Xiexin Tang (XXT) is a classic Chinese medicine formula that can be used to treat Atherosclerosis (AS). This study aimed to investigate the mechanism by which XXT regulated AS lipid levels. Firstly, the mixture components of XXT were analyzed by High-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Then, the AS model based on Apolipoprotein E knockout (ApoE-/-) mice was established. Cytokines related to lipid metabolism and bile acid metabolism were detected by Quantitative Real-time PCR (qRT-PCR). 16S rDNA gene sequencing was performed to analyze differential bacterial populations, and the mechanism of XXT regulation of bile acids affecting lipid metabolism was further explored by targeted metabolomics. Further, antibiotic-treated mice were used to investigate the role of gut microbiota in the anti-AS effect of XXT. The results showed that XXT attenuated the lipid levels and reversed the abnormal elevation of cytokines, such as hepatic lipid metabolism and inflammatory reaction in AS mice. XXT also repaired the gut barrier damage and reversed gut microbiota disorders in AS mice. Furthermore, the metabolic levels of bile acids were reshaped by XXT. Whereas, in the absence of gut microbiota, XXT failed to attenuate lipid levels and inhibit the expression of cytokines related to inflammation and bile acid metabolism in AS mice and failed to play a role in ultimately treating AS. In conclusion, XXT could effectively inhibit the inflammatory reaction and lipid accumulation in AS mice, and this effect was closely related to its remodeling of gut microbiota to regulate bile acid metabolism.

Midkine (MK) is a member of a small protein family that includes pleiotrophin. MK levels are elevated in obese patients and have a pro-arthrogenic effect through various pathophysiological processes including vascular inflammation and atherogenesis. This study aimed to investigate the association between serum MK levels and several atherosclerotic risk factors in patients with type 2 diabetes mellitus (T2DM).

Ninety subjects were enrolled in this study, comprising 60 T2DM patients and 30 age-matched healthy subjects (HS). The patients were categorized into two groups based on dyslipidemia: group 1 consisted of 30 patients with dyslipidemia, while group 2 included 30 patients without dyslipidemia. Laboratory tests were conducted using routine assays at the National Diabetes Center. MK levels were analyzed using enzyme-linked immunosorbent assay (ELISA).

MK levels were significantly higher in patients with dyslipidemia compared to those without dyslipidemia and HS (P ≤ 0.0001). A significant negative correlation was observed between MK levels and the atherogenic index of plasma (AIP), Castelli's risk index-1 (CRI-I), and Castelli's risk index-2 (CRI-II) (r = - 0.489, p = 0.005; r = - 0.465, p = 0.008; r = - 0.421, p = 0.018, respectively) in patients with dyslipidemia. Furthermore, a significant positive correlation was found between MK levels and HDL-C (r = 0.524, p = 0.002) in patients without dyslipidemia. MK, AIP, and CRI-I were identified as predictors of atherosclerosis in DM patients, with MK indicating very good discriminate power (AUC = 0.805) in identifying T2DM patients with dyslipidemia at a cut-off value of ≤ 4.457 ng/ml.

These findings suggest that MK could be considered a predictive biomarker for dyslipidemia associated with DM. MK levels correlate significantly with atherogenic risk factors, indicating its potential as a sensitive risk predictor for atherosclerosis in patients with T2DM.

Hyaluronic acid (HA), the only non-sulfated glycosaminoglycan (GAG), is essential for maintaining the extracellular matrix's structural and functional integrity. Its bioactivity is determined by interactions between HA fragments of different molecular weights and specific receptors, which influence downstream signaling pathways. This review systematic summarizes the correlation between HA molecular weight dynamic changes and bioactivities focusing on imbalance of HA degradation and metabolism due to various pathological processes. Outline the core transduction mechanisms of HA receptors and signaling pathways, and innovatively hypothesize that discrepancies in cellular distribution with HA-molecular weights dependent lead to the activation of different signaling pathways from the perspective of molecular weight affecting cellular distribution. Finally, it addresses challenges in studying HA's biofunctions and provides new perspectives for future research.

Recent research has established a strong link between metabolic abnormalities and an increased risk of dementia. In parallel, there is growing epidemiological evidence supporting the neuroprotective effects of antidiabetic medications against cognitive impairments. Among these, sodium-glucose co-transporter (SGLT2) inhibitors have emerged as pharmacological candidates with promising potential in alleviating the burden of age-related diseases, particularly neurodegenerative diseases (NDD). SGLT2 inhibitor therapies are FDA-approved medications routinely prescribed to manage diabetes. This novel class was initially developed to address cardiovascular disorders and to reduce the risk of hypoglycemia associated with insulin-secretagogue agents. It subsequently attracted growing interest for its beneficial effects on central nervous system (CNS) disorders. However, the molecular mechanisms through which these glucose-lowering therapies mitigate cognitive decline and limit the progression of certain brain degenerative diseases remain largely unexplored. Consequently, the neuroscientific community needs further studies that gather, analyze, and critically discuss the available mechanistic evidence regarding the neuroprotective effects of SGLT2 inhibitors. This review aims to critically examine the most relevant published findings, both in vitro and in vivo, as well as human studies evaluating the impact of SGLT2 inhibitors exposure on Alzheimer's disease (AD). It seeks to integrate the current understanding of their beneficial effects at the molecular level and their role in addressing the pathophysiology and neuropathology of AD. These insights will help extend our knowledge of how SGLT2 inhibitor therapies are associated with reduced risk of dementia and thus shed light on the link between diabetes and AD.

Type 2 diabetes (T2D) and cardiovascular diseases (CVD), part of the metabolic syndrome (MetS), are major contributors to the global health crisis today. A recent report from the World Health Organisation estimates that 17.9 million lives are lost each year to CVD, and one-third of these are premature. The international diabetes federation estimates that around 537 million adults aged between 20 and 79 years are living with diabetes. People with diabetes are suggested to have twice the risk of developing CVD. Epigenetic modifications are being increasingly recognised as the key mediators linking genetic and environmental conditions to metabolic dysfunction. Among these, DNA methylation plays a crucial role in modulating gene expression and influencing pathways involved in glucose homeostasis, inflammation, and vascular integrity. Despite the advances in our understanding of the role of epigenetic alterations in metabolic diseases, including that of T2D, the mechanisms driving selective methylation changes and their long-term impact on cardiovascular health are still not well understood. This review synthesises the current knowledge on DNA methylation dynamics in T2D and their role towards the progression of CVD and explores their potential as biomarkers and therapeutic targets. Understanding the interplay between metabolism and epigenetics in the pathogenesis of T2D and CVD could provide critical insights for early disease identification and the development of novel epigenome-targeted therapeutic strategies.

Identification and stratification of risk factors for stroke among individuals living with HIV (PLWH) will facilitate primary prevention and prognostication, as well as strategies aimed at optimizing neurorehabilitation. This review sought to characterize and stratify the risk factors associated with stroke in PLWH.

