Technology and Health Care最新文献

BackgroundArterial stiffness and endothelial dysfunction are early markers of cardiovascular disease (CVD) risk. While moderate-intensity aerobic exercise has demonstrated vascular benefits in untrained individuals, its acute effects on strength-trained athletes remain unclear.ObjectiveThis study investigates the impact of a single aerobic session on arterial stiffness and endothelial function in strength-trained throwers and untrained controls.MethodsEleven male university throwers and eleven healthy controls participated. Participants completed 30 min of moderate-intensity cycling at 50% of heart rate reserve. Brachial-ankle pulse wave velocity (baPWV) and reactive hyperemia-peripheral arterial tonometry index (RHI) were measured at baseline, immediately after exercise, and 40 min post-exercise.ResultsArterial stiffness decreased significantly in the controls (p = 0.003) but showed no change in the throwers. Endothelial function, as measured by RHI, improved significantly in both groups post-exercise (p < 0.001). There was no significant difference in RHI improvement between groups.ConclusionsIn the throwers group, a single session of moderate-intensity aerobic exercise did not lead to a significant reduction in arterial stiffness but resulted in an improvement in endothelial function. These findings suggest that while endothelial function in strength-trained throwers can benefit acutely from aerobic exercise, their arterial stiffness may require more intensive or longer-duration aerobic interventions to achieve significant improvements.

ObjectiveDuring coronary artery bypass grafting(CABG), surgeons commonly use transit time flow meter (TTFM) to determine the graft patency. This study is to explore the effect of a special "spike waveform" in CABG on graft patency and its hemodynamic environment.MethodsWe collected the data of 1154 patients undergoing CABG, including intraoperative TTFM waveform and coronary CTA at 1 week after surgery. 239 patients had 1-year follow-up CTA. We divided the grafts into spike and non-spike waveform groups, and assessed the patency of grafts. Additionally, we constructed an ideal model of CABG, we also calculated and extracted the hemodynamic parameters of the grafts.ResultsFor immediate patency, the occlusion rates of spike and non-spike waveforms of left internal mammary artery(LIMA) were 0 and 5.13%, those of saphenous vein graft(SVG) were 8.59% and 5.79%. As for medium-long term patency, the occlusion rates of spike and non-spike waveforms were 0 and 12.56% for LIMA, and 42.47% and 16.84% for SVG. Regarding hemodynamics, the relative residence time(RRT) and Max Oscillating shear index(MaxOSI) of the LIMA spike waveform were significantly higher than those of the non-spike waveform, and the mean OSI and MaxOSI of the SVG spike waveform were substantially higher than those of the non-spike waveform.ConclusionsSpike waveform slightly reduces the immediate patency of SVG and significantly reduces the medium-long term patency, while no effect on the patency of LIMA is found. In terms of hemodynamics, both LIMA and SVG with spike waveforms exhibit unfavorable hemodynamic conditions within the grafts.

BackgroundOsteosarcoma (OS) has long presented a formidable challenge to human health and well-being. While traditional treatments, such as clinical chemotherapy and surgical intervention, have shown efficacy, they are frequently accompanied by adverse effects and often lead to a poor prognosis.ObjectiveThymoquinone (TQ) is recognized for its antitumor properties; however, the specific molecular mechanisms underlying its effects against OS remain inadequately understood. Emerging evidence suggests a strong correlation between p53 gene deletion and the onset and progression of various human cancers. This study aimed to elucidate the pharmacological targets and anti-OS mechanisms of TQ using systems bioinformatics approaches, including network pharmacology and molecular docking simulations.MethodsA comprehensive screening process identified 23 potential targets associated with the anti-OS effects of TQ. Subsequent bioinformatics analysis identified 8 core targets involved in TQ's anti-OS activity. Enrichment analysis indicated that these core targets modulate a range of biological processes and may influence multiple molecular pathways.ResultsPreliminary in vitro data indicated that TQ effectively reduces OS cell proliferation, induces apoptosis, and downregulates the expression of P53 and HMOX1 proteins.ConclusionOur findings elucidate the molecular mechanisms underlying TQ's effectiveness against OS, highlighting potential apoptosis-related therapeutic targets, such as P53 and CYCLIN D1, for the treatment of OS with TQ.

