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Splenectomy has been reported to improve liver fibrosis in patients with cirrhosis and hypersplenism. However, the mechanisms remain unclear. Tumor necrosis factor superfamily 14 (TNFSF14; also known as LIGHT) is highly expressed in the context of fibrosis and promotes disease progression in patients with fibrotic diseases such as pulmonary and skin fibrosis. Here, we determined whether splenectomy controls the production of LIGHT to improve liver fibrosis. Splenectomy reduced serum LIGHT levels in cirrhotic patients with hypersplenism and a ConA-induced liver fibrosis mouse model. Blocking LIGHT resulted in the downregulation of TGF-β1 in RAW264.7 cells. LIGHT treatment of RAW264.7 and JS1 cells in coculture regulated transforming growth factor-β1 (TGF-β1) expression through the activation of JNK signaling. Small interfering RNA-mediated silencing of lymphotoxin β receptor (LTβR) in macrophages resulted in pronounced decreases in the levels of fibrosis and αSMA in JS1 cells. These results indicated that LIGHT bound to LTβR and drove liver fibrosis in vitro. Blocking TGF-β1 abolished the effect of LIGHT in vitro. Furthermore, the administration of recombinant murine LIGHT protein-induced liver fibrosis with splenectomy, while blocking LIGHT without splenectomy improved liver fibrosis in vivo, revealing that the decrease in fibrosis following splenectomy was directly related to reduced levels of LIGHT. Thus, high levels of LIGHT derived from the spleen and hepatic macrophages activate JNK signaling and lead to increased TGF-β1 production in hepatic macrophages. Splenectomy attenuates liver fibrosis by decreasing the expression of LIGHT. Liver disease: Splenectomy reduces a factor that fuels fibrosis Surgical removal of the spleen prevents release of a molecular signal that exacerbates liver fibrosis and ultimately contributes to the onset of cirrhosis. Several studies have indicated that splenectomy may protect liver function in cirrhosis patients, but the mechanism underlying this beneficial effect remains unclear. JiKai Yin of the Second Affiliated Hospital of Air Force Military Medical University, Shaanxi Xi’an, China, and colleagues have proposed a signaling protein called LIGHT as a likely factor. This protein is elevated in serum of patients with cirrhosis and mouse models of this disease. The authors subsequently identified molecular pathways triggered by LIGHT that fuel fibrosis. Treatments that interfere with LIGHT function prevent fibrosis, as does the sharp decrease in LIGHT levels that occurs following splenectomy. These results highlight a promising mechanism for protecting liver function in cirrhosis patients.

The authors aimed to characterize the relationships between non‐insulin‐based insulin resistance (IR) indexes and the risk of prehypertension, and to compare their abilities to identify prehypertension. The authors recruited 3274 adults who did not have hypertension and were not taking hypoglycemic or lipid‐lowering medications. The triglyceride‐to‐high‐density lipoprotein‐cholesterol ratio (TG/HDL‐C), fasting triglyceride and glucose index (TyG), and metabolic score for IR (METS‐IR) were calculated. Bivariate Spearman's correlation analysis and multiple logistic analysis were used. The area under the receiver operating characteristic (ROC) curve was used to compare the ability of the three indexes to identify prehypertension. Systolic and diastolic blood pressure (BP) positively correlated with TG/HDL‐C (r = .272, P < .001), TyG (r = .286, P < .001), and METS‐IR (r = .340, P < .001) in the entire cohort. Multiple logistic analysis showed that the proportion of prehypertension in the third and fourth quartiles of the TG/HDL‐C (Q3 vs. Q1: odds ratio (OR) = 1.527, 95% confidence interval (CI): 1.243–1.988; Q4 vs. Q1: OR = 1.580, 95% CI: 1.231–2.028), TyG (Q3 vs. Q1: OR = 1.519, 95% CI: 1.201–1.923; Q4 vs. Q1: OR = 1.658, 95% CI: 1.312–2.614), and METS‐IR (Q3 vs. Q1: OR = 1.542, 95% CI: 1.138–2.090; Q4 vs. Q1:OR = 2.216, 95% CI: 1.474–3.331) were significantly higher than in the lowest quartiles. The areas under the curves and 95% CIs for the identification of prehypertension were .647 (.628–.667) for TG/HDL‐C, .650 (.631–.669) for TyG, and .683 (.664–.702) for METS‐IR, respectively. Thus, non‐insulin‐based IR indexes (TG/HDL‐C, TyG, and METS‐IR) are significantly associated with the risk of prehypertension. Furthermore, METS‐IR is better able to identify prehypertension than TG/HDL‐C and TyG. These non‐insulin‐based IR indexes might assist with the prevention of hypertension in primary care and areas with limited medical resources.