The review was structured in accordance with the preferred items for reporting systematic reviews and meta-analysis (PRISMA) checklist. The epidemiological triangle, Bradford criteria, and Rothman causality model further informed the review. The review outcomes encompassed cardiovascular factors, HIV-related factors, and personal and extrinsic factors associated with stroke in PLWH. We conducted searches in PubMed, Scopus, Medline, Web of Science, Cumulative Index for Nursing and Allied Health Literature, and African Journal (SABINET). Data screening and extraction were independently performed utilizing predefined eligibility criteria and a data-extraction template. Narrative synthesis and risk stratification were employed to analyze the results.

Thirty studies (22 cohorts and eight case-control) with a sample size of 353,995 participants were included in this review. The mean age of the participants was 45.1 ± 10.7 years. The majority of the participants (72.4%) were male. Risk factors for stroke in PLWH include cardiovascular factors (advanced age, tobacco use, hypertension, diabetes, atrial fibrillation, etc.), HIV-related factors (high viral load and low nadir CD4 count), personal factors (advanced age and female sex), and comorbidities (hepatitis C virus infection, chronic kidney disease, coronary artery disease, and liver fibrosis or cirrhosis). Diabetes, atrial fibrillation, smoking habits, hypertension, age, and viral load demonstrated a high likelihood of association with stroke in PLWH and should be prioritized when constructing clinical prediction algorithms for HIV-related stroke.

The most important factors were hypertension and chronic kidney disease, followed by smoking, dyslipidemia, diabetes, HCV, HBV, CD4 count, use of ART, TB, and substance use (cocaine). The least important factors were age, sex, ethnicity, obesity, alcohol use, ART duration, and viral load. The predictive significance of these factors is still evolving, given the average moderate certainty of evidence. Predictive and preventative models should target factors with a high causality index and low investigative costs.

The review is part of a larger review registered with the PROSPERO (ID: CRD42024524494).

Cardiometabolic diseases encompass a group of conditions characterized by metabolic and inflammatory abnormalities that increase the risk of diabetes and cardiovascular disease. These syndromes involve multiple organs, including the heart, arterial system, brain, skeletal muscle, adipose tissue, hematopoietic system, liver, kidneys, and pancreas. The crosstalk between these organs contributes to the development of disease. Advances in imaging techniques, such as magnetic resonance imaging, magnetic resonance spectroscopy, computed tomography, and positron emission tomography, have revolutionized the evaluation of these conditions. Hybrid imaging modalities, such as positron emission tomography/computed tomography and positron emission tomography/magnetic resonance imaging, provide unique insights into the anatomy and metabolic alterations occurring in response to cardiometabolic risk factors. These methods are particularly valuable for assessing multisystemic involvement and interorgan crosstalk, revealing critical interactions such as the brain-heart axis, the heart-liver axis, and the fat-muscle-heart dynamics. This review discusses the role of state-of-the-art imaging techniques in evaluating the pathophysiological mechanisms underlying these complex syndromes and the clinical applications of the different imaging techniques in the assessment of cardiometabolic diseases.

Autoimmune diseases are closely linked to cardiovascular diseases. This study aimed to assess the relationship between cardiovascular health (CVH) defined by Life's Essential 8 (LE8), genetic predisposition, and the risk of 19 autoimmune disorders.

A total of 247 660 participants without prior autoimmune diseases from the UK Biobank were included. CVH was assessed using LE8 scores, categorized into low, moderate, and high. Cox proportional hazards models estimated the association between CVH, genetic susceptibility, and autoimmune disorder risk. Over 13.2 years of follow-up, 11 422 incident autoimmune disorders occurred. Higher CVH levels were associated with reduced risks of overall autoimmune disorders (hazard ratio, 0.68 [95% CI, 0.62-0.74]) and specific conditions, including Graves disease, inflammatory bowel disease, polymyalgia rheumatica, psoriasis, rheumatoid arthritis, and type 1 diabetes. Dose-response analyses revealed a linear negative relationship between continuous LE8 scores and the risks of Graves disease, inflammatory bowel disease, polymyalgia rheumatica, psoriasis, rheumatoid arthritis, and type 1 diabetes (Pnonlinear>0.05). Genetic predisposition to autoimmune disorders (including ankylosing spondylitis, celiac disease, Graves disease, inflammatory bowel disease, polymyalgia rheumatica, psoriasis, rheumatoid arthritis, Sjögren syndrome, systemic lupus erythematosus, systemic sclerosis, and type 1 diabetes) significantly modified these associations (Pinteraction<0.05), with protective effects more pronounced in women, participants aged <65 years, and those with low genetic risk.

LE8 scores inversely and linearly predicted autoimmune disease incidence. Prioritizing CVH optimization through LE8 adherence may reduce the global autoimmune disease burden.

Background/Objectives: MicroRNAs (miRNAs) are molecules involved in biological regulation processes, including type 2 diabetes and its complications development. Single nucleotide polymorphisms (SNPs) can alter miRNA mechanisms, resulting in loss or gain effects. VEGFA is recognized for its role in angiogenesis. However, its overexpression can lead to deleterious effects, such as disorganized and inefficient vasculature. Under hyperglycemic conditions, VEGFA expression seems to increase, which may contribute to the development of microvascular and macrovascular diabetic complications. Several miRNAs are associated with VEGFA regulation and seem to act in the prevention of dysregulated expression. This study aimed to investigate SNPs in miRNA regions related to the loss effect in VEGFA regulation, examining their frequency and potential physiological effects in the development of diabetic complications. Methods: VEGFA-targeting miRNAs were identified using the R package multimiR, with validated and predicted results. Tissue expression analysis and SNP search were data-mined with Python 3 for miRNASNP-v3 SNP raw databases. Allele frequencies were obtained from dbSNP. The miRNA-mRNA interaction comparison was obtained in the miRmap tool through Python 3. MalaCards were used to infer physiological disease association. Results: The variant rs371699284 was selected in hsa-miR-654-3p among 103 potential VEGFA-targeting miRNAs. This selected SNP demonstrated promising results in bioinformatics predictions, tissue-specific expression, and population frequency, highlighting its potential role in miRNA regulation and the resulting loss in VEGFA-silencing efficiency. Conclusions: Our findings suggest that carriers of rs1238947970 may increase susceptibility to diabetic microvascular and macrovascular complications. Furthermore, in vitro and in silico studies are necessary to better understand these processes.

