ABSTRACT
Objective: To observe the clinical efficacy of electroacupuncture in treating spastic paralysis following cerebral infarction. Methods: Sixty patients with spastic paralysis after cerebral infarction were randomly allocated into control group and treatment group, 30 cases each. The control group was treated with conventional acupuncture and the treatment group was treated with conventional acupuncture plus electroacupuncture according to the principle of antagonistic acupuncture. Both groups were given routine drugs and scalp acupuncture treatment. Results: Statistical analysis showed significant differences in NFI score and clinical curative effect score between pretreatment and posttreatment in the treatment and control groups and between the treatment and control groups. Conclusion: Both electroacupuncture and conventional acupuncture have clinical curative effect on spastic paralysis following cerebral infarction, but the curative effect of electroacupuncture is significantly superior to that of conventional acupuncture.
ABSTRACT
<p><b>OBJECTIVE</b>To explore an alternative method for easier and more effective establishment of allergen-specific T-cell clones (TCC) from peripheral blood monouclear cells (PBMCs) of allergic asthma patients with allogeneic feeding cells.</p><p><b>METHODS</b>To determine the optimal condition for T cell growth and effective dose and time of mitomycin-C (MMC) treatment of the feeding cells to prevent their proliferation, the PBMCs were treated with PHA, IL-2 or MMC at different concentrations, and the proliferation rate of the treated cells was analyzed by MTT assay. The effect of IL-4 on the growth and subset selection of TCC was also analyzed. Allergen-specific TCC was established by limiting dilution method with allogeneic PBMCs as the feeding cells, and the proliferation of the allergen-specific TCC was observed to evaluate the feasibility of the feeding cells.</p><p><b>RESULTS</b>PHA at 25 microg/ml and IL-2 at 27 U/ml achieved optimal growth of the T cells, while MMC treatment at the dose of 60 microg/ml for 80 min effectively enriched the non-proliferative feeding cell from the PBMCs. IL-4 could not promote the survival of the TCC, but promoted the formation of CD(4)(+) TCC. Allergen-specific TCC obtained using allogeneic feeding cells required the presence of PHA, but the allergen reactivity of the TCC remained unpredictable.</p><p><b>CONCLUSION</b>IL-4 can promote the formation of CD(4)(+) TCC, but allogeneic feeding cells may fail to produce TCC with high allergen specificity.</p>
Subject(s)
Humans , Allergens , Allergy and Immunology , Asthma , Blood , Cell Culture Techniques , Cell Proliferation , Cells, Cultured , Clone Cells , Cell Biology , Allergy and Immunology , Interleukin-2 , Pharmacology , Leukocytes, Mononuclear , Cell Biology , Allergy and Immunology , Mitomycin , Pharmacology , T-Lymphocyte Subsets , Cell Biology , Allergy and Immunology , T-Lymphocytes , Cell Biology , Allergy and Immunology , T-Lymphocytes, Regulatory , Cell Biology , Allergy and ImmunologyABSTRACT
Summary: The expression of CH50 polypoptide in bladder cancer cell line BIU-87 and the effects on the invasion ability of BIU-87 were investigated. The eukaryotic expressing vector pCH510 of polypeptide CH50 was introduced into BIU-87 cells by gene transfection in vitro. The expression of CH50 polypeptide was detected by using immunohistochemical S-P method. The expression of the transfected gene was identified by RT-PCR. Cell invasion assay kit was applied to detect the effect of CH50 polypeptide on the invasion ability of BIU-87. The results showed that the BIU-87 cells transfected with pCH510 could express the CH50 polypeptide, while in the control group, no CH50 polypeptide was detectable. In the transfection group, the invasion ability of BIU-87 in vitro was lower than in control group (P<0.05). It was concluded that CH50 polypeptide was successfully expressed in BIU-87 cells by gene transfection, by which the in vitro invasion ability of BIU-87 was inhibited.
ABSTRACT
Objective: To demonstrate the influence of HMGB34367,a subfamily member of the high-mobility group protein B1(HMGB1),as a transcriptional factor of the ?-SMA gene expression.Methods: We cloned HMGB34367 cDNA from the fibrotic lung tissue of the Balb/C mouse treated with BLM by RT-PCR,sub-cloned it into a eukaryotic expression vector pcDNA 3.0 or pEGF-N2,and constructed a report plasmid,pDsRed-SMA,encoding red fluorescence(RFP) driven by ?-SMA promoter.Following the co-transfection of pDsRed-SMA and HMGB34367-pcDNA3.0/ pEGF-N2-HMGB34367 in the cultured 16HBE cells,we tested the expression of the RFP in the absence and presence of TGF?1 by fluorescence microscopy.After the transfection of HMGB34367-pcDNA3.0,the nucleus extracts from the transfected cells were subjected to electrophoretic mobility shift assay(EMSA) for the detection of the binding activity of HMGB34367 with ?-SMA promoter CarGB motif.RT-PCR was performed for the evaluation of the ?-SMA gene expression in the cells.Results: The over expression of HMGB34367 activated the ?-SMA promoter and enhances the expression of the ?-SMA gene.An increased binding activity of HMGB34367 with CarGB motif was detected by EMSA in the transfected cells.Conclusion:HMGB34367,a member of HMGB1 family,could act as a transcription factor for the transcriptional activation of the ?-SMA gene,which may play an important role in the development of lung fibrosis.
ABSTRACT
Objective: To investigate the expression and identification of CH50 polypeptide in bladder cancer cell line BIU-87 by gene transfection. Methods:The eukaryotic expressing vector pCH510 of polypeptide CH50 was introduced into BIU-87 cells by gene transfection Lipofectimine TM2000.The expressed product was identified by immunohistochemistry and Western blot method. The expression of the transfected gene was identified by RT-PCR. Results:The BIU-87 cells could produce CH50 polypeptide by transfection. Conclusion:When the vector of pCH510 was transfected into BIU-87 cells in vitro, the cell adhension characteristic would be changed.
ABSTRACT
Objective:To investigate if injury-related myofibroblast induction could occur in bronchial epithelial cells and the role of TGF-?_1(rhTGF-?_1) in epithelial-myofibroblast transdifferentiation. Methods:Cultured bronchial epithelial cells, 16HBE-14o, were exposed to poly-L-arginine(PLA). Using a immunohistochemical method, ?-smooth muscle actin (?-SMA) expression was detected in those cells after being treated with PLA . Relative activity of chloramphenicol acetyltransferase(CAT) was assessed in 16HBE-14o cells, which were transiently transfected with VSMP8 plasmid containing ?-SMA promoter linked to CAT gene, at different time points after rhTGF-?_1(10 ?g/L) treatment. Results:①?-SMA positive, spindle-shaped cells emerged among the regenerated 16HBE-14o epithelial cells following damage. The number of ?-SMA positive 16HBE-14o cells increased and cell repair was delayed under rhTGF-?_1 stimulation.② CAT activity increased significantly in VSMP8 plasmid transfected 16HBE-14o cells 24 h after TGF-?_1 stimulation. (P