Adenosine deaminase acting on double-stranded RNA 1 (ADAR1) mediates adenosine-to-inosine (A-to-I) RNA editing events. ADAR1 is highly expressed in “septic” macrophages and in small intestinal tissues of mice with sepsis. Overexpression of ADAR1 suppresses inflammation and intestinal damage. However, the specific underlying mechanism is unclear. This study was conducted to explore how microRNA (miRNA) regulates the anti-inflammatory mechanism of macrophages following ADAR1 upregulation. A murine sepsis model was established by cecal ligation and puncture (CLP). Mice were randomly assigned to sham, CLP, and CLP+ADAR1 groups. Hematoxylin and eosin (HE) staining and fluorescence isothiocyanate-dextran were used to evaluate intestinal injury and permeability. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR), western blotting, and Luminex assays were performed to detect changes in the expression of inflammatory cytokines. Adenoviruses were used to express ADAR1 in RAW 264.7 cells. Ribonucleoprotein immunoprecipitation analysis was conducted to detect the binding of ADAR1 and miRNAs. A dual-luciferase reporter assay was used to detect the binding of miRNAs and regulatory factors. We observed that ADAR1 significantly increased the expression of suppressor of cytokine signaling 3 (SOCS3) in macrophages and reduced the expression of interleukin-6 in macrophages and the serum, thereby reducing intestinal permeability and mucosal injury in mice with sepsis. The RNA-ribonucleoprotein immunoprecipitation binding assay and qRT-PCR demonstrated a direct interaction between ADAR1 and pri-miR-30a. The luciferase assay demonstrated that SOCS3 was significantly inhibited by miR-30a-5p, the mature product of miR-30a. Thus, ADAR1 exerts a protective effect against sepsis by reducing inflammation and organ damage via the ADAR1-miR-30a-SOCS3 axis.

Data are limited on the relationship between the cardio–ankle vascular index (CAVI) and non-insulin-based insulin resistance (IR) indices, including the triglyceride to high-density lipoprotein cholesterol ratio (TG/HDL-C), fasting triglyceride and glucose index (TyG), and metabolic score for IR (METS-IR). In this study, we explored the relationship between TG/HDL-C, TyG, METS-IR, and the risk of increased arterial stiffness (CAVI ≥ 8.0) and compared their ability to detect arterial stiffness in the non-hypertensive Chinese population. A total of 3,265 non-hypertensive subjects were included. Spearman’s and partial correlation analyses were used to assess the relationship between non-insulin-based IR indices and CAVI. The correlation between these indices and the risk of a CAVI ≥ 8.0 was explored by multiple logistic regression analysis. The area under the receiver-operating characteristic curve was used to compare the ability of TG/HDL-C, TyG, and METS-IR to detect a CAVI ≥ 8.0. After adjustment for confounding factors, linear regression analysis showed that the CAVI changed by 0.092 [95% confidence interval (CI) 0.035–0.149] per standard deviation increase in TyG. While, this linear relationship was not found when analyzing TG/HDL-C and METS-IR. Multiple logistic regression analysis showed that the proportion of patients with CAVI ≥ 8.0 in the fourth quartile of TG/HDL-C [Q4 vs. Q1: odds ratio (OR) 2.434, 95% CI 1.489–3.975], TyG (Q4 vs. Q1: OR 2.346, 95% CI 1.413–3.896), and METS-IR (Q4 vs. Q1: OR 2.699, 95% CI 1.235–5.897) was significantly higher than that in the lowest quartile. The area under the curve that could discriminate CAVI ≥ 8.0 was 0.598 (95% CI 0.567–0.629) for TG/HDL-C, 0.636 (95% CI 0.606–0.667) for TyG, and 0.581 (95% CI 0.550–0.613) for METS-IR. In this study, we demonstrated a significant association between increased arterial stiffness and non-insulin-based IR indices. Among them, TyG showed better discriminatory ability than TG/HDL-C or METS-IR.