BackgroundGround reaction force (GRF) and ground reaction moment (GRM) are critical in gait analysis. While force plates provide accurate measurements, they are costly and spatially limiting.ObjectiveThis study aimed to evaluate the reliability and accuracy of GRF and GRM predictions using a feedforward neural network (FNN) integrating infrared camera-based positional data with accelerometer (ACC) data from wearable devices.MethodsEighty participants walked at their usual pace along a 10-meter walkway over force plates. Positional and ACC data of body segments were used to train the FNN to predict GRF and GRM. Prediction accuracy was assessed using multiple metrics, including root mean square error (RMSE) and normalized RMSE (NRMSE).ResultsCombining positional and ACC data improved GRF prediction in all directions (vertical, anterior-posterior, medial-lateral). The combined dataset achieved a correlation coefficient of 0.979 for medial-lateral GRF and an NRMSE of 6.07%. GRM predictions also benefited from ACC integration, especially in the sagittal plane, where R² reached 0.939, outperforming other models. The vertical direction and transverse axis yielded the lowest RMSE and NRMSE.ConclusionsThese findings surpass many previously reported results, demonstrating the superior performance of the proposed model compared with current state-of-the-art methods. The approach offers a cost-effective, flexible alternative to traditional force plates for clinical and sports assessments.

This study simulated valproic acid (VPA) physiological pharmacokinetics for epilepsy patients via a refined seven-compartmental model. The seven compartments were defined as oral, GI Tract, liver, whole body (WB), cerebrospinal fluid (CSF), kidney, and bladder. A first-order system of seven differential equations was defined according to this specific model and solved by a self-developed program run in MATLAB to evaluate the VPA time-dependent change among compartments. Each compartment's preset dissolving half-life (in hours) was as follows: oral 0.05, GI Tract 0.10, liver 0.5, WB 2.2, CSF 0.8, kidney 1.2, and bladder 0.5, respectively. The derived results were reorganized according to various presets of dissolving half-lives of the liver, WB, CSF, or kidney to analyze the VPA time-dependent changes under various scenarios. Either the liver or WB was the dominant compartment in this model, which mainly controlled the VPA changes. In contrast, others compartments followed the principle of secular equilibrium in the chain decay of radioactive nuclides. Accordingly, the VPA degradation changes in WB ("mother" compartment) mainly affected the VPA changes in other ("daughter") compartments. Thus, the predicted VPA degradation in CSF, kidney, or bladder was always longer than in WB despite its dissolving half-life changes. The predicted results of VPA changes in various compartments were also compared with other studies, and a reasonable agreement was reached on whether the dissolving half-life of the liver or WB ranged from the original 0.2/2.2 to 1.4/0.9 h. The programable capability of this self-developed program allows one to easily modify the primary preset to comply with findings from other studies and has great potential in similar applications.

BackgroundThe cross-organ regulatory relationship between the lung and brain has been suggested. However, the causal associations between lung function and brain neuronal activity remain unclear.ObjectiveIn this study, we aimed to investigate this association using univariable Mendelian randomization (UVMR) and multivariable Mendelian randomization (MVMR) analyses.MethodsWe utilized summary data from genome-wide association studies of European ancestry for three lung function indicators (n = 400,102), including peak expiratory flow (PEF), forced expiratory volume in 1 s (FEV₁), and forced vital capacity, and 68 brain regional neuronal activity amplitude traits (NAATs) (n = 34,691). The inverse-variance weighted method was employed to obtain main causal estimates. Sensitivity analyses were performed.ResultsIn the UVMR analysis, we showed 23 causal associations, including 21 associations with PEF and 2 with FEV₁. The MVMR analysis revealed eight causal associations between PEF and NAATs. These associations were observed across multiple regions, mainly in the precuneus, middle and inferior frontal gyrus, superior and middle occipital gyrus, superior parietal gyrus, inferior parietal lobule, postcentral gyrus, and crus I and II of the cerebellar hemispheres. Among these, causal associations between PEF and the NAAT of the middle occipital gyrus and precuneus (β = -0.146, P = 0.024) and the NAAT of the middle frontal gyrus and crus I and II of the cerebellar hemispheres (β = -0.139, P = 0.024) were observed.ConclusionsWe demonstrated the genetically predicted causal effects of PEF on brain neuronal activity. Closely monitoring PEF reductions in patients with lung disease may be critical for promptly detecting abnormal brain function.

