Search Results (364)

Core body temperature (CBT) is a fundamental physiological parameter tightly regulated by thermoregulatory mechanisms and is critically important for heat stress assessment, clinical management, and circadian rhythm research. Although invasive measurements such as pulmonary artery, esophageal, and rectal temperatures provide high accuracy, their practical use is limited by invasiveness, discomfort, and restricted feasibility for continuous monitoring in daily-life or field environments. Consequently, extensive efforts have been devoted to developing non-invasive CBT measurement and estimation techniques. This review provides an application-oriented synthesis of invasive reference methods and representative non-invasive approaches, including in-ear sensors, infrared thermography, ingestible telemetric sensors, heat-flux-based techniques, and model-based estimation using wearable physiological signals. For each approach, measurement principles, accuracy, invasiveness, usability, and application domains are comparatively examined, with particular emphasis on trade-offs between measurement fidelity and real-world implementability. Rather than ranking methods by absolute performance, this review highlights their relative positioning across clinical, occupational, and daily-life contexts. While no single non-invasive technique can universally replace invasive gold standards, recent advances in wearable sensing, heat-flux modeling, and multimodal estimation demonstrate growing potential for practical CBT monitoring. Overall, the findings suggest that future CBT assessment will increasingly rely on hybrid and context-aware systems that integrate complementary methods to enable reliable monitoring under real-world conditions. This review is intended for researchers and practitioners who need to select or design CBT monitoring systems. Full article

Factor XII is a molecule of unclear physiological function that has attracted increasing research interest across multiple medical disciplines. In recent years, a substantial body of evidence has emerged regarding the contribution of factor XII to the pathogenesis of inflammatory and prothrombotic conditions. FXII has been shown to play a protective role in FXII-driven coagulation during host defence against infections and to protect against multi-organ failure in animal models of sepsis. In acute respiratory distress syndrome (ARDS), FXII activity contributes to the release of pro-inflammatory mediators and is associated with severe clinical outcomes; it also induces fibroblast migration in idiopathic pulmonary fibrosis. FXII deficiency has been associated with reduced neutrophil adhesion and migration in sterile skin wounds and immune complex-induced vasculitis. In neurological conditions, FXII deficiency significantly reduced the number and severity of multiple sclerosis relapses and decreased the volume of post-traumatic brain oedema. In heart failure pathogenesis, FXII deficiency and pharmacological inhibition of FXII activity blocked activation of the renin–angiotensin–aldosterone system (RAAS) in dilated cardiomyopathy, increased median survival, and delayed heart failure onset in murine models. Importantly, FXII inhibition prevented arterial thrombosis without affecting haemostasis. This review summarises the latest findings on the contribution of FXII to inflammatory and prothrombotic states across multiple medical fields, including cardiology. Pharmacological inhibition of FXII has generated considerable interest as a potential future therapeutic strategy; however, to date, human studies remain limited. Full article

Background: Chronic obstructive pulmonary disease (COPD) is a progressive inflammatory lung disorder with limited effective therapies. NRICM102, a traditional multi-herbal formulation originally developed for COVID-19, exhibits anti-inflammatory and immunomodulatory potential. Objectives: The aim of this study was to investigate the therapeutic efficacy of NRICM102 in a COPD-relevant inflammatory lung injury mice model. Methods: Mice were exposed to lipopolysaccharide (LPS) and benzo[a]pyrene (B[a]P) to induce chronic airway inflammation and structural lung damage and treated with NRICM102 (1.5–3.0 g/kg) or dexamethasone. Lung function, histopathology, transcriptomic profiling, and protein expression of key inflammatory markers were assessed. Results: NRICM102 significantly restored LPS+B[a]P-induced enhanced pause (Penh) and arterial oxygen saturation (aO₂%), similar to the effect of dexamethasone. Histological analysis revealed marked alveolar damage, inflammatory cell infiltration, and fibrosis in the model group, all of which were significantly attenuated by NRICM102 in a dose-dependent manner, with high-dose (3.0 g/kg) treatment showing pronounced structural preservation. Transcriptomic profiling revealed that NRICM102, particularly at 3.0 g/kg, partially reversed COPD-associated gene expression patterns, characterized by reduced activation of cytokine signaling, chemokine activity, and antigen presentation pathways. GO, DO, and KEGG enrichment analyses indicated selective modulation of immune-related pathways, with high-dose NRICM102 affecting genes involved in adaptive immunity and cytokine receptor interactions, including a subset of 150 reverted genes. Immunofluorescence analysis confirmed dose-dependent reductions in key inflammatory, immune, and mucus-related markers, including IL-1β, NLRP3, Muc5ac, and MMP12 expression. Conclusions: NRICM102 confers significant protective effects against COPD-relevant inflammatory lung injury by improving pulmonary function, preserving lung architecture, and selectively modulating immune and inflammatory pathways. These results provide preclinical evidence supporting the potential of NRICM102 to modulate inflammation and immune responses associated with COPD-related pathology, although further studies are needed to establish its therapeutic relevance. Full article

