A hybrid method for real-time stimulation artefact removal during functional electrical stimulation with time-variant parameters.

Objective. In this study, a hybrid method combining hardware and software architecture is proposed to remove stimulation artefacts (SAs) and extract the volitional surface electromyography (sEMG) in real time during functional electrical stimulations (FES) with time-variant parameters.Approach. First, an sEMG detection front-end (DFE) combining fast recovery, detector and stimulator isolation and blanking is developed and is capable of preventing DFE saturation with a blanking time of 7.6 ms. The fragment between the present stimulus and previous stimulus is set as an SA fragment. Second, an SA database is established to provide six high-similarity templates with the current SA fragment. The SA fragment will be de-artefacted by a 6th-order Gram-Schmidt (GS) algorithm, a template-subtracting method, using the provided templates, and this database-based GS algorithm is called DBGS. The provided templates are previously collected SA fragments with the same or a similar evoking FES intensity to that of the current SA fragment, and the lengths of the templates are longer than that of the current SA fragment. After denoising, the sEMG will be extracted, and the current SA fragment will be added to the SA database. The prototype system based on DBGS was tested on eight able-bodied volunteers and three individuals with stroke to verify its capacity for stimulation removal and sEMG extraction.Results.The average stimulus artefact attenuation factor, SA index and correlation coefficient between clean sEMG and extracted sEMG for 6th-order DBGS were 12.77 ± 0.85 dB, 1.82 ± 0.37 dB and 0.84 ± 0.33 dB, respectively, which were significantly higher than those for empirical mode decomposition combined with notch filters, pulse-triggered GS algorithm, 1st-order and 3rd-order DBGS. The sEMG-torque correlation coefficients were 0.78 ± 0.05 and 0.48 ± 0.11 for able-bodied volunteers and individuals with stroke, respectively.Significance.The proposed hybrid method can extract sEMG during dynamic FES in real time.

BDNF corrects NLRP3 inflammasome-induced pyroptosis and glucose metabolism reprogramming through KLF2/HK1 pathway in vascular endothelial cells.

NLRP3 inflammasome-mediated vascular EC pyroptosis is a key event in the pathogenesis of atherosclerosis. Dysregulation of glucose metabolism is involved in EC dysfunction. Although BDNF plays a protective role in vascular endothelium physiological activity, the mechanisms underlying this activity are not yet clear. In this study, we investigated the role of BDNF in NLRP3 inflammasome-mediated EC pyroptosis and its associated reprogramming of glucose metabolism. HUVECs were treated with human rBDNF under ox-LDL stimulation. rBDNF alleviated ox-LDL-induced NLRP3 inflammasome formation and HUVEC pyroptosis, as evaluated by NLRP3, caspase1-p10, interleukin-18, and interleukin-1ß protein levels, co-localization of NLRP3 and apoptosis-associated speck-like protein, and lactate dehydrogenase release. These effects were prevented by tropomyosin receptor kinase B inhibition and KLF2 silencing. The hyper-activation of glycolysis induced by ox-LDL-induced was mitigated by rBDNF via KLF2 as assessed by glucose uptake, lactate production, and extracellular acidification rate. In addition, the BDNF/KLF2 pathway preserved the mitochondrial membrane potential, intracellular reactive oxygen species generation, electron transport chain processing, oxygen consumption rate, and adenosine triphosphate production. Furthermore, KLF2 interacted with HK1 and HK1 overexpression evoked NLRP3 inflammasome formation. At the clinical level, plasma BDNF and lactate levels were measured in 274 patients who underwent computed tomography and coronary angiography for CAD diagnosis. Patients with CAD had lower BDNF and increased lactate levels than those without CAD. In 94 patients with CAD, circulating BDNF levels were inversely associated with lactate levels. In the receiver operating characteristic analysis of CAD, the areas under the curves for 1/BDNF, lactate, and 1/BDNF+lactate were 0.707, 0.702, and 0.753 respectively. These results indicate that BDNF and lactate are linked in atherosclerotic patients, and BDNF inhibits ox-LDL induced NLRP3 inflammasome formation and pyroptosis in HUVECs via KLF2/HK1-mediated glucose metabolism modulation and mitochondrial homeostasis preservation.

Involvement of brain-derived neurotrophic factor in exercise­induced cardioprotection of post-myocardial infarction rats.

Exercise induces a number of benefits, including angiogenesis in post­myocardial infarction (MI); however, the underlying mechanisms have not been fully clarified. Neurotrophic brain­derived neurotrophic factor (BDNF) serves a protective role in certain adult cardiac diseases through its specific receptor, BDNF/NT­3 growth factors receptor (TrkB). The present study explored the mechanisms by which exercise improves cardiac function, with a focus on the involvement of the BDNF/TrkB axis. MI rats were assigned to Sham, sedentary, exercise, exercise with K252a (a TrkB inhibitor), and exercise with NG­nitro­L­arginine methyl ester (L­NAME) groups. The exercise group was subjected to 8 weeks of treadmill running. The results demonstrated that the rats in the exercise group exhibited increased myocardial angiogenesis and improved cardiac function, which was attenuated by K252a. Exercise induced activation of the BDNF/TrkB axis in the ischaemic myocardium and increased serum BDNF levels were abated by exposure to L­NAME. Improvements in angiogenesis and left ventricular function exhibited a positive association, with changes in serum BDNF. In the in vitro experiments, human umbilical vein endothelial cells were exposed to shear stress (SS) of 12 dyn/cm2 to mimic the effects of exercise training on vascular tissue. An increased tube­forming capacity, and a nitric oxide (NO)­dependent prolonged activation of the BDNF/TrkB­full­length axis over 12 h, but not the TrkB­truncated axis, was observed. The SS­related angiogenic response was attenuated by TrkB inhibition. Overall, these results demonstrate that exercise confers certain aspects of its cardioprotective effects through the activation of the BDNF/TrkB axis in an NO­dependent manner, a process in which fluid­induced SS may serve a crucial role.