👤 Zemin Ren

Metabolic diseases such as high blood lipids, high blood sugar, and disrupted gut microbiota pose a serious threat to people's physical health. The occurrence of these diseases is closely related to the lack of nutrients in daily rice staple foods, but there is a lack of comprehensive analysis of the underlying mechanisms. This study used fully nutritious brown rice as raw material, and after germination under various stress conditions, it significantly increased the levels of gamma aminobutyric acid (GABA, four carbon non protein amino acid), resistant starch, flavonoids, and other components that regulate metabolic diseases. Using rats as experimental subjects, a model of hyperlipidemia and hyperglycemia was constructed, with rice consumption as the control. The experimental period was 8 weeks. Research has found that feeding sprouted brown rice can significantly improve the accumulation of white fat in the liver caused by a high-fat diet, significantly reduce TC, TG, LDL-C, apoB, HL, LPL, and LCAT, significantly increase HDL-C and apoA1, and significantly reduce the levels of inflammatory factors IL-6 and TNF-α. Therefore, consuming sprouted brown rice can reduce the risk of hyperlipidemia, inflammation, and tumor occurrence by promoting fat breakdown, and can also increase the abundance of metabolic-promoting microorganisms (especially Euryarchaeota and Lactobacillus) in the intestine, improving the entire metabolic ecological network of rats. Show less

Fatty liver hemorrhagic syndrome (FLHS) is a common nutritional and metabolic disease in laying hens, leading to a rapid decline in egg production. This study aims to evaluate the antioxidant effects of dietary supplementation with Pueraria Lobatae Radix polysaccharide (PLRP) on laying hens with FLHS induced by a high-energy low-protein (HELP) diet. A total of 72 thirty-seven-wk-old Hy-Line Brown laying hens were divided into 4 groups: basal diet (CON), HELP diet (HELP), HELP + 100 mg/kg PLRP (HELP-Low), and HELP + 300 mg/kg PLRP (HELP-High), with 6 replicates of 3 hens each. After 4 weeks on the HELP diet, PLRP was added to the diet of the HELP-Low and HELP-High groups for 8 weeks. The results demonstrated that PLRP supplementation significantly improved laying rate compared to the HELP group, with the HELP-Low and HELP-High groups exhibiting respective increases of 23.81% and 28.57% (P < 0.01). PLRP also promoted follicular development, increasing the number of stratified, primary, and secondary follicles and improving the ovarian index. Biochemical analysis revealed enhanced antioxidant activity, with increased levels of T-AOC, T-SOD, and GSH-Px and reduced MDA in the liver and ovaries of PLRP-treated hens (P < 0.05). At the molecular level, PLRP upregulated mRNA expression of ER-α, ER-β, MTTP, APOB, APOVLDL-II, and VTG-II in the liver, as well as VLDLR, LHR, and FSHR in the ovaries, facilitating yolk precursor biosynthesis and follicular development (P < 0.05). It indicated that PLRP supplementation mitigates oxidative stress and enhances yolk precursor synthesis, thereby improving egg production in FLHS-affected hens. PLRP shows promise as an effective feed additive for preventing and alleviating FLHS in laying hens. Future studies will investigate the regulatory effects of PLRP on gut microbiota composition and its potential interactions with FLHS in laying hens. Show less

Lipoprotein subclasses and high-density lipoprotein (HDL) functions are associated with atherosclerotic cardiovascular disease (ASCVD), but researches on them in patients with nephrotic syndrome (NS) are limited. The aims of this study were (1) to analyze the changes in quantity and quality of lipoprotein in patients with idiopathic nephrotic syndrome (INS) and patients in remission from NS, and (2) to evaluate the lipid-related atherosclerotic risk in these patients. 51 patients with idiopathic nephrotic syndrome (NS group), 72 NS patients with complete remission (NS remission group), and 80 healthy controls (control group) were recruited. The levels of conventional lipids, lipoprotein subclasses, including VLDL, IDL (C, B, A), LDL (LDL1-7), HDL (large, intermediate, small) and HDL cholesterol efflux capacity (CEC), were measured and compared across the three groups. Conventional lipid parameters [TG, TC, LDL-C, apo-B and Lp(a)] and lipoprotein subclasses (VLDL, IDL-C, IDL-B, LDL-2 and sdLDL) were higher in NS group when compared to NS remission group and control group (P < 0.05). CEC in NS group was significantly lower than that in control group [21.0 (18.3-27.2) % vs 25.7 (23.3-28.9) %] (P < 0.001) and improved to 22.8 (20.6-23.7) % in NS remission group with the disease recovery. Proatherogenic changes in conventional lipid parameters, lipoprotein subclasses and HDL-CEC were observed in patients with NS, suggesting that more rigorous lipid regulation strategies may help reduce cardiovascular disease risk in patients with NS. Show less

