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BackgroundFall risk prediction is crucial for preventing falls in patients with cerebral small vessel disease (CSVD), especially for those with gait disturbances. However, research in this area is limited, particularly in the early, asymptomatic phase. Wearable sensors offer an objective method for gait assessment. This study integrating wearable sensors and machine learning, aimed to predict fall risk in patients with covert CSVD.MethodsWe employed soft robotic exoskeleton (SRE) to acquire gait characteristics and surface electromyography (sEMG) system to collect sEMG features, constructing three datasets: gait-only, sEMG-only, and their combination. Using Support Vector Machine (SVM), Random Forest (RF), Gradient Boosting Decision Tree (GBDT), and Neural Network (NN) algorithms, we developed twelve predictive models. Furthermore, we integrated the selected baseline data and imaging markers with the three original datasets to create three new integrated datasets, and constructed another twelve optimized predictive models using the same methods. A total of 117 participants were enrolled in the study.ResultsOf the 28 features, ANOVA identified 10 significant indicators. The Gait & sEMG integration dataset, analyzed using the SVM algorithm, demonstrated superior performance compared to other models. This model exhibited an area under the curve (AUC) of 0.986, along with a sensitivity of 0.909 and a specificity of0.923, reflecting its robust discriminatory capability.ConclusionThis study highlights the essential role of gait characteristics, electromyographic features, baseline data, and imaging markers in predicting fall risk. It also successfully developed an SVM-based model integrating these features. This model offers a valuable tool for early detection of fall risk in CSVD patients, potentially enhancing clinical decision-making and prognosis.

Abstract Posttraumatic osteoarthritis (PTOA) is closely related to the inflammatory response caused by mechanical injury and leads to joint degeneration. Herein, we aimed to evaluate the role and underlying mechanism of NUMB in PTOA progression. Anterior cruciate ligament transection (ACLT)-induced rats and interleukin (IL)-1β-treated chondrocytes were used as in vivo and in vitro models of PTOA, respectively. The NUMB overexpression plasmid (pcDNA-NUMB) was administered by intra-articular injection to PTOA model rats, and safranin O-fast green staining, the Osteoarthritis Research Society International (OARSI) scoring system, and HE staining were used to evaluate the severity of cartilage damage. The secretion of inflammatory cytokines (TNF-α, IL-1β, and IL-6) and chondrocyte-specific markers (MMP13 and COL2A1) was detected via ELISA. Cell viability and apoptosis were evaluated by MTT and TUNEL assays. NUMB was expressed at lower levels in ACLT-induced PTOA rats and in IL-1β-treated chondrocytes than in control rats and cells. NUMB overexpression enhanced cell viability and reduced cell apoptosis, inflammation and cartilage degradation in chondrocytes stimulated by IL-1β. NUMB bound to BTRC to promote p-IκBα expression, resulting in NF-κB pathway inactivation. BTRC overexpression reversed the promoting effect of NUMB overexpression on cell viability and the inhibitory effects of NUMB overexpression on apoptosis, inflammation and cartilage degradation in IL-1β-induced chondrocytes. In addition, overexpression of NUMB alleviated articular cartilage damage by repressing inflammation and cartilage degradation in ACLT-induced PTOA rats. Our data indicated that NUMB regulated PTOA progression through the BTRC/NF-κB pathway, which may be a viable therapeutic target in PTOA.

