Beta rebound reduces subsequent movement preparation time by modulating of GABAA inhibition.

Post-movement beta synchronization is an increase of beta power relative to baseline, which commonly used to represent the status quo of the motor system. However, its functional role to the subsequent voluntary motor output and potential electrophysiological significance remain largely unknown. Here, we examined the reaction time of a Go/No-Go task of index finger tapping which performed at the phases of power baseline and post-movement beta synchronization peak induced by index finger abduction movements at different speeds (ballistic/self-paced) in 13 healthy subjects. We found a correlation between the post-movement beta synchronization and reaction time that larger post-movement beta synchronization prolonged the reaction time during Go trials. To probe the electrophysiological significance of post-movement beta synchronization, we assessed intracortical inhibitory measures probably involving GABAB (long-interval intracortical inhibition) and GABAA (short-interval intracortical inhibition) receptors in beta baseline and post-movement beta synchronization peak induced by index finger abduction movements at different speeds. We found that short-interval intracortical inhibition but not long-interval intracortical inhibition increased in post-movement beta synchronization peak compared with that in the power baseline, and was negatively correlated with the change of post-movement beta synchronization peak value. These novel findings indicate that the post-movement beta synchronization is related to forward model updating, with high beta rebound predicting longer time for the preparation of subsequent movement by inhibitory neural pathways of GABAA.

Anesthetic management of a pediatric patient with methylmalonic acidemia combined with hyperhomocysteinemia: A case report.

Methylmalonic acidemia (MMA) combined with hyperhomocysteinemia is an autosomal recessive genetic disease which can lead to metabolic acidosis, elevated lactate, and high blood ammonia level. This anesthetic management was mainly how to maintain the stable state of perioperative physiological metabolism of such patients.

Effects of dural puncture epidural technique with different drug delivery methods for labor analgesia: A randomized controlled clinical trial.

This study aimed to investigate the effect of dural puncture epidural (DPE) combined with small-dose lidocaine for labor analgesia. Parturients were randomly divided into epidural anesthesia (EA), DPE1, and DPE2 groups. In the EA group, 5 mL of 1% lidocaine was administered via conventional L2-L3 puncture catheterization; in the DPE1 group, epidural drug was administered after catheterization using the DPE technique; in the DPE2 group, epidural puncture drug was administered through the epidural puncture needle before catheterization using the DPE technique. The primary outcome was the onset time of analgesia. The secondary outcomes included the numerical rating scale (NRS) scores during uterine contraction before bolus injection of experimental dose (T0) and the second time (T1), the fifth time (T2) and the tenth time (T3) after bolus injection of experimental dose; NRS scores at the second stage of labor (T4) and during perineal suture (T5); operation time of anesthesia; puncture related complications; anesthesia related complications; delivery outcome; use of local anesthesia during vaginal suture; and Apgar score of the neonates. There were 115 women included. The onset time in the DPE2 group was markedly shorter than in the EA and DPE1 groups (P < .001). The NRS scores in the DEP2 group at T1 and T4 were significantly lower than in the EA and DEP1 groups (P < .001). The overall incidence of puncture related complications in the DEP1 and DEP2 groups was markedly higher than in the EA group (P < .05). In dural puncture epidural analgesia, when the experimental dose was injected directly through the epidural puncture needle, the onset time was shorter and the analgesic effect was better as compared to the injection of test dose after inserting the epidural catheter.

Insufficient GDF15 expression predisposes women to unexplained recurrent pregnancy loss by impairing extravillous trophoblast invasion.