Earthworms are valued as a dietary protein source in many regions. Earthworm protein can yield bioactive peptides, but enzymatic hydrolysis is inefficient by commercial proteases, and bioactivity development is still inadequate. This study developed a novel efficient method for degrading earthworm protein and investigated the lipid-lowering activity and mechanism of earthworm peptides. It was found that combining autolysis and alcalase exhibited a higher hydrolysis degree of earthworm protein of 43.64 ± 0.78% compared to using autolysis or alcalase only. The hydrolysate significantly reduced lipid accumulation in steatotic hepatocytes. LC-MS/MS results showed that the primary lipid-lowering peptides (EWPs) in the hydrolysate were small molecule peptides with molecular weights of 500-1000 Da and chain lengths of 4-7 amino acid residues. Western blot results demonstrated that EWP regulated the expression of lipid metabolism-related proteins, including APOC3, HMGCR, PCSK9, SREBP1, C/EBP-α, NPC1L1, PPAR-γ, and CYP7A1. Transcriptomic analysis and validation experiments indicated that the lipid-lowering activity of EWP was associated with its suppression of inflammatory factors, such as IL-6. This study presents an efficient enzymatic hydrolysis strategy for earthworm protein utilization, laying the foundation for its application in functional foods such as protein supplements, nutraceutical capsules, hypoallergenic infant formulas, and sports nutrition products. Show less

Although previous studies have reported associations between gonadotropins, testosterone, and Alzheimer's disease (AD), their longitudinal relationships with cognitive decline and temporal lobe atrophy remain insufficiently characterized. This study examined the association between baseline hormone levels and cognitive decline and temporal lobe volume loss trajectories, and whether these associations vary by sex or This study included 490 participants (378 MCI/112 AD; 311 men/179 women; mean age = 75.01 ± 7.52) from the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort. Baseline plasma levels of gonadotropins (FSH, LH) and total testosterone (TT) were measured using Luminex xMAP multiplex immunoassay. Cognitive decline was assessed longitudinally through MMSE and ADAS-Cog 13 scores. Temporal lobe atrophy was quantified using tensor-based morphometry of 1.5T MRI scans, with bilateral temporal lobe volumes scaled to a normalized reference (1,000 = baseline). Linear mixed effects models were employed to relate baseline plasma hormones to longitudinal cognitive performance and temporal lobe volume. Longitudinal analyses showed that higher baseline FSH levels were associated with faster cognitive decline (MMSE: β = -0.025, The results indicate that in individuals across the AD spectrum, elevated gonadotropin levels may exert deleterious, domain-specific effects on cognitive decline or temporal lobe atrophy. Women with lower TT levels may experience faster cognitive progression. Although future studies incorporating additional longitudinal hormone measurements and cognitive trajectories are warranted, our results underscore the importance of gonadotropins and testosterone in AD progression. Show less

Neurovascular biomarkers have the potential to enhance early diagnosis of Alzheimer's disease (AD) and AD-related dementias (ADRD), as cerebrovascular alterations often precede neurodegeneration. However, their clinical application remains challenging due to insufficient specificity, heterogeneity, and technical limitations. Here, we report that vessel- and cortical layer-specific parameters exhibit promising diagnostic sensitivity for neurovascular impairments in an AD/ADRD mouse model, apolipoprotein E (APOE) 4 knock-in (KI), compared to APOE3-KI at 12 months of age. Using two in vivo imaging modalities, 3D capillary-resolution optical Doppler tomography and laser speckle contrast imaging, we measured 36 morphological and functional vascular parameters and evaluated their diagnostic performance using a machine-learning Support Vector Machine classifier. APOE4 mice showed significant alterations including reduced venular and arterial cerebral blood flow velocities and diameters, increased vascular tortuosity, layer-dependent decreases in vascular density, and impaired cerebrovascular reactivity. Venule- and microcirculation-related parameters and dynamic vasoactivity to brain stimuli demonstrated high diagnostic accuracy (~ 90%). Together, these findings provide in vivo evidence for early, cortical layer-specific neurovascular dysfunction caused by APOE4 that increases the susceptibility to dementia and highlight the potential of combining neurovascular biomarkers from optical imaging with AI-based classifier for identification of increased AD/ADRD risk. Show less

