Quantitative assessment of the association between the GSTM1-null genotype and the risk of childhood asthma.

BACKGROUND: Many studies investigated the association between the glutathione S-transferase M 1 (GSTM1)-null genotype and childhood asthma risk, but there was obvious inconsistence among those studies. The aim of this meta-analysis was to quantify the strength of association between the GSTM1-null genotype and risk of childhood asthma. METHODS: We searched the PubMed, Embase, and Wangfang databases for studies relating the association between the GSTM1-null genotype and risk of childhood asthma. We estimated the pooled odds ratio (OR) with its 95% confidence interval (95% CI) to assess the association. RESULTS: Nineteen case-control studies with 4,543 childhood asthma cases and 19,394 controls were included into this meta-analysis. Meta-analysis of all 19 studies showed that the GSTM1-null genotype was associated with increased risk of childhood asthma (OR=1.17, 95% CI 1.03-1.34, p=0.017). Subgroup analyses by ethnicity suggested that the GSTM1-null genotype was associated with an increased risk of childhood asthma in Caucasians and Africans (for Caucasians, fixed-effects OR=1.16, 95% CI 1.07-1.27, p=0.001; for Africans, fixed-effects OR=1.92, 95% CI 1.35-2.74, p<0.001). The cumulative meta-analyses showed a trend of obvious association between the GSTM1-null genotype and risk of childhood asthma as information accumulated in the analyses of both total studies and Caucasians. No evidence of publication bias was observed. CONCLUSION: Meta-analyses of available data suggest a significant association between the GSTM1-null genotype and the risk of childhood asthma, and the GSTM1-null genotype contributes to increased risk of childhood asthma, especially in Caucasians and Africans.

Effect of ephedrine on neuronal plasticity of hypoxic-ischemic brain damage in neonatal rats.

OBJECTIVE: Study the effect of ephedrine on neural plasticity of hypoxic ischemic brain damaged (HIBD) in neonatal rats, and explore the underlying molecular mechanism. METHODS: 60 Sprats suffered from HIBD (7 days old) were randomly divided into ephedrine group, D-amphetamine (D-AMPH) group, cytidine triphosphate (CTP) group, ganglioside (GM1) group, and spontaneous recovery group. Using immunohistochemical method to test the expression of growth-associated protein-43(GAP-43) and synaptophysin (SYP) on one side of hippocampal CA3 area, then, 4 weeks later, Morris Water Maze test was performed for five days. RESULTS: (1) The expression levels of GAP-43 and SYP on hippocampal CA3 area in ephedrine group were higher than that in spontaneous recovery group (P<0.05). However, there was no statistical difference in ephedrine groups, CTP group, and D-AMPH group. (2) The average time of escape latency was significantly shorter in treating groups than that in spontaneous recovery group (P<0.05), and the frequency of original platform passing was higher than that in spontaneous recovery group (P<0.01). The average time of escape latency was longer in ephedrine group than that in GM1 group. The frequency of original platform passing was significantly less in ephedrine group than that in GM1 group, No statistical difference found in ephedrine groups, CTP group, and D-AMPH group. CONCLUSIONS: Ephedrine may enhance memory, the abilities of spatial orientation and learning in HIBD rats. This protective effect may be associated with increasing synaptic connectivity, as assessed by increased expression of GAP-43 and SYP after HIBD. Ephedrine triggered similar protection against HIBD as treatment of D-AMPH and CTP. However, the amelioration of ability of spatial orientation, learning and memory by ephedrine on HIBD rats in later stage is slightly weaker than that by GM1, which may be related with ephedrine dosage.

[Effect of ephedrine on neuronal plasticity in neonatal rats after hypoxic-ischemic brain injury].

OBJECTIVE: To study the effect of ephedrine on neural plasticity after hypoxic-ischemic brain damage (HIBD) in neonatal rats. METHOD: Sixty SD rats, aged 7 days, were made as HIBD model, which were randomly divided into following 4 groups, an ephedrine group, a D-amphetamine (D-AMPH) group, a cytodine triphosphate-2Na (CTP) group and a ganglioside (GMI) group. Changes in the expression of growth-associated protein-43 (GAP-43) and synaptophysin (SYP) in the hippocampal area CA3 were detected with immunohistochemical method. Four weeks after the operation, learning and memory test in Morris water maze was performed for 5 days. RESULT: (1) The GAP-43 and SYP expression levels in hippocampal area CA3 in the ephedrine group were higher than those in the spontaneous recovery group (P < 0.05), with no significantly different from those the CTP group and the D-AMPH group. (2) The average escape latency in the ephedrine group, the D-AMPH group and the CTP group were significantly shorter than that in the spontaneous recovery group (P < 0.05), and the frequency passing the original platform in the 3 treatment groups were significantly more than those in the spontaneous recovery group (P < 0.01). The escape latency was longer and the frequency passing the original platform was less in the ephedrine group than that in the GM1 group, with no significant differences as compared with the CTP group and the D-AMPH group. CONCLUSION: Ephedrine can enhance spatial orientation and learning and memory abilities of HIBD rats in later life. This protective effect is associated with decrease of neuronal loss after HIBD, and promotion of the expression of GAP43 and SYP. Ephedrine can exert the same protection against HIBD as D-AMPH and CTP do, but the amelioration of spatial orientation and learning and memory abilities by ephedrine in later life in rats after HIBD is slightly weaker than that by GM1, which is possibly related with the dose of ephedrine.