Atherosclerosis is a complex process involving various cells and molecules within the atherosclerotic plaque. Recent evidence suggests that plaque-associated fibroblasts (PAFs), also known as atherosclerosis-associated fibroblasts (AAFs), might play a significant role in the development and progression of the disease. The microenvironment of the atherosclerotic plaque, resembling the tumor microenvironment (TME), includes various cellular populations like plaque-associated macrophages (PAMs), plaque-associated neutrophils (PANs), vascular smooth muscle cells (VSMCs), myeloid-derived suppressor cells (MDSCs), and PAFs. Similar to cancer-associated fibroblasts (CAFs) in tumors, PAFs exhibits a wide range of characteristics and functions. Their interactions with endothelial cells, smooth muscle cells, and other stromal cells, including adventitial fibroblast precursors, significantly influence atherosclerosis progression. Moreover, the ability of PAFs to express various markers such as alpha-SMA, Desmin, VEGF, and GFAP, highlights their diverse origins from different precursor cells, including vascular smooth muscle cells, endothelial cells, glial cells of the enteric nervous system, adventitial fibroblast precursors, as well as resident and circulating fibrocytes. This article explores the molecular interactions between PAFs, cells associated with atherosclerosis, and other stromal cells. It further examines the role of PAFs in the development and progression of atherosclerosis, and compares their features with those of CAFs. The research suggests that studying tumor-associated fibroblasts can help understand fibroblast subpopulations in atherosclerotic plaque. Identifying specific subpopulations could provide new insight into atherosclerosis complexity and lead to the development of innovative drugs for medical intervention.

Microplastics have emerged as persistent organic pollutants, generating significant concerns regarding their potential toxicity. Nevertheless, the impact of microplastics (MPs) on atherosclerosis in mammals remains uncertain. The present study investigated the deleterious effects of polystyrene microplastics (PS-MPs) on the cardiovascular system of mice. A total of thirty-six male ApoE-/- mice were divided into three groups: a control group and two experimental groups. The experimental groups were subjected to the exposure of 5 μm PS-MPs at concentrations of 1 μg/ml and 10 μg/ml, respectively, for twelve weeks. In parallel, HUVECs were treated with the same concentrations of PS-MPs to assess cellular responses. Our results indicate that PS-MPs exposure increased mouse body weight, disrupted lipid metabolism, and exacerbated atherosclerosis. Additionally, both in vivo and in vitro studies indicate that PS-MPs can induce oxidative stress and promote EndMT through the BMP signaling pathway. These findings suggest that PS-MPs may trigcger atherosclerosis and cardiovascular toxicity by activating the BMP pathway and driving EndMT via oxidative stress. In summary, this study elucidates the cardiovascular deleterious effects induced by PS-MPs in mice, providing new insights into the toxicity of PS-MPs in mammalian organisms.

Type 2 diabetes has become a significant global public health issue. Its increasing prevalence is closely linked to sedentary lifestyles, suboptimal diets and high obesity levels. This article provides an overview of type 2 diabetes epidemiology, pathophysiology, clinical presentation, diagnostic tests, risk factors, complications and management. It also describes the role of nurses, which involves: advising patients on weight management, diet, physical activity, smoking cessation and alcohol reduction; encouraging adherence to care plans and drug treatment regimens; and providing ongoing support, education and monitoring to prevent or delay the onset of complications.

Type 2 diabetes significantly increase the risk of cardiovascular disease and mortality. This systematic review and meta-analysis compared cardiovascular and mortality outcomes in type 2 diabetes patients receiving dipeptidyl peptidase-4 inhibitors (DPP-4is) plus metformin versus sulfonylureas (SUs) plus metformin as add-on therapy.

PubMed, Web of Science, Cochrane Central Register of Controlled Trials, Embase, Google Scholar, and Scopus were searched through January 1, 2025, for studies comparing DPP-4is plus metformin versus SUs plus metformin in type 2 diabetes patients. Outcomes of interest were major adverse cardiovascular events and all-cause mortality. Heterogeneity was assessed using Cochran's Q test and I2 statistic. Publication bias was evaluated with Begg's and Egger's tests. Study quality was assessed with the Jadad scale (for randomized controlled trials) and the Newcastle-Ottawa Scale (for observational studies).

Twenty-seven studies (2012-2024), encompassing 1,505,821 participants, were included in the analysis. Major adverse cardiovascular events were reported in 21 studies, and all-cause mortality data were available from 19 studies. Meta-analysis revealed a significantly lower risk of both major adverse cardiovascular events (risk ratio [RR]: 0.79; 95% confidence interval [CI]: 0.73-0.84; p < 0.001) and all-cause mortality (RR: 0.79; 95% CI: 0.71-0.88; p < 0.001) in patients with diabetes treated with DPP-4 inhibitors plus metformin compared to those treated with SUs plus metformin. No publication bias was detected.

In type 2 diabetes patients treated with metformin, adding a DPP-4is is associated with significantly lower risks of major adverse cardiovascular events and all-cause mortality compared to adding an SUs. These findings underscore the potential cardiovascular benefits of DPP-4is and their role in improving patient outcomes.

This study aimed to evaluate the potential of unstructured electronic health records (EHRs) data, analyzed using natural language processing (NLP) and machine learning (ML), to describe the prevalence and clinical spectrum of diabetes mellitus (DM) in hospitals.

A multicenter, retrospective study was conducted using EHRs from eight Spanish hospitals (2013-2018). Unstructured data were extracted using EHRead® (NLP and ML) and SNOMED_CT. Individuals with type 1 or 2 DM (T1DM/T2DM) were identified, and a semi-supervised ML classifier was developed for unregistered types (UrDM). DM prevalence and related complications were analyzed in the final subpopulations (sT1DM/sT2DM).

From 56,181,954 EHRs of 2,582,778 individuals, 638,730 were identified with DM: 75.4 % with UrDM, 21.3 % with T2DM, and 3.3 % with T1DM. The ML model reclassified 93.5 % as T2DM and 6.5 % as T1DM. Over 50 % of relevant variables like anthropometrics, lab values and treatments were missing. The prevalence of sT1DM/sT2DM was 2.6 %/38.4 %. Major comorbidities included hypertension, dyslipidemia, chronic kidney disease (CKD), ischemic heart disease, and chronic heart failure (CHF). CKD and CHF were the most frequent complications for sT1DM/sT2DM at 60 months.

NLP and ML for profiling DM using EHRs unstructured data are helpful, but additional data and better EHR documentation are crucial.

Inflammation plays an essential role in the pathological processes of ischemic stroke (IS). Sulfasalazine is used in clinical practice for the treatment of inflammatory diseases. This study investigated the effects of sulfasalazine in mice with IS and its underlying mechanisms. We employed an in vivo mice model of middle cerebral artery occlusion (MCAO)/reperfusion, investigating the impact of sulfasalazine on MCAO mice using tetrazolium chloride (TTC) staining, behavioral experiments, and pathological staining. Utilizing of network pharmacology methodologies, we speculated that the protective effect of sulfasalazine against IS may be related to inflammation. The effects of sulfasalazine on inflammation and polarization in oxygen-glucose deprivation/re-oxygenation (OGD/R)-induced BV2 cells were examined through immunofluorescence and PCR techniques. Additionally, the influence of sulfasalazine on the STING/NF-κB pathway was assessed using Western blot and immunofluorescence techniques. Sulfasalazine significantly reduced the infarct area in MCAO mice, restored cerebral blood flow, and improved motor function in the MCAO mice. Pathological staining results indicated that sulfasalazine can mitigate neuronal damage in the cerebral cortex of MCAO mice. Immunofluorescence and PCR testing showed that sulfasalazine promotes M1 to M2 polarization, and reduces inflammation in OGD/R-induced BV2 cells. Furthermore, the Western blot and immunofluorescence results both confirmed that sulfasalazine can inhibit the activation of the STING/NF-κB pathway. This study elucidated the potential therapeutic role of sulfasalazine in IS through its anti-inflammatory effects and modulation of STING/NF-κB pathway, offering novel insights into treatment strategies for IS.

