The influence of early nutrition and environmental rearing on brain growth and behaviour

Summary Preweaning malnutrition permanently reduced brain size and cellular content but in spite of changes in the adrenocortical stress response no learning deficit was observed. Differential rearing environments did not influence the effects of malnutrition.This work was supported by a grant from the National Health and Medical Research Council of Australia.We thank Mrs.Jean Williams andDr. A. Miller, Department Maths. Stats., C. S. I. R. O., Sydney for assistance with the statistical analysis.     

Cool heliosheath plasma and deceleration of the upstream solar wind at the termination shock

The solar wind blows outward from the Sun and forms a bubble of solar material in the interstellar medium. The termination shock occurs where the solar wind changes from being supersonic (with respect to the surrounding interstellar medium) to being subsonic. The shock was crossed by Voyager 1 at a heliocentric radius of 94 au (1 au is the Earth-Sun distance) in December 2004 (refs 1-3). The Voyager 2 plasma experiment observed a decrease in solar wind speed commencing on about 9 June 2007, which culminated in several crossings of the termination shock between 30 August and 1 September 2007 (refs 4-7). Since then, Voyager 2 has remained in the heliosheath, the region of shocked solar wind. Here we report observations of plasma at and near the termination shock and in the heliosheath. The heliosphere is asymmetric, pushed inward in the Voyager 2 direction relative to the Voyager 1 direction. The termination shock is a weak, quasi-perpendicular shock that heats the thermal plasma very little. An unexpected finding is that the flow is still supersonic with respect to the thermal ions downstream of the termination shock. Most of the solar wind energy is transferred to the pickup ions or other energetic particles both upstream of and at the termination shock.     

An immunoreactive peptide in milk contains bombesin-like bioactivity

Summary Parallel in vitro biassays using rat uterus and guinea pig large intestine tissues specific for the bombesin family of peptides, demonstrated that the bombesin-like peptides present in bovine milk can produce a dose-related response similar to bombesin and litorin. The bioactivity of this type of milk peptide appeared to be approximately 20–50% as active as the amphibian peptides. These data support the proposal that a bombesin immunoreactive peptide in milk contains bombesin bioactivity.supported in part by a NATO Fellowship and by the Fogarty International Center of the National Institutes of Health, Bethesda, MD, USA.supported by a grant from the Consiglio Nazionale delle Ricerche     

Peptide exosite inhibitors of factor VIIa as anticoagulants

Potent anticoagulants have been derived by targeting the tissue factor-factor VIIa complex with naive peptide libraries displayed on M13 phage. The peptides specifically block the activation of factor X with a median inhibitory concentration of 1 nM and selectively inhibit tissue-factor-dependent clotting. The peptides do not bind to the active site of factor VIIa; rather, they work by binding to an exosite on the factor VIIa protease domain, and non-competitively inhibit activation of factor X and amidolytic activity. One such peptide (E-76) has a well defined structure in solution determined by NMR spectroscopy that is similar to the X-ray crystal structure when complexed with factor VIIa. These structural and functional studies indicate an allosteric 'switch' mechanism of inhibition involving an activation loop of factor VIIa and represent a new framework for developing inhibitors of serine proteases.     

Na+ mechanism of δ-opioid receptor induced protection from anoxic K+ leakage in the cortex

Activation of δ-opioid receptors (DOR) attenuates anoxic K⁺ leakage and protects cortical neurons from anoxic insults by inhibiting Na⁺ influx. It is unknown, however, which pathway(s) that mediates the Na⁺ influx is the target of DOR signal. In the present work, we found that, in the cortex, (1) DOR protection was largely dependent on the inhibition of anoxic Na⁺ influxes mediated by voltage-gated Na⁺ channels; (2) DOR activation inhibited Na⁺ influx mediated by ionotropic glutamate N-methyl-D-aspartate (NMDA) receptors, but not that by non-NMDA receptors, although both played a role in anoxic K⁺ derangement; and (3) DOR activation had little effect on Na⁺/Ca²⁺ exchanger-based response to anoxia. We conclude that DOR activation attenuates anoxic K⁺ derangement by restricting Na⁺ influx mediated by Na⁺ channels and NMDA receptors, and that non-NMDA receptors and Na⁺/Ca²⁺ exchangers, although involved in anoxic K⁺ derangement in certain degrees, are less likely the targets of DOR signal. Received 26 November 2008; received after revision 26 December 2008; accepted 13 January 2009