Systemic lupus erythematosus (SLE) and type 2 diabetes mellitus (T2DM) share inflammatory and metabolic disturbances, yet the molecular mechanism of their overlap remains unclear. This study used integrated bioinformatics to identify transcriptomic signatures and potential biomarkers common to both conditions. Gene expression profiles from publicly available datasets (SLE: 38 patients/32 controls; T2DM: 6 patients/6 controls; validation cohorts: 79/30 and 41/15, respectively) were analyzed to detect shared differentially expressed genes and co-expression modules. Functional enrichment, protein-protein interaction networks, and immune-cell composition analyses were performed. Diagnostic gene panels were constructed using random forest feature selection and logistic regression and evaluated through receiver operating characteristic analysis with external validation. A total of 551 shared differentially expressed genes were identified, enriched predominantly in type I interferon signaling, Toll-like/NOD receptor pathways, TNF signaling, necroptosis, and neutrophil extracellular trap formation. Across analytical methods, a 10-gene interferon-related hub (STAT1, IRF7, OAS1, OAS2, ISG15, MX2, IFI35, RSAD2, SAMD9, SAMD9L) genes demonstrated strong discriminative performance in both SLE and T2DM. A three-gene model further showed potential clinical utility (AUC 0.872-1.00 in discovery; 0.665-0.928 in validation).These signatures align with therapeutic axes in SLE (IFN/JAK-STAT) and intersect inflammatory-metabolic pathways in T2DM, supporting assayable biomarkers and compact diagnostic models that warrant validation in larger, medication-annotated cohorts.

Objective:To investigate the impact of diet on cardiovascular (CV)/all-cause mortality among individuals with diabetes, and to explore whether this relationship changes by gender. Methods:We collected data from the National Health and Nutrition Examination Survey (NHANES) database pertaining to 5,875 individuals with diabetes (3,068 males and 2,807 females) and used the Healthy Eating Index (HEI), the Alternative Healthy Eating Index (AHEI), and the alternative Mediterranean Diet (aMED) index to assess diet quality. Multivariate Cox models were used to determine the association between dietary quality scores and CV/all-cause mortality, stratified by genders. Dose-response relationships were assessed using the Restricted Cubic Spline (RCS). As a secondary objective, a further analysis was conducted on the connection between CV/all-cause mortality and different dietary components. Results:During a median 9.25-year follow-up period, we observed 1,488 all-cause deaths, including 486 CV deaths. Sex-stratified analyses revealed that higher diet quality, as indicated by each standard deviation increase in the score, was significantly associated with a reduced risk of cardiovascular mortality in males (p < 0.05). No significant associations were observed in females (p > 0.05). Among the component scores of the aMED, legume intake was unfavorable for males with diabetes but was remarkably associated with lower CV/all-cause mortality in females. Conclusion:In the diabetic population, high dietary scores are significantly associated with lower CV/all-cause mortality in males but not in females.

BACKGROUND:Patients with multivessel disease and ST-elevation myocardial infarction (MVD-STEMI) have a poor prognosis but benefit from quantitative flow ratio (QFR)-based revascularization. The influence of chronic kidney disease (CKD) on this benefit is unclear. This study aimed to evaluate differences in clinical outcomes of QFR-based revascularization in MVD-STEMI patients with or without CKD. METHODS:A total of 495 patients with MVD-STEMI who underwent primary percutaneous coronary intervention (PCI) were included in the study. Patients were divided into nonCKD and CKD cohort, and were further stratified into functional complete revascularization (FCR) and functional incomplete revascularization (FIR) layer based on QFR assessments. The primary outcomes were 3-year major adverse cardiovascular events (MACEs). RESULTS:The incidence of MACEs was lower in FCR than FIR layers in both nonCKD and CKD cohorts (p = 0.014, p = 0.008), but the percentage decrease in MACEs from FIR to FCR in CKD was greater than that in nonCKD cohort (53.1 % vs 49.7 %). The baseline QFR measurements were significantly lower in FIR patients with CKD than with nonCKD (p < 0.001). The residual SYNTAX score derived from QFR (RSSQFR) was significantly associated with the increased risk of MACEs in both cohorts (p < 0.001). Incorporating RSSQFR into prognostic models improved MACE prediction, especially in CKD cohort than in nonCKD cohort (difference in area under the curve = -0.143 vs difference in area under the curve = -0.133). CONCLUSIONS:In MVD-STEMI patients, the CKD population showed greater absolute risk reduction, which could be attributed to either their higher baseline risk or possible enhanced QFR efficacy. The ability of the QFR-based scoring system to predict prognosis was stronger in the CKD population than in the nonCKD population.