In recent years, endocan has emerged as a potential biomarker in various medical conditions. This multifaceted molecule, involved in key processes such as inflammation and endothelial dysfunction, has shown promise in predicting disease progression and therapeutic response across a spectrum of pathologies. However, the heterogeneity of studies and the complexity of endocan's role in different diseases necessitate a comprehensive review. This umbrella review aimed to systematically synthesize and evaluate the evidence from multiple meta-analyses, offering a view of endocan's effectiveness as a predictive biomarker in medical diseases.

An extensive search was carried out on March 12, 2024, using the following four databases: PubMed, Scopus, Web of Science, and Cochrane Library. The goal was to identify meta-analyses that assess endocan's predictive efficacy. The pooled effect size and its 95% confidence interval were taken out of each discovered meta-analysis. Furthermore, power analyses were performed to assess the robustness and dependability of the results. An additional GRADE assessment was carried out to gauge the epidemiological reliability of the findings.

In the final analysis, 12 meta-analyses were included in the current umbrella review. The results showed that there is a significant correlation between a higher endocan level and COVID-19 (SMD: 1.40, 95% CI 0.21-2.58, P = 0.02), followed by chronic kidney disease (SMD: 1.34, 95% CI 0.20 to 2.48, P < 0.01), obstructive sleep apnea (SMD: 1.30, 95% CI 1.06-1.54, P < 0.01), diabetes mellitus (SMD: 1.00, 95% CI 0.81 to 1.19, P < 0.01), coronary artery disease (SMD: 0.99, 95% CI 0.58-1.39, P < 0.01), hypertension (SMD: 0.91, 95% CI 0.44-1.38, P < 0.01), and preeclampsia (SMD: 0.37, 95% CI 0.13-0.62, P < 0.01).

Endocan has emerged as a highly promising biomarker with considerable potential across various medical conditions. Its relevance spans critical areas such as COVID-19, chronic kidney disease, obstructive sleep apnea, diabetes mellitus, coronary artery disease, and preeclampsia. The broad applicability of endocan highlights its value in improving diagnostic accuracy and enhancing our understanding of these diseases. Clinically, incorporating endocan testing could aid in early detection, monitoring disease progression, and refining patient management, particularly for high-risk populations. However, additional research is needed to fully assess its specificity, sensitivity, and overall clinical utility, paving the way for its integration into routine healthcare practices and enabling more precise, individualized treatment strategies.

Adults with Type 1 diabetes (T1DM) have increased cardiovascular risk. Most of the Polish general population fails to meet lipid goals. Recent data on the effectiveness of dyslipidemia treatment in T1DM population is lacking. We aimed to investigate which part of adults with T1DM met the dyslipidemia treatment goals according to the European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS) 2016 and 2019 guidelines.

We recruited adult people with T1DM, for whom a cross-sectional assessment of disease progression was performed. Anthropometric measurements and a basic panel of laboratory tests were conducted for each person. We assessed cardiovascular risk and lipid goals according to the ESC/EAS dyslipidemia guidelines from 2016 to 2019. Among the n = 233 participants, only 34.3 % met the lipid goal according to the 2016 guidelines, while for the 2019 guidelines, merely 13.3 %. Only 12.8 % of individuals with very high cardiovascular risk met the LDL cholesterol goals according to ESC/AES 2016, and 4.9 % when ESC/EAS 2019 guidelines were considered. The median difference between the LDL cholesterol value and the target value was 18.0 (-16.0 to 49.0) mg/dl [20.4 % (-19.8 %-41.2 %)], when considering the 2016 ESC/EAS guidelines, whereas for the 2019 guidelines, it was 36.0 (11.0-60.0) mg/dl [36.3 % (13.9 %-48.0 %)].

Therapeutic inertia results in the failure to meet the lipid goals according to the ESC/EAS guidelines for 2016 and 2019 in most Polish adults with T1DM. Many adults with T1DM may require intensification of lipid-lowering interventions.

Myocardial infarction (MI) poses a serious health threat to diabetic patients, who are particularly vulnerable due to heightened oxidative stress. The dietary oxidative balance score (DOBS) quantifies the overall oxidative profile of the diet and may reflect diet-related cardiovascular risk.

This study aimed to evaluate the association between DOBS and the risk of MI among diabetic individuals using a nationally representative U.S.

We analyzed data from 5,002 diabetic participants in the NHANES 1999-2018 cycles. DOBS was calculated based on 16 pro- and antioxidant nutrients using two 24-hour dietary recalls. Logistic regression models and 1:1 propensity score matching (PSM) were employed to assess the association between DOBS and self-reported history of MI, adjusting for demographic, clinical, and lifestyle covariates. Restricted cubic spline (RCS) models were used to evaluate potential nonlinear relationships.

A one-point increase in DOBS was associated with a 3% lower odds of MI in both unadjusted and fully adjusted models (adjusted OR = 0.97, 95% CI: 0.95-0.99). Participants in the highest DOBS tertile had a 38% lower odds of MI compared to the lowest tertile (OR = 0.62, 95% CI: 0.43-0.87), and this association remained consistent in the matched cohort (OR = 0.72, 95% CI: 0.48-0.88). While formal tests for nonlinearity were not significant, RCS curves suggested a threshold effect with diminishing benefits at higher DOBS levels. Subgroup and sensitivity analyses confirmed the robustness of the findings.

Higher DOBS is associated with a lower likelihood of MI among diabetic patients. These findings highlight the potential value of antioxidant-rich dietary patterns in cardiovascular risk assessment. However, given geographic and cultural variability in diet, further validation is needed in diverse populations and prospective study settings.

Ischemic heart disease (IHD) is the leading cause of mortality in the world with an increasing incidence. One of the interventions to treat IHD is coronary artery bypass grafting (CABG) and people with diabetes mellitus (DM) account for approximately one quarter of all patients who undergo coronary revascularization. Furthermore, people with DM have a higher risk of mortality due to heart failure (HF).

We aim to describe the risk of developing HF after CABG in patients with versus without DM.

Through a large nationwide register-based cohort study, patients who underwent CABG from January 1, 2000 to December 31, 2020 were included. In addition to Cox regression, g-formula methods based on multivariable Cox regression were performed to estimate the absolute risk (AR) and risk difference (RD) of the association between DM status and HF outcome, and between DM status and mortality.

A total of 34,855 patients were included in this study, consisting of 6909 (19.8%) DM patients. The AR of HF after CABG in the 10th year was 35.1% versus 26.4% for patients with versus without DM (p < 0.001), respectively. The RD of HF for each exceeding year (3.7 percentage point (pp.) in the 1st year versus 8.6 pp. in the 10th year) was higher for patients with DM compared to those without DM.

