Radial Evolution of Thermal and Suprathermal Electron Populations in the Slow Solar Wind from 0.13 to 0.5 au: Parker Solar Probe Observations

We develop and apply a bespoke fitting routine to a large volume of solar wind electron distribution data measured by Parker Solar Probe (PSP) over its first five orbits, covering radial distances from 0.13 to 0.5 au. We characterise the radial evolution of the electron core, halo and strahl populations in the slow solar wind during these orbits. The fractional densities of these three electron populations provide evidence for the growth of the combined suprathermal halo and strahl populations from 0.13 to 0.17 au. Moreover, the growth in the halo population is not matched by a decrease of the strahl population at these distances, as has been reported for previous observations at distances greater than 0.3 au. We also find that the halo is negligible at small heliocentric distances. The fractional strahl density remains relatively constant ~1% below 0.2 au, suggesting that the rise in the relative halo density is not solely due to the transfer of strahl electrons into the halo

The Stability of the Electron Strahl against the Oblique Fast-magnetosonic/Whistler Instability in the Inner Heliosphere

We analyze the micro-kinetic stability of the electron strahl in the solar wind depending on heliocentric distance. The oblique fast-magnetosonic/whistler (FM/W) instability has emerged in the literature as a key candidate mechanism for the effective scattering of the electron strahl into the electron halo population. Using data from the Parker Solar Probe (PSP) and Helios, we compare the measured strahl properties with the analytical thresholds for the oblique FM/W instability in the low- and high-β ∥c regimes, where β ∥c is the ratio of the core parallel thermal pressure to the magnetic pressure. Our PSP and Helios data show that the electron strahl is on average stable against the oblique FM/W instability in the inner heliosphere. Our analysis suggests that the instability, if at all, can only be excited sporadically and on short timescales. We discuss the caveats of our analysis and potential alternative explanations for the observed scattering of the electron strahl in the solar wind. Furthermore, we recommend the numerical evaluation of the stability of individual distributions in the future to account for any uncertainties in the validity of the analytical expressions for the instability thresholds

Radial Evolution of Thermal and Suprathermal Electron Populations in the Slow Solar Wind from 0.13 to 0.5 au: Parker Solar Probe Observations

We develop and apply a bespoke fitting routine to a large volume of solar wind electron distribution data measured by Parker Solar Probe over its first five orbits, covering radial distances from 0.13 to 0.5 au. We characterize the radial evolution of the electron core, halo, and strahl populations in the slow solar wind during these orbits. The fractional densities of these three electron populations provide evidence for the growth of the combined suprathermal halo and strahl populations from 0.13 to 0.17 au. Moreover, the growth in the halo population is not matched by a decrease in the strahl population at these distances, as has been reported for previous observations at distances greater than 0.3 au. We also find that the halo is negligible at small heliocentric distances. The fractional strahl density remains relatively constant at ∼1% below 0.2 au, suggesting that the rise in the relative halo density is not solely due to the transfer of strahl electrons into the halo

The Kinetic Expansion of Solar-wind Electrons: Transport Theory and Predictions for the Very Inner Heliosphere

We propose a transport theory for the kinetic evolution of solar-wind electrons in the heliosphere. We derive a gyro-averaged kinetic transport equation that accounts for the spherical expansion of the solar wind and the geometry of the Parker spiral magnetic field. To solve our three-dimensional kinetic equation, we develop a mathematical approach that combines the Crank–Nicolson scheme in velocity space and a finite-difference Euler scheme in configuration space. We initialize our model with isotropic electron distribution functions and calculate the kinetic expansion at heliocentric distances from 5 to 20 solar radii. In our kinetic model, the electrons evolve mainly through the combination of ballistic particle streaming, the magnetic mirror force, and the electric field. By applying fits to our numerical results, we quantify the parameters of the electron strahl and the core part of the electron velocity distributions. The strahl fit parameters show that the density of the electron strahl is around 7% of the total electron density at a distance of 20 solar radii, the strahl bulk velocity and strahl temperature parallel to the background magnetic field stay approximately constant beyond a distance of 15 solar radii, and β∥s (i.e., the ratio of the strahl parallel thermal pressure to the magnetic pressure) is approximately constant with heliocentric distance at a value of about 0.02. We compare our results with data measured by the Parker Solar Probe. Furthermore, we provide theoretical evidence that the electron strahl is not scattered by the oblique fast-magnetosonic/whistler instability in the near-Sun environment

A multinational case series describing successful treatment of persistent SARS-CoV-2 infection caused by Omicron sublineages with prolonged courses of nirmatrelvir/ritonavir.

