Osteoporosis is a highly prevalent disease among older adults. Chronic obstructive pulmonary disease (COPD) and associated hypoxia may contribute to the development of osteoporosis. This study aimed to further investigate the impact of CO₂ retention (another key pathophysiological feature of COPD) on osteoporosis, providing a novel perspective for understanding COPD-related bone metabolic disorders. A total of 611 older patients with acute exacerbation (AE) of COPD were enrolled from the hospital’s emergency department and completed a 1-year follow-up. Arterial PaO₂, PaCO₂, FEV₁

Cognitive impairment is a major complication in individuals with hypertension. Emerging evidence suggests that metabolic abnormalities may contribute to its pathogenesis. This study examined the association between the atherogenic index of plasma (AIP) and risk of cognitive impairment in middle-aged and older adults with hypertension. Data were from the 2011 baseline and 2018 follow-up waves of the China Health and Retirement Longitudinal Study (CHARLS). Multivariable logistic regression was used to assess the association between baseline AIP and subsequent cognitive impairment. Dose-response patterns were explored using restricted cubic spline (RCS) models, and subgroup analyses evaluated effect modification. Predictive performance of AIP versus traditional lipids was assessed by receiver operating characteristic (ROC) curves. Among 3,739 hypertensive participants (mean age: 60.5 ± 9.1 years; 50.0

Background:The atherogenic index of plasma (AIP) has been implicated in various disease processes, yet its relationship with depression, particularly in the context of differing glucose metabolism status, remains underexplored. This study aimed to investigate the association between AIP and depression in middle-aged and older adults with varying glucose metabolism profiles. Methods:Data were derived from the China Health and Retirement Longitudinal Study (CHARLS) conducted in 2011 and 2018, encompassing 7,723 participants aged 45 years and above. Depression was defined using a cutoff score of ≥12 on the 10-item Center for Epidemiologic Studies Depression Scale (CESD-10). The primary outcome of interest was incident depression. Logistic regression and restricted cubic spline (RCS) models were applied to assess the relationship between baseline AIP levels and depression risk across distinct glucose metabolism categories. Results:Elevated AIP was strongly associated with increased odds of depression. In fully adjusted models, a graded relationship was observed, with higher quartiles of AIP corresponding to greater depression risk. Participants in the highest AIP quartile (Q4) had significantly increased odds of depression (odds ratio [OR]: 3.36, 95% confidence interval [CI]: 2.67-4.24, P < 0.001) compared to those in the lowest quartile (Q1). Furthermore, RCS analyses revealed a significant positive association between AIP and incident depression among individuals with prediabetes mellitus (Pre-DM) and diabetes mellitus (DM) (P < 0.001), whereas no such association was found in participants with normal glucose regulation (NGR) (P = 0.086). These findings suggest that glucose metabolism status modifies the relationship between AIP and depression risk. Conclusion:Higher baseline AIP levels are significantly associated with an increased risk of depression in middle-aged and older adults, with distinct effects modulated by glucose metabolism status. These results highlight the potential utility of AIP as a biomarker for depression risk and suggest that metabolic health should be considered in the development of targeted strategies for depression prevention and intervention.

BackgroundSepsis remains a leading cause of mortality in intensive care units (ICUs), with high morbidity and healthcare costs worldwide. The serum anion gap (AG), a marker of metabolic acidosis, has been associated with adverse outcomes in various critical illnesses. However, the prognostic value of longitudinal AG trajectories in sepsis remains underexplored. This study explored the link between dynamic AG trajectories and all-cause mortality in critically ill septic patients.MethodsA retrospective cohort study utilized data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. Adult patients meeting Sepsis-3 criteria for sepsis were included. Group-based trajectory modeling was used to identify AG trajectories during the initial five days of ICU admission. Patients were classified into three trajectory groups: normal-level-stable trajectory (Class 1), high-level-decline trajectory (Class 2), and progressive acidosis trajectory (Class 3). Cox proportional hazards models evaluated the link between AG trajectories and ICU/hospital mortality, controlling for demographic, laboratory, and clinical severity factors. Subgroup and sensitivity analyses were performed to validate the findings.ResultsAmong 6,110 septic patients, three distinct AG trajectory groups were identified. Patients in Class 3 (decreasing high AG) had the highest mortality, with ICU mortality of 30.61% and hospital mortality of 35.85%, compared to Class 1 (ICU mortality: 14.46%, hospital mortality: 19.41%) and Class 2 (ICU mortality: 21.88%, hospital mortality: 31.88%). In fully adjusted models, Class 3 exhibited a significantly increased risk of ICU mortality [HR=1.72, (95% CI 1.43-2.07), P<0.001] and hospital mortality [HR=1.64, (95% CI 1.39-1.94), P<0.001] relative to Class 1. Subgroup analysis revealed a significant interaction between AG trajectories and heart failure status. Sensitivity analysis excluding patients with malignancies confirmed the robustness of the findings.ConclusionContinuous monitoring of AG levels is crucial for risk assessment and personalized treatment, as rising AG levels significantly increase mortality risk. These findings underscore the potential of AG trajectories as a dynamic biomarker to improve sepsis management and patient outcomes.