The risk of HF was significantly higher up to ten years after CABG in patients with DM compared to those without DM.

Metabolic syndrome (MetS) is a prevalent health condition characterized by central obesity, insulin resistance, hypertension, and dyslipidemia, increasing the risk of cardiovascular disease and type 2 diabetes. Lifestyle interventions, particularly plant-based nutrition and exercise, are essential for managing MetS. While both strategies are well-documented independently, their synergistic effects remain less explored. This narrative review integrates findings from both domains to evaluate their combined impact on metabolic syndrome. The review examines the individual and combined impacts of plant-based nutrition and exercise on MetS-related metabolic dysfunction.

A comprehensive review of 114 peer-reviewed studies was conducted to assess the role of plant-based diets and structured physical activity in improving insulin sensitivity, lipid profiles, inflammation, and weight management. Studies investigating the mechanisms through which dietary components and exercise modalities influence metabolic health were analyzed, along with behavioral and psychological factors affecting long-term adherence.

Plant-based diets, particularly those high in fiber, polyphenols, and healthy fats, improve glucose metabolism, reduce inflammation, and enhance cardiovascular health. Exercise complements these benefits by increasing insulin sensitivity, promoting fat oxidation, and improving lipid metabolism. When combined, plant-based nutrition and exercise provide superior metabolic outcomes, including greater reductions in visceral adiposity, improved endothelial function, and enhanced glycemic control.

Plant-based nutrition and structured exercise are effective strategies for managing MetS. Their synergistic effects highlight the importance of integrated lifestyle interventions for long-term metabolic health.

S100A12 acts as a pro-inflammatory agent in vivo, with a close relationship with plaque formation in patients with acute coronary syndrome (ACS), end-stage renal disease, and diabetes. Peripheral arterial disease (PAD) can lead to mobility difficulties and ultimately disability and amputation. The association between S100A12 and risk of peripheral arterial disease remains unclear. This study aims to investigate the association between S100A12 and the risk of PAD in patients with dyslipidemia.

From March 2023 to June 2024, 478 patients were included in this cross-sectional study. They were divided into PAD group (n = 105) and control group (n = 373) according to the presence or absence of PAD (The diagnosis of PAD is a combination of the patient's clinical symptoms, imaging evidence and ankle-brachial index). Plasma S100A12 was detected by available kit. General information, disease history, smoking history, and laboratory indicators were collected from both groups. The relationship between S100A12 and the risk of PAD was analyzed using statistical methods.

Levels of S100A12 were significantly higher in the PAD group of dyslipidemia [0.22 (0.13,1.49) ng/cL vs. 0.13 (0.10,0.18)ng/cL, p value < 0.001]. Univariate and multivariate logistic regression analyses suggested that the risk of PAD was significantly higher with increasing levels of S100A12 [Odd ratio (OR) (95%CI) = 2.264 (1.681, 3.047), p value < 0.05]. In addition, lower high-density lipoprotein cholesterol (HDL-C) level and diabetes mellitus (DM) were independent risk factors for PAD [OR (95%CI) = 0.388 (0.186,0.809), p value = 0.012; OR = 2.375 (1.527,3.695), p value < 0.001]. Subgroup analysis suggested that S100A12 was significantly and positively associated with the risk of PAD in all subgroups, regardless of whether HDL-C levels < 1.03 mmol/L, age > 60 years, and presence of diabetes or hypertension. Restricted cubic spline (RCS) curves suggested that the correlation between S100A12 and the risk of PAD was nonlinear (p-non-linear value < 0.05). The RCS curves showed that the positive correlation between S100A12 and the risk of PAD was stronger when the S100A12 level was less than 1.00ng/cL.

In conclusion, elevated S100A12 level is an independent risk factor for PAD in patients with dyslipidemia. In different subgroups, S100A12 was significantly and positively associated with the risk of PAD after adjusting for different factors. There is a non-linear relationship between S100A12 and the risk of PAD, with a stronger positive correlation at S100A12 levels below 1.00ng/cL. These findings implied that S100A12 is a potential biomarker for identifying patients with dyslipidemia who are at high risk of developing PAD. They also implied that S100A12 levels can be routinely monitored in dyslipidemic populations for the early detection of PAD and to guide the management of PAD. Finally, the results of this study emphasize that inflammation in dyslipidemia patients plays an important role in the development of PAD, suggesting that lipid control and immunomodulation may be effective in the prevention of PAD.

MR-35-24-038431.

The non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio (NHHR) represents a novel composite lipid marker for atherosclerosis and cardiovascular disease (CVD). Nevertheless, the correlation between NHHR and mortality in the non-diabetic population remains indistinct.

This study included 20,774 non-diabetic individuals from the 1999-2018 National Health and Nutrition Examination Survey (NHANES). We employed a weighted multivariate Cox proportional hazards model and restricted cubic splines to assess the associations between NHHR, its combination with obesity indicators, and all-cause and CVD mortality.

During a mean follow-up period of 62 months, a total of 897 participant deaths were recorded, of which 155 were attributed to cardiovascular causes. The restricted cubic splines revealed a U-shaped association between NHHR and all-cause mortality, while an L-shaped association was observed for CVD mortality. The analysis of threshold efects revealed that the infection points for NHHR and all-cause and CVD mortality were 2.65 and 2.07, respectively. The cubic spline revealed a nonlinear correlation was observed between NHHR-BMI, NHHR-WC and NHHR-WHtR and all-cause and CVD mortality.

NHHR and its combination with obesity indicators can be a meaningful predictor of all-cause mortality and CVD mortality in non-diabetic individuals.

BAY55-9837, a potential therapeutic peptide for the treatment of type 2 diabetes mellitus (T2DM), can induce glucose (GLC)-dependent insulin secretion. Our previous study has demonstrated that the use of superparamagnetic iron oxide nanoparticle-decorated exosome (exosome-SPION) and external magnetic force (MF) enables BAY 55-9837 to target pancreatic islets. However, the initial burst release of BAY 55-9837 loaded within exosome-SPION shortens its in vivo half-life and consequently reduces the frequency of GLC responsiveness. Therefore, in our study, the transmembrane hydrophobic structure of the exosome signature protein CD81 was fused with BAY 55-9837 to obtain MBAY with sustained-release capability.

MBAY was fabricated via genetic engineering, and the dissociation constant (Kd) was determined to assess its affinity for vasoactive intestinal peptide receptor type 2 (VPACII). Subsequently, MABY was incorporated into exosomes through electroporation to obtain MBAY-exosome, and SPOIN was adorned on MBAY-exosome by means of the self-assembly of transferrin (Tf) and the transferrin receptor (TfR). The in vitro release profile and in vivo pharmacokinetic profile of MBAY-Exosome-SPION were detected using high-performance liquid chromatography (HPLC). The L9(34) orthogonal design approach was utilized to optimize the drug administration mode in vivo. The therapeutic effect of MBAY-exosome-SPIONs/MF on T2DM was assessed both in vitro and in vivo.

