ObjectiveTo investigate the single nucleotide polymorphisms (SNPS) in the coding regions of the human ABCA2 gene and to determine the association of some of these SNPs with gallstone disease in a Chinese population. MethodsThe exons and part of the introns of the ABCA2 gene were sequenced using a fluorescent labeling automatic method in 24 patients with gallstone disease to identify and characterize the SNPs in a Chinese population. For SNPs in the exons, case-control studies were performed on patients and controls. ResultsTwelve SNPs were found within a 16911 bp region of the ABCA2 gene. Among them, two were in the exons, ten in the introns and five were novel SNPs. There was no significant difference in the SNPs genotype between the patients and the controis. ConclusionsThere is an important ethnic difference in the SNPs distribution of the human ABCA2 gene. The distribution of SNPs in the coding regions of the human ABCA2 gene is not significantly different between the patients and the controls.

Objective:To investigate the mechanism of human placenta derived mesenchymal stem cells (hPMSCs) in the inhibition of TNF-α secretion in CD4 + IFN-γ + T cells (Th1) through CD73/nuclear factor-erythroid 2-related factor 2(Nrf2) pathway to reduce liver injury in mice with graft versus-host disease (GVHD). Methods:Flow cytometry (FCM) was used to analyze the expression of TNF-α in Th1 cells and the expression of PD-1 on CD4 + IFN-γ + TNF-α + T cells (TNF-α + Th1 cells) isolated from peripheral blood and liver tissues of mice with GVHD. Hematoxylin-hosin (HE) staining, Masson staining and immunofluorescence staining were used to observe the pathological changes in liver tissues of GVHD mice in each group. HE staining was also used to observe the pathological changes in skin and lung tissues of GVHD mice. A nonconditional protocol to induce the differentiation of peripheral blood mononuclear cells (PBMCs) into Th1 cells in vitro was established. The proportion of TNF-α + Th1 cells and the mean fluorescence intensity (MFI) of Nrf2 and phosphorylated nuclear factor-kappa B (p-NF-κB) in this T cell subgroup were detected. Results:Compared with the normal control group, the proportion of TNF-α + Th1 cells and the expression of PD-1 on this T cells in peripheral blood and liver tissues of mice in the GVHD high group increased significantly ( P<0.01). The proportion of TNF-α + Th1 cells in peripheral blood and liver tissues decreased after hPMSCs treatment ( P<0.001), but the expression of PD-1 on this T cell subset was promoted in peripheral blood and liver tissues ( P<0.01, P<0.001). However, the intervention effects of shCD73 on TNF-α + Th1 cells in peripheral blood and liver tissues were significantly weakened ( P<0.05, P<0.01). Liver histopathological analysis showed that the proportion of TNF-α + Th1 cells in liver was positively correlated with Suzuki′s score, collagen area and the MFI of α-SMA ( P<0.001). Similarly, histopathological analysis of skin and lung tissues also showed that the proportion of TNF-α + Th1 cells in peripheral blood was positively correlated with skin Marina score and lung Shukai Qiao score ( P<0.001). In vitro experiment also showed that hPMSCs down-regulated the proportion of TNF-α + Th1 cells ( P<0.01) and up-regulated the expression of PD-1 on them ( P<0.05). Further analysis showed that hPMSCs could enhance the MFI of Nrf2 ( P<0.05) and weaken the MFI of p-NF-κB ( P<0.01) in TNF-α + Th1 cells. Conclusions:hPMSCs could up-regulate the expression of PD-1 through CD73/Nrf2 pathway to inhibit the formation of TNF-α + Th1 cells, thereby alleviating liver injury in GVHD mice.