Background:Sudden infant death syndrome (SIDS) remains a leading cause of infant mortality globally. Although the global burden has generally declined over recent decades, the COVID-19 pandemic may have influenced these trends. This study investigates whether the global SIDS burden has changed, particularly during the COVID-19 pandemic. Methods:Data from the Global Burden of Disease (GBD) 2021 study were analyzed to estimate SIDS mortality and disability-adjusted life years (DALYs) globally, regionally, and nationally. Rates were stratified by sex, age group, socio-demographic index (SDI), and health system level. Projections were made using the Bayesian Age-Period-Cohort model and the the autoregressive integrated moving average (ARIMA) model. Results:In 2021, global SIDS deaths totaled 30,608, with a mortality rate of 24.16 per 100,000 infants (95% UI, 14.06-32.44). Global DALYs were 2,746,174, at a rate of 2,167.56 per 100,000 infants (95% UI, 1,261.44-2,909.59). Mortality and DALYs rates decreased by 59% from 1990 to 2021, with marked regional differences. Regions with Low SDI and Minimal health systems, particularly Sub-Saharan Africa, had the highest burden, while higher SDI and advanced health system regions reported significant declines. Male infants aged 1-5 months showed higher rates than females. Despite a global decline during the pandemic, temporary increases occurred in countries including China, the Russian Federation, and Monaco. Projections suggest continued declines, predicting a mortality rate of 16.86 per 100,000 infants and DALYs rate of 1,400.41 per 100,000 infants by 2035. Conclusions:The global SIDS burden has consistently declined since 1990, including during COVID-19, yet significant regional disparities remain. Enhanced healthcare interventions and targeted public health initiatives are crucial, particularly in regions with Low SDI and Minimal health system resources.

AIMS:To investigate the expression characteristics, clinical implications, and underlying mechanisms of miR-491-3p in patients with acute myocardial infarction (AMI). METHODS:Serum samples were collected from patients with AMI and healthy controls. miR-491-3p expression was measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Receiver operating characteristic (ROC) curves evaluated its diagnostic accuracy for AMI. Correlations between miR-491-3p levels and myocardial injury markers or inflammatory factors were analyzed. A one-year follow-up assessed its predictive value for major adverse cardiovascular events (MACE). A hypoxia/reoxygenation (H/R) model of human AC16 cardiomyocytes was established to explore the mechanism of miR-491-3p in H/R-induced injury via targeting aquaporin 9 (AQP9). RESULTS:Serum miR-491-3p was significantly downregulated in AMI patients, with an AUC of 0.893 for AMI diagnosis (sensitivity 83 %, specificity 79.5 %). Levels were negatively correlated with myocardial injury markers and inflammatory factors. AMI patients with low miR-491-3p expression had a higher incidence of MACE, and low expression was identified as a risk factor. In the H/R model, miR-491-3p was downregulated. Overexpression of miR-491-3p improved cell proliferation, reduced apoptosis, and decreased inflammatory factors by targeting and inhibiting AQP9. CONCLUSIONS:miR-491-3p may be involved in the pathological process of AMI by targeting and regulating AQP9. This makes it a promising candidate as both a diagnostic and prognostic marker for AMI, as well as a potential therapeutic target.

