Học Viện Công Nghệ Bưu Chính Viễn Thông Cơ sở TP. Hồ Chí Minh

Detecting new or worsening hypomobility in acute ischemic cerebrovascular patients is challenging, especially when asleep or unattended. This study used a wearable movement acceleration monitoring system to identify changes in these patients, aiming to improve early detection. Continuous bilateral upper limb acceleration data, clinical characteristics, specific treatments, stroke etiology, and in-hospital outcomes were collected from patients. The primary outcome was newly emerging or worsening hypomobility during monitoring. An XGBoost model, trained with synthetic minority oversampling to address class imbalance and validated via 5-fold cross-validation, analyzed movement acceleration features to diagnose hypomobility timing. Model performance was evaluated through AUC and feature importance metrics. From April 2023 to February 2025, 85 patients with acute ischemic cerebrovascular events were enrolled; three were excluded due to data errors. A total of 82 patients were included in the analysis, comprising 76 (92.7%) with ischemic stroke and 6 (7.3%) with transient ischemic attack. Among them, 26 (31.7%) were women. The median monitoring duration was 26.9 hours (IQR: 24.6–46.5), with 15 patients (18.3%) developing hypomobility. The XGBoost model achieved an AUC of 0.975 (95% CI: 0.965–0.985) and a mean AUC of 0.975 (SD 0.003) across folds. Optimized with a learning rate of 0.1, maximum depth of 6, and 200 boosting rounds, the model, at a cutoff of 0.587, recorded an average sensitivity of 0.969 and specificity of 0.900, accurately detecting 96.9% of the hypomobility cases. The overall metrics included a sensitivity of 0.966, specificity of 0.900, positive predictive value of 0.896, negative predictive value of 0.968, and F1-score of 0.930. The SHAP (SHapley Additive exPlanations) analysis revealed the significant contributions of the interaction terms (mean |SHAP| = 3.475) and slope features for movement changes (e.g., 1-min RSMA and LSMA slopes), while elevating the importance of the ‘Likely weak side’ predictor (mean |SHAP| = 2.053) in orienting asymmetry. This wearable movement acceleration monitoring system, by continuously tracking upper limb acceleration data, effectively detects the onset of hypomobility in acute ischemic cerebrovascular patients, highlighting its substantial potential for clinical application in enabling timely interventions and improving patient outcomes.

To investigate the efficacy and safety of Cerebrolysin and Cerebrolysin plus nootropics in the routine treatment of patients with acute ischemic stroke (AIS). Acute ischemic stroke (AIS) is a leading cause of disability with unmet treatment needs lacking effective drug therapy. Multimodal drugs modulating stroke pathophysiology as Cerebrolysin constitute a good therapeutic option. In this study, we assessed the effects of Cerebrolysin and Cerebrolysin plus nootropics, in comparison with other nootropic drugs alone, on functional, neurological and cognitive recovery of patients with AIS in Vietnam. This non-interventional, controlled, open-label, prospective and multicenter study included 398 AIS patients (234 males) treated with Cerebrolysin (n=190; 20 i.v. infusions of 10 ml), other nootropics (comparator group; n=86), or a combination of both (n=122). The study primary endpoint was the modified Ranking Scale (mRS) score on day 90. Secondary endpoints included study-period change in NIHSS score; percentage of well-recovered (mRS 0-2) patients, the proportion of good NIHSS response (≥6 points) cases, and MoCA scores at day 90; and safety indicators. Compared with other nootropics, both Cerebrolysin and combined therapy induced significant improvements (p<0.001) in: Functional recovery (mRS scores); percentage of well-recovered patients (Cerebrolysin: 81.6%; combination: 93.4%; comparator: 43.0%); neurological recovery (study- period NIHSS change); proportion of good NIHSS responders (Cerebrolysin: 77.5%; combination: 92.5%; comparator: 47.6%); and MoCA scores (Cerebrolysin: 23.3±4.8; combination: 23.7±4.1; comparator: 15.9±7.7). Compared to Cerebrolysin, combined therapy improved (p<0.01) mRS outcomes and NIHSS change, but not MoCA scores, in moderate-severe stroke (NIHSS>11) cases only. No drug-related adverse events were reported. Cerebrolysin alone or combined with other nootropics was effective and safe in routine AIS treatment, during both acute and recovery phases, which supports its use in daily clinical practice. Others: According to the results of this multicenter study, the importance of reducing differences in the treatment regimens of AIS in Vietnam should be further emphasized.