The optimum treatment for persistent infection with SARS-CoV-2 is not known. Our case series, across 5 hospitals in 3 countries, describes 11 cases where persistent SARS-CoV-2 infection was successfully treated with prolonged courses (median 10 days, range 10-18) of nirmatrelvir/ritonavir (Paxlovid). Most cases (9/11) had haematological malignancy and ten (10/11) had received CD20 depleting therapy. The median duration of infection was 103 days (IQR 85-138). The majority (10/11) were hospitalised, and seven (7/11) had severe/critical disease. All survived and 9/11 demonstrated viral clearance, almost half (4/9) of whom received nirmatrelvir/ritonavir as monotherapy. This case series suggests prolonged nirmatrelvir/ritonavir has a role in treating persistent infection

Association of a de novo 16q copy number variant with a phenotype that overlaps with Lenz microphthalmia and Townes-Brocks syndromes

<p>Abstract</p> <p>Background</p> <p>Anophthalmia and microphthalmia are etiologically and clinically heterogeneous. Lenz microphthalmia is a syndromic form that is typically inherited in an X-linked pattern, though the causative gene mutation is unknown. Townes-Brocks syndrome manifests thumb anomalies, imperforate anus, and ear anomalies. We present a 13-year-old boy with a syndromic microphthalmia phenotype and a clinical diagnosis of Lenz microphthalmia syndrome.</p> <p>Case Presentation</p> <p>The patient was subjected to clinical and molecular evaluation, including array CGH analysis. The clinical features included left clinical anophthalmia, right microphthalmia, anteriorly placed anus with fistula, chordee, ventriculoseptal defect, patent ductus arteriosus, posteriorly rotated ears, hypotonia, growth retardation with delayed bone age, and mental retardation. The patient was found to have an approximately 5.6 Mb deletion of 16q11.2q12.1 by microarray based-comparative genomic hybridization, which includes the <it>SALL1 </it>gene, which causes Townes-Brocks syndrome.</p> <p>Conclusions</p> <p>Deletions of 16q11.2q12.2 have been reported in several individuals, although those prior reports did not note microphthalmia or anophthalmia. This region includes <it>SALL1</it>, which causes Townes-Brocks syndrome. In retrospect, this child has a number of features that can be explained by the <it>SALL1 </it>deletion, although it is not clear if the microphthalmia is a rare feature of Townes-Brocks syndrome or caused by other mechanisms. These data suggest that rare copy number changes may be a cause of syndromic microphthalmia allowing a personalized genomic medicine approach to the care of patients with these aberrations.</p

Midbrain-Hindbrain Involvement in Septo-Optic Dysplasia

BACKGROUND AND PURPOSE: Midbrain-hindbrain involvement in septo-optic dysplasia has not been well described, despite reported mutations of genes regulating brain stem patterning. We aimed to describe midbrain-hindbrain involvement in patients with septo-optic dysplasia and to identify possible clinical-neuroimaging correlations. MATERIALS AND METHODS: Using MR imaging, we categorized 38 patients (21 males) based on the presence (group A, 21 patients) or absence (group B, 17 patients) of visible brain stem anomalies. We measured height and anteroposterior diameter of midbrain, pons, and medulla, anteroposterior midbrain/pons diameter (M/P ratio), vermian height, and tegmento-vermian angle, and compared the results with 114 healthy age-matched controls. Furthermore, patients were subdivided based on the type of midline anomalies. The associations between clinical and neuroradiological features were investigated. Post hoc tests were corrected according to Bonferroni adjustment (pB). RESULTS: Patients with brain stem abnormalities had smaller anteroposterior pons diameter than controls (pB CONCLUSION: Midbrain-hindbrain abnormalities are a significant, albeit underrecognized, component of the septo-optic dysplasia spectrum, and are significantly associated with developmental delay in affected patients

Loss of the BMP Antagonist, SMOC-1, Causes Ophthalmo-Acromelic (Waardenburg Anophthalmia) Syndrome in Humans and Mice

Ophthalmo-acromelic syndrome (OAS), also known as Waardenburg Anophthalmia syndrome, is defined by the combination of eye malformations, most commonly bilateral anophthalmia, with post-axial oligosyndactyly. Homozygosity mapping and subsequent targeted mutation analysis of a locus on 14q24.2 identified homozygous mutations in SMOC1 (SPARC-related modular calcium binding 1) in eight unrelated families. Four of these mutations are nonsense, two frame-shift, and two missense. The missense mutations are both in the second Thyroglobulin Type-1 (Tg1) domain of the protein. The orthologous gene in the mouse, Smoc1, shows site- and stage-specific expression during eye, limb, craniofacial, and somite development. We also report a targeted pre-conditional gene-trap mutation of Smoc1 (Smoc1tm1a) that reduces mRNA to ∼10% of wild-type levels. This gene-trap results in highly penetrant hindlimb post-axial oligosyndactyly in homozygous mutant animals (Smoc1tm1a/tm1a). Eye malformations, most commonly coloboma, and cleft palate occur in a significant proportion of Smoc1tm1a/tm1a embryos and pups. Thus partial loss of Smoc-1 results in a convincing phenocopy of the human disease. SMOC-1 is one of the two mammalian paralogs of Drosophila Pentagone, an inhibitor of decapentaplegic. The orthologous gene in Xenopus laevis, Smoc-1, also functions as a Bone Morphogenic Protein (BMP) antagonist in early embryogenesis. Loss of BMP antagonism during mammalian development provides a plausible explanation for both the limb and eye phenotype in humans and mice

P4 1 Lightning in Inazuma, the Devastation of the Musou no Hitotachi

In this paper, we examine Genshin Impact’s Raiden Shogun’s ability to split a mountain in half and simulate the resultant plasma from the release of 1.7×1023J of energy. Our models suggest that the large pressure gradient primarily drives the cooling of this plasma, overshadowing other radiative processes