Accurate cardiac output (CO) measurement is vital for hemodynamic management; however, it usually requires invasive monitoring, which limits its continuous and out-of-hospital use. Wearable sensors integrated with deep learning offer a noninvasive alternative. This study developed and validated a lightweight deep learning model using wearable electrocardiography (ECG) and photoplethysmography (PPG) signals to predict CO and examined whether cardiac index-based normalization (Cardiac Index (CI) = CO/body surface area) improves performance. Twenty-seven patients who underwent cardiac surgery and had pulmonary artery catheters were prospectively enrolled. Single-lead ECG (HiCardi+ chest patch) and finger PPG (WristOx2 3150) were recorded simultaneously and processed through an ECG–PPG fusion network with cross-modal interaction. Three models were trained as follows: (1) CI prediction, (2) direct CO prediction, and (3) indirect CO prediction. The total number of CO = predicted CI × body surface area. Reference values were derived from thermodilution. The CI model achieved the best performance, and the indirect CO model showed significant reductions in error/agreement metrics (MAE/RMSE/bias; p < 0.0001), while correlation-based metrics are reported descriptively without implying statistical significance. The Pearson correlation coefficient (PCC) and percentage error (PE) for the indirect CO estimates (PCC = 0.904; PE = 23.75%). The indirect CO estimates met the predefined PE < 30% agreement benchmark for method-comparison; this is not a universal clinical standard. These results demonstrate that wearable ECG–PPG fusion deep learning can achieve accurate, noninvasive CO estimation and that CI-based normalization enhances model agreement with pulmonary artery catheter measurements, supporting continuous catheter-free hemodynamic monitoring. Full article

Background: Accurate risk stratification in acute pulmonary embolism (PE) is critical for guiding management. This study assessed the prognostic value of computed tomography (CT) indicators of right-heart strain and thrombus burden for predicting in-hospital adverse events. Methods: In this retrospective cohort of 300 patients with CT-confirmed acute PE, the right-to-left ventricular (RV/LV) diameter ratio, Pulmonary Artery Obstruction Index (PAOI), and inferior vena cava (IVC) contrast reflux were measured. The primary endpoint was in-hospital adverse events, including hemodynamic collapse, vasopressor or ventilatory support, rescue reperfusion therapy, or death. Logistic regression and receiver operating characteristic (ROC) analyses were performed. Results: Adverse events occurred in 106 patients (35.3%). Compared with stable patients, those with events had higher RV/LV ratios (1.45 vs. 1.03), higher PAOI (38.8 vs. 24.3), and more frequent IVC reflux (74% vs. 7%) (all p < 0.001). Independent predictors were RV/LV ratio (aOR 3.22 per 0.1), PAOI (aOR 5.53 per 10 points), and IVC reflux (aOR 428.5; all p < 0.001). The model showed excellent discrimination (AUC = 0.96). Conclusions: CT-derived indices of right-heart strain and thrombus burden are strong, independent predictors of in-hospital adverse events in acute PE and should be integrated into routine CT-based risk assessment. Full article

Connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH) is a severe form of pulmonary hypertension with poor prognosis. It most commonly arises in systemic sclerosis (SSc), followed by systemic lupus erythematosus (SLE) and mixed connective tissue disease (MCTD). Its pathogenesis involves a complex interplay of immune dysregulation, chronic inflammation, endothelial injury, vascular remodeling, and fibrosis. Although vasodilators targeting the endothelin, nitric oxide, and prostacyclin pathways remain the therapeutic backbone, newer agents—including the activin signal inhibitor sotatercept and inhaled treprostinil—have expanded treatment options. Immune-targeted therapies such as glucocorticoids, cyclophosphamide, mycophenolate mofetil, rituximab, and IL-6 receptor inhibitors may benefit inflammation-dominant PAH phenotypes, while fibrotic phenotypes continue to demonstrate limited responsiveness. In addition to brain natriuretic peptide (BNP), N-terminal (NT)-proBNP and disease-specific autoantibodies, emerging biomarkers show promise for early detection, risk stratification, and personalized treatment, though validation in CTD-PAH is lacking. Advances in animal models replicating immune-mediated vascular injury and fibrosis have further improved mechanistic understanding. Despite these developments, substantial unmet needs remain, including the absence of disease-specific therapeutic strategies, limited biomarker integration into clinical practice, and a scarcity of large, well-designed trials targeting individual CTD subtypes. Addressing these gaps will be essential for improving prognosis in patients with CTD-PAH. Full article

Vascular remodeling and progressive lung vessel obliteration are a histopathological cornerstone for the onset of pulmonary arterial hypertension (PAH). However, the role of vascular endothelial growth factor (VEGF) signaling pathways in the development of histopathological vascular changes in PAH is still incompletely understood. This educational review aims to untangle the opposing and heterogeneous actions of VEGF and the receptors it engages in triggering lung angio-proliferative lesions, driving hemodynamic changes in PAH. A proposed ‘VEGF-oriented’ approach attempts to untangle some of the contrasting and complementary actions of VEGF in the pathogenesis of the disease. Experimental models provide a cogent explanation for dysfunctional angiogenesis and the paradox of VEGF-receptor-blockade-induced PAH. The multifaced properties of VEGF, whether angiogenic or nonangiogenic, vary depending on the nature of the ligand, receptor-dependent and -independent signaling pathways, and the duration of the ligand–receptor engagement. Further investigation is needed to translate the knowledge acquired to human subjects and to confirm the pathogenic mechanisms surrounding the phenotypic shift to apoptosis-resistant, hyperproliferative cellular subset and the development of angio-obliterative lesions in PAH. Full article

Objectives: To develop and validate a transthoracic lung ultrasound (TLUS)-integrated clinical nomogram for predicting pulmonary arterial hypertension (PAH) in patients with connective tissue disease-associated interstitial lung disease (CTD-ILD). Methods: This multicenter retrospective study included 550 patients with CTD-ILD from the Second Affiliated Hospital of Fujian Medical University and 169 external cases from the Xijing Hospital, Fourth Military Medical University. Patients were randomly divided into a training cohort (n = 385) and an internal validation cohort (n = 165); the external dataset served as a testing cohort. Demographic, physiological, laboratory, pulmonary function, and TLUS data were collected. Univariate and multivariate logistic regression analyses identified independent predictors of PAH, which were used to construct a nomogram model. Discrimination was assessed using receiver operating characteristic (ROC) curves and area under the curve (AUC) values. Calibration, decision curve analysis (DCA), and clinical impact curves (CIC) were performed to evaluate model accuracy and clinical utility. Results: Five independent predictors were identified: respiratory rate, diffusing capacity of the lung for carbon monoxide (DLCO% predicted), TLUS score, red blood cell (RBC) count, and brain natriuretic peptide (BNP). The model achieved excellent discrimination with AUCs of 0.952 (95% confidence interval [CI]: 0.927–0.977) in the training cohort, 0.935 (95% CI: 0.885–0.985) in the validation cohort, and 0.874 (95% CI: 0.806–0.942) in the testing cohort, outperforming individual predictors. Calibration plots showed close agreement between predicted and observed probabilities, while DCA and CIC confirmed strong clinical benefit and applicability across all thresholds. Conclusions: This TLUS-integrated nomogram provides a noninvasive and reliable tool for individualized PAH risk assessment in CTD-ILD patients. By combining ultrasound findings with physiological and laboratory markers, the model enables accurate detection of high-risk cases and may assist clinicians in optimizing surveillance and management strategies. Full article