BACKGROUND:The association between rheumatoid arthritis (RA) and blood lipids remains controversial. OBJECTIVE:This study aimed to investigate the association between RA and blood lipids by integrating observational and Mendelian randomization (MR) analyses. METHODS:The association between the prevalence of RA and blood lipid levels was examined using data from the National Health and Nutrition Examination Survey (NHANES) (n = 24,345). Subsequently, the causality between RA and lipid and apolipoprotein levels was inferred in a 2-sample MR framework. Genetic instruments for RA (13,261 RA cases and 43,823 controls), lipids (n = 121,577), and apolipoproteins (n = 121,577) were obtained from large-scale genome-wide association studies. The statistical significance of the MR effect estimates was determined using a false discovery rate (FDR) with a <5% threshold to adjust for multiple testing. RESULTS:In the NHANES cohort, RA was associated with lower total cholesterol (TC) (β -0.08; 95% CI -0.15, -0.02) and low-density lipoprotein cholesterol (LDL-C) (β -0.11; 95% CI -0.18, -0.05) levels after adjusting for potential confounders. In the 2-sample MR analyses, genetic liability to RA was associated with lower levels of TC (β -0.013; 95% CI -0.022, -0.004, FDR 0.011), LDL-C (β -0.017; 95% CI -0.027, -0.008, FDR 0.003), and apolipoprotein B (Apo B) (β -0.016; 95% CI -0.028, -0.004, FDR 0.015). CONCLUSION:RA is causally associated with lower TC, LDL-C, and Apo B levels. Clinicians should cautiously interpret lower atherogenic lipid levels in patients with RA, as these may indicate underlying disease processes.

The role of noise pollution in chronic obstructive pulmonary disease (COPD) remains unclear. The aim of this study was to investigate the correlation between nighttime sleep noise levels and the risk of acute exacerbations of this lung disease. A total of 518 stable COPD patients were enrolled in the study. A portable sound level meter was used to measure the nighttime sleep noise levels. Subsequently, based on a threshold of 40 dB, the patients were divided into a high-noise group (n = 210) and a low-noise group (n = 308). The Pittsburgh Sleep Quality Index was employed to assess the sleep quality of the patients. During the 12-month follow-up, the events of acute exacerbation (i.e., Escalated therapy, Urgent hospitalization, and Admitted to intensive care unit) in these COPD patients were recorded. Multivariate logistic regression was utilized for data analysis. When most potential confounding factors (i.e., demographic variable, chronic disease, risk factor of COPD, status of COPD, and inflammatory indicator) were adjusted, a higher nighttime sleep noise level was found to be associated with acute exacerbations of COPD during the follow-up period. After adjusting the sleep quality score, although the P-value of the above-mentioned correlation was still statistically significant, its level increased significantly, that is, the level of the P-value became closer to the threshold at which it would not be statistically significant. There is a significant correlation between relatively high nighttime sleep noise level and acute exacerbations of COPD. Sleep disorders might potentially contribute in some way to the above-mentioned correlation. The exact role of nighttime sleep noise in acute exacerbations of this lung disease and the underlying mechanisms still need further research.

Sepsis is a life-threatening condition characterized by a dysregulated host response to infection, resulting in high mortality rates and complex clinical management. This study leverages transcriptomics and machine learning (ML) to identify critical biomarkers and therapeutic targets in sepsis. Analyzing microarray data from the Gene Expression Omnibus (GEO) datasets GSE28750, GSE26440, GSE13205, and GSE9960, we discovered three pivotal biomarkers that BMX (bone marrow tyrosine kinase gene on chromosome X), GRB10 (growth factor receptor bound protein 10), and GADD45A (growth arrest and DNA damage inducible alpha), exhibiting exceptional diagnostic accuracy (AUC >0.9). Functional enrichment analyses revealed that these genes play key roles in reactive oxygen species metabolism and immune response regulation. Specifically, GADD45A was positively correlated with eosinophils and inversely associated with activated NK cells, CD8 T cells, and activated memory CD4 T cells. BMX showed positive correlations with eosinophils, mast cells, and neutrophils, while GRB10 was linked to eosinophils and M2 macrophages. Additionally, we constructed a comprehensive mRNA-miRNA-lncRNA regulatory network, identifying key interactions that may drive sepsis pathogenesis. Molecular docking and dynamics simulations validated Bendroflumethiazide, Cianidanol, and Hexamidine as promising therapeutic agents targeting these biomarkers. In conclusion, this integrated approach provides profound insights into the molecular mechanisms underlying sepsis, pinpointing BMX, GRB10, and GADD45A as pivotal biomarkers and therapeutic targets. These findings significantly enhance our understanding of sepsis pathophysiology and lay the groundwork for developing personalized diagnostic and therapeutic strategies aimed at improving patient outcomes.