BackgroundSchizophrenia (SCZ) pharmacotherapy relies on Western medications with limited efficacy/significant adverse effects. Baicalin (BA), a purified botanical monomer, shows promise as a safer multitarget antipsychotic candidate.ObjectiveTo study the effect and mechanism of Baicalin on MK-801 induced schizophrenia model mice.MethodsBehavioral assessments (water maze, open field, dark avoidance, forced swimming tests) evaluated emotional/cognitive functions in MK-801 induced schizophrenia mice. Histological staining analyzed hippocampal, prefrontal cortical, and striatal morphology. Serum inflammatory markers (NF-κB, IL-6, IL-1β, TNF-α) and oxidative stress indicators (SOD, MDA) were quantified by ELISA, alongside hippocampal neurotransmitter levels (DA, 5-HT, GABA, AChE). This study employed a network pharmacology approach to screen the mechanisms of action of baicalin in the treatment of schizophrenia. Western blotting determined hippocampal PI3K/Akt/GSK3β pathway protein expression.ResultsNetwork pharmacology analysis revealed that baicalin may exert its therapeutic effects in the treatment of schizophrenia through modulation of the PI3K-Akt signaling pathway. Versus model group, BA doses significantly decreased: IL-1β, IL-6, GABA, AChE, MDA, TNF-α, NF-κB; open field total distance; forced swimming immobility; dark avoidance errors (p < 0.05). Increased: DA, 5-HT; water maze platform crossings; dark avoidance latency (p < 0.05). Staining confirmed BA reduced cerebral oxidative stress/neuroinflammation. Western blot showed dose-dependent elevation of p-Akt/Akt and p-GSK3β/GSK3β ratios.ConclusionBaicalin may improve cognitive impairments in MK801-induced schizophrenia model mice through the PI3K/Akt/GSK3β signaling pathway, exhibiting anti-neuroinflammatory and neuroprotective effects.

BackgroundNear-infrared (NIR) imaging technology has been increasingly applied in clinical and biomedical engineering fields for subcutaneous vein detection and vascular guidance. However, most existing systems still face limitations such as inconsistent visualization under various skin tones and difficulties in achieving real-time projection alignment.ObjectiveThe objective of this study is to develop a near-infrared (NIR)-based vascular detection system and to evaluate its performance.MethodsThe developed system provides intuitive visualization by projecting vascular images in real time onto the same skin region. Performance validation was conducted using a vascular model and the abdominal vessels of rabbits.ResultsIn the vascular model experiment, the localization accuracy was 98.9%, and in the rabbit experiment, the detection success rate for vessels with a diameter of ≥1 mm was 100%.ConclusionsThe proposed method was confirmed to reduce the time required for acquiring anatomical knowledge and to minimize complications by preventing incorrect venipuncture.

BackgroundExtracellular matrix (ECM) stiffness is increasingly recognized as a key pathological factor in musculoskeletal and aging-related disorders. Although cell-based therapies-particularly mesenchymal stem cells (MSCs)-hold regenerative potential, their effectiveness is significantly reduced in fibrotic and mechanically rigid environments.ObjectiveThis review compares ECM-targeted and cell-based therapies, with a focus on their mechanistic basis, limitations, and potential for integration in regenerative strategies.SummaryPathological ECM stiffening, driven by lysyl oxidase (LOX)-mediated collagen crosslinking, chronic inflammation, and Piezo channel activation, alters cell-matrix interactions and promotes tissue degeneration. Therapeutic interventions such as LOX inhibitors, low-intensity pulsed ultrasound (LIPUS), and antifibrotic agents show promise in reversing matrix rigidity and restoring tissue biomechanics. In contrast, the success of MSC therapies is often hindered by impaired viability, reduced paracrine activity, and disrupted immunomodulation in stiffened ECM. Mechanosensitive pathways-including YAP/TAZ, integrins, and Piezo1/2-play critical roles in mediating this dysfunction.ConclusionEffective tissue regeneration requires a permissive mechanical and biochemical microenvironment. Rather than treating ECM remodeling as ancillary, it should be prioritized as a foundational therapeutic target. Preconditioning the ECM enhances the efficacy of cell-based therapies, suggesting that matrix normalization is essential for long-term regenerative success. Targeting ECM stiffness may therefore represent the most decisive step in overcoming barriers to musculoskeletal and aging-related tissue repair.