Histone deacetylase 3 (HDAC3) is an epigenetic modifying enzyme closely linked to the development of atherosclerosis. Endothelial inflammation is a critical factor in atherosclerosis. However, the role of HDAC3 in mediating epigenetic modifications and regulating endothelial inflammation in atherosclerosis remains unclear. This study aims to investigate the impact of HDAC3 on endothelial inflammation and its contribution to atherosclerosis. Firstly, single-cell transcriptomic analysis identified elevated expression of HDAC3 and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) in inflammatory endothelial cells of atherosclerotic plaques in symptomatic patients. Endothelial-specific knockout HDAC3 in an apolipoprotein E knockout (ApoE Show less

In recent years, polysaccharides from Codonopsis pilosula (CPs) have received increasing attention for their excellent behaviors in immune-regulation. However, the relationship between the structure and immunomodulatory activity has rarely been reported. In this work, four fractions purified from crude CPs (CPW, CPS0.2, CPS0.5, CPS1) by chromatographic column separation were explored with both structure and immunomodulatory effects by THP-1 cells. The results showed that the monosaccharide composition, chain conformation, molecular weight (M Show less

The Mpox virus (MPXV) has emerged as a formidable orthopoxvirus, posing an immense challenge to global public health. An understanding of the regulatory mechanisms of MPXV infection, replication and immune evasion will benefit the development of novel antiviral strategies. Despite the involvement of G-quadruplexes (G4s) in modulating the infection and replication processes of multiple viruses, their roles in the MPXV life cycle remain largely unknown. Here, we found a highly conservative and stable G4 in MPXV that acts as a positive regulatory element for viral immunodominant protein expression. Furthermore, by screening 42 optically pure chiral metal complexes, we identified the Λ enantiomer of a pair of chiral helical compounds that can selectively target mRNA G4 and enhance expression of the 39-kDa core protein encoded by the MPXV Show less

Dietary guidelines recommend replacing saturated fatty acid with unsaturated fats, particularly polyunsaturated fatty acids. Cohort studies do not suggest a clear benefit of higher intake of polyunsaturated fatty acids but, in contrast, higher circulating linoleic acid (LA) levels-reflective of dietary LA intake, are associated with a reduced risk of type 2 diabetes. However, genetic variants in the fatty acid desaturase 1 gene (FADS1) may influence individual responses to plant-based fats. We explored whether FADS1 variants influence the relationships of LA and α-linolenic acid (ALA) intakes and nut consumption with plasma phospholipid fatty acid profiles and type 2 diabetes risk in a large-scale cohort study and a randomized controlled trial. In the EPIC-InterAct case-cohort (7,498 type 2 diabetes cases, 10,087 subcohort participants), we investigated interactions of dietary and plasma phospholipid fatty acids and nut consumption with FADS1 rs174547 in relation to incident type 2 diabetes using weighted Cox regression. In PREDIMED (492 participants in the Mediterranean Diet + Nuts intervention group, 436 participants in the control group), we compared changes in plasma phospholipid FAs from baseline to year 1. In EPIC-InterAct and PREDIMED, nut consumption was positively associated with LA plasma levels and inversely with arachidonic acid, the latter becoming stronger with increasing number of the minor rs174547 C allele (p interaction EPIC-InterAct: 0.030, PREDIMED: 0.003). Although the inverse association of nut consumption with diabetes seemed stronger in participants with rs174547 CC-genotype (HR: 0.73, 95% CI: 0.54-1.00) compared with CT (0.94, 0.81-1.10) or TT (0.90, 0.78-1.05) in EPIC-InterAct, this interaction was not statistically significant. FADS1 variation modified the effect of nut consumption on circulating FAs. We did not observe clear evidence that it modified the association between nut consumption and type 2 diabetes risk. Show less

