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Introduction: We sought to translate, cross-culturally adapt, and evaluate the internal consistency and validity of the Chinese version of the 15-Item Myasthenia Gravis Quality of Life (MG-QOL15).Methods: Translation and cross-cultural adaptation of the MG-QOL15 were performed. We used Cronbach's α to test internal consistency, one-way analysis of variance to test construct validity, and Pearson or Spearman correlations to test discriminant and concurrent validity.Results: We enrolled 168 outpatients. Internal consistency was excellent (Cronbach's α = 0.928). The MG-QOL15 discriminated MG severity as stratified by the MG Composite (MGC; P < 0.001) and Osserman class (P = 0.01). Concurrent validity was low to moderate with the subscales of the 36-item Short Form (-0.31 to ∼-0.59), MGC (r = 0.46), and Myasthenia Gravis Activities of Daily Living profile (r = 0.54).Discussion: The Chinese MG-QOL15 showed comparable construct, discriminant and concurrent validity, and internal consistency with to the original version. Muscle Nerve 59:95-99, 2019. [ABSTRACT FROM AUTHOR]

In ischemia-reperfusion injury in ischemic stroke, mitophagy, which can remove damaged mitochondria, reduce cytotoxic damage, and enhance neurological recovery, is crucial. Jionoside A1 is a substance found in the traditional Chinese herb Rehmannia glutinosa, which may have neuroprotective effects. The fundamental objective of this work was to find out Jionoside A1's contribution to ischemia/reperfusion injury in ischemic stroke. The oxygen-glucose deprivation/reperfusion (OGD-Rep) model and the right transient middle cerebral artery occlusion (tMCAO) model were established. Jionoside A1 was used for treatment. We utilized a tiny interfering RNA (siRNA) to lower Nix expression. The results suggest that Jionoside A1 may reduce ischemic stroke. By lowering the consequences of ischemia/reperfusion injury, Rehmannia glutinosa can be utilized to treat ischemic stroke. These discoveries provide fresh experimental information for the investigation of ischemic stroke ischemia/reperfusion injury and provide some theoretical justification for their application.

Currently, no data are available regarding the expression levels of CD40L on CD4 + T cells in patients with neuromyelitis optica spectrum disorders (NMOSD). The percentage of circulating CD40L + CD4 + T cells was measured by flow cytometry in 23 NMOSD patients and 10 healthy controls. The ratio of CD40L + CD4 + to CD4 + T cells in patients at acute phase (18.28 ± 15.56%) was significantly higher than that in healthy controls (7.23 ± 5.94%, P = .032) and was positively correlated with disease severity (r = 0.532, P = .041). Thus, our results suggest an important role of this molecule in acute attacks of NMOSD., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Objective: To investigate the effect of monocyte chemoattractant protein 1 (MCP-1) on the migration of the induced and differentiated mouse bone marrow mesenchymal stem cells (BMSCs) for raising the efficacy of intravenous transplantation of BMSCs., Methods: The BMSCs were cultured with the method of differential adhesion and density gradient centrifugation of C57/BL10 mice, and were identified by alkaline phosphatase Gomori modified staining after osteogenic inducing. At the 3rd passage, the BMSCs were induced to the myoblasts with 5-azacytidine (5-Aza). The chemotaxis of MCP-1 in the induced and differentiated BMSCs in vitro at concentrations of 25, 50, 100, 200, and 400 ng/mL was observed through the migration test, by counting the number of the migrated cells. The expression of the chemokine receptor 2 (CKR-2) in the induced and differentiated BMSCs was detected with the flow cytometry., Results: The cells could be cultured with the methods of differential adhesion and density gradient centrifugation and still had higher proliferative and differentiative potency; the induced cells at the 3rd passage could differentiate to the osteoblasts, confirming that the cells were BMSCs; the myogenic induced BMSCs possessed the sarcotubule structure. The number of the migrating BMSCs at MCP-1 concentrations of 25-400 ng/mL were respectively 35.066 7 +/- 6.584 2, 43.200 0 +/- 6.460 8, 44.466 7 +/- 4.823 5, 45.600 0 +/- 8.650 3, and 50.733 3 +/- 7.582 5; showing significant difference when compared with control group (28.333 3 +/- 8.917 6, P < 0.05), and presenting significant difference among 25, 50, 400 ng/mL groups compared with each other (P < 0.05). The expression of CKR-2 in the mouse BMSCs (48.0%) was significantly higher (P < 0.001) than those of blank control (0.6%) and negative control (17.0%)., Conclusion: The results indicate that the MCP-1 can induce the migration of mouse BMSCs by MCP-1/CKR-2 pathway.