Demonstration of an electric field conjugation algorithm for improved starlight rejection through a single mode optical fiber

Linking a coronagraph instrument to a spectrograph via a single mode optical fiber is a pathway towards detailed characterization of exoplanet atmospheres with current and future ground- and space-based telescopes. However, given the extreme brightness ratio and small angular separation between planets and their host stars, the planet signal-to-noise ratio will likely be limited by the unwanted coupling of starlight into the fiber. To address this issue, we utilize a wavefront control loop and a deformable mirror to systematically reject starlight from the fiber by measuring what is transmitted through the fiber. The wavefront control algorithm is based on the formalism of electric field conjugation (EFC), which in our case accounts for the spatial mode selectivity of the fiber. This is achieved by using a control output that is the overlap integral of the electric field with the fundamental mode of a single mode fiber. This quantity can be estimated by pair-wise image plane probes injected using a deformable mirror. We present simulation and laboratory results that demonstrate our approach offers a significant improvement in starlight suppression through the fiber relative to a conventional EFC controller. With our experimental setup, which provides an initial normalized intensity of $3\times10^{-4}$ in the fiber at an angular separation of $4\lambda/D$, we obtain a final normalized intensity of $3\times 10^{-6}$ in monochromatic light at $\lambda=635$~nm through the fiber (100x suppression factor) and $2\times 10^{-5}$ in $\Delta\lambda/\lambda=8\%$ broadband light about $\lambda=625$~nm (10x suppression factor). The fiber-based approach improves the sensitivity of spectral measurements at high contrast and may serve as an integral part of future space-based exoplanet imaging missions as well as ground-based instruments

Rare missense variants in the SH3 domain of PSTPIP1 are associated with hidradenitis suppurativa

Summary: Hidradenitis suppurativa (HS) is a chronic, debilitating skin disease for which few treatment options are available. While most HS is sporadic, some rare kindred show a high-penetrance, autosomal-dominant inheritance. We wanted to identify rare variants that could contribute to HS risk in sporadic cases using candidate gene sequencing. We ultimately identified 21 genes for our capture panel. We included genes of the γ-secretase complex (n = 6) because rare variants in these genes sometimes cause familial HS. We added Notch receptor and ligand genes (n = 13) because γ-secretase is critical for processing Notch receptor signaling. Clinically, some people with PAPA (pyogenic arthritis, pyoderma gangrenosum, and acne) syndrome, a rare inflammatory disease, have concurrent HS. Rare variants in PSTPIP1 are known to cause PAPA syndrome, so we included PSTPIP1 and PSTPIP2 in the capture panel. We screened 117 individuals with HS for rare variations and calculated the expected burden using Genome Aggregation Database (gnomAD) allele frequencies. We discovered two pathogenic loss-of-function variants in NCSTN. This class of NCSTN variant can cause familial HS. There was no increased burden of rare variations in any γ-secretase complex gene. We did find that individuals with HS had a significantly increased number of rare missense variants in the SH3 domain of PSTPIP1. This finding, therefore, implicates PSTPIP1 variation in sporadic HS and further supports dysregulated immunity in HS. Our data also suggests that population-scale HS genetic research will yield valuable insights into disease pathology

Destroying activity of magnetoferritin on lysozyme amyloid fibrils

Presence of protein amyloid aggregates (oligomers, protofilaments, fibrils) is associated with many diseases as diabetes mellitus or Alzheimer's disease. The interaction between lysozyme amyloid fibrils and magnetoferritin loaded with different amount of iron atoms (168 or 532 atoms) has been investigated by small-angle X-rays scattering and thioflavin T fluorescence measurements. Results suggest that magnetoferritin caused an iron atom-concentration dependent reduction of lysozyme fibril siz