Insufficient extravillous trophoblast (EVT) invasion during early placentation has been shown to contribute to recurrent pregnancy loss (RPL). However, the regulatory factors involved and their involvement in RPL pathogenesis remain unknown. Here, we found aberrantly decreased growth differentiation factor 15 (GDF15) levels in both first-trimester villous and serum samples of unexplained recurrent pregnancy loss (URPL) patients as compared with normal pregnancies. Moreover, GDF15 knockdown significantly reduced the invasiveness of both HTR-8/SVneo cells and primary human EVT cells and suppressed the Jagged-1 (JAG1)/NOTCH3/HES1 pathway activity, and JAG1 overexpression rescued the invasion phenotype of the GDF15 knockdown cells. Induction of a lipopolysaccharide-induced abortion model in mice resulted in significantly reduced GDF15 level in the placenta and serum, as well as increased rates of embryonic resorption, and these effects were reversed by administration of recombinant GDF15. Our study thus demonstrates that insufficient GDF15 level at the first-trimester maternal-foetal interface contribute to the pathogenesis of URPL by impairing EVT invasion and suppressing JAG1/NOTCH3/HES1 pathway activity, and suggests that supplementation with GDF15 could benefit early pregnancy maintenance and reduce the risk of early pregnancy.

Gating at cortical level contributes to auditory-motor synchronization during repetitive finger tapping.

Sensory integration contributes to temporal coordination of the movement with external rhythms. How the information flowing of sensory inputs is regulated with increasing tapping rates and its function remains unknown. Here, somatosensory evoked potentials to ulnar nerve stimulation were recorded during auditory-cued repetitive right-index finger tapping at 0.5, 1, 2, 3, and 4 Hz in 13 healthy subjects. We found that sensory inputs were suppressed at subcortical level (represented by P14) and primary somatosensory cortex (S1, represented by N20/P25) during repetitive tapping. This suppression was decreased in S1 but not in subcortical level during fast repetitive tapping (2, 3, and 4 Hz) compared with slow repetitive tapping (0.5 and 1 Hz). Furthermore, we assessed the ability to analyze temporal information in S1 by measuring the somatosensory temporal discrimination threshold (STDT). STDT increased during fast repetitive tapping compared with slow repetitive tapping, which was negatively correlated with the task performance of phase shift and positively correlated with the peak-to-peak amplitude (% of resting) in S1 but not in subcortical level. These novel findings indicate that the increased sensory input (lower sensory gating) in S1 may lead to greater temporal uncertainty for sensorimotor integration dereasing the performance of repetitive movement during increasing tapping rates.

The pathophysiological nature of sarcomeres in trigger points in patients with myofascial pain syndrome: A preliminary study.

BACKGROUND: Myofascial pain syndrome (MPS) has a high global prevalence and is associated with myofascial trigger points (MTrPs) in taut bands or nodules. Little is known about the aetiology. The current study assessed the pathophysiological characteristics of MTrPs in MPS patients. METHODS: Biopsies of the trapezius muscle were collected from the MTrPs of MPS patients (MTrP group; n = 29) and from healthy controls (control group; n = 24), and their morphologies were analysed via haematoxylin-eosin (H&E) and Masson staining. A protein microarray was used to detect the receptor tyrosine kinase (RTK) family proteins. mRNA and long non-coding RNA (lncRNA) sequencing and analysis were conducted, and immunohistochemistry and Western blotting were used to examine the expression of EphB and Rho family proteins. RESULTS: Abnormally contracted sarcomeres showed enlarged, round fibres without inflammation or fibrosis. An lncRNA-mRNA network analysis revealed activation of muscle contraction signalling pathways in MTrP regions. Among RTK family proteins, 15 exhibited increased phosphorylation, and two exhibited decreased phosphorylation in the MTrP regions relative to control levels. In particular, EphB1/EphB2 phosphorylation was increased on the muscle cell membranes of abnormal sarcomeres. RhoA and Rac1, but not cell division control protein 42 (Cdc42), were activated in the abnormal sarcomeres. CONCLUSIONS: EphB1/EphB2 and RhoA/Rac1 might play roles in the aetiology of abnormally contracted sarcomeres in MTrPs without inflammatory cell infiltration and fibrotic adhesion. SIGNIFICANCE: Contracted sarcomeres were found in MTrP regions, which is consistent with the MTrP formation hypothesis. EphB1/EphB2 and RhoA/Rac1 might play roles in the sarcomere contractile sites of MTrPs, which may be promising therapeutic targets.

