Inclusion formation by ataxins -1, -2, -3, and -7

The authors studied inclusion formation in vitro using transiently transfected PC12 cells, with epitope-tagged and untagged full-length and truncated wild-type and expanded ataxins -1, -2, -3, and -7. At 72 hours, no inclusions were seen with wild-type full-length or truncated ataxins -2, -3, or -7, and only one with ataxin-1. Truncation abolished nuclear localization of ataxins -1 and -7, and allowed nuclear entry of ataxin-2. Of the expanded ataxins, only -1 and -2 formed inclusions, and those of ataxin-2 were rare and exclusively cytoplasmic. Truncation resulted in inclusion formation by ataxins -3 and -7, increased ataxin-1 inclusions, and enabled formation of nuclear ataxin-2 inclusions. There was no recruitment of wild-type ataxin-1 to expanded ataxin-1 inclusions.     

INCLUSION FORMATION BY ATAXINS -1, -2, -3, AND -7

The authors studied inclusion formation in vitro using transiently transfected PC12 cells, with epitope-tagged and untagged full-length and truncated wild-type and expanded ataxins -1, -2, -3, and -7. At 72 hours, no inclusions were seen with wild-type full-length or truncated ataxins -2, -3, or -7, and only one with ataxin-1. Truncation abolished nuclear localization of ataxins -1 and -7, and allowed nuclear entry of ataxin-2. Of the expanded ataxins, only -1 and -2 formed inclusions, and those of ataxin-2 were rare and exclusively cytoplasmic. Truncation resulted in inclusion formation by ataxins -3 and -7, increased ataxin-1 inclusions, and enabled formation of nuclear ataxin-2 inclusions. There was no recruitment of wild-type ataxin-1 to expanded ataxin-1 inclusions.     

硬脑膜动脉血管融通术治疗成人烟雾病

目的 探讨成人烟雾病的临床特征,观察脑硬膜动脉血管融通术(EDAS)对成人烟雾病的治疗作用.方法 回顾分析在我院接受EDAS治疗的312例成人烟雾病患者的临床资料.结果 缺血型和出血型患者分别占79.8%(249例)、20.2%(63例).2例出血型患者术后发生再出血;219例缺血型患者术后临床症状明显缓解或完全消失.术后76.2%的患者糖代谢明显改善;56.6%的患者显示良好的颅内外血管重建,糖代谢减低、低龄、缺血型患者预示更好的血管重建.结论 中国成人烟雾病患者有自身的发病特征;应用EDAS术能明显改善和预防成人烟雾病患者脑缺血发作,对出血型患者再发脑出血也可能有一定的预防作用.     

Effects of (R)-(-)-1-(benzofuran-2-yl)-2-propylaminopentane hydrochloride [(-)-BPAP] in animal models of mood disorders

(R)-(-)-1-(Benzofuran-2-yl)-2-propylaminopentane hydrochloride [(-)-BPAP] is a highly potent enhancer of impulse propagation-mediated monoamine release and an inhibitor of monoamine uptake. We evaluated the efficacy of (-)-BPAP as a drug for mood disorders by using two animal models. (1) Acute, but not chronic, administration of (-)-BPAP and imipramine significantly attenuated immobility in mice induced by forced swimming. Chronic, but not acute, administration of (-)-BPAP ameliorated the impairment of social interaction (SI) behavior following forced swimming, without affecting locomotor activity. The ameliorating effect of (-)-BPAP on the impairment of SI behavior was suppressed by dopamine receptor antagonists, which suggests that the effect was mediated through the activation of the dopaminergic system. Chronic administration of imipramine tended to attenuate the impairment of SI behavior in stressed mice, but not significantly. (2) In the olfactory bulbectomized (OB) rat, chronic (-)-BPAP treatment significantly ameliorated the impairment of SI behavior, prepulse inhibition, and tone-cue fear learning, without affecting locomotor activity in an open field and circadian activity pattern. Furthermore, (-)-BPAP tended to improve sexual dysfunction in OB rats, but imipramine had no such effect. These findings suggest that (-)-BPAP may be clinically effective in treating mood disorders, including comorbid anxiety and depression that are poorly responsive to imipramine.