Local charge of the ν = 5/2 fractional quantum Hall state

Electrons moving in two dimensions under the influence of strong magnetic fields effectively lose their kinetic energy and display exotic behaviour dominated by Coulomb forces. When the ratio of electrons to magnetic flux quanta in the system (ν) is near 5/2, the electrons are predicted to condense into a correlated phase with fractionally charged quasiparticles and a ground-state degeneracy that grows exponentially as these quasiparticles are introduced. The only way for electrons to transform between the many ground states would be to braid the fractional excitations around each other. This property has been proposed as the basis of a fault-tolerant quantum computer. Here we present observations of localized quasiparticles at ν = 5/2, confined to puddles by disorder. Using a local electrometer to compare how quasiparticles at ν = 5/2 and ν = 7/3 charge these puddles, we were able to extract the ratio of local charges for these states. Averaged over several disorder configurations and samples, we found the ratio to be 4/3, suggesting that the local charges are = e/3 and = e/4, where e is the charge of an electron. This is in agreement with theoretical predictions for a paired state at ν = 5/2. Confirming the existence of localized e/4 quasiparticles shows that proposed interferometry experiments to test statistics and computational ability of the state at ν = 5/2 would be possible.     

p53 mutant mice that display early ageing-associated phenotypes.

The p53 tumour suppressor is activated by numerous stressors to induce apoptosis, cell cycle arrest, or senescence. To study the biological effects of altered p53 function, we generated mice with a deletion mutation in the first six exons of the p53 gene that express a truncated RNA capable of encoding a carboxy-terminal p53 fragment. This mutation confers phenotypes consistent with activated p53 rather than inactivated p53. Mutant (p53+/m) mice exhibit enhanced resistance to spontaneous tumours compared with wild-type (p53+/+) littermates. As p53+/m mice age, they display an early onset of phenotypes associated with ageing. These include reduced longevity, osteoporosis, generalized organ atrophy and a diminished stress tolerance. A second line of transgenic mice containing a temperature-sensitive mutant allele of p53 also exhibits early ageing phenotypes. These data suggest that p53 has a role in regulating organismal ageing.     

An intelligent model selection and forecasting system

In this paper we present an intelligent decision‐support system based on neural network technology for model selection and forecasting. While most of the literature on the application of neural networks in forecasting addresses the use of neural network technology as an alternative forecasting tool, limited research has focused on its use for selection of forecasting methods based on time‐series characteristics. In this research, a neural network‐based decision support system is presented as a method for forecast model selection. The neural network approach provides a framework for directly incorporating time‐series characteristics into the model‐selection phase. Using a neural network, a forecasting group is initially selected for a given data set, based on a set of time‐series characteristics. Then, using an additional neural network, a specific forecasting method is selected from a pool of three candidate methods. The results of training and testing of the networks are presented along with conclusions. Copyright © 1999 John Wiley & Sons, Ltd.     

Thiamine deficiency and protein secretion by pancreatic slices in vitro

Summary Pancreatic slices incubated in glucose medium take up oxygen and glucose and liberate pentose, pyruvate and proteins. Thiamine deficiency decreases oxygen consumption but increases liberation of pentose, pyruvate and proteins by pancreatic slices.     

Mutations in sodium-borate cotransporter SLC4A11 cause recessive congenital hereditary endothelial dystrophy (CHED2)

Congenital hereditary endothelial dystrophy (CHED) is a heritable, bilateral corneal dystrophy characterized by corneal opacification and nystagmus. We describe seven different mutations in the SLC4A11 gene in ten families with autosomal recessive CHED. Mutations in SLC4A11, which encodes a membrane-bound sodium-borate cotransporter, cause loss of function of the protein either by blocking its membrane targeting or nonsense-mediated decay.