Sepsis poses a global health challenge, necessitating effective predictors for risk stratification and timely intervention. Serum calcium, involved in vital physiological processes, has shown potential associations with sepsis outcomes, but the evidence remains limited and conflicting. This retrospective study included 1000 sepsis patients admitted to the intensive care unit. Serum calcium levels were measured within 1 hour of emergency room (ER) admission. Clinical data, including demographics, comorbidities, vital signs, laboratory results, and severity scores, were collected. Logistic regression and receiver operating characteristic curve analyses were conducted to assess the association between serum calcium levels and 28-day mortality. Kaplan–Meier analysis assessed the effect of serum calcium on 28-day survival. Lower serum calcium levels within 1 hour of ER admission were significantly associated with higher 28-day mortality (adjusted odds ratio: 0.1097, 95% CI: 0.04024–0.2912, P < .0001), even after adjusting for confounders. The area under the curve for serum calcium in predicting 28-day mortality was 0.5885 ( P < .0001). Combining serum calcium with other predictors, such as the Charlson comorbidity index, red cell distribution width, lactic acid levels, and Acute Physiology and Chronic Health Evaluation II score, improved predictive accuracy (area under the curve: 0.7245, P < .0001). Kaplan–Meier analysis demonstrated a significant association between lower serum calcium levels and reduced 28-day survival ( P < .0001). Low serum calcium levels within 1 hour of ER admission are significantly associated with increased 28-day mortality in sepsis patients. It complements existing predictors, showcasing its potential role in a comprehensive prognostic framework.

Background: This study aimed to examine the associations of cystatin C, cystatin C estimated glomerular filtration rate (eGFRcys), and the difference between eGFRs (eGFRdiff) using cystatin C and creatinine levels with incident motoric cognitive risk syndrome (MCR). Methods: We utilized data from two nationally representative cohort studies, the China Health and Retirement Longitudinal Study (CHARLS, 2011-2015) and the US Health and Retirement Study (HRS, 2010-2018). Baseline serum cystatin C and creatinine levels were measured, and eGFRcys and creatinine estimated GFR (eGFRcr) were calculated. MCR was defined as subjective cognitive complaints plus objectively measured slow gait speed. Multivariable logistic models were used to investigate the longitudinal associations between kidney function measurements and incident MCR. Results: In CHARLS (N = 2,085) and HRS (N = 1,240) cohorts, 7.4% and 7.2% developed MCR over follow-up. Each SD increment in serum cystatin C level was associated with elevated incident MCR odds, and an inverse association of eGFRcys with incident MCR was observed in both cohorts after multivariable adjustment and meta-analyses. The association between serum cystatin C and incident MCR remained significant even after adjusting for serum creatinine, suggesting that cystatin C is independently associated with MCR, regardless of kidney function levels. Additionally, each SD decrease in the absolute value of eGFRdiff was associated with lower odds of incident MCR among CHARLS participants. Conclusions: Cystatin C and eGFRcys were correlated with an elevated MCR risk in two distinct populations. Specifically, eGFRdiff also related to incident MCR among Chinese older adults. Monitoring cystatin C-based kidney function could have significant clinical utility for identifying incident MCR risk, and represents a potential intervention target for healthier cognitive aging. (c) 2025 Published by Elsevier Masson SAS on behalf of SERDI Publisher. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

