Galaxy-Galaxy Flexion: Weak Lensing to Second Order

In this paper, we develop a new gravitational lensing inversion technique. While traditional approaches assume that the lensing field varies little across a galaxy image, we note that this variation in the field can give rise to a ``Flexion'' or bending of a galaxy image, which may then be used to detect a lensing signal with increased signal to noise. Since the significance of the Flexion signal increases on small scales, this is ideally suited to galaxy-galaxy lensing. We develop an inversion technique based on the ``Shapelets'' formalism of Refregier (2003). We then demonstrate the proof of this concept by measuring a Flexion signal in the Deep Lens Survey. Assuming an intrinsically isothermal distribution, we find from the Flexion signal alone a velocity width of v_c=221\pm 12 km/s for lens galaxies of r < 21.5, subject to uncertainties in the intrinsic Flexion distribution.Comment: 11 pages, Latex, 4 figures. Accepted by ApJ, changes include revision of errors from previous draf

Strategies for the treatment of Hepatitis C in an era of interferon-free therapies: what public health outcomes do we value most?

Objective: The expense of new therapies for HCV infection may force health systems to prioritise the treatment of certain patient groups over others. Our objective was to forecast the population impact of possible prioritisation strategies for the resource-rich setting of Scotland. Design: We created a dynamic Markov simulation model to reflect the HCV-infected population in Scotland. We determined trends in key outcomes (e.g. incident cases of chronic infection and severe liver morbidity (SLM)) until the year 2030, according to treatment strategies involving prioritising, either: (A) persons with moderate/advanced fibrosis or (B) persons who inject drugs (PWID). Results: Continuing to treat the same number of patients with the same characteristics will give rise to a fall in incident infection (from 600 cases in 2015 to 440 in 2030) and a fall in SLM (from 195 cases in 2015 to 145 in 2030). Doubling treatment-uptake and prioritising PWID will reduce incident infection to negligible levels (&#60;50 cases per year) by 2025, while SLM will stabilise (at 70–75 cases per year) in 2028. Alternatively, doubling the number of patients treated, but, instead, prioritising persons with moderate/advanced fibrosis will reduce incident infection less favourably (only to 280 cases in 2030), but SLM will stabilise by 2023 (i.e. earlier than any competing strategy). Conclusions: Prioritising treatment uptake among PWID will substantially impact incident transmission, however, this approach foregoes the optimal impact on SLM. Conversely, targeting those with moderate/advanced fibrosis has the greatest impact on SLM but is suboptimal in terms of averting incident infection

Monolayer MoS2 strained to 1.3% with a microelectromechanical system

We report on a modified transfer technique for atomically thin materials integrated onto microelectromechanical systems (MEMS) for studying strain physics and creating strain-based devices. Our method tolerates the non-planar structures and fragility of MEMS, while still providing precise positioning and crack free transfer of flakes. Further, our method used the transfer polymer to anchor the 2D crystal to the MEMS, which reduces the fabrication time, increases the yield, and allowed us to exploit the strong mechanical coupling between 2D crystal and polymer to strain the atomically thin system. We successfully strained single atomic layers of molybdenum disulfide (MoS2) with MEMS devices for the first time and achieved greater than 1.3% strain, marking a major milestone for incorporating 2D materials with MEMS We used the established strain response of MoS2 Raman and Photoluminescence spectra to deduce the strain in our crystals and provide a consistency check. We found good comparison between our experiment and literature.Published versio

Unfair competition governs the interaction of pCPI-17 with myosin phosphatase (PP1-MYPT1).

The small phosphoprotein pCPI-17 inhibits myosin light-chain phosphatase (MLCP). Current models postulate that during muscle relaxation, phosphatases other than MLCP dephosphorylate and inactivate pCPI-17 to restore MLCP activity. We show here that such hypotheses are insufficient to account for the observed rapidity of pCPI-17 inactivation in mammalian smooth muscles. Instead, MLCP itself is the critical enzyme for pCPI-17 dephosphorylation. We call the mutual sequestration mechanism through which pCPI-17 and MLCP interact inhibition by unfair competition: MLCP protects pCPI-17 from other phosphatases, while pCPI-17 blocks other substrates from MLCP\u27s active site. MLCP dephosphorylates pCPI-17 at a slow rate that is, nonetheless, both sufficient and necessary to explain the speed of pCPI-17 dephosphorylation and the consequent MLCP activation during muscle relaxation