Technology and Health Care最新文献

BackgroundAcupoint thread embedding treatment (ATET) is a traditional therapeutic approach used in stroke rehabilitation.ObjectiveTo explore the application of ATET in combination with modern medical technology, examining its effects on neurological function and key serum biomarkers in stroke patients.MethodsA total of 108 stroke patients were randomly assigned to ATE treatment group (n = 52) and Control Group (n = 56). Various parameters including baseline characteristics, levels of inflammatory markers, macrophage efferocytosis-related factors, the National Institutes of Health Stroke Scale (NIHSS) scores, therapeutic efficacy, and adverse events were assessed and compared between the two groups.ResultsA significant improvement in NIHSS scores was observed in the treatment group compared to the control group. Additionally, serum levels of SIRT1, HIF-1α, and macrophage efferocytosis-related factors were significantly altered, suggesting that ATET may influence biological pathways involved in stroke recovery.ConclusionThe application of ATET, supported by advanced diagnostic technologies, shows promising effects in stroke rehabilitation. This study highlights the potential for integrating traditional therapies with modern medicine to improve clinical outcomes in stroke patients.

BackgroundMagnetic Resonance Imaging (MRI) is a cornerstone in diagnosing brain tumors. However, the complex nature of these tumors makes accurate segmentation in MRI images a demanding task.ObjectiveAccurate brain tumor segmentation remains a critical challenge in medical image analysis, with early detection crucial for improving patient outcomes.MethodsTo develop and evaluate a novel UNet-based architecture for improved brain tumor segmentation in MRI images. This paper presents a novel UNet-based architecture for improved brain tumor segmentation. The UNet model architecture incorporates Leaky ReLU activation, batch normalization, and regularization to enhance training and performance. The model consists of varying numbers of layers and kernel sizes to capture different levels of detail. To address the issue of class imbalance in medical image segmentation, we employ focused loss and generalized Dice (GDL) loss functions.ResultsThe proposed model was evaluated on the BraTS'2020 dataset, achieving an accuracy of 99.64% and Dice coefficients of 0.8984, 0.8431, and 0.8824 for necrotic core, edema, and enhancing tumor regions, respectively.ConclusionThese findings demonstrate the efficacy of our approach in accurately predicting tumors, which has the potential to enhance diagnostic systems and improve patient outcomes.

BackgroundThis study was designed to investigate the mechanism of Circ_0046336 in oral squamous cell carcinoma (OSCC).MethodsThe expression pattern of Circ_0046336 and its distribution in OSCC cell lines (SCC-9 and CAL-27) were identified. Fluorescence in situ hybridization was applied to determine the location of Circ_0046336. Circ_0046336 silencing was detected by methylthiazolyldiphenyl-tetrazolium bromide (MTT), flow cytometry and transwell assays. The binding relation between Circ_0046336 and miR-181d-3p or ADAM12 and miR-181d-3p was investigated using bioinformatics and dual luciferase reporter assay. ADAM12 and miR-181d-3p expressions in OSCC cells with Circ_0046336 knockdown were quantified. Rescue assays were carried out, and the expressions of epithelial-mesenchymal transition (EMT)-related proteins were measured via Western blot.ResultsCirc_0046336 was overexpressed and mainly distributed in the cytoplasm of OSCC cells. Circ_0046336 targeted miR-181d-3p and miR-181d-3p targeted ADAM12 in OSCC cells. Circ_0046336 silencing facilitated apoptosis, and suppressed viability, migration and invasion of OSCC cells, while upregulating miR-181d-3p and downregulating ADAM12. MiR-181d-3p deficiency reversed the regulatory role of Circ_0046336 in biological behaviors of OSCC cells. Circ_0046336 silencing promoted E-cadherin expression and inhibited N-cadherin and Vimentin expressions, but such effects were reversed by miR-181d-3p downregulation.ConclusionCirc_0046336 acts as a ceRNA to regulate apoptosis, migration, invasion and EMT of OSCC cells via miR-181d-3p/ADAM12 axis.

BackgroundBortezomib is the first-line drug in the treatment of multiple myeloma (MM) and its resistance is the main obstacle to cure MM. MicroRNA-361-5p (MiRNA-361-5p) in bone marrow mesenchymal stem cells (BMSCs) might participate in the bortezomib resistance via paracrine pathway. The study was to characterize the role and molecular mechanism of miR-361-5p in bortezomib resistance in MM.MethodsThe exosomes of BMSCs were obtained and characterized by transmission electron microscopy and nanoparticle tracking analysis. The MM cell U266 was treated with bortezomib, bortezomib and BMSC exosomes, bortezomib and BMSC exosomes transfected with miR-361-5p inhibitor. The cell viability was measured by cell counting kit. Protein expression of PDPK1, PI3K, p-PI3K, mTOR, p-mTOR, AKT, and Pan-AKT was detected by western blot. The apoptosis level of bortezomib resistant cell lines was detected by flow cytometry.ResultsLow expression of miR-361-5p promoted the survival of U266 cells and inhibited cell apoptosis, reversing the inhibitory effect of bortezomib on U266 cells. PDPK1 may be a downstream target of miR-361-5p. Low expression of BMSCs-derived exosomal miR-361-5p may reverse the effect of bortezomib on U266 cells by regulating the PDPK1/PI3K/AKT/mTOR axis.ConclusionLow expression of BMSCs-derived exosomal miR-361-5p may overcome bortezomib resistance in MM by regulating PDPK1/PI3K/AKT/mTOR axis.