To explore whether sarcopenia, a common disease among the elderly, could promote the hypercoagulable state in elderly patients with chronic obstructive pulmonary disease (COPD). There is a significant correlation between sarcopenia and blood hypercoagulability in elderly patients with COPD. Sarcopenia seemingly has the potential to be a risk factor for the blood hypercoagulable state in such patients. The findings provide a new perspective for the prevention and intervention of the hypercoagulable state in elderly COPD patients, which is conducive to improving the prognosis of these patients. Blood hypercoagulability is associated with poor prognosis in elderly patients with chronic obstructive pulmonary disease (COPD). The aim of this study was to explore whether sarcopenia, a common disease among the elderly, could promote the hypercoagulable state in such patients. Elderly patients with stable-phase COPD were divided into the sarcopenia group (n = 192) and the non-sarcopenia group (n = 264). Sarcopenia was diagnosed according to the criteria for risk assessment, muscle mass measurement, muscle strength evaluation, and muscle function assessment. All patients were followed up for 18 months, and the acute exacerbation of COPD was recorded. The characteristics of COPD, coagulation function, and potential confounding factors during the stable and acute exacerbation phases were collected. Multivariate logistic or linear regression was used for data analysis. Compared with the non-sarcopenia group, the levels of PLT and AT-III in patients of the sarcopenia group were significantly lower, while the levels of PAR, PT, APTT, FIB, and D-dimer were significantly higher during both the stable phase and the acute exacerbation phase of COPD. More importantly, compared with the non-sarcopenia group, the deterioration amplitudes of most coagulation indicators in patients of the sarcopenia group were significantly greater during the process of COPD developing from the stable phase to the acute exacerbation phase. There is a significant correlation between sarcopenia and blood hypercoagulability in elderly patients with COPD. Sarcopenia seemingly has the potential to be a risk factor for the blood hypercoagulable state in such patients, but further verification is still needed.

OBJECTIVE:Comparing the effects of extracorporeal cardiopulmonary resuscitation (ECPR) and conventional cardiopulmonary resuscitation (CCPR) on outcomes in patients with in-hospital cardiac arrest (IHCA) in China. The benefits of ECPR over CCPR in patients with IHCA remain controversial. DESIGN:This article analyzed data from the BASeline Investigation of In-hospital Cardiac Arrest (BASIC-IHCA) study, which consecutively enrolled patients with IHCA from July 1, 2019, to December 31, 2020. Patients who received ECPR were selected as the case group and matched with patients who received CCPR as the control group by propensity score at a ratio of 1:4. A parallel questionnaire survey of participating hospitals was conducted, to collect data on ECPR cases from January 1, 2021 to November 30, 2021. The primary outcome was survival to discharge or 30-day survival. SETTING:We included 39 hospitals across 31 provinces in China. PATIENTS:Patients receiving cardiopulmonary resuscitation and without contraindications to ECPR were selected from the BASIC-IHCA database. Patients older than 75 years, not witnessed, or with cardiopulmonary resuscitation duration less than 10 min were excluded. INTERVENTIONS:None. MEASUREMENTS AND MAIN RESULTS:A total of 4853 patients met the inclusion criteria before matching, with 34 undergoing ECPR (median age, 56.5 yr; 67.65% male) and 4819 underwent CCPR (median age, 59 yr; 64.52% male). There were 132 patients receiving CCPR and 33 patients receiving ECPR who were eventually matched. The ECPR group had significantly higher survival rates at discharge or 30-day survival (21.21% vs. 7.58%, p = 0.048). The ECPR group had significantly lower mortality rates (hazard ratio 0.57; 95% CI, 0.38-0.91) than the CCPR group at discharge or 30 days. Besides the BASIC-IHCA study, the volume of ECPR implementations and the survival rate of patients with ECPR (29.4% vs. 10.4%. p = 0.004) in participating hospitals significantly improved. CONCLUSIONS:ECPR may be beneficial compared with CCPR for patient survival after IHCA and should be considered for eligible patients with IHCA.