Cirrhotic cardiomyopathy encompasses structural and functional cardiac abnormalities occurring in patients with liver cirrhosis despite the absence of pre-existing heart disease, yet its diagnosis remains challenging. Although echocardiography is the standard diagnostic tool, circulating biomarkers may provide complementary value when imaging findings are inconclusive. This study evaluated the association between N-terminal pro-B-type natriuretic Peptide (NT-proBNP), soluble Suppression of Tumorigenicity 2 (sST2), and diastolic dysfunction in cirrhotic patients without known cardiac disease. We conducted a prospective case–control study including 83 participants (43 patients with non-alcoholic cirrhosis and 40 healthy controls), assessed clinically, biochemically, and echocardiographically between June 2020 and July 2021. Cirrhotic patients showed significantly higher NT-proBNP (94.17 ± 151.36 pg/mL vs. 19.2 ± 5.47 pg/mL, p < 0.001) and sST2 levels (5.4 ± 2.31 ng/mL vs. 2.4 ± 0.99 ng/mL, p < 0.001). NT-proBNP demonstrated limited diagnostic accuracy for diastolic dysfunction (accuracy 52.6%, sensitivity 50%, specificity 60%, AUC 0.51), but it correlated modestly with congestion markers such as left atrial volume and pulmonary artery systolic pressure. A multimarker model combining age, NT-proBNP, and sST2 substantially improved diagnostic performance for diastolic dysfunction (accuracy 75%, sensitivity 77.1%, specificity 71.4%, AUC 0.925). In conclusion, NT-proBNP is associated with diastolic dysfunction but is influenced by cirrhosis congestion status. A combined NT-proBNP and sST2 assessment enhances diagnostic precision and may aid therapeutic decision-making, particularly regarding congestion and diuretic management in cirrhotic patients. Full article

Objective: In this study, we aimed to determine the most significant risk factors for 5-year mortality in patients with paroxysmal and persistent drug-refractory tachysystolic atrial fibrillation after undergoing atrioventricular node ablation (AVNA) in combination with the implantation of a permanent three-chamber pacemaker with an implantable cardioverter–defibrillator function (CRT-D). Methods: This prospective single-center cohort study included 101 patients with chronic heart failure (mean age 62 ± 15.5 years; 70.3% male) with paroxysmal or persistent drug-refractory atrial fibrillation who underwent atrioventricular node ablation and CRT-D implantation. All patients received optimal medical therapy before and after undergoing the procedure. Predictors of 5-year mortality were assessed using exploratory machine-learning methods, including random forest and Shapley additive explanations. Results: During 5-year follow-up, 13 cardiovascular deaths were recorded. Five key predictors of mortality were identified: left ventricular ejection fraction, 6 min walk distance, mean pulmonary artery pressure, systolic relaxation coefficient, and degree of mitral regurgitation. The exploratory predictive model showed high accuracy (92%) in terms of classifying the outcomes. Conclusions: Atrioventricular node ablation (AVNA) combined with CRT-D was associated with the observed long-term clinical outcomes observed in patients with drug-refractory tachysystolic atrial fibrillation. The exploratory machine learning analysis identified key mortality-associated factors, which may support future efforts in personalized risk stratification and hypothesis generation. The combination of AVNA and CRT-D was associated with the observed long-term outcomes in this real-world cohort. Full article