BackgroundDespite its clinical relevance, there is a relative lack of research examining flexibility and stability based on the acceleration or speed of localized limb segments, such as the shank and thigh.ObjectiveThis study aimed to evaluate gait characteristics based on acceleration in the thigh and shank to identify differences between the affected and unaffected sides in stroke hemiplegic patients.MethodForty individuals with stroke-induced hemiplegia were assessed during a 5-meter walk using a 3D motion analysis system and Inertial Measurement Units (IMUs). Spatial-temporal and acceleration parameters were calculated.ResultsSignificant differences were observed between the affected and unaffected sides in stance time, swing time, swing phase, and stance phase. In terms of acceleration, the mean acceleration in the anterior-posterior (AP) direction of the thigh and the mean value of the center of mass (CoM) in the AP direction differed significantly. These spatial-temporal findings were consistent with known characteristics of hemiplegic gait. A notable posterior shift of the thigh CoM on the affected side was identified, likely reflecting impaired propulsion and reduced stability.ConclusionThe posterior displacement of the thigh CoM on the affected side may represent a compensatory mechanism to maintain balance during gait. Clinically, this posterior CoM shift could serve as a meaningful indicator of hemiplegic gait and a potential target for rehabilitation interventions aimed at restoring gait symmetry and improving functional mobility.

ObjectiveThis study aims to enhance cybersecurity by implementing a robust biometric-based authentication approach. A Multimodal Biometric System (MBS) is proposed, utilizing feature-level fusion of human facial (physiological) and speech (behavioral) features to improve security, accuracy, and user convenience. The system addresses the limitations of traditional authentication methods, including unimodal biometrics and password-based security.BackgroundIn the modern digital landscape, human-computer interaction and digital platforms play a crucial role in daily life. With billions of users engaging in social media, financial transactions, and e-commerce, the demand for secure authentication mechanisms has intensified. However, the increasing sophistication of cyber threats poses significant risks, undermining trust, security, and confidence in digital systems.Method: The proposed MBS incorporates improved proposed techniques for feature extraction, feature level fusion strategies and an ensemble classification model combining Bi-LSTM and DCNN. To optimize performance, the system is enhanced using an improved bio-inspired Manta Ray Foraging Optimization (MRFO) algorithm.ResultsThe system's performance was evaluated using two publicly available Voxceleb1 and VidTIMIT datasets, achieving accuracy rates of 98.23% and 97.92%, with Equal Error Rates (EERs) of 3.23% and 3.62%, respectively.ConclusionThe proposed approach outperforms conventional optimization techniques and existing state-of-the-art MBS. As a contactless and non-intrusive authentication system, it enables seamless data acquisition through devices equipped with cameras and microphones, such as smartphones, ensuring real-time processing of biometric modalities.Application: This contactless MBS presents a viable solution for secure and hygienic authentication in applications requiring high cyber resilience, including banking, e-commerce and other digital security domains.Precis/Table of Contents: This research enhances cybersecurity by proposing a Multimodal Biometric System (MBS) that integrates feature-level fusion of facial (physiological) and speech (behavioral) traits. The approach improves security, accuracy, and user convenience while addressing hygiene concerns. It overcomes the limitations of traditional authentication methods, including unimodal biometrics and password-based security vulnerabilities.

BackgroundTargeted regulation of drug-resistant gene expression through lncRNA has emerged as a novel research direction for overcoming immune resistance in osteosarcoma. However, the specific effects and regulatory mechanisms of lncRNA-TIL1H on immune resistance in osteosarcoma remain unclear.ObjectiveTo explore the mechanism by which lncRNA-TIL1H targets the regulation of the drug-resistant genes MDR1 and RAD21.MethodsClinical samples including osteosarcoma tissues and adjacent tissues were collected for qPCR and WB analysis of lncRNA-TIL1H expression as well as MDR1 and RAD21. Acquisition of drug-resistant osteosarcoma cells by cisplatin treatment MG-63/R. The cells were divided into four groups: MG-63, MG-63/R, si-NC-MG-63/R, and si-TIL1H-MG-63/R group. Cell proliferation and colony formation, and migration and invasion were detected by CCK-8, Transwell and scratch assays. In addition, the effects on osteosarcoma after interfering with lncRNA-TIL1H were further explored by the animal experiments, including HE staining and immunohistochemistry.ResultsThe expression of lncRNA-TIL1H and the drug-resistant genes MDR1 and RAD21 significantly increased in osteosarcoma. si-TIL1H effectively inhibited cell proliferation, invasion, migration and decreased the expression of drug-resistant genes in MG-63/R. Finally, the animal experiments revealed that si-lncRNA-TIL1H inhibited tumor proliferation.ConclusionThe expression of lncRNA-TIL1H in MG-63/R promotes the upregulation of drug-resistant genes MDR1 and RAD21, leading to the occurrence of immune resistance and accelerating osteosarcoma progression.