Background: Parkinson's disease (PD) is a prevalent neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons. This study aims to discover potential new genetic biomarkers for PD. Methods: Transcriptome data from a total of 56 patients with PD and 61 healthy controls were downloaded from the Gene Expression and three machine learning algorithms (LASSO, Random Forest, SVM-RFE) were employed to identify pivotal PD-associated genes. Additionally, RT-qPCR experiments were conducted to validate our findings in clinical specimens. Functional enrichment analysis and Gene Set Enrichment Analysis (GSEA) were performed to explore the functional and pathway mechanisms of the identified genes in PD. Molecular docking studies revealed potential small-molecule drug targets for the key genes. Results: The results from the three machine learning algorithms identified ELL-Associated Factor 2 (EAF2) as a key gene in PD. Gene expression analysis indicated that EAF2 is significantly downregulated in PD patients, and the receiver operating characteristic (ROC) analysis validated the diagnostic potential of EAF2. The results from RT-qPCR on clinical specimens confirmed the findings from public database analyses. Functional enrichment analysis suggested that EAF2 is involved in dopamine biosynthesis and synaptic transmission for PD pathology. Additionally, EAF2 expression correlated significantly with immune cell infiltration. Furthermore, molecular docking results indicated that Acalabrutinib, Tirabrutinib Hydrochloride, and Ibrutinib are potential targeted therapeutic agents for EAF2. Conclusion: These findings underscore EAF2 as a novel diagnostic biomarker and potential therapeutic target for PD, warranting further mechanistic studies and clinical validation.

Background: S epsis-associated encephalopathy (SAE) is a complex condition with variable outcomes. This study investigates the potential of the Triglyceride-glucose (TyG) index as a marker for disease severity and prognosis in SAE patients. Methods: Our cohort comprised 1578 SAE patients from the MIMIC-IV database, stratified based on TyG index tertiles. We analyzed baseline characteristics, disease severity, and prognostic outcomes. The Kaplan-Meier method and Cox regression analyses were employed for survival analysis, while Spearman rank correlation and various statistical tests were used to assess correlations between TyG index and clinical outcomes. Results: The study population's median age was 65.96 years, predominantly male (60.1%). Higher TyG index scores correlated with elevated clinical severity scores (APSIII, LODS, OASIS, SAPSII, and CCI) and increased ICU and hospital stay durations. TyG index categorization revealed significant differences in 90-day survival probabilities, with "high TyG" associated with a 25% increased mortality risk compared to "low TyG". Furthermore, TyG index showed a moderate positive correlation with ICU stay duration and use of norepinephrine and vasopressin, but not with dopamine and epinephrine use. Conclusions: The TyG index is a significant independent predictor of disease severity and prognosis in SAE patients. High TyG levels correlate with worse clinical outcomes and increased mortality risk, suggesting its potential as a valuable tool in managing SAE.

BACKGROUND:There is still no study on the use of the SARC-CalF questionnaire for older critically ill patients. Moreover, there is limited evidence on whether a combination of sarcopenia and frailty can provide incremental improvements in risk stratification for older critically ill patients. METHODS:A total of 653 patients older than 60 years were recruited. We used the clinical frailty scale (CFS) and SARC-CalF questionnaire to assess the frailty status and sarcopenia risk, respectively, of older patients shortly after admission to the ICU. The effect of frailty and sarcopenia risk on ICU mortality and 30-day mortality was evaluated. RESULTS:A total of 147 (22.5%) patients died in the ICU, and 187 (28.6%) patients died within 30 days after ICU admission. The CFS score was associated with increased ICU mortality [per 1-score increase: odds ratio (OR) = 1.222, 95% confidential interval (CI): 1.003-1.489] and 30-day mortality (per 1-score increase: OR = 1.307, 95% CI: 1.079-1.583). The SARC-CalF score was also associated with increased ICU mortality (per 1-score increase: OR = 1.204, 95% CI: 1.120-1.294) and 30-day mortality (per 1-score increase: OR = 1.247, 95% CI: 1.163-1.337). The addition of the CFS + SARC-CalF score to Acute Physiology and Chronic Health Evaluation (APACHE) II improved discrimination and reclassified ICU and 30-day mortality risk. CONCLUSIONS:Sarcopenia risk assessed by the SARC-CalF questionnaire provided independent prognostic information for older critically ill patients. A combination of sarcopenia and frailty improved the prediction of mortality for older critically ill patients and thus might be useful in the clinical decision-making process.