This study aimed to investigate the associations between the Dietary Inflammatory Index (DII) and cardiovascular (CV)/non-CV mortality in hypertensive individuals, and to explore sex-specific differences. Sixteen thousand six hundred twenty-three individuals with hypertension were selected from the National Health and Nutrition Examination Survey (NHANES) from 2001 to 2018 and divided into groups of males and females. We used multivariate Cox proportional hazards models, competing risk regression, restricted cubic splines (RCS), propensity score matching (PSM), and decision curve analysis (DCA) to evaluate the associations between the DII and CV/non-CV mortality. After fully adjusting for potential confounders, individuals with the highest DII score had a 35 percent higher CV mortality than those with the lowest DII score, observed in females but not in males. Across the cohort, there was a significant association between DII and non-CV mortality. RCS results showed that DII had an S-shaped association with CV mortality and a J-shaped association with non-CV mortality in hypertensive individuals. In patients with hypertension, we found sex differences in the association between DII and CV mortality. High DII was only associated with increased CV mortality in females with hypertension, but not in males. Higher DII was also associated with increased non-CV mortality.

Background Diet-related inflammation and metabolic dysfunction may influence long-term outcomes in hypertension. Objectives The objective of the study was to evaluate whether the DII (Dietary Inflammatory Index) and TyG-BMI (triglyceride-glucose body mass index), individually and jointly, are associated with cardiovascular and all-cause mortality in adults with hypertension. Methods The authors analyzed 8,024 hypertensive adults (≥18 years) from National Health and Nutrition Examination Survey 2001 to 2018 with a median follow-up of 9.91 years. DII was calculated from 27 nutrient intakes (24-hour recalls) and categorized into tertiles; TyG-BMI was derived from fasting triglycerides, fasting glucose, and BMI. Results Proinflammatory diets were associated with higher risks of cardiovascular disease (CVD) mortality (HR: 1.36; 95% CI: 1.00-1.85) and all-cause mortality (HR: 1.29; 95% CI: 1.08-1.54). Elevated TyG-BMI was associated with higher CVD mortality (HR: 1.46; 95% CI: 1.10-1.94), whereas its association with all-cause mortality was not statistically significant (HR: 1.12; 95% CI: 0.96-1.32). Participants with both high DII and high TyG-BMI had nearly a 2-fold higher risk of CVD mortality (HR: 1.98; 95% CI: 1.33-2.94). In subgroup analyses, risks appeared stronger in men (CVD HR: 2.15; 95% CI: 1.27-3.63) and among adults ≥60 years, where the highest CVD risk was observed for high DII + low TyG-BMI (HR: 1.91; 95% CI: 1.41-2.59; reference: low DII + middle TyG-BMI). Conclusions DII and TyG-BMI are significant indices that may enhance personalized strategies for CVD prevention and management.

Both alkaline phosphatase (ALP) and serum creatinine (sCr) have been individually associated with adverse outcomes in patients with diabetes. This study investigates a novel composite indicator-ln[ALP × sCr]-to predict all-cause and CVD mortality risk among U.S. adults with diabetes. We analyzed data from 82,091 U.S. adults enrolled in NHANES (1999-2014), with mortality follow-up through December 31, 2019. A deep learning model identified ALP, sCr, and vitamin D as top mortality-related biomarkers. Based on these results, we derived a composite index, ln[ALP × sCr], to reflect integrated cardiac-renal dysfunction. Restricted cubic spline analysis was used to define risk thresholds. Cox proportional hazards models assessed the association between ln[ALP × sCr] and all-cause, cardiovascular, and diabetes-related mortality. Over a median follow-up of 11.4 years, 4,839 T2DM patients in the highest quartile of ln[ALP × Scr] exhibited significantly elevated risks of all-cause (HR 1.47, 95