Context AMD3100, a CXCR4 antagonist, has beneficial effects immaculate in the treatment of acute lung injury (ALI). Objective ALI is a severe inflammatory condition associated with poor prognosis and limited treatment options. AMD3100, has therapeutic effects that reduce ALI. Our study explored the regulatory mechanisms of AMD3100 in alleviating the injury of lipopolysaccharide (LPS)-induced ALI in mice. Materials and Methods Male ICR mice were randomly divided into control, LPS-treated, AMD3100-treated, and LPS + AMD3100-treatment groups. The histological changes of lung tissues from different groups were evaluated using hematoxylin and eosin staining. Lung injury was measured by ELISA and lung wet/dry ratio. Moreover, lung tissues from the four groups were subjected to transcriptome sequencing followed by differential expression, functional enrichment, protein-protein interaction (PPI) networks, and transcription factor analyses. The validation of mRNAs and protein levels were conducted with qRT-PCR and ELISA. Results Hematoxylin and eosin staining combined with the concentration of IL-1 and IL1-β and lung wet/dry ratios revealed that AMD3100 reduced the level of LPS-induced lung injury. Analysis of the transcriptome sequencing data identified 294 differentially expressed genes in the LPS-induced ALI mouse model. Based on the PPI network and module analysis, hub targets of AMD3100, such as Cxcl10 and Cxcl9, were identified in module 1, and hub targets, such as Cxcl12 and Cxcl1, were identified in module 2. Cxcl10 and Cxcl9 are involved in the Toll-like receptor signaling pathway, and Cxcl12 and Cxcl1 arae enriched in the nuclear factor-kappa B signaling pathway. Cxcl19, Cxcl10, and Cxcl1 are targeted by transcription factors like NF-κB. The validation of mRNAs and protein levels conducted by PCR and ELISA supported our transcriptome data. Conclusions Our findings indicate that AMD3100 may exhibit a therapeutic effect on LPS-induced ALI in mice by modulating multiple chemokines to inhibit the Toll-like receptor/nuclear factor-kappa B signaling pathway.

Background Sepsis is a significant contributor to both intensive care unit (ICU) admissions and mortality among patients in ICU, with a rising prevalence of obesity. There is a lack of extensive research on the correlation between TyGI and findings in patients with sepsis, especially in obese patients.Methods This study used a retrospective cohort design and included patients with sepsis (≥18 years) from the Medical Information Mart for Intensive Care IV database. The association between TyGI and outcome was examined using multivariable logistic regression analysis.Results 8,840 patients with sepsis were included in the analysis. The in-ICU mortality rate was 9.7%. Non-survivors exhibited significantly greater TyGI levels than survivors [9.19(8.76–9.71) vs. 9.10(8.67–9.54), p

BackgroundThe choice of postoperative weight bearing protocol after uncemented total hip arthroplasty (THA) remains controversial. The aim of this study was to assess the efficacy and safety of immediate unrestricted weight bearing (UWB) compared with partial weight bearing (PWB) in patients undergoing uncemented THA.MethodsRelevant articles were retrieved from electronic databases. Both randomized controlled trials (RCTs) and non-RCTs were included but analyzed separately. All functional and clinical outcomes with at least 2 independent study outcomes were meta-analyzed.ResultsA total of 17 studies were investigated. No adverse effect was found regarding micromotion of the femoral stem with immediate UWB following uncemented THA. There was also no correlation between immediate UWB and failure of ingrowth fixation and higher risks of femoral stem subsidence and surgical revision in RCTs. Harris hip score was better in patients with immediate UWB than those with PWB at 1 year post surgery, but the difference was not statistically significant.ConclusionsImmediate UWB did not have extra harm compared with PWB in patients undergoing uncemented THA. UWB was not superior to PWB. Considering the improvement of Harris score and the compliance of patients, UWB can be encouraged in THA rehabilitation.

Context Salidroside, a compound extracted from Rhodiola rosea L. (Crassulaceae), possesses many beneficial pathological effects. Objective To explore the effect of salidroside on ventilator-induced lung endothelial dysfunction in vivo and in vitro. Materials and methods In vivo, male ICR mice were divided into sham, ventilation, salidroside, and ventilation plus salidroside groups. The mice were ventilated for 4 h, salidroside (50 mg/kg) was administrated intraperitoneally before ventilation, dexamethasone (Dex) (5 mg/kg) was used as a positive control. In vitro, mouse lung vascular endothelial cells (MLVECs) were treated with salidroside, MMP-9 siRNA, and BAY11-7082 (10 μM), and then exposed to cyclic stretch for 4 h. Afterward, lung tissues and MLVECs were collected for further analysis. Results Salidroside pre-treatment significantly reversed the expression of vascular endothelial cadherin (VE-cadherin) and zonula occluden-1 (ZO-1) proteins in cyclic stretch-treated MLVECs (0.46 ± 0.09 vs. 0.80 ± 0.14, 0.49 ± 0.05 vs. 0.88 ± 0.08) and ventilated lung tissues (0.56 ± 0.06 vs. 0.83 ± 0.46, 0.49 ± 0.08 vs. 0.80 ± 0.12). The results further indicated that salidroside inhibited the expression of matrix metalloproteinase-9 (MMP-9), whereas knockdown of its expression restored the expression levels of VE-cadherin (0.37 ± 0.08 vs. 0.85 ± 0.74) and ZO-1 (0.48 ± 0.08 vs. 0.81 ± 0.11) in stretched MLVECs. Meanwhile, salidroside inhibited the NF-κB signalling pathway and alleviated lung injury. Conclusions Salidroside protected against stretch-induced endothelial barrier function, improving lung injury after ventilation. Thus, salidroside may be a promising therapeutic agent for patients with MV-induced lung injury.

