Enhancements of energetic particles near the heliospheric termination shock

The spacecraft Voyager 1 is at a distance greater than 85 au from the Sun, in the vicinity of the termination shock that marks the abrupt slowing of the supersonic solar wind and the beginning of the extended and unexplored distant heliosphere. This shock is expected to accelerate 'anomalous cosmic rays', as well as to re-accelerate Galactic cosmic rays and low-energy particles from the inner Solar System. Here we report a significant increase in the numbers of energetic ions and electrons that persisted for seven months beginning in mid-2002. This increase differs from any previously observed in that there was a simultaneous increase in Galactic cosmic ray ions and electrons, anomalous cosmic rays and low-energy ions. The low-intensity level and spectral energy distribution of the anomalous cosmic rays, however, indicates that Voyager 1 still has not reached the termination shock. Rather, the observed increase is an expected precursor event. We argue that the radial anisotropy of the cosmic rays is expected to be small in the foreshock region, as is observed.     

Inactivation of superoxide dismutase by several thiocarbamic acid derivatives

Summary 4 thiocarbamic acid derivatives inhibited superoxide dismutase (SOD) activity in vitro. Dimethyldithiocarbamate also inhibited tissue SOD in mice in vivo. These data extend previously published results on the inhibitory action of diethyldithiocarbamate on SOD activity.Supported by the Clinical Research Center for the study of Parkinson's and Allied Diseases, Grant NS-05184 from the US Public Health Service.     

In vivo generation of hydrogen peroxide from 6-hydroxydopamine

Zusammenfassung Es gelang, die Erythrocytenkatalase der Maus durch Injektion von 6-Hydroxydopamin und in Gegenwart von 3-Amino-1,2,4-triazol zu hemmen, was auf die Wasserstoffperoxyd-Entwicklung hinweist und mit der Rolle des H₂O₂ bei der Degeneration der Nervenenden durch 6-Hydroxydopamin in Einklang steht.     

An asymmetric solar wind termination shock

Voyager 2 crossed the solar wind termination shock at 83.7 au in the southern hemisphere, approximately 10 au closer to the Sun than found by Voyager 1 in the north. This asymmetry could indicate an asymmetric pressure from an interstellar magnetic field, from transient-induced shock motion, or from the solar wind dynamic pressure. Here we report that the intensity of 4-5 MeV protons accelerated by the shock near Voyager 2 was three times that observed concurrently by Voyager 1, indicating differences in the shock at the two locations. (Companion papers report on the plasma, magnetic field, plasma-wave and lower energy particle observations at the shock.) Voyager 2 did not find the source of anomalous cosmic rays at the shock, suggesting that the source is elsewhere on the shock or in the heliosheath. The small intensity gradient of Galactic cosmic ray helium indicates that either the gradient is further out in the heliosheath or the local interstellar Galactic cosmic ray intensity is lower than expected.     

Heat shock protein gene expression during Xenopus development

Stress-induced heat shock protein gene expression is developmentally regulated during early embryogen esis of the frog, Xenopus laevis. For example, a number of heat shock protein genes, such as hsp70, hsp90, and ubiquitin are not heat-inducible until after the midblastula stage of embryogenesis. Furthermore, the family of small heat shock protein genes, hsp30, are differentially expressed after the midblastula stage as well as being regulated at the level of mRNA stability. Many of these stress proteins are also synthesized constitutively during oogenesis and embryogenesis during which they may act as molecular chaperones as well as being involved in sequestering proteins in an inactive state until required by the developing embryo. Furthermore the induction of these stress protein genes has been correlated with enhanced thermoresistance. During stressful conditions heat shock proteins probably prevent aggregation or misfolding of damaged protei ns within the embryo.     

Protection against the dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine by monoamine oxidase inhibitors

1-Methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) causes degeneration of the dopaminergic nigrostriatal pathway in several animal species, including humans, monkeys and mice. Changes observed after MPTP administration include marked decrements in the neostriatal content of dopamine and its major metabolites, dihydroxyphenylacetic acid and homovanillic acid, and a greatly diminished capacity of neostriatal synaptosomes to take up 3H-dopamine. In contrast, there is no pronounced loss of serotonin in the neostriatum or of dopamine and its metabolites in other brain areas in MPTP-treated animals. The oxidative metabolism of MPTP to 1-methyl-4-phenyl pyridine, a positively charged species, has been suggested as a critical feature in the neurotoxic process. Moreover, in rat brain preparations, the monoamine oxidase (MAO) inhibitor pargyline and the specific MAO-B inhibitor deprenil can prevent the formation of 1-methyl-4-phenyl-pyridine from MPTP, while the specific MAO-A inhibitor clorgyline has no such effect, suggesting that MAO, and specifically MAO-B, is responsible for the oxidative metabolism of MPTP. We now report that pargyline, nialamide and tranylcypromine, which inhibit both MAO-A and MAO-B, when administered to mice before MPTP, protect against MPTP-induced dopaminergic neurotoxicity. Deprenil is also protective, but clorgyline is not. Our data are consistent with the premise that MAO-B has a crucial role in MPTP-induced degeneration of the nigrostriatal dopaminergic neuronal pathway.     

The generation of the superoxide radical by 2-amino-4-hydroxy-6,7-dimethyl-5,6,7,8-tetrahydropteridine (DMPH4)

Zusammenfassung Es werden neue Befunde beigebracht, die für die Bildung von Superoxyd-Radikal durch DMPH₄, ein biologisch wichtiges Pterinderivat, sprechen.

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This work was supported by the Clinical Research Center for Parkinsons and Allied Diseases and USPHS Grant No. NS-05184.     

The prevention of alloxan-induced diabetes in mice by the iron-chelator detapac: Suggestion of a role for iron in the cytotoxic process

Summary DETAPAC, an iron-chelating agent, given to male Swiss-Webster mice prior to alloxan, was able to protect the mice from the diabetogenic actions of alloxan. In contrast EDTA, another chelating agent, offered no protection. Possible mechanisms for these effects, including inhibition of hydroxyl radical formation, will be discussed.Supported in part by grant AM-27328 from the US Public Health Service.