In vitro studies showed that the release rate of MBAY from exosome-SPION was slower compared with BAY 55-9837. Meanwhile, MBAY still maintained high affinity and selectivity for VPAC II and MBAY-exosome-SPIONs/MF could effectively promote insulin secretion in response to elevated GLC as BAY-exosome-SPIONs/MF. In vivo studies indicated that MBAY-exosome-SPIONs had a prolonged half-life and improved pharmacokinetic parameters compared to BAY-exosome-SPIONs, which further alleviated the symptoms of T2DM model mice.

Thus, the reconstructed MBAY loaded in SPION-exosome realized sustained-release and exosomes-SPIONS achieved pancreatic targeting which led to ideal therapeutic effect in T2DM mice.

Coronary atherosclerosis in patients with diabetes mellitus is the most significant pathophysiological mechanism responsible for ischemic heart disease. Atherosclerosis in diabetes is premature, more diffuse, and more progressive, and it affects more coronary blood vessels compared to non-diabetics. Atherosclerosis begins with endothelial dysfunction, continues with the formation of fatty streaks in the intima of coronary arteries, and ends with the appearance of an atherosclerotic plaque that expands centrifugally and remodels the coronary artery. If the atherosclerotic plaque is injured, a thrombus forms at the site of the damage, which can lead to vessel occlusion and potentially fatal consequences. Diabetes mellitus and atherosclerosis are connected through several pathological pathways. Among the most significant factors that lead to atherosclerosis in diabetics are hyperglycemia, insulin resistance, oxidative stress, dyslipidemia, and chronic inflammation. Chronic inflammation is currently considered one of the most important factors in the development of atherosclerosis. However, to date, no adequate anti-inflammatory therapeutic measures have been found to prevent the progression of the atherosclerotic process, and they remain a subject of ongoing research. In this review, we summarize the most significant pathophysiological mechanisms that link atherosclerosis and diabetes mellitus.

The significance of thiamine in human health is linked to its role in several pathways that control different disease processes. Significant improvements in cardiometabolic diseases, substantially impacted by thiamine imbalances, are observed with thiamine supplementation. Diabetic patients could see a reduction in cardiovascular (CV) risk due to thiamine's significant impact on glucose metabolism. Specifically, increased ventricular filling pressures and oxygen consumption, indicative of CV dysfunction, are caused by oxidative and inflammatory damage to blood vessels, diabetic nephropathy, and elevated lactic acid production. Despite promising pre-clinical results for thiamine, clinical trials have yielded conflicting and contradictory findings due to limitations like small sample sizes and insufficient follow-up. To provide a summary of clinical study results, this systematic review assessed the impact of thiamine supplementation on diabetes and its CV complications. The studies included in this systematic review were retrieved from PubMed and Medline databases, in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement and following the Population Intervention Comparison Outcome (PICO) framework. Seven clinical studies were identified, which enlighten the association between thiamine supplementation, hyperglycemia, and cardiovascular disease (CVD). Although large-scale, multicenter studies with longer follow-up periods are needed, the association between thiamine and chronic metabolic dysfunction related to CV risk suggests its crucial role in preventing severe heart failure (HF).

Carotid atherosclerosis (CAS) is a complex cardiovascular disease linked to inflammatory response and oxidative stress. This study aimed to develop and assess the therapeutic efficacy of Phlorizin liposomes (Phlorizin-Lips) in repairing CAS in rats. Phlorizin-Lips were prepared using the film dispersion method and evaluated for controlled release, antioxidant properties, and biocompatibility. The methodology included preparing Phlorizin-Lips, conducting in vitro and in vivo experiments, observing histopathological changes in carotid arteries in a rat model, and detecting inflammatory markers and antioxidant gene expression in arterial endothelial cells using immunoblotting and ELISA. Results showed that Phlorizin-Lips significantly lowered inflammatory markers TNF-α and IL-1β in endothelial cells while upregulating Nrf2 and its downstream antioxidant genes, enhancing the cells' antioxidant capacity and reducing oxidative damage by activating the Nrf2 signaling pathway. Additionally, Phlorizin-Lips reduced carotid plaque formation, improved vascular endothelial function, and promoted CAS repair. This study underscores Phlorizin's potential as a therapeutic agent for CAS and highlights the Nrf2 pathway's role in regulating inflammation and oxidative stress. Future research will explore the clinical potential of Phlorizin-Lips.

The ratio of non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol (NHHR) has been introduced as a novel indicator to evaluate lipid metabolism. The study explored the association between NHHR and cardiovascular disease (CVD).

A cross-sectional study was achieved by utilizing data obtained from the NHANES (2003-2016). The association between NHHR and CVD was assessed by multivariate logistic regression analysis (LRA) and the restricted cubic spline (RCS) analysis. Also, interaction tests and subgroup analyses were employed to explore whether the associations differ by subgroups. Then, threshold analysis were conducted for interval delineation and detection of threshold effects with two-segment piecewise LR model.

A cohort of 11,471 individuals was involved. The results indicated that the linear relationship between NHHR and CVD was not significant (P for trend >0.05). The RCS analysis revealed a non-linear J-shaped association of NHHR with CVD risk. A two-segment LR model was established to assess the threshold effect of the NHHR. A log-likelihood ratio test (P < 0.001) suggested that the two-segment LR model exhibited better performances compared with the single-line LR model. Additionally, a tangent point of the NHHR occurred at 2.82, and the likelihood of CVD increased by 21% as the NHHR increased by one unit (OR = 1.21, 95% CI = 1.10-1.34).

A J-shaped association was detected between NHHR and the prevalence of CVD, suggesting that NHHR could serve as a novel assessment marker for identifying high-risk CVD populations. However, further cohort studies are needed to confirm this finding.

Stress hyperglycemia ratio (SHR), which adjusts blood glucose levels using glycated hemoglobin to eliminate the influence of chronic hyperglycemia, has been demonstrated to have superior predictive value than absolute hyperglycemia. However, its predictive value for sepsis-associated acute kidney injury (SA-AKI) remains unclear. This study aimed to investigate the relationship between the SHR and the risk of developing SA-AKI.

Data were extracted from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. Restricted cubic splines (RCS) were employed to depict the relationship between SHR and the likelihood of SA-AKI, determining an optimal cut-off value. Based on this threshold, patients were categorized into two groups. Logistic regression was utilized to evaluate SHR's predictive value for SA-AKI, with adjustments for confounding variables. Propensity score matching (PSM) was applied to balance baseline characteristics. Subgroup and sensitivity analyses were conducted.