This retrospective study evaluated the clinical utility of Virtual Reality (VR) in visualizing extracardiac CHD (eCHD) abnormalities involving great vessels, pericardium, or structures outside the heart in nine pediatric patients. Anonymized computed tomography angiography (CTA) DICOM images were processed using Elucis (Version 1.10 elucis next) software to generate interactive 3D models via segmentation. VR models were reviewed for a variety of cases: vascular rings (two with right aortic arch, aberrant left subclavian artery, and diverticulum of Kommerell; two with double aortic arch), pericardial teratomas (n = 2), right superior vena cava draining into the left atrium (n = 1), left pulmonary artery sling (n = 1), and aortopulmonary window (n = 1). VR video images were presented during weekly heart center conferences. A survey conducted among heart center staff assessed the perceived value of VR in clinical practice. A total of 62% found traditional diagnostic modalities very effective, 100% considered VR a valuable diagnostic tool, 65% responded positively to VR image resolution, 50% highlighted its educational benefit, 81% believed VR enhanced diagnostic accuracy and surgical planning, and 100% would recommend its use to colleagues. This study demonstrates the successful integration of VR-based segmentation into clinical workflows, underlining its potential as both an educational resource and a tool to support diagnostic and surgical decision-making. Full article

Background: Noble gases, such as argon, have been observed to exhibit cytoprotective effects. The non-anesthetic properties, abundance, and cost-effectiveness of argon suggest its clinical potential. While its efficacy in mitigating ischemia–reperfusion injury has been demonstrated in cellular and small animal models, data on its effects in large animals remain limited. This study evaluated the effects of argon inhalation on pulmonary ischemia–reperfusion injury in miniature swine with potential applications in transplantation. Methods: The left bronchial and pulmonary artery and veins were clamped for 90 min, and then the clamps were released to induce lung ischemia–reperfusion injury in 10 CLAWN miniature swine. The argon group (n = 5) inhaled a mixture of 30% oxygen and 70% argon for 360 min, whereas the control group (n = 5) inhaled a mixture of 30% oxygen and 70% nitrogen for an equivalent duration. Lung function was evaluated using chest X-ray, lung biopsies, and blood gas analysis. Results: The PaO₂/FiO₂ ratio significantly decreased in the control group 2 h post-reperfusion (568 ± 12 to 272 ± 39 mmHg), but was better preserved in the argon group (562 ± 17 to 430 ± 48 mmHg). Blood gas from the left pulmonary vein showed a superior PvO₂/FiO₂ ratio in the argon group (331 ± 40 vs. 186 ± 17 mmHg at 2 h; 519 ± 19 vs. 292 ± 33 mmHg at 2 days). Chest X-ray revealed reduced infiltration in the left lung. The lung biopsy histological scores improved in the argon group at 2 h and 2 days. Serum superoxide dismutase analysis and tissue TUNEL assays suggested that antioxidant and anti-apoptotic mechanisms, respectively, were involved. Conclusions: Perioperative argon inhalation attenuates ischemia–reperfusion injury in swine lungs, likely via anti-apoptotic and antioxidant effects. Full article

Background: Inflammatory bowel disease (IBD) is associated with systemic inflammation and potential cardiovascular complications. This meta-analysis evaluates long-term cardiovascular risks in IBD. Methods: Electronic databases were searched for studies examining cardiovascular, cerebrovascular, and thromboembolic risks in IBD. Adjusted hazard ratios (aHRs) with 95% confidence intervals (CIs) were pooled using a random-effects model. Results: Fifty-three studies comprising 1,406,773 patients were analyzed. IBD was linked to increased risk of ischemic heart disease (aHR 1.25; p = 0.001) myocardial infarction (aHR 1.25; p = 0.01), acute coronary syndrome (aHR 1.43; p < 0.00001), heart failure (aHR 1.24; p < 0.00001), atrial fibrillation (aHR 1.20; p < 0.00001), and stroke (aHR 1.13; p < 0.00001). Elevated risks were also observed for peripheral arterial disease (aHR 1.41; p < 0.00001), diabetes mellitus (aHR 1.40; p < 0.00001), venous thromboembolism (aHR 1.98; p < 0.00001), deep vein thrombosis (aHR 2.85; p = 0.0004), and pulmonary embolism (aHR 1.98; p = 0.03). Importantly, IBD was associated with increased cardiovascular (aHR 1.14; p = 0.03) and all-cause mortality (aHR 1.53; p < 0.00001). Conclusions: IBD patients face higher risk for adverse cardiovascular outcomes, thromboembolic disease, and mortality, necessitating early cardiovascular risk assessment and targeted interventions in this population. Full article