BackgroundRadiotherapy has become a fundamental treatment modality of head and neck (HN) malignancies, which provides a chance of long-term survival. However, radiation also amplifies the risk of developing radiation-induced sarcoma (RIS) in the irradiated tissue. Radiation-induced maxillary sinus sarcoma (RIMSS) is an extremely rare and highly lethal malignancy of the HN. RIS is mainly treated with surgery, but the anatomical district and the infiltrative nature of RIS make it challenging to achieve negative margins, resulting in high fatality rate with the mean survival time of approximately one year. Immunotherapy, as an effective treatment option is rapidly evolving for HN tumors. However, checkpoint Blockade Immunotherapy (CBI) combined with chemotherapy as maintenance therapy for RIS of HN is rarely reported.Case presentationThe study presents a 36-year-old female with numerous recurrences of RIMSS, who experienced a dramatic response to checkpoint blockade immunotherapy after rapidly progressing on involved-field radiotherapy and multiple surgeries. After using immunotherapy combined with chemotherapy, the patient had a nearly complete response (CR) and maintained with single-agent programmed cell death 1 (PD-1) inhibitors.ResultsThe patient achieved a durable response, with progression-free survival (PFS) lasting 18 months.ConclusionUsing CBI as maintenance therapy for RIMSS represents a novel treatment option, especially for unresectable patients. Further investigation is warranted to optimize a multimodal treatment and improve response.

BackgroundCow's milk protein allergy (CMPA) is a common food allergy in children, affecting growth, development, and quality of life. The pathogenesis involves immune dysregulation, particularly CD4+ T lymphocyte subsets, which play a key role in immune responses. The JAK2-STAT3 signaling pathway is critical for immune cell regulation, but its role in CMPA-associated immune changes remains unclear.MethodsA total of 103 CMPA patients and 100 healthy controls were enrolled. Peripheral blood samples were collected from patients before and after a 3-month CMPA avoidance diet. Flow cytometry, ELISA, western blotting, and qRT-PCR were used to analyze CD4+ T cell subsets (Th1, Th2, Th17), cytokine levels, and JAK2-STAT3 pathway activity.ResultsCMPA patients exhibited increased Th2 and Th17 proportions and reduced Th1 cells compared to controls. JAK2 and STAT3 phosphorylation levels were elevated, while SOCS1/SOCS3 expression was downregulated. After dietary avoidance, Th2 and Th17 proportions decreased, Th1 increased, and JAK2-STAT3 activation normalized. Pearson correlation analysis revealed positive associations between JAK2-STAT3 activation and Th2/Th17 proportions and a negative correlation with Th1.ConclusionsThe JAK2-STAT3 signaling pathway is abnormally activated in CMPA and correlates with CD4+ T lymphocyte subset imbalances. Targeting this pathway may offer therapeutic potential for CMPA management.

Background and ObjectiveBudd-Chiari syndrome (BCS) presents challenges in postoperative restenosis risk prediction due to unclear hemodynamic pathophysiology. Despite advances in interventional therapies, tools linking hemodynamic abnormalities to vascular remodeling are lacking. This study aimed to evaluate hemodynamic changes in BCS patients with inferior vena cava (IVC) stenosis using patient-specific MRI and computational fluid dynamics (CFD) to establish predictive biomarkers and optimize management.Methods3D IVC models were reconstructed from preoperative, postoperative, and healthy control MRI data. Dynamic hemodynamic parameters, including flow velocity, pressure gradients, wall shear stress (WSS), and vortex patterns, were analyzed via CFD simulations under physiologically accurate boundary conditions.ResultsPreoperative IVC stenosis caused severe disturbances. Post-intervention, parameters decreased (e.g., peak stenotic velocity from 1.91 m/s to 0.97 m/s; trans-stenotic pressure gradient from 3562 Pa to 1404 Pa) but remained higher than normal (peak velocity: 0.27 m/s; pressure fluctuation: Δ1225 Pa). Persistent vortices near stent edges and incomplete pressure normalization were observed, correlating with restenosis incidence. These findings highlight unresolved WSS (post-op peak WSS: 18.2 Pa vs normal: 6.18 Pa) and abnormal flow dynamics (e.g., prolonged vortex duration) as key recurrence risks.ConclusionThis study provides a hemodynamic framework for BCS, showing that intervention alleviates stenosis but doesn't restore normal flow. Residual stress emphasizes the need for adjunct therapies. The CFD approach offers predictive insights, advocating personalized monitoring for improved BCS outcomes.