Delirium frequently manifests in hospitalized geriatric patients and is associated with negative health outcomes. Available large-scale data regarding its prevalence rate and impact on older Thai patients are limited. This study aimed to analyze trends in the prevalence rate, its consequences, and the factors contributing to death at discharge among this population.

A retrospective study of inpatients over the age of 60 who received a diagnosis of delirium was conducted, utilizing inpatient medical expense documentation for the fiscal years 2019-2023. The identification of delirium was conducted by the National Health Security Office using the International Statistical Classification of Diseases and Related Health Problems, 10th Revision, Thai Modification (ICD-10-TM) code F05.

The 5-year prevalence rate and mortality rate of delirium were 215.1 and 18.7/100,000 population, respectively, and tended to rise over the studied periods. The average hospitalization was 10 days, and the average healthcare expenditure was about 1470 USD/visit. Respiratory disease emerged as the most common primary diagnosis in delirious patients (23.5%). Factors associated with mortality were individuals aged >80 years when juxtaposed with the cohort aged 61-70 years (adjusted odds ratio [AOD] 1.07), being female (AOR 1.13), and a primary diagnosis of respiratory disease (AOR 2.72), cardiovascular disease (AOR 1.68), musculoskeletal disease (AOR 0.61), systemic infection/septicemia (AOR 2.08); or malignancy (AOR 2.97).

There was an upward trend in rates of both prevalence and mortality associated with delirium among hospitalized geriatric patients. Advancing age, gender, and particular primary diagnoses were associated with mortality at hospital discharge.

Erythropoietin-producing hepatoma A2 (EphA2), a receptor for progranulin (PGRN), which is a growth factor associated with metabolic disorders, is implicated in inflammation and atherosclerotic diseases. Since both EphA2 and PGRN play roles in diabetic kidney disease (DKD) and cardiovascular disease (CVD), this study examined their association with renal function and CVD markers in individuals with diabetes. In addition, the diagnostic value of EphA2 and PGRN in predicting renal impairment was evaluated.

Circulating EphA2 and PGRN levels were measured using enzyme-linked immunosorbent assay in 735 participants with diabetes. Clinical data, including biometric parameters, physiological measurements, and comorbidities, were collected for analysis.

Both EphA2 and PGRN levels positively correlated with older age, elevated blood pressure, higher urinary albumin-to-creatinine ratio (UACR), and brain natriuretic peptide (BNP) levels but negatively correlated with estimated glomerular filtration rate (eGFR). Multivariate logistic regression analysis revealed that EphA2 was an independent predictor of eGFR <60 mL/min/1.73 m², even after adjusting for UACR and CVD risk factors and glycated hemoglobin. Although PGRN was also independently associated with eGFR <60 mL/min/1.73 m², its association was weaker than that of EphA2. Conversely, when UACR ≥30 mg/g was used as the dependent variable, PGRN emerged as a stronger independent determinant than EphA2, even after adjusting for eGFR and CVD risk factors.

EphA2 and PGRN levels are significantly associated with renal function in individuals with diabetes. These findings suggest that EphA2 and PGRN could serve as novel biomarkers for kidney impairment, independent of established CVD markers in this population.

Epigenetic biomarkers offer promising potential for early identification and risk stratification of frail individuals susceptible to adverse cardiovascular outcomes. This scope review aimed to identify and evaluate epigenetic biomarkers concurrently associated with frailty and increased cardiovascular risk, potentially facilitating more precise patient stratification and treatment decisions. A two-stage literature search was performed using PubMed, Scopus, Web of Science, and Embase databases from the year 2000 through 27 December 2024. Stage 1 identified studies reporting epigenetic biomarkers associated with frailty in blood-derived human samples. Stage 2 assessed cardiovascular relevance by screening the frailty biomarkers identified in Stage 1 for their documented association with cardiovascular diseases. Two independent reviewers conducted screening, data extraction, and risk-of-bias assessments, resolving disagreements via a third reviewer. The primary outcomes were the association of biomarkers with frailty severity and cardiovascular risk. Key epigenetic biomarkers identified included microRNAs (particularly miR-21, miR-146a, miR-451, and miR-92a) and DNA methylation markers (LINE-1 methylation, epigenetic clocks like GrimAge and DunedinPACE, and possibly novel, emerging clocks like DNAmCVDscore and the Smoking Index). Due to specificity limitations, these biomarkers are most promising when used collectively as part of multimarker panels rather than individually. Future research should validate multimarker panels, explore novel biomarkers, and assess clinical integration to optimize precision medicine in frail cardiovascular populations.

