ABSTRACT
Objective:To observe the effect of genetic inactivation of adenosine A 2A receptor on apoptosis in the prefrontal cortex and on the expression of phosphorylated p38 mitogen-active protein kinase (p38MAPK) in mice with chronic hypoxic hypercapnia. Methods:Sixteen male wild-type mice and 16 male mice in which the adenosine A 2A receptor gene had been knocked out were randomly divided into a 4 weeks group (including 4HH+ /+ and 4HH-/- subgroups) and a normal control group (including NC+ /+ and NC-/- subgroups). The 4HH+ /+ and 4HH-/- group mice were exposed to an atmosphere containing 9-11% O 2 and 5-6% CO 2 8 hours a day, 6 days a week for 4 weeks. The apoptosis index (AI) in their prefrontal cortices was then evaluated using terminal-deoxynucleoitide transferase mediated nick end labelling (TUNEL) staining. The expression of p38MAPK protein in the prefrontal cortices was measured using western blotting. Results:The average AI had increased significantly in the 4HH+ /+ and 4HH-/- groups compared with the controls, with significantly more apoptotic cells in the 4HH+ /+ group than in the 4HH-/- group. In the 4HH+ /+ and 4HH-/- groups the average expression of p38 protein in the prefrontal cortex was significantly higher than among their controls. Moreover, the average expression of p-p38MAPK protein in the prefrontal cortex of the 4HH-/- group was significantly lower than in the 4HH+ /+ group.Conclusion:Adenosine A 2A receptor knockout inhibits apoptosis in the prefrontal cortex and down-regulates the p38MAPK activation of mice after exposure to chronic hypoxic hypercapnia.
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Objective To explore the effects of transcranial magnetic stimulation (TMS) on motor function in patients with Parkinson's disease (PD) using meta-analysis. Methods Eight comparative studies of the effects of TMS were meta-analyzed. Results The combined studies confirmed a significant difference before and after TMS treatment. Between the experimental and control groups the effect was also highly significant. Conclusion TMS may play an active role in the rehabilitation of motor function for patients with Parkinson's disease.
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<p><b>OBJECTIVE</b>To explore the strategies which reduce the amount of xenoantigen Galalpha1,3Gal.</p><p><b>METHODS</b>Human alpha-galactosidase gene and alpha1,2-fucosyltransferase gene were transferred into cultured porcine vascular endothelial cells PEDSV.15 and human alpha-galactosidase transgenic mice were produced. The Galalpha1,3Gal on the cell surface and susceptibility of cells to human antibody-mediated lysis were analyzed.</p><p><b>RESULTS</b>Human alpha-galactosidase gene alone reduced 78% of Galalpha1,3Gal on PEDSV.15 cell surface while human alpha-galactosidase combined with alpha1,2-fucosyltransferase genes removed Galalpha1,3Gal completely. Decrease of Galalpha1,3Gal could reduce susceptibility of cells to human antibody-mediated lysis, especially during co-expression of alpha-galactosidase gene and alpha1,2-fucosyltransferase gene. RT-PCR indicated positive human alpha-galactosidase gene expression in all organs of positive human alpha-galactosidase transgenic F1 mice including heart, liver, kidney, lung, and spleen, the amount of Galalpha1,3Gal antigens on which was reduced largely. 58% of spleen cells from F1 mice were destroyed by complement-mediated lysis compared with 24% of those from normal mice.</p><p><b>CONCLUSIONS</b>Human alpha-galactosidase gene and alpha1,2-fucosyltransferase gene effectively reduce the expression of Galalpha1,3Gal antigens on endothelial cell surface and confers resistance to human serum-mediated cytolysis. The expression of human alpha-galactosidase in mice can also eliminate the Galalpha1,3Gal antigens in most tissues and decrease the susceptibility of spleen cells to human serum-mediated cytolysis.</p>
Subject(s)
Animals , Humans , Mice , Antigens, Heterophile , Metabolism , Cell Death , Cells, Cultured , Disaccharides , Metabolism , Endothelial Cells , Metabolism , Fucosyltransferases , Genetics , Metabolism , Graft Rejection , Genetics , Mice, Transgenic , Spleen , Cell Biology , Swine , Transfection , alpha-Galactosidase , Genetics , MetabolismABSTRACT
Objectives:To establish hybridomas secreting monoclonal antibodies(McAbs) against O6-methylguanine-DNA methyltransferase(MGMT) and to observe the relationship between MGMT expression and clinical responses to ACNU and BCNU in human brain tumors.Methods:The hybridomas were established by cell fusion.MGMT expression in 60 glioma specimens was detected by means of immunohistochemical assay.Results: Seven hybridomas secreting McAbs against MGMT were obtained.Thirty tumor specimens had no detectable or low level of MGMT expression(Mer-), while 30 specimens had high level of MGMT expression(Mer+). The Mer- patients showed more sensitive to ACNU and BCNU than the Mer+ patients.Conclusions: The high specific hybridomas secreting monoclonal antibodies(McAbs) against MGMT were established.The preliminary study indicated that MGMT negative tumors were sensitive to ACNU and BCNU, whereas MGMT positive ones were more resistant to nitrosourea drugs.