patients with the highest DAL scores had the highest TyG-BMI, TyG, TG/HDL-C ratio, and METS-IR. After adjusting for confounders, there was a significant positive association between DAL and TyG-BMI and METS-IR.