Biomechanical forces, including vascular shear stress, cyclic stretching, and extracellular matrix stiffness, which influence mechanosensitive channels in the plasma membrane, determine cell function in atherosclerosis. Being highly associated with the formation of atherosclerotic plaques, endocytosis is the key point in molecule and macromolecule trafficking, which plays an important role in lipid transportation. The process of endocytosis relies on the mobility and tension of the plasma membrane, which is sensitive to biomechanical forces. Several studies have advanced the signal transduction between endocytosis and biomechanics to elaborate the developmental role of atherosclerosis. Meanwhile, increased plaque growth also results in changes in the structure, composition and morphology of the coronary artery that contribute to the alteration of arterial biomechanics. These cross-links of biomechanics and endocytosis in atherosclerotic plaques play an important role in cell function, such as cell phenotype switching, foam cell formation, and lipoprotein transportation. We propose that biomechanical force activates the endocytosis of vascular cells and plays an important role in the development of atherosclerosis.

Currently, there is a lack of clinical studies on how to stratify endothelial dysfunction based on the severity of co-existing hypertension and OSAHS. This evidence gap hinders clinicians' ability to accurately assess disease burden and determine the best timing and intensity of intervention for these high-risk patients. This study aimed to investigate the impact of hypertension combined with OSAHS on vascular endothelial function. Patients aged 35-60 years with hypertension and OSAHS were consecutively recruited from the outpatient department of the Department of Cardiology at the Chengdu Pidu District People's Hospital, from July 1, 2023, to December 31, 2023. AHI, RHI and endothelial damage-related markers [Von Willebrand Factor (VWF), Vascular Endothelial Growth Factor (VEGF), and Endothelial Microparticles (EMPs)] were measured. Routine examination data were collected. The correlation analysis between AHI, RHI, and hypertension grade and hypertension stage showed correlation coefficients less than 0.2, indicating almost no linear relationship. The correlation coefficient between AHI and RHI was -0.58 (  < 0.001). The correlation coefficients between AHI and VWF, VEGF, and EMPS were 0.56 (  < 0.001), 0.49 (  < 0.001), and 0.66 (  < 0.001). The correlation coefficients between RHI and VWF, VEGF, and EMPS were -0.62 (  < 0.001), -0.63 (  < 0.001), and -0.67 (  < 0.001). The RHI showed significant inverse associations with the studied variables.A 1-SD increase in AHI, vWF, VEGF, and EMPs was associated with a decrease in RHI of 0.02, 0.62, 0.63, and 0.67 units, respectively. (  = -0.02, adjusted  = -0.60,  < 0.01;  = -0.62, adjusted  = -0.64,  < 0.01;  = -0.63, adjusted  = -0.64,  < 0.01;  = -0.67, adjusted  = -0.71,  < 0.01). In patients with hypertension combined with OSAHS, RHI can be used as an important indicator in routine tests of vascular endothelial function to predict the degree of vascular endothelial injury.

