Parallel-propagating Fluctuations at Proton-kinetic Scales in the Solar Wind are Dominated by Kinetic Instabilities

We use magnetic helicity to characterise solar wind fluctuations at proton-kinetic scales from Wind observations. For the first time, we separate the contributions to helicity from fluctuations propagating at angles quasi-parallel and oblique to the local mean magnetic field, $\mathbf{B}_0$. We find that the helicity of quasi-parallel fluctuations is consistent with Alfv\'en-ion cyclotron and fast magnetosonic-whistler modes driven by proton temperature anisotropy instabilities and the presence of a relative drift between $\alpha$-particles and protons. We also find that the helicity of oblique fluctuations has little dependence on proton temperature anisotropy and is consistent with fluctuations from the anisotropic turbulent cascade. Our results show that parallel-propagating fluctuations at proton-kinetic scales in the solar wind are dominated by proton temperature anisotropy instabilities and not the turbulent cascade. We also provide evidence that the behaviour of fluctuations at these scales is independent of the origin and macroscopic properties of the solar wind.Comment: Accepted for publication in ApJL. 6 Pages, 3 figures, 1 tabl

Anesthesia for Pediatric Deep Brain Stimulation

In patients refractory to medical therapy, deep brain stimulations (DBSs) have emerged as the treatment of movement disorders particularly Parkinson's disease. Their use has also been extended in pediatric and adult patients to treat epileptogenic foci. We here performed a retrospective chart review of anesthesia records from 28 pediatric cases of patients who underwent DBS implantation for dystonia using combinations of dexmedetomidine and propofol-based anesthesia. Complications with anesthetic techniques including airway and cardiovascular difficulties were analyzed

Solar Cycle Variation of 0.3-1.29 MeV/nucleon Heavy Ion Composition during Quiet Times near 1 AU in Solar Cycles 23 and 24

We report on the annual variation of quiet-time suprathermal ion composition for C through Fe using Advanced Composition Explorer (ACE)/Ultra-Low Energy Isotope Spectrometer (ULEIS) data over the energy range 0.3 MeV/nuc to 1.28 MeV/nuc from 1998 through 2019, covering solar cycle 23's rising phase through Solar Cycle 24's declining phase. Our findings are (1) quiet time suprathermal abundances resemble CIR-associated particles during solar minima; (2) quiet time suprathermals are M/Q fractionated in a manner that is consistent with M/Q fractionation in large gradual solar energetic particle events (GSEP) during solar maxima; and (3) variability within the quiet time suprathermal pool increases as a function of M/Q and is consistent with the analogous variability in GSEP events. From these observations, we infer that quiet time suprathermal ions are remnants of CIRs in solar minima and GSEP events in solar maxima. Coincident with these results, we also unexpectedly show that S behaves like a low FIP ion in the suprathermal regime and therefore drawn from low FIP solar sources.Comment: Accepted in Astrophysical Journal. 19 pages, 10 figures, 4 table

A Majority of Solar Wind Intervals Support Ion-Driven Instabilities

We perform a statistical assessment of solar wind stability at 1 AU against ion sources of free energy using Nyquist's instability criterion. In contrast to typically employed threshold models which consider a single free-energy source, this method includes the effects of proton and He$^{2+}$ temperature anisotropy with respect to the background magnetic field as well as relative drifts between the proton core, proton beam, and He$^{2+}$ components on stability. Of 309 randomly selected spectra from the Wind spacecraft, $53.7\%$ are unstable when the ion components are modeled as drifting bi-Maxwellians; only $4.5\%$ of the spectra are unstable to long-wavelength instabilities. A majority of the instabilities occur for spectra where a proton beam is resolved. Nearly all observed instabilities have growth rates $\gamma$ slower than instrumental and ion-kinetic-scale timescales. Unstable spectra are associated with relatively-large He$^{2+}$ drift speeds and/or a departure of the core proton temperature from isotropy; other parametric dependencies of unstable spectra are also identified.Comment: 6 pages, 3 figures, 2 tables, accepted in Physical Review Letters; fixed typos in version

Loss of huntingtin function slows synaptic vesicle endocytosis in striatal neurons from the htt(Q140/Q140) mouse model of Huntington\u27s disease

Huntington\u27s disease (HD) is caused by CAG repeat expansion within the HTT gene, with the dysfunction and eventual loss of striatal medium spiny neurons a notable feature. Since medium spiny neurons receive high amounts of synaptic input, we hypothesised that this vulnerability originates from an inability to sustain presynaptic performance during intense neuronal activity. To test this hypothesis, primary cultures of either hippocampal or striatal neurons were prepared from either wild-type mice or a knock-in HD mouse model which contains 140 poly-glutamine repeats in the huntingtin protein (htt(Q140/Q140)). We identified a striatum-specific defect in synaptic vesicle (SV) endocytosis in htt(Q140/Q140) neurons that was only revealed during high frequency stimulation. This dysfunction was also present in neurons that were heterozygous for the mutant HTT allele. Depletion of endogenous huntingtin using hydrophobically-modified siRNA recapitulated this activity-dependent defect in wild-type neurons, whereas depletion of mutant huntingtin did not rescue the effect in htt(Q140/Q140) neurons. Importantly, this SV endocytosis defect was corrected by overexpression of wild-type huntingtin in homozygous htt(Q140/Q140) neurons. Therefore, we have identified an activity-dependent and striatum-specific signature of presynaptic dysfunction in neurons derived from pre-symptomatic HD mice, which is due to loss of wild-type huntingtin function. This presynaptic defect may render this specific neuronal subtype unable to operate efficiently during high frequency activity patterns, potentially resulting in dysfunctional neurotransmission, synapse failure and ultimately degeneration