A total of 2,249 patients were included. The RCS curve indicated a non-linear positive association between SHR and the likelihood of SA-AKI (P for non-linearity < 0.001), with an optimal cut-off at 1.55. Accordingly, patients were divided into SHR ≤ 1.55 and SHR > 1.55 subgroups, comprising 1,131 and 1,118 individuals, respectively. A higher incidence of SA-AKI was observed in the SHR > 1.55 group (38.64% vs. 27.23%, P < 0.001). This association persisted after baseline adjustment through PSM. Logistic regression analysis confirmed that SHR > 1.55 was linked to increased odds of SA-AKI in both unadjusted (OR: 1.68, P < 0.001) and adjusted models (OR: 1.73, P < 0.001), with SHR ≤ 1.55 serving as the reference. In subgroup analysis, all subgroups consistently demonstrated a significant association between SHR > 1.55 and elevated odds of SA-AKI (all OR > 1). Sensitivity analysis validated that SHR > 1.55 remained significantly correlated with SA-AKI occurrence in the survival subgroup (OR: 1.46, P < 0.001) and the non-CKD subgroup (OR: 1.69, P < 0.001).

The findings indicate a non-linear positive relationship between SHR and the likelihood of SA-AKI in patients with sepsis, suggesting that SHR could be a potential predictor for SA-AKI.

Diabetic retinopathy (DR) is a severe complication of diabetes, and lipid imbalances play a key role in its progression. The non-high-density lipoprotein cholesterol-to-high-density lipoprotein cholesterol ratio (NHHR) has been identified as a predictor of cardiovascular diseases, but its link to DR remains unclear. This study aimed to assess the association between NHHR and DR risk in diabetic patients.

Data from the 2005-2018 National Health and Nutrition Examination Survey (NHANES) were analyzed. Multivariate logistic regression models were used to evaluate the relationship between NHHR and DR. Nonlinear associations were assessed using restricted cubic spline analysis.

Of the 4,935 participants, 1,193 had DR. Higher NHHR was strongly associated with increased DR risk. Each unit rise in NHHR increased the risk by 19% (OR = 1.19, 95% CI: 1.07-1.31, p < 0.05). In quartile analysis, participants in the highest NHHR quartile had nearly double the risk of DR compared to those in the lowest quartile (OR = 1.84, 95% CI: 1.62-2.06, p < 0.001). Subgroup analysis showed this association was consistent across different demographic groups, including age, gender, BMI, and smoking status.

NHHR is significantly linked to DR risk in diabetic patients and may be a valuable biomarker for early detection and prevention strategies in clinical settings.

A substantial body of research has underscored the intricate nature of diagnosing oral disorders in conjunction with chronic inflammatory diseases.

Diabetes mellitus (DM) is a chronic endocrine and metabolic disorder characterized by persistent hyperglycemia that poses serious threats to human health and quality of life. The morbidity, disability, and mortality rates of cardiovascular complications stemming from chronic hyperglycemia are primary factors affecting the lifespan of patients with diabetes. Currently, there is no cure for DM. Standard biomedical treatments mostly control the symptoms using insulin injections or oral hypoglycemic drugs. Although the effect of standard biomedical therapy is remarkable, its long-term use is prone to toxic side effects. Numerous studies have recently found that Traditional Chinese Medicine (TCM) has strong advantages in the prevention and treatment of DM and cardiovascular complications (DACC). The collection, processing, preparation and clinical use of TCM are guided by the theory of TCM and follow the "holistic concept." Multiple components, pathways, and targets form the basis for the use of TCM in treating multiple parts and organs of the body simultaneously. TCM is mainly derived from natural medicines and their processed products and has fewer side effects. TCM is clinically used as compound prescriptions, botanical drugs, and monomers. TCM, either independently or in combination with standard biomedical treatments, has shown unique therapeutic advantages. This review aimed to explore the recently reported mechanisms of action of TCM in the prevention and treatment of DACC. These findings will aid the optimization of the current therapy or formation of a therapeutic schedule for integrated TCM and standard biomedical treatments.

Diabetes is one common clinical symptoms of metabolic disorders. The peel of Zea mays L. is a folk remedy for diabetes that has not been thoroughly studied. The effects and mechanisms on diabetes complicated glucose and lipid metabolism disorders are still unknown now.

The research is intended to elucidate the constituent of phenylpropanoid enriched of Zea mays L. (YMP), and investigate the treatment and mechanism on amending glucose and lipid metabolism disorders.

The constituents of YMP were systematacially identified by HPLC-Q-TOF-MS/MS and NMR. To assess the effects of varying YMP doses, diabetic mice induced by streptozotocin and a high-fat diet were divided into groups. Targeted serum metabolomics investigations were conducted using UHPLC-LTQ-Orbitrap MS. Moreover, 16S rRNA analysis was employed to elucidate the intricate mechanisms through the gut microbiota modulates lipid and glucose metabolism.

It demonstrated that the primary component of YMP was luteolin. At a high dosage of 160 mg/kg/day, YMP considerably reduced the values of the oral glucose tolerance test, insulin, and blood glucose (p < 0.001). After administration, insulin resistance indexes decreased. YMP reversed the accumulation of glycogen in the liver and reduced hepatic lipid deposition. Compared to MOD group, the concentration of luteolin is higher and its metabolite, indicating that luteolin may be adequately absorbed and have an influence on the circulatory system. The results of 16S rRNA sequencing demonstrated that YMP and gut microbiota interacted to positively regulate beneficial bacteria such as Bifidobacterium, Ligilactobacillus, and Lactobacillus.

This work investigated the regulating effect of YMP on the liver glycolipid metabolism for the first time, and it also showed the underlying mechanism through gut microbiota. According to these studies, YMP has a lot of potential to be used as a supplemental treatment for complex metabolic illnesses like diabetes. It offered empirical support for the use of alternative medicine in the area to treat complex problems of glucose and lipid metabolism in diabetes.

Sexual dysfunction (SD) is a complication of poorly managed diabetes mellitus (DM). To prevent SD, patients should develop sexual health literacy (SHL).

This study investigated the relationship between SHL and SD in women with DM.

This cross-sectional study was performed between 1 October 2023 and 1 June 2024. The sample comprised 400 participants. The inclusion criteria were (1) being 18-65 years of age, (2) having been diagnosed with DM, and (3) having a sex partner. Data were collected using a personal information form, the Female Sexual Function Index (FSFI), and the Sexual Health Literacy Scale (SHLS).

The data were analyzed using the Mann-Whitney test, Kruskal-Wallis H test, Spearman correlation coefficients, and binary logistic regression.

Over half of the participants experienced SD (68,2%). Participants with higher education, those whose partners had higher education, those who did not have any chronic disease other than DM, and those who did not take hormone replacement therapy had a lower rate of SD (P < 0.05). Participants with higher income, those who used family planning, those with DM I, and non-menopausal participants had lower SD and higher SHL (P < 0.05). Insulin-only participants had higher SD and lower SHL than those who were on other types of medications (P < 0.05). There was a significant negative correlation between scale scores (FSFI and SHLS) and age (r = -0.388; P < 0.001 r = -0.326; P < 0.001, respectively), age of partner (r = -0.383; P < 0.001, r = -0.274; P < 0.001, respectively), duration of romantic relationship (r = -0.326; P < 0.001, r = -0.328; P < 0.001, respectively), number of children (r = -0.109; P < 0.001, r = -0.290; P < 0.001, respectively), and duration of DM (r = -0.254; P < 0.001, r = -0.125; P < 0.013, respectively). There was a significant positive correlation between scale scores (FSFI and SHLS) and number of sexual intercourse (r = 0,493; P < 0.001, r = 0.127; P < 0.011, respectively). A one-unit increase in DM duration resulted in a 3.7% increase in SD rate (OR = 1.037). A one-unit increase in the number of sexual intercourses reduced the SD rate by 35.5% (OR = 0.645).

