Simulation of ion cyclotron wave heating in the EXL-50U spherical tokamak based on dispersion relations

This study investigates the single-pass absorption(SPA) of ion cyclotron range of frequency(ICRF) heating in hydrogen plasma of the EXL-50U spherical tokamak,which is an upgraded EXL-50 device with a central solenoid and a stronger magnetic field.The reliability of the kinetic dispersion equation is confirmed by the one-dimensional full-wave code,and the applicability of Porkolab's simplified theoretical SPA model is discussed based on the kinetic dispersion equation.Simulations are conducted to investigate the heating effects of the fundamental and second harmonic frequencies.The results indicate that with the design parameters of the EXL-50U device,the SPA for second harmonic heating is 63%,while the SPA for fundamental heating is 13%.Additionally,the optimal injection frequencies are 23 MHz at 0.9 T and 31 MHz at 1.2 T.The wave vector of the antenna parallel to the magnetic field,with a value of k_‖=7.5 m^(-1),falls within the optimal heating region.Simulations reveal that the ICRF heating system can play an important role in the ion heating of the EXL-50U.

Combination therapy of scalp electro-acupuncture and medication for the treatment of Parkinson's disease: A systematic review and meta-analysis

Objective:To summarize the current clinical evidence related to the therapeutic effects and safety of adjuvant scalp electro-acupuncture (SEA) treatment for Parkinson's disease in China.Methods:Following the PRISMA statement,seven electronic databases were searched to retrieve randomized controlled clinical trials that used SEA combined with medication as the treatment intervention,and medication as the control.RevMan 5.3 was used to analyze outcomes,including the Unified Parkinson's Disease Rating Scale (UPDRS),Webster scale,effectiveness rate,and UPDRS III.Results:Nine randomized controlled trials,with certain methodological flaws and risks of bias,were included that involved 474 participants.SEA combined with medication was more effective than medication alone in overall therapeutic effects,as evidenced by total UPDRS scores (mean difference (MD):7.15,95% confidence interval [CI] 0.24 to 14.07,P =.04),Webster scores (MD:1.60,95% CI 0.20 to 2.99,P =.03),and effectiveness rate (risk ratio:1.35,95% CI 1.19 to 1.54,P <.001).In addition,there was significant improvement in pooled motor function results after adjuvant SEA treatment compared with medication alone (MD:5.75,95% Cl 4.18 to 7.32,P <.001).Conclusion:The combination of SEA and medication may be a promising intervention for patients with Parkinson's disease,especially to improve motor function.However,results were inconclusive,and additional studies with rigorous experimental design and larger sample sizes are needed to verify these results.

Protective effects of Buyinqianzheng Formula on mitochondrial morphology by PINK1/Parkin pathway in SH-SY5Y cells induced by MPP^(+)

Objective:Buyinqianzheng Formula(BYQZF)is clinically employed in traditional Chinese medicine to treat Parkinson's disease(PD)by improving mitochondrial dysfunction.However,the underlying mechanisms by which BYQZF affects mitochondrial morphology remain unknown.Therefore,we observed the effects of BYQZF on mitochondria from the perspective of the PINK1/Parkin pathway.Methods:Cell survival rates were assessed by Cell Counting Kit-8 assay.Expression levels of PINK1 and Parkin mRNA were examined by qRT-PCR.Protein expression levels of PINK1,PINK1-Ser228,Parkin,Parkin-Ser65,Drp1,and Drp1-Ser637 were examined by western blotting.PINK1,Parkin,and MitoTracker?Red CMXRos(MTR)were stained by triple-labeled immunofluorescence,and observed under laser confocal microscopy.Results:Cell survival rate,mitochondrial form factor,mean length and number of mitochondrial network branches,mitochondrial activity,m RNA expression levels of PINK1 and Parkin,and protein expression levels of PINK1,Parkin,and Drp1-Ser637 were reduced after 1-methyl-4-phenylpyridinium(MPP^(+))intervention.In contrast,Pearson's correlation coefficients between PINK1 and Parkin,and between Parkin and MTR,as well as protein expression levels of PINK1-Ser228,Parkin-Ser65,and Drp1 increased significantly after MPP^(+) intervention.Treatment with BYQZF increased cell survival rate,mitochondrial form factor,mean length and number of mitochondrial network branches,mitochondrial activity,m RNA expression levels of PINK1 and Parkin,and expression of PINK1,Parkin,and Drp1-Ser637 proteins.Pearson's correlation coefficients between PINK1 and Parkin,and between Parkin and MTR,as well as protein expression levels of PINK1-Ser228,Parkin-Ser65,and Drp1 decreased after BYQZF treatment.Conclusion:These results demonstrate that BYQZF has a protective effect on mitochondrial molecular mechanisms in the PD cell model,and the mechanism is related to the PINK1/Parkin pathway.

Mechanism of mitochondrial protection by the Buyin Qianzheng formula in a Parkin overexpression cell model

Objective:To identify the molecular mechanisms of the effects of the Buyin Qianzheng formula(BYQZF)on the mitochondrial dynamics in a Parkin overexpression Parkinson's disease(PD)cell model.Methods:First,a stable Parkin overexpression cell model was constructed using plasmid transfection.Then,we examined the protective effect of BYQZF on the mitochondrial dysfunction of the Parkin overexpression PD cell model induced by neurotoxin 1-methyl-4-phenylpyridinium ion(MPPþ).The mRNA expression level of Parkin was evaluated using real-time quantitative PCR.The cell survival rate was detected using the Cell Counting Kit-8 assay.We evaluated the cellular adenosine triphosphate(ATP)levels using luciferase assays.A laser scanning confocal microscope was used to observe the mitochondrial morphology,activity,and mitochondrial membrane potential(DJm).Western blot was conducted to evaluate the levels of the fusion proteins mitofusin1,mitofusin2,optic atrophy 1,dynaminrelated protein 1,and mitochondrial fission protein 1.Results:Parkin overexpression attenuated MPPþ-induced mitochondrial damage,increased mitochondrial activity and DJm.BYQZF increased the survival of MPPþ-induced cells that overexpressed Parkin and upregulated the mitochondrial form factor and activity.It also inhibited a decrease in the DJm and ATP levels.These findings suggested that BYQZF protected against MPPþ-induced mitochondrial dysfunction and enhanced the protective effect of Parkin overexpression.Furthermore,the formula upregulated the expression of the fusion proteins mitofusin1,mitofusin2,and optic atrophy 1(closely related to mitochondrial quality remodeling),and reduced the expression of the fission protein dynamicrelated protein 1,as well as mitochondrial fission protein 1.Conclusion:The mechanism by which BYQZF increased the mitochondrial protective effect of Parkin gene overexpression in MPPþ-induced cells may be related to improving mitochondrial function and regulating the balance of mitochondrial division and fusion proteins.