Heliolatitude and time variations of solar wind structure from in situ measurements and interplanetary scintillation observations

The 3D structure of solar wind and its evolution in time is needed for heliospheric modeling and interpretation of energetic neutral atoms observations. We present a model to retrieve the solar wind structure in heliolatitude and time using all available and complementary data sources. We determine the heliolatitude structure of solar wind speed on a yearly time grid over the past 1.5 solar cycles based on remote-sensing observations of interplanetary scintillations, in situ out-of-ecliptic measurements from Ulysses, and in situ in-ecliptic measurements from the OMNI-2 database. Since the in situ information on the solar wind density structure out of ecliptic is not available apart from the Ulysses data, we derive correlation formulae between solar wind speed and density and use the information on the solar wind speed from interplanetary scintillation observations to retrieve the 3D structure of solar wind density. With the variations of solar wind density and speed in time and heliolatitude available we calculate variations in solar wind flux, dynamic pressure and charge exchange rate in the approximation of stationary H atoms.Comment: Accepted for publication in Solar Physic

Astroglial-targeted expression of the fragile X CGG repeat premutation in mice yields RAN translation, motor deficits and possible evidence for cell-to-cell propagation of FXTAS pathology

The fragile X premutation is a CGG trinucleotide repeat expansion between 55 and 200 repeats in the 5′- untranslated region of the fragile X mental retardation 1 (FMR1) gene. Human carriers of the premutation allele are at risk of developing the late-onset neurodegenerative disorder, fragile X-associated tremor/ataxia syndrome (FXTAS). Characteristic neuropathology associated with FXTAS includes intranuclear inclusions in neurons and astroglia. Previous studies recapitulated these histopathological features in neurons in a knock-in mouse model, but without significant astroglial pathology. To determine the role of astroglia in FXTAS, we generated a transgenic mouse line (Gfa2-CGG99-eGFP) that selectively expresses a 99-CGG repeat expansion linked to an enhanced green fluorescent protein (eGFP) reporter in astroglia throughout the brain, including cerebellar Bergmann glia. Behaviorally these mice displayed impaired motor performance on the ladder-rung test, but paradoxically better performance on the rotarod. Immunocytochemical analysis revealed that CGG99- eGFP co-localized with GFAP and S-100ß, but not with NeuN, Iba1, or MBP, indicating that CGG99-eGFP expression is specific to astroglia. Ubiquitin-positive intranuclear inclusions were found in eGFP-expressing glia throughout the brain. In addition, intracytoplasmic ubiquitin-positive inclusions were found outside the nucleus in distal astrocyte processes. Intriguingly, intranuclear inclusions, in the absence of eGFP mRNA and eGFP fluorescence, were present in neurons of the hypothalamus and neocortex. Furthermore, intranuclear inclusions in both neurons and astrocytes displayed immunofluorescent labeling for the polyglycine peptide FMRpolyG, implicating FMRpolyG in the pathology found in Gfa2-CGG99 mice. Considered together, these results show that Gfa2-CGG99 expression in mice is sufficient to induce key features of FXTAS pathology, including formation of intranuclear inclusions, translation of FMRpolyG, and deficits in motor function