ABSTRACT
Objective:To study the effects of transcranial direct current stimulation (tDCS) in different intensities on dysphagia after cerebral infarction and its neurological mechanism. Methods:From January, 2016 to December, 2018, 60 inpatients with dysphagia after cerebral infarction were randomly equally divided into low-, medium- and high-intensity groups, in which the intensities of tDCS were 1.0 mA, 1.5 mA and 2.0 mA, respectively, for 30 days. They were observed with video fluoroscopic swallowing study and α waves of electroencephalography before and after treatment. Results:The score of oral stage increased in the high-intensity group after treatment (t = -2.196, P < 0.05), while the dominant frequency of α wave increased (t = -6.488, P < 0.001). Conclusion:High-intensity tDCS may improve the excitability of the brain for patients with dysphagia after cerebral infarction, to improve the swallowing.
ABSTRACT
Disuse atrophy of skeletal muscle is a common clinical problem and its exact mechanisms have not been fully understood. Previous studies suggested that disuse muscle atrophy is realized through the activation of one or more cell signaling pathways, but studies have shown that disuse atrophy is the activation of the ubiquitin-proteasome caused extensive decomposition of the protein. The present researches for disuse atrophy mainly focus on regulatory role in the upstream signaling molecules MuRF1 and Atroginl/MAFbx by NF-kappaB, IGF-1/PI3K/Akt, TGF-beta/Smad and MAPK signal pathway and a plurality of signal pathway activation or inhibition and interaction,and then through the ubiquitin--proteasome to influence the metabolism of protein. But regulation of expression of MuRF1 and Atroginl/MAFbxs still to be studied. Participate in disuse atrophy also needs to be further studied with atrophy confirmation and functional gene verification. The paper summarized recent original articles about the researches of skeletal muscle disuse atrophy and reviewed the various signal pathways and related u-biquitin-proteasome protein metabolism of disuse muscle atrophy.
Subject(s)
Animals , Humans , Muscle, Skeletal , Metabolism , Muscular Disorders, Atrophic , Metabolism , Proteins , Metabolism , Signal TransductionABSTRACT
L-glutamate (Glu) is an excitatory neurotransmitter in the mammalian central nervous system. Relatively much attention has been paid to functional expression of Glu signaling molecules in peripheral tissues very recently. The present study tested the hypothesis that the activation of group I metabotropic glutamate receptor (mGluRI) in neutrophils stimulated neutrophils adherence to endothelial cells by increasing the surface expression of certain adhesion molecules. Peripheral blood was obtained by venipuncture from healthy donors, and the neutrophils were isolated by Ficoll-Hypaque gradient centrifugation. Neutrophils floating into DMEM/F12 culture medium containing 10% fetal bovine serum were then used immediately. Immunocytochemistry and real-time quantitative RT-PCR were used to detect the expression of mGluRI (mGluR1 and mGluR5) in neutrophils. The adherence of neutrophils to cultured human normal umbilical vein endothelial cells (HUVE-12) was measured by the colorimetric method. Cell surface expression of adhesion molecule CD11a in the neutrophils was determined by flow cytometry. Immunocytochemistry and real-time quantitative RT-PCR showed that mGluR1 and mGluR5 were constitutively expressed in neutrophils. Application of mGluRI agonist S-3,5-dihydroxyphenylglycine (S-DHPG) (1x10(-8)-1x10(-6) mol/L) showed a dose-dependent stimulatory effect on the adherence of neutrophils to HUVE-12 (P<0.05 or P<0.01), with a maximum effect at 1x10(-6) mol/L (P<0.01). Incubations as short as 30 min were sufficient to induce increased adherence after the beginning of S-DHPG treatment. Following time extension (0.5-5 h), S-DHPG (1x10(-6) mol/L) increased the rate of neutrophils adhesion to HUVE-12 with a maximum effect at 0.5 h (P<0.01). However, a time-dependent effect of S-DHPG on the rate of neutrophils adhesion to HUVE-12 was not observed during the experimental period. 1x10(-6) mol/L of S-DHPG also induced an increased surface expression of adhesion molecule CD11a (P<0.01) when neutrophils were preincubated with 1x10(-6) mol/L of S-DHPG for 1 h. Furthermore, the specific mGluRI antagonist (RS)-alpha-methyl-4-carboxyphenylglycine ((+/-)-MCPG, 0.5 mmol/L) significantly abolished the stimulatory effect of S-DHPG (1x10(-6) mol/L) on the adherence of neutrophils to HUVE-12 (P<0.01). These results suggest that the activation of mGluRI in neutrophils results in increased adhesion molecule CD11a expression and thereby promotes the adherence of neutrophils to endothelial cells.