Gal-3, also known as galectin-3, a lectin that binds β-galactosides, has gained attention as a novel biomarker and pathophysiological mediator in cardiovascular disease, where it contributes to inflammation, fibrosis, metabolic dysregulation and cardiac remodeling. This narrative review, developed following SANRA (Scale for the Assessment of Narrative Review Articles) guidelines, aims to integrate current clinical and experimental findings on gal-3 into the American Heart Association Life's Simple 7 (LS7) and Life's Essential 8 (LE8). By thematically organizing our review across modifiable domains of cardiovascular health, including glucose regulation, lipid metabolism, physical activity, blood pressure, diet, sleep, tobacco use, and body weight (BMI, body mass index), we highlight the role of gal-3 in linking environmental, behavioral and molecular risk factors to cardiometabolic outcomes. Particular attention is given to the oxidative stress, inflammatory-fibrotic axis, and immune activation as mechanistic pathways underlying gal-3-associated cardiovascular damage. We also discuss its relevance to public health and prevention, considering gal-3's potential for early risk stratification, monitoring lifestyle interventions and personalized prevention strategies. This review bridges molecular mechanisms with clinical and public health relevance, particularly in the context of environmental and lifestyle-related cardiovascular risk.

Alpha-lipoic acid (ALA) is an essential organosulfur compound with a wide range of therapeutic applications, particularly in conditions involving inflammation and oxidative stress. In this review, we describe our current understanding of the multifaceted role of ALA in several inflammatory diseases (acute pancreatitis, arthritis, osteoarthritis, asthma, and sepsis), cardiovascular disorders (CVDs), and neurological conditions. The dual redox nature of ALA, shared with its reduced form dihydrolipoic acid (DHLA), underpins its powerful antioxidant and anti-inflammatory properties, including reactive oxygen species scavenging, metal chelation, and the regeneration of endogenous antioxidants such as glutathione. A substantial body of evidence from preclinical and clinical studies suggests that ALA modulates the key signaling pathways involved in inflammation and cellular stress responses, making it a promising candidate for mitigating inflammation and its systemic consequences. Notably, we also discuss a novel perspective that attributes some of the therapeutic effects of ALA to its ability to release hydrogen sulfide (H₂S), a gaseous signaling molecule. This mechanism may offer further insights into the efficacy of ALA in the treatment of several diseases. Together, these findings support the potential of ALA as a multifunctional agent for managing inflammatory and oxidative stress-related diseases.

Fraxin is a bioactive compound derived from Cortex Fraxini. It is known for its diverse biological activities and numerous benefits, including anti-inflammatory, antioxidant, analgesic, antimicrobial, antiviral, and immunomodulatory effects. Despite growing interest in natural compounds for cardiovascular diseases Fraxin's atheroprotective properties and molecular targets have not yet been fully elucidated. To address this gap, our research employed an integrated approach combining network pharmacology, molecular docking simulations, and in vitro biological validation to systematically unravel Fraxin's therapeutic mechanisms against atherosclerosis (AS). The results showed that 84 potential targets for Fraxin against AS were predicted through public databases, and the key target TLR4 was identified by protein-protein interaction and molecular docking analysis. GO enrichment and KEGG pathway analysis revealed that these potential targets were significantly enriched in the PI3K-Akt and oxidative stress responses pathways. Subsequently conducted in vitro studies validated that Fraxin modulates the TLR4/PI3K/Akt signaling pathway to suppress reactive oxygen species generation and downregulate pro-inflammatory cytokines including Il1b, Il6, and Tnf thereby slowing atherosclerotic disease advancement. This investigation methodically delineates Fraxin's therapeutic targets and underlying molecular mechanisms in AS management, establishing a scientific foundation for its potential translation into clinical practice.

Sleep disorders increase the risk of cardiovascular diseases. However, the underlying mechanisms remain unclear. This study aims to examine the critical role of oxytocin neurons in the paraventricular nucleus (PVN^OXT) in regulating the cardiovascular system and to elucidate potential mechanisms through which sleep disturbance may contribute to cardiovascular diseases. In this study, using an automated sleep deprivation system, mice were given chronic sleep deprivation (cSD) for 7 days, 6 h per day. cSD induced blood transcriptomic alterations accompanied by lower heart rate, higher blood pressure, and elevated cardiac autophagy/apoptosis. Instant optogenetic activation of oxytocin neurons in the paraventricular nucleus (PVN^OXT) provoked heart rate suppression in normal mice, whereas in cSD mice, activation precipitated intermittent cardiac arrest. On the contrary, inhibition of PVN^OXT showed no influence on the cardiovascular system of normal mice, but it attenuated cSD-induced rise in blood pressure. Long-term low-frequency stimulation (LTF) of PVN^OXT decreased neuronal excitability and oxytocin release, effectively reversing cSD-mediated cardiovascular responses. Mechanistically, cSD triggered the upregulation of blood-derived 3-mercaptopyruvate sulfurtransferase (mPST), and a suppression of PVN^OXT postsynaptic activity to a certain extent. The quick and long-term decrease of oxytocin by LTF could lead to feedback inhibition in mPST expression and thus reverse cSD-mediated cardiovascular responses. Altogether, modulation of PVN^OXT could mediate cSD-induced cardiovascular abnormalities without affecting normal mice. Our research provided potential targets and key mechanisms for cardiovascular diseases associated with sleep disorders.