Inhibition of histone deacetylases (HDACs) attenuates cardiac fibrosis. In this study, we evaluated whether the inhibition of class I HDACs can attenuate angiotensin II (ANG II)-induced fibrogenesis and mitochondrial malfunction through its effects on reactive oxygen species (ROS) and calcium dysregulation in human cardiac fibroblasts (CFs). Seahorse XF24 extracellular flux analyser, fluorescence staining, Western blotting, HDAC activity assays and Transwell migration assay were used to study mitochondrial respiration, adenosine triphosphate (ATP) production, mitochondrial calcium uptake and ROS, HDAC expression and activity and fibroblast activity in CFs without (control) or with ANG II (100nM) and/or MS-275 (HDAC class 1 inhibitor, 10μM) for 24h. ANG II increased HDAC activity without changing protein expression in CFs. Compared with controls, ANG II-treated CFs had greater migration activity, higher ATP production, maximal respiration and spare capacity with higher mitochondrial Ca2+ uptake and ROS generation, which was attenuated by the administration of MS-275. ANG II activated CFs by increasing mitochondrial calcium content and ATP production, which may be caused by increased HDAC activity. Inhibition of HDAC1 attenuated the effects of ANG II by reducing mitochondrial ROS generation and calcium overload. Modulating mitochondrial function by regulation of HDAC may be a novel strategy for controlling CF activity.

Introduction: Acute coronary syndrome (ACS) is caused by rupture of coronary plaques. What triggers these ruptures? Hypothesis: In the field of hydraulics, in a setting of a tank and draining pipe, if the valve at the distal end of the pipe is open, the fluid flows normally. If the valve closes abruptly, the flow next to the valve stops. However the fluid from the tank continues to flow forward and can collide with the distal stationary fluid. This is called water hammer shock. Could the same event happen in coronary arteries? The contraction of the left ventricle (LV) is similar to the abrupt closure of a valve, stopping the myocardial capillary flow. Could the systolic LV contraction trigger water hammer shock? Methods: Angiograms with culprit lesions of ACS (recorded at 15 images/second or 0.06 second per image) were reviewed. The first image was of the artery completely filled with contrast. The subsequent images showed the blood in white color blood moving in over a background of black contrast. The normal flow was laminar. When there was retrograde on top of turbulent flow, this was evidence of a collision between antegrade and retrograde flow (or water hammer shock). The measurements by visual angiographic evaluation and by Machine Learning (ML) included (1) the duration and (2) size of coronary segment with turbulence. The ML program had 2 models (build on Python). Model 1 was built based on U-net and Densenet-121 for vessel segmentation. Model 2 was used for classification of flow. The model 2 was trained based on the convolutional neural network. Results: Angiograms of 20 ACS patients showed laminar flow (90%) in diastole. The flow became turbulent during systole with retrograde flow. The area of collision or water hammer shock showed diffuse coarse mixing of black (contrast) and white (blood). The presence of turbulence matched the location of 85% of ruptured plaques. The duration of turbulence lasted 80% of systole. Special protocols were used successfully to train AI to recognize the lesions, retrograde and turbulent flow. Conclusions: With the new angiographic technique, detailed images of water hammer shock matched the location of ruptured plaques in ACS patients. These results may help to understand the genesis and offer precise prevention and treatment for ACS