This paper presents a versatile multi-sensor fusion method and decision-making algorithm for ambulatory and continuous patient monitoring purposes via a body sensor network (BSN). Gait features including spatio-temporal parameters, gait asymmetry, and regularity were identified and estimated from individual patients data collected from clinical trials. Hence, a continuous assessment and diagnosis of the improvement or the deterioration of the lower limb rehabilitation process is ensured. The experimental results from 10-m free walking trials indicated that the proposed method has a good consistency with the clinically used observational method. The gait assessment results were comparable with previous studies. Gait segmentation succeed even when the pace deviates significantly from the healthy subjects' reference value, which provides proof of objectivity and effectiveness of this preliminary research, namely, using wearable inertial measurement unit (IMUs) as an indicator to detect gait abnormality in subjects with neurological disorders. The hypothesis of gait quality-related clinical trials were designed and validated via both machine learning approach and feature layer data fusion. With further validations, the proposed inertial sensor-based gait assessment approach has the potential to be applied both routinely in clinical practice and for tele-health scenes such as fall detection of the elder at home.
BackgroundPlatycodin D (PD) is one of the major bioactive components of the roots of Platycodon grandiflorum and possesses multiple biological and pharmacological properties, such as antiviral, anti-inflammatory, and anti-cancer activities. However, whether it affects platelet function remains unclear. This study aims to evaluate the role of PD in platelet function and thrombus formation.MethodsPlatelets were treated with PD followed by measuring platelet aggregation, activation, spreading, clot retraction, expression of glycoprotein receptors. Moreover, mice platelets were treated with PD and infused into wild-type mice for analysis of in vivo hemostasis and arterial thrombosis.ResultsPlatycodin D treatment significantly inhibited platelet aggregation in response to collagen, ADP, arachidonic acid and epinephrine, reduced platelet P-selectin expression, integrin αIIbβ3 activation, spreading on fibrinogen as well as clot retraction, accompanied with decreased phosphorylation of Syk and PLCγ2 in collagen-related peptide or thrombin-stimulated platelets. Moreover, PD-treated mice platelets presented significantly impaired in vivo hemostasis and arterial thrombus formation. Interestingly, PD induced internalization of glycoprotein receptors αIIbβ3, GPIbα and GPVI. However, GM6001, cytochalasin D, BAPTA-AM and wortmannin did not prevent PD-induced internalization of receptors.ConclusionsOur study demonstrates that PD inhibits platelet aggregation, activation and impairs hemostasis and arterial thrombosis, suggesting it might be a potent anti-thrombotic drug.
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