High-density lipoprotein(a) (Lp(a)) is a well-established independent risk factor for atherosclerotic cardiovascular diseases (ASCVD). However, the interaction between Lp(a), low-density lipoprotein cholesterol (LDL-C), and polygenic risk score (PRS) in cardiovascular diseases has been the subject of relatively limited research. The present study included a total of 346,751 participants from the UK Biobank. According to the guideline of Lp(a), the study subjects were divided into 3 groups: the first group was <75 mmol/L (n = 272,643), the second group was 75 to 125 mmol/L (n = 35,792), and the third group was >125 mmol/L (n = 38,316). Elevated Lp(a) levels were associated with a progressively increased risk of overall cardiovascular events (CVEs), including ischemic stroke (IS), coronary heart disease (CHD), angina pectoris, and myocardial infarction (MI). In contrast, the risks of atrial fibrillation (AF) and heart failure (HF) decreased with higher Lp(a) levels. Additive interaction analyses revealed significant synergistic effects between Lp(a) and LDL-C for CHD (relative excess risk interaction [RERI] = 0.081, attributable proportion of interaction [AP] = 0.046, synergy index [SI] = 1.117), angina pectoris (RERI = 0.112, AP = 0.055, SI = 1.121), and MI (RERI = 0.183, AP = 0.079, SI = 1.161), with MI showing the strongest synergy. Incorporating PRS further amplified these effects, and the RERI (CHD: RERI = 0.721; angina pectoris: RERI = 0.781; MI: RERI = 1.318) and SI (CHD: SI = 2.218; angina pectoris: SI = 1.97; MI: SI = 2.326) were significantly higher than those of the interaction model containing only Lp(a) and LDL-C. In conclusion, Lp(a) and LDL-C show a significant synergistic effect in ASCVD, and this effect is more prominent in individuals with a higher PRS, suggesting that dual lipid management should be strengthened for such populations. While AF and HF may require alternative risk factor management.

Previous findings have indicated the potential benefits of the Chinese traditional medicine Qiliqiangxin (QLQX) in heart failure. Here we performed a double-blind, randomized controlled trial to evaluate the efficacy and safety of QLQX in patients with heart failure and reduced ejection fraction (HFrEF). This multicenter trial, conducted in 133 hospitals in China, enrolled 3,110 patients with HFrEF with NT-proBNP levels of ≥450 pg ml −1 and left ventricular ejection fraction of ≤40%. Participants were randomized to receive either QLQX capsules or placebo (four capsules three times daily) alongside standard heart failure therapy. The trial met its primary outcome, which was a composite of hospitalization for heart failure and cardiovascular death: over a median follow-up of 18.3 months, the primary outcome occurred in 389 patients (25.02%) in the QLQX group and 467 patients (30.03%) in the placebo group (hazard ratio (HR), 0.78; 95% confidence interval (CI), 0.68−0.90; P  < 0.001). In an analysis of secondary outcomes, the QLQX group showed reductions in both hospitalization for heart failure (15.63% versus 19.16%; HR, 0.76; 95% CI, 0.64−0.90; P  = 0.002) and cardiovascular death (13.31% versus 15.95%; HR, 0.83; 95% CI, 0.68−0.996; P  = 0.045) compared to the placebo group. All-cause mortality did not differ significantly between the two groups (HR, 0.84; 95% CI, 0.70−1.01; P  = 0.058) and adverse events were also comparable between the groups. The results of this trial indicate that QLQX may improve clinical outcomes in patients with HFrEF when added to conventional therapy. ChiCTR registration: ChiCTR1900021929 . In a randomized controlled trial involving patients with heart failure with reduced ejection fraction, treatment with Qiliqiangxin, a traditional Chinese medicine derived from 11 types of plants, decreased the incidence of cardiac events, as compared to placebo.