Background and aims: Disparities in serum biomarker levels related to mortality persist within the US diabetic population. We conducted a study to explore the impact of alkaline phosphatase (ALP) on all-cause mortality and cardiovascular disease (CVD) mortality in type 2 diabetes patients. Methods: We analyzed a nationally representative sample of individuals aged 20 years and above from the National Health and Nutrition Examination Survey (NHANES) conducted in the United States between 1999 and 2018. Baseline demographic information and biochemical markers, including blood glucose, gamma-glutamyltranspeptidase, vitamin D and albumin, were collected. Participants were divided into four groups based on ALP levels and linked to the National Death Index to assess mortality. Follow-up continued until December 2019, and multiple mediation analyses were performed to assess the combined impact of different indicators on ALP differences in all-cause mortality and cardiovascular mortality risk. Results: Our analysis included 6481 NHANES participants, categorized as follows: 1626 (21.9%) had ALP levels below 58 U/L, 1674 in the second quartile (58-72 U/L), 1569 in the third quartile (72-88.3 U/L), and 1612 in the fourth quartile (above 88.3U/L). Significantly higher all-cause mortality and cardiovascular mortality rates were observed among participants in the 4th ALP quartile compared to other levels. The all-cause mortality rate was 38.06 per 1000 person-years (95% CI 34.89-41.51), and the cardiovascular mortality rate was 10.67 (9.06-12.57). Mediation analysis indicated that Vitamin D and albumin played a mediating role in the association between all-cause mortality, cardiovascular mortality, and ALP levels, with mediation proportions ranging from 10.33% to 27.64%. Conclusions: Our study suggests that ALP levels have clinical value in predicting all-cause and CVD mortality risk in T2DM patients. The upregulation of Vitamin D and albumin might play a significant role in improving risk prediction and enable targeted interventions for reducing mortality risk in this population.

BACKGROUND:Among patients with multivessel disease and ST-elevation myocardial infarction (MVD-STEMI), complete revascularization (CR) has been shown with improved outcomes. However, it is controversial whether diabetes mellitus (DM) status affects the outcomes. Quantitative flow ratio (QFR), as a newer non-invasive tool for identifying functional coronary stenosis and determining the presence of functional CR (FCR), may open up a new perspective for studying the above issues. The aim of this retrospective study was to investigate an association between QFR-based FCR and clinical outcomes in MVD-STEMI patients under DM status. METHODS:A total of 623 patients were included in the final analysis. The patients were divided into nonDM cohort and DM cohort. Within each cohort, patients were further stratified into functional CR (FCR) layer and functional incomplete revascularization (FIR) layer based on QFR assessment. The primary outcomes were 3-year major adverse cardiovascular events (MACEs), encompassing cardiac death, ischemia-driven revascularization (target vessel and non-target vessel), rehospitalization due to unstable angina pectoris, and non-fatal myocardial infarction. RESULTS:The incidence of MACEs was significantly lower in the FCR layer than in the FIR layer (12.6% vs 24.0%, log-rank P<0.001). In the nonDM cohort, the incidence of MACEs was also lower in the FCR layer than in the FIR layer (9.8% vs 18.5%, log-rank P = 0.032). Similar situations occurred in the DM cohort (16.1% vs 27.9%, log-rank P = 0.017). In addition, the multivariate Cox analysis showed that rSSQFR (QFR-derived residual SYNTAX score) was significantly associated with the increased risk of MACEs in the nonDM cohort (HR (95% CI) = 1.18 (1.10-1.26), P<0.001) and DM cohort (HR (95% CI) = 1.13 (1.09-1.18), P<0.001). ROC analysis showed adding rSSQFR into the model of clinical risk factors yielded a significant improvement in prediction of MACEs, especially in the DM cohort (AUC (95% CI) = 0.747 (0.675-0.819), P = 0.001) than in the nonDM cohort (AUC (95% CI) = 0.697 (0.602-0.791), P = 0.033). Furthermore, additional multivariate Cox analysis showed that rSSQFR was associated with the increased risk of MACEs in patients with moderate lesions (DS of 50%-89%) after procedure (HR (95% CI) = 1.16 (0.11-1.22), P<0.001). CONCLUSIONS:In patients with MVD-STEMI, the incidence of MACEs was lower in FCR than in FIR, and the decrease was particularly significant in the DM cohort. The association between QFR-derived rSSQFR and MACEs was independent of baseline characteristic differences, and rSSQFR provided higher prognostic predictive ability in DM cohort than in nonDM cohort. Additionally, QFR had the additional utility of identifying moderate residual lesions that require revascularization.