Background/Objectives: This study investigated the influence of long-term medications and patient conditions on pulmonary arterial enhancement and image quality in computed tomography pulmonary angiography (CTPA). A cohort matched for age was divided into two main groups: a medication group (Captopril, Albuterol, and control) and a condition group (obesity, COPD, and control). Methods: Temporal enhancement (Hounsfield Units, HU), area under the curve (AUC), and washout rates were analyzed alongside image quality metrics (signal-to-noise ratio, SNR; contrast-to-noise ratio, CNR). Results: The results demonstrated significant intergroup differences. In the medication group, Albuterol was associated with significantly higher peak enhancement (368.9 ± 16.3 HU) compared to control (327.1 ± 13.8 HU; p = 0.001), while Captopril showed significantly lower baseline HU (153.5 ± 7.3 vs. 185.3 ± 9.3; p < 0.001) and reduced total AUC. In the condition group, both obesity and COPD exhibited significantly lower peak HU values, slower washout rates, and reduced total AUC compared to controls (p < 0.0001). Consequently, SNR and CNR were significantly lower in the obesity and COPD groups (p = 0.001). Linear mixed-effects models confirmed significant group × time interactions for both medication and condition groups after adjustment for confounders. Furthermore, pulmonary arterial enhancement (HU) showed a very strong positive correlation with both SNR (R² = 0.9956) and CNR (R² = 0.9848, p < 0.001). Conclusions: The findings indicate that patient-specific factors significantly impact CTPA image quality. Albuterol was associated with peak vascular opacification, whereas conditions like obesity and COPD were consistently associated with reduced enhancement and inferior image quality. The strong correlation between HU and objective image quality metrics underscores vascular enhancement as a key determinant of diagnostic CTPA quality. Full article

Background: Despite the increasing adoption of minimally invasive direct coronary artery bypass (MIDCAB), data on its long-term outcomes—particularly regarding sex-based differences—remain limited. This study presents a robust 20-year analysis comparing males and females, assessing perioperative outcomes, long-term survival, and independent predictors of mortality to inform sex-sensitive clinical decision-making. Methods: A retrospective cohort analysis of 676 patients (138 females, 538 males) undergoing MIDCAB was performed. Propensity score matching (PSM) generated balanced female and male cohorts (n = 129 each). Preoperative demographics, short-term outcomes, and long-term survival were assessed using Kaplan–Meier analysis and Cox regression modelling. Results: In unmatched cohorts, females exhibited significantly lower NYHA class distribution (p = 0.011) and higher atrial fibrillation prevalence (p = 0.038), with otherwise comparable comorbidities. Propensity score matching achieved cohort balance, and short-term outcomes—including 30-day mortality, stroke/TIA, and reoperation—were similar across sexes. Kaplan–Meier analysis of matched cohorts revealed no significant survival difference (log-rank p = 0.3370), though females demonstrated greater 20-year survival than males (77.6% versus 55.8%). In females, age 70–79 (HR 2.66; 95% CI: 1.02–6.95; p = 0.046) and cerebrovascular disease (HR 5.33; 95% CI: 1.49–19.03; p = 0.010) were independently associated with mortality. In males, significant predictors included diabetes (HR 1.86; 95% CI: 1.02–3.38; p = 0.042), chronic kidney disease (HR 4.92; 95% CI: 1.21–20.02; p = 0.026), pulmonary disease (HR 2.35; 95% CI: 1.20–4.60; p = 0.013), cerebrovascular disease (HR 4.77; 95% CI: 1.97–11.56; p < 0.001), and reduced left ventricular ejection fraction (HR 0.17; 95% CI: 0.06–0.43; p < 0.001). Conclusions: This 20-year study, the longest to date, demonstrates that MIDCAB achieves durable and equivalent long-term survival in males and females. It highlights sex-specific predictors of mortality, emphasizing the necessity for personalized preoperative risk assessment and postoperative management. Full article