Wave acceleration of electrons in the Van Allen radiation belts

The Van Allen radiation belts are two regions encircling the Earth in which energetic charged particles are trapped inside the Earth's magnetic field. Their properties vary according to solar activity and they represent a hazard to satellites and humans in space. An important challenge has been to explain how the charged particles within these belts are accelerated to very high energies of several million electron volts. Here we show, on the basis of the analysis of a rare event where the outer radiation belt was depleted and then re-formed closer to the Earth, that the long established theory of acceleration by radial diffusion is inadequate; the electrons are accelerated more effectively by electromagnetic waves at frequencies of a few kilohertz. Wave acceleration can increase the electron flux by more than three orders of magnitude over the observed timescale of one to two days, more than sufficient to explain the new radiation belt. Wave acceleration could also be important for Jupiter, Saturn and other astrophysical objects with magnetic fields.     

A new interpretation of the sex determining mechanism of the European earwig,Forficula auricularia

Riassunto Osservazioni su femmine diForficula auricularia L. indicano che esse possiedono un solo cariotipo formato da 22 autosomi e da 2 cromosomiX. Sulla base di questo studio, suggeriamo che i maschi con 3 cromosomi sessuali sono del tipoXYY, e nonXXY come precedentemente ritenuto da varii autori. Ci sono maschiXY ₁t, XY₂, XY₂Y₂ e mosaiciXY ₂/XY₂Y₂ nella popolazione. Inoltre viene dimostrato che solamente il più grande dei due cromosomi Y, che caratterizzano questa specie, viene accumulato nei maschi con un meccanismo multiple di cromosomi sessuali.

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Supported by a postgraduate award from the Commonwealth of Australia to G.C.W. and by Public Health Service Grant No. GM-07212 from the Division of General Medical Sciences, U.S. National Institutes of Health and by a grant from the Australian Research Grants Committee.     

Effect of decapacitation factor on the oxygen uptake of rabbit spermatozoa recovered from the uterus

Résumé L'addition d'un facteur de décapacitation préparé à partir du plasma séminal de lapin et de taureau a généralement produit une augmentation supplémentaire de l'absorption d'oxygène, quand il a été ajouté à la suspension de spermatozoïdes enlevée de l'utérus. Le facteur de décapacitation n'a exercé aucun effet stimulant similaire sur les spermatozoïdes de lapin avant l'incubation dans l'utérus et n'a montré lui-même aucune absorption d'oxygène appréciable.

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Dr.I. G. White is indebted to the Population Council for a fellowship and to the Australian Research Grants Committee for financial support. The authors are indebted to ProfessorC. W. Emmens for his interest and advice.     

Bleeding due to disruption of a cargo-specific ER-to-Golgi transport complex

Mutations in LMAN1 (also called ERGIC-53) result in combined deficiency of factor V and factor VIII (F5F8D), an autosomal recessive bleeding disorder characterized by coordinate reduction of both clotting proteins. LMAN1 is a mannose-binding type 1 transmembrane protein localized to the endoplasmic reticulum-Golgi intermediate compartment (ERGIC; refs. 2,3), suggesting that F5F8D could result from a defect in secretion of factor V and factor VIII (ref. 4). Correctly folded proteins destined for secretion are packaged in the ER into COPII-coated vesicles, which subsequently fuse to form the ERGIC. Secretion of certain abundant proteins suggests a default pathway requiring no export signals (bulk flow; refs. 6,7). An alternative mechanism involves selective packaging of secreted proteins with the help of specific cargo receptors. The latter model would be consistent with mutations in LMAN1 causing a selective block to export of factor V and factor VIII. But approximately 30% of individuals with F5F8D have normal levels of LMAN1, suggesting that mutations in another gene may also be associated with F5F8D. Here we show that inactivating mutations in MCFD2 cause F5F8D with a phenotype indistinguishable from that caused by mutations in LMAN1. MCFD2 is localized to the ERGIC through a direct, calcium-dependent interaction with LMAN1. These findings suggest that the MCFD2-LMAN1 complex forms a specific cargo receptor for the ER-to-Golgi transport of selected proteins.     

Monoclonal antibodies inhibit prion replication and delay the development of prion disease

Prion diseases such as Creutzfeldt-Jakob disease (CJD) are fatal, neuro-degenerative disorders with no known therapy. A proportion of the UK population has been exposed to a bovine spongiform encephalopathy-like prion strain and are at risk of developing variant CJD. A hallmark of prion disease is the transformation of normal cellular prion protein (PrP(C)) into an infectious disease-associated isoform, PrP(Sc). Recent in vitro studies indicate that anti-PrP monoclonal antibodies with little or no affinity for PrP(Sc) can prevent the incorporation of PrP(C) into propagating prions. We therefore investigated in a murine scrapie model whether anti-PrP monoclonal antibodies show similar inhibitory effects on prion replication in vivo. We found that peripheral PrP(Sc) levels and prion infectivity were markedly reduced, even when the antibodies were first administered at the point of near maximal accumulation of PrP(Sc) in the spleen. Furthermore, animals in which the treatment was continued remained healthy for over 300 days after equivalent untreated animals had succumbed to the disease. These findings indicate that immunotherapeutic strategies for human prion diseases are worth pursuing.