Background: Salidroside (SDS) is the main effective ingredient of Rhodiola rosea L with a variety of pharmacologic properties. We aim to investigate the effects of SDS on ventilation induced lung injury (VILI) and explore the possible underlying molecular mechanism. Methods: Lung injury was induced in male ICR mice via mechanical ventilation (30 ml/kg) for 4h. The mice were divided in four groups:(1) Control group; (2) Ventilation group; (3) SDS group; (4) Ventilation with SDS group. SDS (50 mg/kg) was injected intraperitoneally 1h before operation. Mouse lung vascular endothelial cells (MLVECs) were subjected to cyclic stretch for 4h. Results: It was found that SDS attenuated VILI as shown in HE staining, cell count and protein content levels in BAL fluid, W/D and Evans blue dye leakage into the lung tissue. SDS treatment inhibited the activation of NLRP3 inflammasome and subsequent caspase-1 cleavage as well as interleukin (IL)-1β secretion both in vivo and in vitro. Moreover, SDS administration up-regulated SIRT1 expression. Importantly, knockdown of SIRT1 reversed the inhibitory effect of SDS on NLRP3 inflammasome activation. Conclusions: Taken together, these findings indicate that SDS may confer protection against ventilation induced lung injury via SIRT1-de-pendent inhibition of NLRP3 inflammasome activation.

A battery’s state-of-charge (SOC) can be used to estimate the mileage an electric vehicle (EV) can travel. It is desirable to make such an estimation not only accurate, but also economical in computation, so that the battery management system (BMS) can be cost-effective in its implementation. Existing computationally-efficient SOC estimation algorithms, such as the Luenberger observer, suffer from low accuracy and require tuning of the feedback gain by trial-and-error. In this study, an algorithm named lazy-extended Kalman filter (LEKF) is proposed, to allow the Luenberger observer to learn periodically from the extended Kalman filter (EKF) and solve the problems, while maintaining computational efficiency. We demonstrated the effectiveness and high performance of LEKF by both numerical simulation and experiments under different load conditions. The results show that LEKF can have 50% less computational complexity than the conventional EKF and a near-optimal estimation error of less than 2%.

Growing research reveals that circular RNAs (circRNAs) play a major part in the progression and development of cancer. Here, we investigated the oncogenic function and regulatory mechanisms of the circRNA circACTN4 in hepatocellular carcinoma (HCC), particularly in the tumor epithelial-mesenchymal transition (EMT). In vitro functional assays (Cell Counting Kit 8, TUNEL, scratch wound healing, and invasion assays) of HCC cell lines, alongside in vivo analyses of subcutaneous tumors in nude model mice, were employed to assess the impact of circACTN4 on HCC proliferation. Interactions concerning circACTN4, microRNA (miR)-424-5p, and non-SMC condensing I complex subunit G (NCAPG) have been assessed deploying luciferase reporter assays and also quantitative reverse transcription PCR investigation of circACTN4 transcripts in HCC tissues. Findings indicated a high expression of circACTN4 in HCC, promoted proliferation, while inhibiting apoptosis of HCC cells, and correlated with poor prognosis. Mechanistically, circACTN4 served as a rival internal RNA for miR-424 5p, controlling NCAPG level and initiating the Wnt/β-catenin signaling routes, which in turn impacted the EMT machinery in HCC. According to our surveys, the circACTN4/miR-424 5p/NCAPG axis could be an intriguing candidate for therapy to address the treatment of HCC. [ABSTRACT FROM AUTHOR]