Over the course of several decades, robust research has firmly established the significance of mitochondrial pathology as a central contributor to the onset of skeletal muscle atrophy in individuals with diabetes. However, the specific intricacies governing this process remain elusive. Extensive evidence highlights that individuals with diabetes regularly confront the severe consequences of skeletal muscle degradation. Deciphering the sophisticated mechanisms at the core of this pathology requires a thorough and meticulous exploration into the nuanced factors intricately associated with mitochondrial dysfunction.

Over the course of several decades, robust research has firmly established the significance of mitochondrial pathology as a central contributor to the onset of skeletal muscle atrophy in individuals with diabetes. However, the specific intricacies governing this process remain elusive. Extensive evidence highlights that individuals with diabetes regularly confront the severe consequences of skeletal muscle degradation. Deciphering the sophisticated mechanisms at the core of this pathology requires a thorough and meticulous exploration into the nuanced factors intricately associated with mitochondrial dysfunction.

Diabetes poses a significant threat to human health. There is a lack of large-scale cohort studies to explore the association between mortality risk and indicators beyond blood glucose monitoring in diabetic populations. Multivariable Cox proportional hazards regression models were performed to investigate the association of 13 blood biomarkers with mortality risk in the National Health and Nutrition Examination Survey (NHANES) and biomarker levels were log-transformed and correlated with mortality. During a median follow-up of 7.42 years, 1783 diabetic patients were enrolled. Compared to traditional risk factors, the addition of hs-cTnT, hs-cTnI, NT-proBNP, creatinine, cystatin C, and β-2 microglobulin biomarkers increased the predictive ability for all-cause mortality by 56.4 Question: Is blood glucose monitoring the most effective predictor of long-term survival in the diabetic population? Findings: Among 1783 diabetic patients, the addition of hs-cTnT, hs-cTnI, NT-proBNP, creatinine, cystatin C, and β-2 microglobulin biomarkers increased the predictive ability for all-cause mortality by 56.4 Meaning: Among individuals with diabetes, the utilization of plasma cardiac and renal biomarkers as primary predictors for overall mortality is recommended.

BackgroundEmerging evidence shows that exosomes play a crucial role in the occurrence and development of diabetes and its complications. The molecules in exosomes can be regarded as important markers for the diagnosis of diseases. However, it is presently unclear the pathological association mechanism between exosomes and diabetes.ResultsIn this study, transcriptome data and lncRNA regulatory association data of human pancreatic islet-derived exosome were integrated to construct the ceRNA network. Network analysis revealed that lncRNA with differential expression were primarily involved in islet insulin secretion signaling pathways, including Hippo, TGF-beta, Wnt, FOXO, Neurotrophin and ErbB signaling pathway. Further, combined with miRNA mediated competitive regulation and differential expression analysis results, potential markers of diabetes were revealed and validated in independent datasets. Finally, we analyzed the mechanisms of diabetes based on the competitive regulatory association and function of lncRNA.ConclusionOur results suggest that lncRNA such as lncRNA PVT1, LINC00960 and hsa-miR-107 might be involved in inflammation response in T1DM, and the former lncRNA chose in the present study may serve as novel biomarkers and potential targets for the diagnosis and treatment of T1DM.