Objective:To investigate the mechanism of IL-6 affecting the expression of CD73 on human placenta-derived mesenchymal stem cells (hPMSCs) and regulating their migration, adhesion and proliferation.Methods:Flow cytometry (FCM) and Western blot were used to analyze the effects of exogenous IL-6 or IL-6 secreted by hPMSCs on the expression of CD73 on hPMSCs. The influence of IL-6 on the phosphorylation of signal transducer and activator of transcription 3 (p-STAT3) in hPMSCs was detected by monoclonal antibody blocking test and Western blot. Real-time cellular analysis (RTCA) was used to analyze the changes in the migration, adhesion and proliferation of hPMSCs after knockdown of CD73 expression or APCP pretreatment.Results:FCM and Western blot showed that both exogenous and autocrine IL-6 from hPMSCs promoted the expression of CD73 on hPMSCs ( P<0.001, P<0.01). Moreover, CD73 expression decreased significantly with the presence of IL-6R inhibitor ( P<0.01). IL-6 could up-regulate the levels of both p-STAT3 and CD73 in hPMSCs ( P<0.05, P<0.01), while CD73 expression decreased after adding STAT3 inhibitor ( P<0.01). RTCA showed that knockdown of CD73 expression on hPMSCs significantly inhibited the adhesion and proliferation ability of hPMSCs( P<0.01, P<0.05), but promoted the migration ability of hPMSCs ( P<0.05). Similarly, inhibiting the hydrolase activity of CD73 on hPMSCs by APCP also resulted in a significant decrease in the adhesion and proliferation capacities of hPMSCs, and an increase in the migration capacity of hPMSCs ( P<0.05). Conclusions:IL-6 enhanced the expression of CD73 on hPMSCs via the JAK/STAT3 pathway, thus affecting the migration, adhesion and proliferation of hPMSCs.

ObjectiveTo investigate the effects of an intelligent aerobic bicycle training on lower limb motor function, cardiopulmonary function and activities of daily living (ADL) in patients with ischemic stroke at different courses. MethodsFrom November, 2019 to November, 2021, 138 ischemic stroke patients were stratified-randomly divided into control group (n = 69) and experimental group (n = 69). All the patients received medication and routine rehabilitation training, and the experimental group additionally received intelligent aerobic bicycle training, for eight weeks. They were assessed with Fugl-Meyer Assessment-Lower Extremities (FMA-LE), peak oxygen uptake (VO₂peak), Six-minute Walk Test (6MWT) and modified Barthel Index (MBI) before, and four weeks and eight weeks after treatment. ResultsThe performances of FMA-LE, VO₂peak, 6MWT and MBI improved in both groups after treatment (|t| > 6.763, P < 0.001), and improved more in the experimental group than in the control group (|t| > 2.439, P < 0.05). For the patients beginning training less than one month after stroke, the performances of FMA-LE, VO₂peak and 6MWT improved more in the experimental group than in the control group (|t| > 2.036, P < 0.05); for those during one to three months, the performances of 6MWT and MBI improved more (|t| > 2.005, P < 0.05); for those during three to six months, the performances of all the tests were not significantly different (|t| < 1.303, P > 0.05). ConclusionIntelligent aerobic bicycle training may improve the lower limb motor function, cardiopulmonary function and ADL for patients with ischemic stroke, especially intervening earlier.

ObjectiveTo visually analyze the current status, hot spots and frontiers of the researches on transcranial magnetic stimulation for stroke in recent five years. MethodsLiterature related to transcranial magnetic stimulation for stroke were retrieved from the Web of Science Core Collection from January 1, 2018 to December 31, 2022, and a visualized analysis was performed using CiteSpace 6.1.R6 software. ResultsThe number of published papers increased year by year, the most prolific author was Abo Masahiro, the country with the largest number of articles was China, and Sun Yat-sen University published the most papers. The hot keywords were cerebral cortex, functional magnetic resonance imaging, cortical excitability, plasticity, etc. The top five keywords of bursting strength were unilateral spatial neglect, poststroke, neuropathic pain, cortical plasticity, and trancallosal inhibition. ConclusionThe popularity of studies on transcranial magnetic stimulation in the treatment of stroke is increasing year by year. In the future, attention can be paid to the therapeutic effect of transcranial magnetic stimulation on unilateral spatial neglect, neuropathic pain, etc. Additionally, the influence of transcranial magnetic stimulation on cortical plasticity can be further studied.