Alpha Frequency Intervention by Electrical Stimulation to Improve Performance in Mu-Based BCI.

The accuracy of brain-computer interfaces (BCIs) is important for effective communication and control. The mu-based BCI is one of the most widely used systems, of which the related methods to improve users' accuracy are still poorly studied, especially for the BCI illiteracy. Here, we examined a way to enhance mu-based BCI performance by electrically stimulating the ulnar nerve of the contralateral wrist at the alpha frequency (10 Hz) during left- and right-hand motor imagination in two BCI groups (literate and illiterate). We demonstrate that this alpha frequency intervention enhances the classification accuracy between left- and right-hand motor imagery from 66.41% to 81.57% immediately after intervention and to 75.28% two days after intervention in the BCI illiteracy group, while classification accuracy improves from 82.12% to 91.84% immediately after intervention and to 89.03% two days after intervention in the BCI literacy group. However, the classification accuracy did not change before and after the sham intervention (no electrical stimulation). Furthermore, the ERD on the primary sensorimotor cortex during left- or right-hand motor imagery tasks was more visible at the mu-rhythm (8-13 Hz) after alpha frequency intervention. Alpha frequency intervention increases the mu-rhythm power difference between left- and right-hand motor imagery tasks. These results provide evidence that alpha frequency intervention is an effective way to improve BCI performance by regulating the mu-rhythm which might provide a way to reduce BCI illiteracy.

Enhancing Mu-based BCI Performance with Rhythmic Electrical Stimulation at Alpha Frequency.

The accuracy of brain-computer interfaces (BCIs) is important for effective communication and control. The mu-based BCI is one of the widely used systems, of which the related methods to improve users' accuracy is still poorly studied. Here, we examined the way to enhance the mu-based BCI performance by rhythmic electrical stimulation on the ulnar nerve at the contralateral wrist at the alpha frequency (10 Hz) during the left-and right-hand motor imagery. Time-frequency analysis, spectral analysis, and discriminant analysis were performed on the electroencephalograph (EEG) data before and after the intervention of electrical stimulation in 9 healthy subjects. We found that the ERD/S on the somatosensory and motor cortex during left-or right-hand imagination was more obvious at the mu rhythm after intervention. Furthermore, average classification accuracy between left-and right-hand imagery significantly increased from 78.43% to 88.17% after intervention, suggesting that the electrical stimulation at alpha frequency effectively regulates the brain's mu rhythm and enhances the discriminability of the left-hand and right-hand imagination tasks. These results provide evidence that the electrical stimulation at the alpha frequency is an effective way to improve the mu-based BCI performance.

Upregulation of miR-126-3p promotes human saphenous vein endothelial cell proliferation in vitro and prevents vein graft neointimal formation ex vivo and in vivo.

Poor long-term patency of vein grafts remains an obstacle in coronary artery bypass grafting (CABG) surgery using an autologous saphenous vein graft. Recent studies have revealed that miR-126-3p promotes vascular integrity and angiogenesis. We aimed to identify the role of miR-126-3p in the setting of vein graft disease and investigate the value of miR-126-3p agomir as a future gene therapy in vein graft failure. Expression analysis of circulating miR-126-3p in plasma from CABG patients established the basic clues that miR-126-3p participates in CABG. The in vitro results indicated that elevated miR-126-3p expression significantly improved proliferation and migration in human saphenous vein endothelial cells (HSVECs) by targeting sprouty-related protein-1 (SPRED-1) and phosphatidylinositol-3-kinase regulatory subunit 2 (PIK3R2), but not in human saphenous vein smooth muscle cells (HSVSMCs). Moreover, the therapeutic potential of miR-126-3p agomir was demonstrated in cultured human saphenous vein (HSV) ex vivo. Finally, local delivery of miR-126-3p agomir was confirmed to enhance reendothelialization and attenuate neointimal formation in a rat vein arterialization model. In conclusion, we provide evidence that upregulation of miR-126-3p by agomir possesses potential clinical value in the prevention and treatment of autologous vein graft restenosis in CABG.