High-density lipoprotein(a) (Lp(a)) is a well-established independent risk factor for atherosclerotic cardiovascular diseases (ASCVD). However, the interaction between Lp(a), low-density lipoprotein cholesterol (LDL-C), and polygenic risk score (PRS) in cardiovascular diseases has been the subject of relatively limited research. The present study included a total of 346,751 participants from the UK Biobank. According to the guideline of Lp(a), the study subjects were divided into three groups: the first group was < 75 mmol/L (n = 272,643), the second group was 75 - 125 mmol/L (n = 35,792), and the third group was > 125 mmol/L (n = 38,316). Elevated Lp(a) levels were associated with a progressively increased risk of overall cardiovascular events (CVEs), including ischemic stroke (IS), coronary heart disease (CHD), angina pectoris, and myocardial infarction (MI). In contrast, the risks of atrial fibrillation (AF) and heart failure (HF) decreased with higher Lp(a) levels. Additive interaction analyses revealed significant synergistic effects between Lp(a) and LDL-C for CHD [relative excess risk interaction (RERI) = 0.081, attributable proportion of interaction (AP) = 0.046, synergy index (SI) = 1.117], angina pectoris [RERI = 0.112, AP = 0.055, SI = 1.121], and MI [RERI = 0.183, AP = 0.079, SI = 1.161], with MI showing the strongest synergy. Incorporating PRS further amplified these effects, and the RERI [CHD: RERI = 0.721; angina pectoris: RERI = 0.781; MI: RERI = 1.318] and SI [CHD: SI = 2.218; angina pectoris: SI = 1.97; MI: SI = 2.326)] were significantly higher than those of the interaction model containing only Lp(a) and LDL-C. In conclusion, Lp(a) and LDL-C show a significant synergistic effect in ASCVD, and this effect is more prominent in individuals with a higher PRS, suggesting that dual lipid management should be strengthened for such populations. While AF and HF may require alternative risk factor management.High-density lipoprotein(a) (Lp(a)) is a well-established independent risk factor for atherosclerotic cardiovascular diseases (ASCVD). However, the interaction between Lp(a), low-density lipoprotein cholesterol (LDL-C), and polygenic risk score (PRS) in cardiovascular diseases has been the subject of relatively limited research. The present study included a total of 346,751 participants from the UK Biobank. According to the guideline of Lp(a), the study subjects were divided into three groups: the first group was < 75 mmol/L (n = 272,643), the second group was 75 - 125 mmol/L (n = 35,792), and the third group was > 125 mmol/L (n = 38,316). Elevated Lp(a) levels were associated with a progressively increased risk of overall cardiovascular events (CVEs), including ischemic stroke (IS), coronary heart disease (CHD), angina pectoris, and myocardial infarction (MI). In contrast, the risks of atrial fibrillation (AF) and heart failure (HF) decreased with higher Lp(a) levels. Additive interaction analyses revealed significant synergistic effects between Lp(a) and LDL-C for CHD [relative excess risk interaction (RERI) = 0.081, attributable proportion of interaction (AP) = 0.046, synergy index (SI) = 1.117], angina pectoris [RERI = 0.112, AP = 0.055, SI = 1.121], and MI [RERI = 0.183, AP = 0.079, SI = 1.161], with MI showing the strongest synergy. Incorporating PRS further amplified these effects, and the RERI [CHD: RERI = 0.721; angina pectoris: RERI = 0.781; MI: RERI = 1.318] and SI [CHD: SI = 2.218; angina pectoris: SI = 1.97; MI: SI = 2.326)] were significantly higher than those of the interaction model containing only Lp(a) and LDL-C. In conclusion, Lp(a) and LDL-C show a significant synergistic effect in ASCVD, and this effect is more prominent in individuals with a higher PRS, suggesting that dual lipid management should be strengthened for such populations. While AF and HF may require alternative risk factor management.

The structural integrity of poultry eggs is essential for food safety, economic value, and hatchability. External eggshell quality—measured by thickness, strength, cracks, color, and cleanliness—is a key criterion for grading and sorting. Traditional assessment methods, although simple, suffer from subjectivity, low efficiency, and destructive nature. In contrast, recent developments in nondestructive testing (NDT) technologies have enabled precise, automated, and real-time evaluation of eggshell characteristics. This review systematically summarizes state-of-the-art NDT techniques including acoustic resonance, ultrasonic imaging, terahertz spectroscopy, machine vision, and electrical property sensing. Deep learning and sensor fusion methods are highlighted for their superior accuracy in microcrack detection (up to 99.4%) and shell strength prediction. We further discuss emerging challenges such as noise interference, signal variability, and scalability for industrial deployment. The integration of explainable AI, multimodal data acquisition, and edge computing is proposed as a future direction to develop intelligent, scalable, and cost-effective eggshell inspection systems. This comprehensive analysis provides a valuable reference for advancing nondestructive quality control in poultry product supply chains.