Osteosarcoma is the most prevalent primary malignant bone tumor in children and adolescents. However, its underlying pathogenesis and mechanisms driving metastasis remain poorly understood. Here, we identified a novel super-enhancer-associated long noncoding RNA (SE-lncRNA), Zinc Finger MIZ-Type Containing 1 Antisense RNA 1 (ZMIZ1-AS1), which is highly expressed in osteosarcoma and promoted tumor cell proliferation, migration, and invasion. Mechanistically, the m⁶A demethylase ALKBH5 post-transcriptionally stabilized ZMIZ1-AS1 through m⁶A demethylation. Furthermore, ZMIZ1-AS1 directly bound to the RNA-binding protein Polypyrimidine Tract Binding Protein 1 (PTBP1), facilitating the translocation of PTBP1 from the nucleus to the cytoplasm. The relocalized PTBP1 then bound to and stabilized fibroblast growth factor receptor 1 (FGFR1) mRNA. In nude mouse models, ZMIZ1-AS1 overexpression promoted tumor growth and lung metastasis. Notably, combined inhibition of ALKBH5 (using ALKBH5-IN-5) and FGFR1 (using BGJ398/infigratinib) synergistically suppressed ZMIZ1-AS1-driven oncogenesis in vivo. Our study establishes the ALKBH5/ZMIZ1-AS1/PTBP1/FGFR1 signaling axis as a key driver of osteosarcoma progression and a promising target for therapeutic intervention. Show less

Drug resistance severely hinders the clinical application of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) in the treatment of non-small cell lung cancer (NSCLC). Notably, resistance caused by rare target mutations (with a mutation incidence rate below 5 %) accounts for approximately 15 % of total resistance cases in NSCLC. Due to the diversity and complexity of these mutations, targeted therapies against them are currently very limited. To address the challenge of multi-driver resistance in NSCLC, this study aimed to explore a novel therapeutic strategy that can simultaneously inhibit multiple resistance drivers and enhance drug resensitization to EGFR-TKIs, overcoming the limitations of conventional single-protein inhibitors. Established gefitinib-resistant HCC827 cell models driven by rare co-activation of two EGFR-independent membrane proteins. Developed a strategy targeting lipid raft cholesterol to destabilize raft integrity, leveraging the cholesterol-modulating properties of ginsenosides. Evaluated the synergistic effect of co-administering ginsenoside Rg3 with gefitinib in both in vitro and in vivo models. Explored the mechanism of Rg3 action, including its binding to lipid raft cholesterol, disruption of membrane anchoring of resistance-associated receptor tyrosine kinases, and acceleration of their endocytic degradation. Co-administration of ginsenoside Rg3 with gefitinib synergistically restored antitumor efficacy in both in vitro and in vivo models, outperforming conventional single-protein inhibitors. Mechanistically, Rg3 specifically binds to lipid raft cholesterol, disrupting the membrane anchoring of resistance-associated receptor tyrosine kinases (e.g., FGFR1 and VEGFR2) and accelerating their endocytic degradation. Structural-activity relationship analyses revealed that the cholesterol-binding capacity of ginsenosides-critical for resistance reversal-is modulated by the stereochemical configuration of sugar moieties at C3, C6, and C20 positions. This study elucidates a novel membrane-centric paradigm for overcoming multi-driver resistance in NSCLC, where pharmacological perturbation of cholesterol-lipid raft interactions by natural compounds like Rg3 enables broad-spectrum suppression of coexisting resistance mechanisms. It not only provides novel insights into the mechanisms underlying resistance in NSCLC but also presents a promising clinical strategy that could significantly improve treatment outcomes for patients. Show less

The selective inhibition of fibroblast growth factor receptors (FGFR) presents a significant challenge due to the high degree of sequence and the close structural similarity of the subtypes. Herein, we designed selective dual FGFR2/3 inhibitors based on the in-depth understanding of protein-ligand interaction contributions. We efficiently identified ISM7594 ( Show less

Fibroblast growth factor receptors (FGFRs) are established oncogenic drivers in various solid tumors. However, the approved FGFR inhibitors face challenges with acquired resistance and dose-limiting adverse effects associated with FGFR1/4 inhibition, limiting therapeutic efficacy. Herein, we systematically explored linker and electrophile moieties based on the pyrrolopyrazine carboxamide core and identified aniline α-fluoroacrylamide as an effective covalent warhead. Compound Show less