目的 研究五味子乙素(Sch.B)是否可通过降低活性氧(ROS)的生成保护糖尿病状态下心肌细胞;是否通过抑制细胞凋亡减轻高糖诱导的心肌细胞损伤.方法 链脲佐菌素诱导Wistar大鼠制备1型糖尿病模型.口服药物Sch.B 4周后进行取材和检测.心肌细胞分为低糖组和高糖组,高糖+Sch.B组和高糖+氧自由基清除剂组.DHE染色检测各组细胞ROS的生成,并用Hoechst 33258检测各组细胞凋亡情况.结果 Sch.B组大鼠心肌组织排列相对规整,染色均一.Sch.B组与糖尿病组大鼠相比凋亡相关蛋白半胱天冬酶-3/9和线粒体中细胞色素C表达下降.DHE染色可发现,Sch.B处理后能明显降低高糖诱导心肌细胞的ROS生成.Hoechst 33258染色可发现,Sch.B和氧自由基清除剂处理后可明显降低高糖处理心肌细胞凋亡的比例.结论 Sch.B可抑制糖尿病状态下心肌细胞胞浆和线粒体中ROS的生成,抑制心肌细胞氧化应激反应,降低线粒体途径的细胞凋亡,保护心肌细胞.

Background Type 2 diabetes mellitus (T2DM) is a common chronic disease that is strongly associated with cardiovascular risk. Long-term high blood glucose levels may induce cardiomyocyte apoptosis, cardiac dysfunction and suppress fetal cardiomyocyte proliferation. Recent epidemiological studies have shown a link between antioxidant carotenoids and T2DM, but a comprehensive longitudinal study of this association has not yet been conducted. Methods We included participants with biological measurements for both serum cis-β-carotene and fasting glucose from NHANES (2001–2006). We divided the participants into quartiles according to serum cis-β-carotene levels and determined the association between these levels and glucose metabolism by using multivariable regression models adjusted for confounding factors. The mechanism through which β-carotene levels regulate plasma glucose levels was further investigated in vivo and in vitro. In addition, we performed a preliminary exploration of the effects of β-carotene on diabetic rats and primary cardiomyocytes. Results Higher cis-β-carotene (quartile 4) was associated with higher LDL-cholesterol levels but lower fasting blood glucose levels. However, T2DM rats subjected to β-carotene treatment showed diminished total triglycerides and LDL-cholesterol, and their β-carotene levels were associated with better cardiac function than that in the T2DM group (P<0.05). Moreover, β-carotene was found to be an important protective factor improving cardiac and mitochondrial function in diabetes. At non-cytotoxic doses, β-carotene clearly improved glucose uptake in insulin-resistant cells. Treatment with β-carotene increased GLUT4 and p-Akt expression, and attenuated the phosphorylation of IRS-1. Our data demonstrated that β-carotene improved cardiac mitochondria biogenesis in diabetes due to activation of PGC-1β. Conclusion Our results indicate that β-carotene can be used to treat metabolic disorders through inhibition of the insulin-resistance pathway in diabetes.

冠状动脉粥样硬化斑块破裂或侵蚀引起的血栓形成造成心肌梗死事件的发生.了解斑块是如何从稳定型转变为危及生命的高危易损斑块的过程并寻求有效的早期干预是临床亟需解决的问题.目前,临床中使用的腔内影像学技术可以识别斑块的形态特征,但不能可靠预测哪些稳定型斑块会转变为高危易损斑块发生破裂继发心肌梗死.本文从高危斑块单模态成像进展、血管内分子成像到多模态血管内成像技术的进展作相关整理,并总结近年来多项评估高危易损斑块的研究,对冠脉内高危易损斑块识别的多模态成像在临床转化的可能性和潜力进行综述.