The data show that the prevalence of SD in diabetic women is directly affected by the number of sexual intercourses per week, menopausal status, and duration of DM.

This is the first study to examine the relationship between SHL and SD in women with DM. Second, the results are sample-specific and cannot be generalized to all women with DM.

Healthcare professionals should ensure that women with DM have high levels of SHL to prevent SD and improve their quality of sexual life.

Lung cancer is a leading cause of cancer-related morbidity and mortality worldwide. Diabetes, as a common metabolic disorder, further increases the risk of cardiovascular damage. Studies have shown that myocardial cells in diabetic patients are more vulnerable to the toxic effects of cancer treatments, thereby raising the risk of heart failure. Therefore, cardiovascular risk assessment in lung cancer patients with diabetes is particularly important. The Inflammatory Burden Index (IBI) is a biomarker that reflects systemic inflammation, combining the levels of C-reactive protein (CRP), neutrophils, and lymphocytes. It has been shown to be a significant prognostic indicator in various cancer populations. This study aims to investigate the predictive ability of IBI and the triglyceride-glucose (TyG) index for cardiac injury in lung cancer patients with diabetes undergoing antitumor therapy. A single-center retrospective case-control study was conducted, including clinical data of 192 lung cancer patients with diabetes who received anti-tumor therapy from July 2018 to January 2023.Cardiac injury was assessed by measuring high-sensitivity cardiac troponin T (hs-cTnT) levels. The Inflammatory Burden Index (IBI) was calculated using the formula: IBI = (C-reactive protein [CRP] × Neutrophils)/Lymphocytes. Univariate and multivariate logistic regression analyses were performed to assess the relationship between clinical factors, IBI, TyG index, and cardiac injury. The clinical predictive value of these factors was further evaluated using receiver operating characteristic (ROC) curves, and the relationship between IBI and cardiac injury was explored using the Restricted Cubic Spline (RCS) model. In the 192 patients, 101 (52.6%) developed cardiac injury during follow-up. Univariate analysis showed that age, male, hypertension, smoking, D-dimer, CKMB, IBI, TNM stage: III/IV, and Immunotherapy were significantly associated with cardiac injury (P < 0.001). Multivariate analysis identified IBI (P = 0.007), age (P = 0.01), smoking (P < 0.001), CKMB (P < 0.001), TNM stage (P = 0.014), and hypertension (P = 0.007) as independent predictors of cardiac injury. ROC analysis revealed an area under curve (AUC) of 0.722 for IBI (cut-off: 8.408), indicating good predictive value. RCS analysis showed a significant nonlinear positive correlation between IBI and cardiac injury (P = 0.0079), with the risk of cardiac injury increasing significantly as IBI levels rose. The TyG index was not significantly associated with cardiac injury. IBI, as a simple and accessible biomarker, can effectively predict cardiac injury in lung cancer patients with diabetes undergoing antitumor therapy. Although the TyG index did not show a significant association with cardiac injury in this study, IBI demonstrated strong predictive ability in this patient group. Future studies should further validate the use of IBI across different cancer types and evaluate its prognostic role in long-term follow-up.

Malignant melanoma, a highly malignant tumor predominantly found on the skin surface, has exhibited an alarming rise in both incidence and mortality rates annually since 2012. Despite its relatively low occurrence among skin malignancies, the mortality rate of malignant melanoma remains disproportionately high. The prognosis relies heavily on early stage detection, with a significant disparity in survival rates between stage I and stage IV patients. Studies exploring insulin resistance (IR) as a potential risk factor for malignant melanoma are scarce. The present study therefore investigated the association between the triglyceride glucose (TyG) index, an indicator of IR, and malignant melanoma incidence. Retrospective data from patients diagnosed with malignant melanoma at the First Affiliated Hospital of Nanjing Medical University (Nanjing, China) between January 2019 and January 2024 were collected. Basic information, including age, sex and body mass index, and hematological test results, such as those for fasting triglycerides and fasting blood glucose, were analyzed. Logistic regression analysis and receiver operating characteristic (ROC) curve analysis were employed to explore the association between melanoma risk and the TyG index. A total of 403 participants, including 272 patients with malignant melanomas and 131 patients with nevi, were included in the study. The melanoma group exhibited significantly higher levels of the TyG index compared with the control group (P<0.001). Univariate and multivariable logistic regression analyses revealed the TyG index as an independent risk factor for melanoma incidence (OR, 6.33; 95% CI, 3.56-11.27; P<0.001). Incidence rates of melanoma significantly increased across tertiles of the TyG index (P<0.001). The ROC curve analysis identified a clinically acceptable predictive cutoff point for the TyG index. The present study therefore provides evidence that the TyG index is a significant risk factor for the incidence of malignant melanoma. The findings underscore the potential utility of the TyG index as a biomarker for diagnosing melanoma and suggest new avenues for melanoma treatment strategies.

Atherosclerosis (AS) is the pathological basis of many cardiovascular and cerebrovascular diseases. To further the investigation of treatments for AS, this research analyzed the role of lncRNA MBNL1-AS1.

MBNL1-AS1 expression in the serum of AS patients and healthy controls were detected by qPCR. Its diagnostic value in AS was assessed by receiver operating characteristic curve (ROC). Additionally, the link between MBNL1-AS1, carotid intima-media thickness (CIMT) and C-reactive protein (CRP) was examined using the Spearman correlation coefficient. The prognostic value of MBNL1-AS1 in AS was assessed using the Kaplan-Meier survival curve and univariate and multivariate Cox regression analysis.

The present study consisted of 103 patients with AS and 92 healthy patients (HC) and comparison of baseline data between the two groups revealed no remarkable difference (P>0.05) except for CRP (P<0.0001). The serum of AS patients exhibited a considerably higher expression of MBNL1-AS1 in comparison to the HC group. Furthermore, MBNL1-AS1 was highly expressed in patients following higher CIMT and CRP values, which was positively linked with both, respectively (r>0.5, P<0.001). Meanwhile. MBNL1-AS1 has enhanced diagnostic accuracy in AS patients (AUC=0.893) and can be utilized as an independent prognostic factor for AS. Patients with high MBNL1-AS1 expression have a higher likelihood of cardiovascular events. (log rang P=0.0025).

Elevated MBNL1-AS1p can be used as a potential marker for the clinical diagnosis of AS and is linked to a poor prognosis of AS.