Association analysis of the parkin gene in patients with sporadic Parkinson's disease from a Han population of Sichuan province / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To determine whether there are any associations between the -258T/G polymorphism of the promoter and the IVS3 -20T/C polymorphism in parkin gene and Parkinson's disease (PD) from a Han population in Sichuan province.</p><p><b>METHODS</b>Polymerase chain reaction (PCR), restriction fragment length polymorphism, denaturing high performance liquid chromatography(dHPLC) and sequence analysis were used to determine the genotype of each subject. The -258T/G polymorphism and IVS3 -20T/C polymorphism were analysed in 198 patients with sporadic PD and 187 healthy controls, matched for age and gender.</p><p><b>RESULTS</b>There were significant differences in allele frequency of the -258T/G polymorphism between PD patients and controls, with the G allele more common in cases than controls (52.5% vs 43.3%; chi square is 6.17, P< 0.025, OR is 1.45, 95% CI 1.04-1.86). There were also significant differences in G allele frequency between PD patients with onset age over 50 years old and controls(chi square is 9.048, P< 0.01, OR is 1.57, 95% CI:1.08-2.06). The frequency of TG+GG genotype was significantly higher in PD patients than in controls (78.79% vs 69.51%; chi square is 3.854, P< 0.05, OR is 1.63, 95% CI:0.88-2.38). In addition, there were significant differences in age of onset between PD patients with different genotypes (P< 0.05). The average age of onset in group of GG genotype was later about 5 years compared with the group of TT or TG genotype. The frequency of CC genotype in IVS3 -20T/C polymorphism was much higher than that of TC genotype. No TT genotype was found.</p><p><b>CONCLUSION</b>This study suggests that the parkin promoter -258T/G polymorphism might be a risk factor for late onset PD in Sichuan. CC genotype for IVS3 -20T/C polymorphism is common in Sichuan Han population. No TT genotype for IVS3 -20T/C polymorphism is found in Sichuan Han population.</p>

Effect of the Ca2+ -activated K+ channel in veratridine-induced cortex neurons damage / 中国应用生理学杂志

<p><b>AIM</b>To observe the effects of Ca2+ -activated K+ channel of primary cultured fetal SD rat cortex neurons in the veratridine triggered neuronal damage.</p><p><b>METHODS</b>The patch clamp technique of cell-attach and inside-out mode for these two kinds of single channel recordings were used.</p><p><b>RESULTS</b>Extracellular veratridine activated the Kca. In Ca2+ bath solution of cell-attach mode, Vp + 30 mV, when the concentration (micromol/L) of veratridine were 15,25,50 and 75, the open probabilities of the channel were 0.014 +/- 0.003, 0.085 +/- 0.010, 0.132 +/- 0.016 and 0.059 +/- 0.006 (P < 0.01) respectively. It appeared concentration-dependent within 50 micromol/L veratridine. In Ca2+ free bath solution of cell-attach mode, Vp = +50 mV, when the concentration (micromol/L) of veratridine were 15, 40,60 and 100, the open probabilities of the channel were 0.014 +/- 0.010, 0.113 +/- 0.006, 0.141 +/- 0.004 and 0.295 +/- 0.009 (P < 0.05) respectively. In the 6 cases of inside-out mode patch clamp, Vp = +40 mV, when the concentration of veratridine were 0, 25 micromol/L and 50 micromol/L, the open probabilities of the channel were 0.011 +/- 0.008, 0.010 +/- 0.010 and 0.012 +/- 0.007 (P > 0.05) respectively. There were no significant difference on open probabilities, average open/close times and amplitudes at different intracellular veratridine concentration.</p><p><b>CONCLUSION</b>Veratridine can affect the activation of the Kca channel through regulating the concentration of cytoplasmic free Ca2+. The opening of Kca activated by increase of intracellular Ca2+ during the early stage of anoxia may be a protection reaction of ischemic neurons.</p>