Chemoresistance is one ofthe main challenges for advanced NPCtreatment.We previouslyproved LHX2 transcriptionally regulates FGF1 and promotes cancer progression through activating FGF1/FGFR axis,which prompted us toexplore the potential inhibitors for FGFR to improve the therapy response. RT-qPCR, immunohistochemistry, western blot assayand immunofluorescencewere applied to verify the gene expression levels. Xenograftmodel as well as lung metastasis model was performed forin vitroassays. Flow cytometry and Tunel stainingwere used to determine the apoptosis of NPC cells.The interaction between β-eudesmol and FGFR1/2 was analyzed by Autodock software. β-eudesmol inhibited the growth and metastasisof NPCin vivoandin vitro.In addition,β-eudesmol treatment promoted NPC apoptosis and sensitized NPC to cisplatin. β-eudesmol putatively bound to FGFR and blocked the Akt signaling, STAT3 signalingandERKsignaling,which in turn restrainedABCC1 transcription. β-eudesmol suppressed cell growth, metastasis and chemoresistance in NPC through targetingFGF1/FGFR signaling, thereby blocking the Akt signaling, STAT3 signaling andERKsignaling, as well as down-regulating ABCC1 expression. Our findings provided a novel potential drug for NPC treatment. Show less

Notch2 activation promotes kidney cyst growth. Silencing Notch2 ameliorated cyst growth in mice with autosomal dominant polycystic kidney disease. Notch signaling, a conserved mechanism of cell-to-cell communication, plays a crucial role in regulating cellular processes, such as proliferation and differentiation, in a context-dependent manner. However, the specific contribution of Notch signaling to the progression of polycystic kidney disease (PKD) remains unclear. We investigated the changes in Notch signaling activity (Notch1–4) in the kidneys of patients with autosomal dominant PKD (ADPKD) and two ADPKD mouse models (early and late onset). Multiple genetic and pharmacologic approaches were used to explore Notch2 signaling during kidney cyst formation in PKD. Notch2 expression was significantly increased in the kidney tissues of patients with ADPKD and ADPKD mice. Targeted expression of Notch2 intracellular domain in renal epithelial cells resulted in cyst formation and kidney failure in neonatal and adult mice. Mechanistically, Notch2/Hey2 signaling promoted renal epithelial cell proliferation by driving the expression of the E26 transformation–specific homologous factor (Ehf). Depletion of Ehf delayed Notch2 intracellular domain overexpression–induced cyst formation and kidney failure in mice. A gain-of-function mutation in exon 34 of Notch2 signaling promoted kidney cyst growth, partially by upregulating Ehf expression. Show less

Interleukin-27 (IL-27), an Interleukin-12 (IL-12) family heterodimeric cytokine, plays a central yet complex role in immunoregulation within the intestinal mucosa, where its context-dependent actions can promote both protective and pathogenic outcomes. Although its cellular sources, receptor structure (IL-27Rα/gp130 complex), and involvement in regulating key immune cells (e.g., T-cell subsets, macrophages, neutrophils) and epithelial functions are established, the precise mechanisms underlying its paradoxical effects-balancing homeostasis with inflammation-remain incompletely resolved. This review synthesizes current understanding of IL-27 biology to clarify its multifaceted role. Crucial insights into these dual functions have emerged from preclinical models, including murine colitis (e.g., DSS-, TNBS-induced), enteric infection (e.g., Toxoplasma gondii, Citrobacter rodentium), and colorectal cancer models. These studies demonstrate that IL-27 critically orchestrates gut immunity, maintaining homeostasis through antimicrobial defense and barrier enhancement while suppressing immunopathology. Conversely, its dysregulation drives chronic inflammation and carcinogenesis. Clinically, IL-27 expression correlates with disease activity in inflammatory bowel disease (IBD), colorectal cancer (CRC), and infections, highlighting its biomarker potential. Consequently, targeting the IL-27 pathway presents promising therapeutic avenues: augmenting signaling may mitigate IBD hyperinflammation, while inhibition could bolster antitumor immunity or resolve infection-driven pathology. Future research must prioritize defining context-specific IL-27 functions, optimizing delivery strategies, and integrating IL-27 targeting with existing biologics to translate its immunomodulatory potential into novel therapies for intestinal diseases. Show less

The genetic foundations underlying the observed disease resistance in certain indigenous pig breeds, notably the Min pigs of China, present a compelling underexplored subject of study. Exploring the mechanisms of disease resistance in these breeds could lay the groundwork for genetic improvements in pig immunity, potentially augmenting overall pig productivity. In this study, whole blood samples were collected from pre- and post- swine fever vaccinated Min and Large White pigs for transcriptome sequencing. The mRNA and lncRNA in both pig breeds were analyzed, and intra-group and inter-group comparisons were also conducted. The results indicated that a greater number of immune-related pathways such as the JAK-STAT and PI3K-AKT signaling were enriched in Min pigs. Furthermore, genes involved in inflammation and antiviral responses, including IL16, IL27, USP18, and DHX58, were upregulated in post-vaccination Min pigs compared to post-vaccination Large White pigs. This heightened immune responsiveness could contribute to the observed differences in disease resistance between Min pigs and Large White pigs. Show less

