Terahertz-driven positron acceleration assisted by ultra-intense lasers.

Generation and acceleration of energetic positrons based on laser plasma have attracted intense attention due to their potential applications in medical physics, high energy physics, astrophysics and nuclear physics. However, such compact positron sources face a series of challenges including the beam dispersion, dephasing and unstability. Here, we propose a scheme that couples the all-optical generation of electron-positron pairs and rapid acceleration of copious positrons in the terahertz (THz) field. In the scheme, nanocoulomb-scale electrons are first captured in the wakefield and accelerated to 2.5 GeV. Then these energetic electrons emit strong THz radiation when they go through an aluminum foil. Subsequently, abundant γ photons and positrons are generated during the collision of GeV electron beam and the scattering laser. Due to the strong longitudinal acceleration field and the transvers confining field of the emitted THz wave, the positrons can be efficiently accelerated to 800 MeV, with the peak beam brilliance of 2.26 × 1012s-1mm-2mrad-2eV-1. This can arouse potential research interests from PW-class laser facilities together with a GeV electron beamline.

A Modified Power-on Programming Method after Deep Brain Stimulation for Parkinson Disease.

OBJECTIVE: To explore the feasibility of using a modified power-on programming method in deep brain stimulation (DBS) for Parkinson disease (PD). METHODS: We conducted a retrospective cohort study including 151 PD patients with bilateral robot-assisted DBS surgery from July 2017 to June 2020. Ninety-seven patients were adopted to the modified power-on programming method (Group I) and 54 patients were adopted to the traditional power-on programming method (Group II). In one-year follow-up, power-on programming duration, stimulation parameters, scores of Unified PD Rating Scale (UPDRS) and UPDRS-III of the 2 groups were recorded and compared. RESULTS: There were no significant differences in the postoperative UPDRS, UPDRS-III improvement rate, and stimulation parameters between the 2 groups. The duration of power-on programming of Group I (1.7 ± 1.1 hours) was significantly less than that of Group II (3.5 ± 1.8 hours, P < 0.0001). CONCLUSIONS: The modified power-on programming method can achieve a similar clinical effect to the traditional method, with the advantage of more efficiency.

Corrigendum: Neuroprotective Effects of Celastrol on Transient Global Cerebral Ischemia Rats via Regulating HMGB1/NF-κB Signaling Pathway.

[This corrects the article DOI: 10.3389/fnins.2020.00847.].

Neuroprotective Effects of Celastrol on Transient Global Cerebral Ischemia Rats via Regulating HMGB1/NF-κB Signaling Pathway.

Cerebral ischemia is a major cause of brain dysfunction, neuroinflammation and oxidative stress have been implicated in the pathophysiological process of cerebral ischemia/reperfusion injury. Celastrol is a potent inhibitor of inflammation and oxidative stress that has little toxicity. The present study was designed to evaluate whether celastrol has neuroprotective effects through anti-inflammatory and antioxidant actions, and to elucidate the possible involved mechanisms in transient global cerebral ischemia reperfusion (tGCI/R) rats. Celastrol (1, 2, or 4 mg/kg) was administrated intraperitoneally immediately after reperfusion and the effect of celastrol on reverting spatial learning and memory impairment was determined by Morris water maze (MWM) task. Inflammatory response and oxidative stress, hippocampal neuronal damage and glial activation, and HMGB1/NF-κB signaling pathway proteins were also examined. Our results indicated that celastrol dose-dependently reduced hippocampal and serum concentration of pro-inflammatory markers (TNF-α, IL-1ß, and IL-6) and oxidative stress marker (MDA), whereas the anti-inflammatory marker IL-10 and antioxidant markers (GSH, SOD, and CAT) were increased significantly in celastrol treated tGCI/R rats. Celastrol alleviated apoptotic neuronal death, inhibited reactive glial activation and proliferation and improved ischemia-induced neurological deficits. Simultaneously, we found that mechanisms responsible for the neuroprotective effect of celastrol could be attributed to its anti-inflammatory and antioxidant actions via inhibiting HMGB1/NF-κB signaling pathway. These findings provide a proof of concept for the further validation that celastrol may be a superior candidate for the treatment of severe cerebral ischemic patients in clinical practice in the future.