肺动脉高压(PAH)是一种以肺动脉远端进行性狭窄为特征的复杂疾病,其最终可导致患者右心衰竭甚至死亡.近年研究表明,肺动脉平滑肌细胞(PASMCs)可诱导血管收缩和血管重塑,引起肺血管病理结构异常及肺血管阻力持续升高,进而促进PAH的发生发展.与一氧化氮(NO)和一氧化碳(CO)相似,硫化氢(H2S)可以内源性生成并通过细胞膜扩散,其对心血管系统具有保护作用.笔者通过检索、分析文献发现,H2S调控PASMCs的机制可能为通过血管内皮细胞生长因子(VEGF)/Akt/内皮型一氧化氮合酶(eNOS)途径释放NO,进而扩张血管,或通过CHOP/活化转录因子6(ATF-6)途径减轻内质网应激,还可能通过激活核因子相关因子2(Nrf-2)而影响抗氧化系统,这可能为PAH的治疗提供新的思路.

Background: Bone metabolism can be influenced by sex steroid hormones. However, the relationship between sex steroid hormones and bone mineral density (BMD) remains inconsistent. Our study explored existing evidence of the association between sex hormones, blood glucose and BMD. Methods: We conducted a cross-sectional study of 6434 participants aged 18-80 years in the National Health and Nutrition Examination Survey (NHANES) 2013-2016 to assess the association between SHBG and BMD. The multivariable linear regression models were performed to evaluate the associations between testosterone, estrogen, sex hormone binding globulin (SHBG) and BMD. Results: On adjustment for traditional risk factors (age, BMI, ALB, ALK, ASP, calcium, cholesterol, potassium, sodium, total protein, uric acid), SHBG could be regarded as an independent predictor for BMD, while fasting blood glucose did not. SHBG levels were significant associated with BMD in the multivariate model; however, it will be a different effect between the genders. On comparative analysis, high level SHBG was predictive of lumbar BMD irrespective of other two sex steroid hormones. Conclusion: This study indicated that SHBG may improve the predictive value for bone loss in adults.

Objective To investigate the clinical significance of tricuspid annular plane systolic excursion (TAPSE) in patients with rheumatic mitral stenosis and regurgitation.Methods We prospectively studied the consecutive patients who were diagnosed as rheumatic mitral stenosis and regurgitation in the Fourth Hospital of Harbin Medical University between January 1,2014 and December 31,2015.No patients had been performed heart surgery ever.The biochemical markers,6-minute walking distance test and echocardiography were measured.Clinical data was obtained by clinical visits or telephone interviews.The end point date was taken as the occurrence date of endpoint events or a censor date of 10 June,2016.The primary endpoint events:rehospitalized for heart failure;secondary endpoint events:death or cardiac surgery.Results We enrolled 74 rheumatic mitral stenosis and regurgitation patients,including 9 males and 65 females.Of which 53 cases of patients had atrial fibrillation.TAPSE had good relation with serum BNP level and 6 minutes walking distance.The cut point of TAPSE was 13.5mm which was selected by receiver operating characteristic analysis (area under the curve 0.721,P =0.002).The patients with TAPSE ＜ 13.5mm had higher plasma BNP levels and poor 6-minute walk distance.By Kaplan-Meier survival curves,the survival of the subjects with TAPSE ＜ 13.5mm was significantly poor than those with TAPSE ≥ 13.5mm (P =0.005).Conclusion TAPSE is a powerful variable to reflect heart function and predict the survival of re-hospitalization in patients with rheumatic mitral stenosis and regurgitation.

目的 研究中国汉族遗传性出血性毛细血管扩张症(hereditary haemorrhagic telangiectasia,HHT)合并肺动脉高压(pulmonary hypertension,PAH)患者的基因突变及其治疗.方法 总结中国汉族HHT合并PAH 14例家系其临床和分子遗传学特征,及相应治疗经验.结果 总体基因突变率为71.4％,包括8个ACVRL-1突变和2个ENG突变,其中6个为新发突变.大多数患者接受PAH靶向药物治疗.结论 HHT合并PAH中国汉族患者ACVRL-1和ENG突变是遗传易感因素;初步总结了该类患者的临床管理经验,为治疗提供一定临床依据.