Epidemiological studies have suggested that dried fruit intake may be associated with a lower risk of breast cancer (BC), yet the genetic mechanisms underlying this association remain unclear. This study aimed to explore the potential genetic relationship between dried fruit intake and BC susceptibility. We conducted a comprehensive genetic analysis using genome-wide association study (GWAS) data for dried fruit intake and BC, focusing on individuals of European ancestry. We assessed genome-wide and region-specific genetic correlations using several complementary methods, including linkage disequilibrium score regression and regional genetic mapping. To identify shared genetic regions, we applied statistical approaches that integrate information across traits and improve the detection of common genetic signals. Modest but statistically significant negative genetic correlations were observed between dried fruit intake and BC, including its subtypes. Regional analysis revealed shared signals across multiple chromosomal regions. Five candidate loci were consistently identified as shared between the traits, including BCL11A, MAD1L1, MLLT10, JMJD1C, and RP11-795H16.2. This study provides evidence for a genome-wide genetic link between dried fruit intake and BC risk, identifying several loci that may be shared between the traits. These findings may help improve our understanding of BC development and offer preliminary leads for future dietary prevention and personalized interventions, pending further experimental validation. Show less

Cardiovascular disease (CVD) is the leading cause of mortality in patients with metabolic dysfunction-associated steatotic liver disease (MASLD), yet traditional risk predictors remain limited in clinical practice. To develop machine learning (ML) models for classifying prevalent atherosclerotic cardiovascular disease (ASCVD) risk in MASLD patients, and to enhance model interpretability using SHapley Additive exPlanations (SHAP). Methods: This retrospective study included 590 MASLD patients diagnosed at the Affiliated Hospital of Qingdao University between December 2019 and December 2024. Patients were randomly divided into a training set (n=413) and a validation set (n=177), and further stratified based on ASCVD status. Least absolute shrinkage and selection operator (LASSO) regression was used for feature selection. Six ML models were developed and evaluated using sensitivity, specificity, accuracy, area under the receiver operating characteristic curve (AUC), and F1 score. SHAP analysis was performed to interpret feature contributions. ASCVD was present in 434 of 590 patients (73.6%). The Gradient Boosting (GB) model achieved the best performance, with AUCs of 0.918 (95% CI: 0.890-0.944) in the training set and 0.817 (95% CI: 0.739-0.883) in the validation set. SHAP analysis identified the top predictors as the Cholesterol-HDL-Glucose (CHG) index, Castelli Risk Index II (CRI-II), lipoprotein(a) [Lp(a)], serum creatinine (Scr), and uric acid (UA). The GB model demonstrated strong high accuracy in identifying existing ASCVD in MASLD patients and may serve as a useful tool for early risk stratification in clinical settings. Show less