There is growing evidence that programmed cell death plays a significant role in the pathogenesis of chronic thromboembolic pulmonary hypertension (CTEPH). Anoikis is a newly discovered type of programmed death and has garnered great attention. However, the precise involvement of Anoikis in the progression of CTEPH remains poorly understood. The goal of this study was to identify Anoikis-related genes (ARGs) and explore potential therapeutic drugs for CTEPH. Differentially expressed genes were identified by limma and weighted gene co-expression network analysis (WGCNA) packages, and functional analyses were conducted based on the differentially expressed genes. Subsequently, a combination of protein-protein interaction (PPI), Least Absolute Shrinkage and Selection Operator (LASSO), and Support Vector Machine Recursive Feature Elimination (SVM-RFE) methodologies was employed to screen hub genes associated with CTEPH, which were further verified by dataset GSE188938, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. CIBERSORT was utilized to evaluate the infiltration of immune cells and the relationship between infiltration-related immune cells and ARGs. Finally, targeted drug analysis and molecular docking were used to predict drugs targeting Anoikis process to treat CTEPH. Thirty-two differentially expressed genes related to Anoikis and CTEPH were screened through WGCNA analysis. Then, the key ARGs FASN, PLAUR, BCL2L1, HMOX1 and RHOB were screened by PPI, Lasso and SVM-RFE machine learning. Validation through dataset GSE188938, qRT-PCR, and Western blot analyses confirmed HMOX1 and PLAUR as powerful and promising biomarkers in CTEPH. In addition, CIBERSORT immunoinfiltration revealed that Mast_cells_activated and Neutrophils were involved in the pathological regulation of CTEPH. Correlation analysis indicated that HMOX1 was positively correlated with Neutrophils, while PLAUR was negatively correlated with Mast_cells_activated. Finally we used targeted drug analysis and molecular docking to identify that STANNSOPORFIN as a potential drug targeting HMOX1 for the treatment of CTEPH. HMOX1 and PLAUR emerge as potential biomarkers for CTEPH and may influence the development of CTEPH by regulating Anoikis. Mast_cells_activated and Neutrophils may be involved in Anoikis resistance in CTEPH patients, presenting novel insights into CTEPH therapeutic targets. STANNSOPORFIN is a potential agents targeting Anoikis process therapy for CTEPH.

We present an exceptional case of a 53-year-old female, initially misdiagnosed with fulminant myocarditis, but later correctly diagnosed with pheochromocytoma. The presentation of the patient included a spectrum of symptoms such as headache, chest discomfort, palpitations, and dyspnea, following the intake of Domperidone. Two weeks prior to admission, the patient had experienced episodes of diarrhea and a low-grade fever. Unresolved symptoms and an unmanageable surge in blood pressure despite comprehensive fulminant myocarditis treatment prompted further investigation. The discovery of an adrenal mass via a CT scan and subsequent biochemical tests led to the confirmation of pheochromocytoma. Implementation of alpha-blockade therapy and a successful laparoscopic adrenalectomy resulted in significant clinical improvement. This case underscores the diagnostic intricacies of pheochromocytoma and highlights the need for vigilance when faced with severe, unresponsive cardiovascular symptoms.

Background:This study aimed to assess whether integrating handgrip strength (HGS) into the concept of motoric cognitive risk (MCR) would enhance its predictive validity for incident dementia and all-cause mortality. Methods:A cohort of 5, 899 adults from the Health and Retirement Study underwent assessments of gait speed, subjective cognitive complaints, and HGS were involved. Over a 10-year follow-up, biennial cognitive tests and mortality data were collected. Cox proportional hazard analyses assessed the predictive power of MCR alone and MCR plus HGS for incident dementia and all-cause mortality. Results:Patients with MCR and impaired HGS (MCR-HGS) showed the highest adjusted hazard ratios (AHR) for dementia (2.33; 95% CI, 1.49-3.65) and mortality (1.52; 95% CI, 1.07-2.17). Even patients with MCR and normal HGS (MCR-non-HGS) experienced a 1.77-fold increased risk of incident dementia; however, this association was not significant when adjusted for socioeconomic status, lifestyle factors, and medical conditions. Nevertheless, all MCR groups demonstrated increased risks of all-cause mortality. The inclusion of HGS in the MCR models significantly improved predictive discrimination for both incident dementia and all-cause mortality, as indicated by improvements in the C-statistic, integrated discrimination improvement (IDI) and net reclassification indices (NRI). Conclusion:Our study underscores the incremental predictive value of adding HGS to the MCR concept for estimating risks of adverse health outcomes among older adults. A modified MCR, incorporating HGS, could serve as an effective screening tool during national health examinations for identifying individuals at risk of dementia and mortality.