The Effects of Electroacupuncture in a Rat Model of Cerebral Ischemia-Reperfusion Injury Following Middle Cerebral Artery Occlusion Involves MicroRNA-223 and the PTEN Signaling Pathway.

BACKGROUND In China, electroacupuncture (EA) is used to treat the symptoms of ischemic stroke. However, the mechanisms involved in the effects of EA in cerebral ischemia remain to be investigated. This study aimed to investigate the molecular mechanism underlying the effects of EA in a rat model of cerebral ischemia-reperfusion injury (CIRI) induced by middle cerebral artery occlusion (MCAO). MATERIAL AND METHODS Seventy-five male Sprague-Dawley rats were divided into five groups: the sham group (with sham surgery), the model group (the MCAO model), the EA group (treated with EA), the EA control group, and the EA+antagomir-223-3p group. Rats in the model of CIRI underwent MCAO for 90 minutes. EA was performed on the second postoperative day and was performed at the Waiguan (TE5) and Zusanli (ST36) acupoints. The rat brains were evaluated for structural and molecular markers. RESULTS EA treatment significantly upregulated the expression of microRNA-223 (miR-223), NESTIN, and NOTCH1, and downregulated the expression of PTEN in the subventricular zone (SVZ) and hippocampus. The luciferase reporter assay supported that PTEN was a direct target of miR-223, and antagomiR-223-3p reversed the effects of EA and reduced the increase in NESTIN and inhibition of PTEN expression associated with EA treatment. There was a negative correlation between PTEN expression and the number of neural stem cells (NSCs). CONCLUSIONS In a rat model of CIRI following MCAO, EA activated the NOTCH pathway, promoted the expression of miR-223, increased the number of NSCs, and reduced the expression of PTEN.

Electroacupuncture Alleviates Ischemic Brain Injury by Inhibiting the miR-223/NLRP3 Pathway.

BACKGROUND Electroacupuncture (EA) has been commonly used to treat stroke in China. However, the underlying mechanism remains largely unknown. The present study investigated the neuroprotective effects of EA in middle cerebral artery occlusion (MCAO) rats and elucidated the possible anti-inflammatory mechanisms. MATERIAL AND METHODS In this study, modified neurological severity scoring (mNSS) was used to assess neurological deficits, and TTC staining and brain water content were measured to evaluate the degree of brain damage. HE staining, Nissl staining, and TUNEL staining were employed to evaluate apoptotic neuronal death. Molecular biological methods were used to measure the levels of miR-233, NLRP3, caspase-1, IL-1ß, and IL-18 in the peri-infarct cortex. RESULTS Our results showed that EA treatment significantly decreased the neurological deficit score and infarct volume of MCAO rats. The level of miR-223 was increased, while the levels of NLRP3, caspase-1, IL-1ß, and IL-18 were decreased in the peri-infarct cortex of EA-treated MCAO rats. However, the neuroprotective effect of EA was partially blocked by antagomir-223. CONCLUSIONS These data suggest that EA treatment can alleviate neuroinflammation by inhibiting the miR-223/NLRP3 pathway, thus playing a neuroprotective role in MCAO in rats.

Repetitive transcranial magnetic stimulation promotes functional recovery and differentiation of human neural stem cells in rats after ischemic stroke.

Stem cells hold great promise as a regenerative therapy for ischemic stroke by improving functional outcomes in animal models. However, there are some limitations regarding the cell transplantation, including low rate of survival and differentiation. Repetitive transcranial magnetic stimulation (rTMS) has been widely used in clinical trials as post-stroke rehabilitation in ischemic stroke and has shown to alleviate functional deficits following stroke. The present study was designed to evaluate the therapeutic effects and mechanisms of combined human neural stem cells (hNSCs) with rTMS in a middle cerebral artery occlusion (MCAO) rat model. The results showed that human embryonic stem cells (hESCs) were successfully differentiated into forebrain hNSCs for transplantation and hNSCs transplantation combined with rTMS could accelerate the functional recovery after ischemic stroke in rats. Furthermore, this combination not only significantly enhanced neurogenesis and the protein levels of brain-derived neurotrophic factor (BDNF), but also rTMS promoted the neural differentiation of hNSCs. Our findings are presented for the first time to evaluate therapeutic benefits of combined hNSCs and rTMS for functional recovery after ischemic stroke, and indicated that the combination of hNSCs with rTMS might be a potential novel therapeutic target for the treatment of stroke.