Cardiovascular diseases remain one of the leading causes of mortality worldwide, with atrial fibrillation emerging as a clinically significant arrhythmia. The increasing prevalence of atrial fibrillation calls for advanced diagnostic tools for accurate detection to reduce adverse consequences, such as stroke and heart failure. Cardiovascular advancements in artificial intelligence have improved the detection and management of atrial fibrillation.

This review examines recent advancements in atrial fibrillation detection using artificial intelligence-driven tools-such as wearables, neural networks, and machine learning-and highlights their clinical relevance, limitations, and potential to transform cardiovascular care.

A systematic review was conducted using PubMed, IEEE Xplore, and ScienceDirect to identify peer-reviewed studies between 2020 and 2024. Original clinical studies using artificial intelligence were included for the diagnosis of atrial fibrillation. Studies on conditions other than atrial fibrillation or incomplete data were excluded. Factors analyzed across all studies included diagnostic application, key findings, clinical implications, and limitations of artificial intelligence approaches.

This review evaluated 11 studies on artificial intelligence-enhanced tools for atrial fibrillation diagnostics. Neural networks showed the highest diagnostic accuracy, outperforming clinicians in retrospective electrocardiogram analyses (80% vs. 75%). Wearable artificial intelligence-integrated devices, such as electrocardiogram wristbands, offer the highest accessibility and real-time monitoring, with sensitivities exceeding 94%, although they are limited by single-lead input and patient compliance. Machine learning models, including random forest and XGBoost, showed moderate performance (AUROC 0.74-0.89) with strengths in risk prediction and stratification. Key challenges included limited generalizability, small-sample sizes, and varying model accuracy.

This review highlights the potential of artificial intelligence to improve atrial fibrillation diagnostics through wearable technologies, neural networks, and machine learning. While these tools often outperform traditional methods, real-world use is limited by small, retrospective studies and a lack of validation. Future work should focus on equity, transparency, and expanding artificial intelligence use beyond atrial fibrillation diagnosis, with collaboration needed to ensure safe, effective clinical integration.

Atherosclerotic cardiovascular disease (ASCVD), influenced by elevated plasma low-density lipoprotein (LDL) and cholesterol levels, is important to various acute cardiovascular and cerebrovascular diseases, causing life-threatening deaths worldwide. Early intervention for atherosclerosis is both essential and beneficial. As members of a class of transcription factors, sterol regulatory element-binding proteins (SREBPs) regulate the expression of most genes involved in lipid metabolism. This review aimed to present three aspects of SREBP regulation in the Endoplasmic Reticulum (ER), Golgi apparatus, and nucleus after maturation. Different subcellular localizations play integral roles in regulating the maturation and activity of SREBPs. Moreover, several drugs that target SREBPs for the treatment of atherosclerosis are described, with the aim of exploring SREBPs as new targets for treating atherosclerosis.

There are three members of the SREBP family, namely, SREBP-1a, SREBP-1c, and SREBP-2, all of which have differing functions. SREBP-1a and SREBP-1c regulate the synthesis of fatty acids, while SREBP-2 regulates cholesterol metabolism. SREBPs combine with the SREBP Cleavage-Activating Protein (SCAPs) to form the SCAP/SREBP complex. This complex can bind to and is regulated by insulin-induced genes (INSIG), affecting endoplasmic reticulum (ER)-to-Golgi translocation. SREBPs are sheared by 1-site protease (S1P) and 2-site protease (S2P) in a regular sequence on arrival at the Golgi apparatus, and are processed, matured, and transported to the nucleus for action. The review focuses on how SREBPs, crucial regulators of cholesterol and fatty acid metabolism, are controlled at different cellular locations (ER, Golgi, Nucleus), and explores their potential as drug targets for treating atherosclerosis, a major global health threat driven by high LDL cholesterol.

To develop a pericardiocentesis (PCT) simulation model applied for undergraduate medical training.

A PCT simulator consisted of a torso mannequin, a silicone rubber heart (SRH), a container, and a filling system. The mannequin was submitted to a coronal section and an 18 × 18-cm precordial area opening. The SRH was prepared in accordance with structural dimensions of a normal heart. The elaboration of a structure container to simulate the pericardial cavity consisted of a non-leakable unit inside a cardboard (PcavBox). The PcavBox filling system was connected to a 10-mm diameter tube and a total of 2.5 L of saline solution. This structure was adapted inside the mannequin and covered with a thermoformable rubber material of 2 mm in skin color. For PCT simulation, we used a 10-mL syringe connected to a 14G needle for an imaging guided puncture facilitated by a portable ultrasound.

A SRH was successfully developed and fixed inside the Pcav Box, connected to the fluid pressure system. It was able to simulate a cardiac tamponade scenario identified by ultrasound. A series of 50 punctures was successively performed without liquid leak.

A low-cost PCT simulator was developed and coan be applied to healthcare education.