The decay and collisions of dark solitons in superfluid Fermi gases

We study soliton collisions and the decay of solitons into sound in superfluid Fermi gases across the Bose-Einstein condensate to Bardeen-Cooper-Schrieffer (BEC-BCS) crossover by performing numerical simulations of the time-dependent Bogoliubov-de Gennes equations. This decay process occurs when the solitons are accelerated to the bulk pair-breaking speed by an external potential. A similar decay process may occur when solitons are accelerated by an inelastic collision with another soliton. We find that soliton collisions become increasingly inelastic as we move from the BEC to BCS regimes, and the excess energy is converted into sound. We interpret this effect as being due to evolution of Andreev bound states localized within the soliton.Comment: 9 pages, 5 figure

Grey solitons in a strongly interacting superfluid Fermi Gas

The Bardeen-Cooper-Schrieffer to Bose-Einstein condensate (BCS to BEC) crossover problem is solved for stationary grey solitons via the Boguliubov-de Gennes equations at zero temperature. These \emph{crossover solitons} exhibit a localized notch in the gap and a characteristic phase difference across the notch for all interaction strengths, from BEC to BCS regimes. However, they do not follow the well-known Josephson-like sinusoidal relationship between velocity and phase difference except in the far BEC limit: at unitary the velocity has a nearly linear dependence on phase difference over an extended range. For fixed phase difference the soliton is of nearly constant depth from the BEC limit to unitarity and then grows progressively shallower into the BCS limit, and on the BCS side Friedel oscillations are apparent in both gap amplitude and phase. The crossover soliton appears fundamentally in the gap; we show, however, that the density closely follows the gap, and the soliton is therefore observable. We develop an approximate power law relationship to express this fact: the density of grey crossover solitons varies as the square of the gap amplitude in the BEC limit and a power of about 1.5 at unitarity.Comment: 10 pages, 6 figures, part of New Journal of Physics focus issue "Strongly Correlated Quantum Fluids: From Ultracold Quantum Gases to QCD Plasmas," in pres

Association between age at disease onset of anti-neutrophil cytoplasmic antibody-associated vasculitis and clinical presentation and short-term outcomes

Objectives: ANCA-associated vasculitis (AAV) can affect all age groups. We aimed to show that differences in disease presentation and 6 month outcome between younger- A nd older-onset patients are still incompletely understood. Methods: We included patients enrolled in the Diagnostic and Classification Criteria for Primary Systemic Vasculitis (DCVAS) study between October 2010 and January 2017 with a diagnosis of AAV. We divided the population according to age at diagnosis: <65 years or ≥65 years. We adjusted associations for the type of AAV and the type of ANCA (anti-MPO, anti-PR3 or negative). Results: A total of 1338 patients with AAV were included: 66% had disease onset at <65 years of age [female 50%; mean age 48.4 years (s.d. 12.6)] and 34% had disease onset at ≥65 years [female 54%; mean age 73.6 years (s.d. 6)]. ANCA (MPO) positivity was more frequent in the older group (48% vs 27%; P = 0.001). Younger patients had higher rates of musculoskeletal, cutaneous and ENT manifestations compared with older patients. Systemic, neurologic,cardiovascular involvement and worsening renal function were more frequent in the older-onset group. Damage accrual, measured with the Vasculitis Damage Index (VDI), was significantly higher in older patients, 12% of whom had a 6 month VDI ≥5, compared with 7% of younger patients (P = 0.01). Older age was an independent risk factor for early death within 6 months from diagnosis [hazard ratio 2.06 (95% CI 1.07, 3.97); P = 0.03]. Conclusion: Within 6 months of diagnosis of AAV, patients >65 years of age display a different pattern of organ involvement and an increased risk of significant damage and mortality compared with younger patients

The genomic landscape of balanced cytogenetic abnormalities associated with human congenital anomalies

Despite the clinical significance of balanced chromosomal abnormalities (BCAs), their characterization has largely been restricted to cytogenetic resolution. We explored the landscape of BCAs at nucleotide resolution in 273 subjects with a spectrum of congenital anomalies. Whole-genome sequencing revised 93% of karyotypes and demonstrated complexity that was cryptic to karyotyping in 21% of BCAs, highlighting the limitations of conventional cytogenetic approaches. At least 33.9% of BCAs resulted in gene disruption that likely contributed to the developmental phenotype, 5.2% were associated with pathogenic genomic imbalances, and 7.3% disrupted topologically associated domains (TADs) encompassing known syndromic loci. Remarkably, BCA breakpoints in eight subjects altered a single TAD encompassing MEF2C, a known driver of 5q14.3 microdeletion syndrome, resulting in decreased MEF2C expression. We propose that sequence-level resolution dramatically improves prediction of clinical outcomes for balanced rearrangements and provides insight into new pathogenic mechanisms, such as altered regulation due to changes in chromosome topology