重元素:一次非常短暂的邂逅

人们对于元素周期表边缘范围的重元素知之甚少。然而人们如何研究在瞬间就衰变的子原呢?肯德尔·鲍威尔(Kendall Powell)找到了解决方法。     

Mechanism for the learning deficits in a mouse model of neurofibromatosis type 1.

Neurofibromatosis type I (NF1) is one of the most common single-gene disorders that causes learning deficits in humans. Mice carrying a heterozygous null mutation of the Nfl gene (Nfl(+/-) show important features of the learning deficits associated with NF1 (ref. 2). Although neurofibromin has several known properties and functions, including Ras GTPase-activating protein activity, adenylyl cyclase modulation and microtubule binding, it is unclear which of these are essential for learning in mice and humans. Here we show that the learning deficits of Nf1(+/-) mice can be rescued by genetic and pharmacological manipulations that decrease Ras function. We also show that the Nf1(+/-) mice have increased GABA (gamma-amino butyric acid)-mediated inhibition and specific deficits in long-term potentiation, both of which can be reversed by decreasing Ras function. Our results indicate that the learning deficits associated with NF1 may be caused by excessive Ras activity, which leads to impairments in long-term potentiation caused by increased GABA-mediated inhibition. Our findings have implications for the development of treatments for learning deficits associated with NF1.     

Experimental immunity against trypanosomiasis

Summary 9 groups of 6 female rats were used in an experiment using fraction 3 ofTrypanosoma rhodesiense. 500 g gave 100% immunoprotection and 1000 and 1500 g gave 66% immunoprotection when challenged with 5×10² T. brucei. 2 groups of 10 female rats were tested for a short period inoculation immune response. In this, 750 g of fraction 3 ofT. rhodesiense gave 70% immunoprotection when challenged withT. brucei.I thank the University of Zambia for support; Dr M. A. Q. Awan, Mazabuka, Zambia, forT. rhodesiense andT. brucei; Prof. J. W. Kibukamusoke, Dr O. Okong'o and Dr W. W. Anokbonggo for advice; Mr L. Nyaliti for technical help.     

'Rejuvenation' protects neurons in mouse models of Parkinson's disease

Why dopamine-containing neurons of the brain's substantia nigra pars compacta die in Parkinson's disease has been an enduring mystery. Our studies suggest that the unusual reliance of these neurons on L-type Ca(v)1.3 Ca2+ channels to drive their maintained, rhythmic pacemaking renders them vulnerable to stressors thought to contribute to disease progression. The reliance on these channels increases with age, as juvenile dopamine-containing neurons in the substantia nigra pars compacta use pacemaking mechanisms common to neurons not affected in Parkinson's disease. These mechanisms remain latent in adulthood, and blocking Ca(v)1.3 Ca2+ channels in adult neurons induces a reversion to the juvenile form of pacemaking. Such blocking ('rejuvenation') protects these neurons in both in vitro and in vivo models of Parkinson's disease, pointing to a new strategy that could slow or stop the progression of the disease.