Patients suffering coronary artery disease (CAD) with calcific aortic valve disease (CAVD) are facing worse prognosis with more complex operation strategies. As the primary stage of CAVD, it is helpful to confirm the risk factors of aortic valve calcification (AVC) in advance for exploring the secondary prevention as well as early intervention strategies of CAVD for CAD patients. Lipoprotein(a) [Lp(a)] has been confirmed as the risk factor of both CAD and CAVD. But whether Lp(a) level still affects the occurrence and development of CAVD in CAD patients has not been demonstrated yet. We firstly investigate the predictive value of Lp(a) for new-onset AVC in patients with CAD. Patients who were admitted to the Department of Cardiology, Zhujiang Hospital, Southern Medical University from March 2021 to December 2022 and diagnosed with CAD by elective coronary angiography(CAG)were included when met the criteria. Baseline data were collected through the electronic medical record system. Patients were followed up to repeat echocardiography with an interval at least 6 months, which was up to September 2023. The primary endpoint was new-onset AVC, according to which patients were divided into new-onset AVC group (n = 43) and the opposite(n = 165). Analyses were conducted using SPSS 26.0 and GraphPad Prism 10.1.2. A total of 208 patients with CAD were included, with a median follow-up time of 16 (12, 20) months. Compared with AVC-free group, patients with new-onset AVC had higher body mass index (BMI) (p = 0.003), higher proportion of tree-vessel disease(p < 0.001), higher rates of diabetes (p = 0.001) and atrial fibrillation (p = 0.017), higher Lp(a) levels(p < 0.001), lower left ventricular systolic function (LVEF) (p < 0.001) and thicker left ventricular posterior wall (LVPW) (p < 0.001). Increased BMI, three-vessel disease, Lp(a) > 26.65 nmol/L, increased LVPW were found independent risk factors for new-onset AVC. Using a cutoff level of 26.65 nmol/L, Lp(a) predicted new-onset AVC with a sensitivity of 79.1% and a specificity of 59.4% (AUC: 0.740, 95% CI: 0.657-0.823, p < 0.001). When combined with BMI, there present a higher AUC value of 0.752(95%CI: 0.668-0.836, p < 0.001); however, the statistical significance remains limited (p = 0.732). High-level serum Lp(a) was independently associated with new-onset AVC in patients with CAD. Lp(a) demonstrates a significant predictive value for the onset of new AVC in CAD patients, with an established cut-off threshold of 26.65 nmol/L. Show less

To investigate the risk factors associated with coronary heart disease (CHD) in patients with metabolic-associated fatty liver disease (MAFLD) and develop a nomogram prediction model. This study included 394 patients with MAFLD who underwent coronary angiography at The Affiliated Hospital of Qingdao University between December 2019 and December 2024. The study cohort was divided in a 7:3 ratio into training and validation sets comprising 277 and 117 cases, respectively. The training group was further divided into the MAFLD-only ( Of the 394 MAFLD cases, 313 had CHD-related complications. Of the 277 patients in the training set, 220 had CHD, and of the 117 patients in the validation set, 93 had CHD. LASSO regression analysis revealed that the following variables were associated with the risk of CHD: sex, lipoprotein(a) (Lp[a]), low-density lipoprotein cholesterol, white blood cell count (WBC), glycated triglyceride-glucose index (TyG), and atherosclerosis index (AIP). Multivariate logistic regression analysis revealed that sex, Lp(a), WBC, TyG, and AIP were independent risk factors for CHD in MAFLD cases. A nomogram was constructed and an ROC curve was plotted, based on which the optimal cutoff value was determined as 0.698. The area under the curve of the nomogram in the training and validation cohorts was 0.860 (95% CI = 0.807-0.913) and 0.843 (95% CI = 0.757-0.929), respectively. Calibration curves for CHD risk probability showed good agreement between the nomogram's predicted probabilities and the observed event rates. DCA demonstrated the net clinical benefit of the constructed nomogram. Sex, Lp(a), WBC, TyG, and AIP emerged as independent risk factors for CHD in patients with MAFLD and the nomogram prediction model constructed using these factors could effectively predict CHD occurrence. Show less

This study aimed to investigate the association between objectively and subjectively measured 24-hour movement behaviors and physical fitness, and explore how the reallocation of time between 24-hour movement behaviors is associated with changes in physical fitness in adolescents. A total of 690 adolescents aged 14-17 years (55% girls) were included in this cross-sectional study conducted in Foshan, China. Moderate-to-vigorous physical activity (MVPA), light physical activity (LPA), sedentary behavior, and sleep were assessed using accelerometers in combination with a questionnaire. Physical fitness was tested through body mass index, forced vital capacity, 50-m sprint, standing long jump, sit-and-reach, gender-specific 800/1000-m run, and pull-ups/sit-ups. MVPA was significantly associated with better performance in the 50-m sprint ( Show less

Lymphoplasmacytic Lymphoma (LPL) with immunoglobulin (Ig)A paraprotein is rare. When plasma cells dominate, the diagnosis becomes more challenging. We reported a case of a 71-year-old male with elevated creatinine, splenomegaly, monoclonal IgA, and MYD88 mutation. Only monoclonal plasma cells were detected first, leading to a misdiagnosis of multiple myeloma. When progressive spleen enlargement was observed, re-evaluation revealed the emergence of monoclonal lymphocytes and the diagnosis was revised to LPL. The addition of rituximab to DVD regimen led to a partial response. For cases where an initial definitive diagnosis cannot be established, close follow-up is required for timely diagnosis revision and therapeutic adjustment. Show less