The price of being SM-like in SUSY

We compute the tuning in supersymmetric models associated with the constraints from collider measurements of the Higgs couplings to fermions and gauge bosons. In supersymmetric models, a CP-even state with SM Higgs couplings mixes with additional, heavier CP-even states, causing deviations in the Higgs couplings from SM values. These deviations are reduced as the heavy states are decoupled with large soft masses, thereby exacerbating the tuning associated with the electroweak scale. This new source of tuning is different from that derived from collider limits on stops, gluinos and Higgsinos. It can be offset with large tan beta in the MSSM, however this compensating effect is limited in the NMSSM with a large Higgs-singlet coupling due to restrictions on large tan beta from electroweak precision tests. We derive a lower bound on this tuning and show that the level of precision of Higgs coupling measurements at the LHC will probe naturalness in the NMSSM at the few-percent level. This is comparable to the tuning derived from superpartner limits in models with a low messenger scale and split families. Instead the significant improvement in sensitivity of Higgs coupling measurements at the ILC will allow naturalness in these models to be constrained at the per-mille level, beyond any tuning derived from direct superpartner limits.Comment: 29 pages, 6 figure

Microsecond Lifetimes and Low Interface Recombination Velocities in Moderately Doped n-GaAs Thin Films

We have observed lifetimes greater than 1 ps in moderately doped, thin film, n-GaAs/A1a,Gae,As double heterostructure membranes formed by etching away the substrate. We attribute these ultralong lifetimes to enhanced photon recycling caused by the removal of the substrate. Nonradiative recombination in the bulk and at the interfaces is very low; the upper limit of the interface recombination velocity is 25 cm/S.-Such long lifetimes in GaAs doped at N,= 1.3 X 10” cme3 suggest that thin-film solar cells offer a potential option for achieving very high efficiencies

The Extrasolar Planet epsilon Eridani b - Orbit and Mass

Hubble Space Telescope observations of the nearby (3.22 pc), K2 V star epsilon Eridani have been combined with ground-based astrometric and radial velocity data to determine the mass of its known companion. We model the astrometric and radial velocity measurements simultaneously to obtain the parallax, proper motion, perturbation period, perturbation inclination, and perturbation size. Because of the long period of the companion, \eps b, we extend our astrometric coverage to a total of 14.94 years (including the three year span of the \HST data) by including lower-precision ground-based astrometry from the Allegheny Multichannel Astrometric Photometer. Radial velocities now span 1980.8 -- 2006.3. We obtain a perturbation period, P = 6.85 +/- 0.03 yr, semi-major axis, alpha =1.88 +/- 0.20 mas, and inclination i = 30.1 +/- 3.8 degrees. This inclination is consistent with a previously measured dust disk inclination, suggesting coplanarity. Assuming a primary mass M_* = 0.83 M_{\sun}, we obtain a companion mass M = 1.55 +/- 0.24 M_{Jup}. Given the relatively young age of epsilon Eri (~800 Myr), this accurate exoplanet mass and orbit can usefully inform future direct imaging attempts. We predict the next periastron at 2007.3 with a total separation, rho = 0.3 arcsec at position angle, p.a. = -27 degrees. Orbit orientation and geometry dictate that epsilon Eri b will appear brightest in reflected light very nearly at periastron. Radial velocities spanning over 25 years indicate an acceleration consistent with a Jupiter-mass object with a period in excess of 50 years, possibly responsible for one feature of the dust morphology, the inner cavity

A study of minority carrier lifetime versus doping concentration in n‐type GaAs grown by metalorganic chemical vapor deposition

Time‐resolved photoluminescence decay measurements are used to explore minority carrier recombination in n‐type GaAs grown by metalorganic chemical vapor deposition, and doped with selenium to produce electron concentrations from 1.3×1017 cm−3 to 3.8×1018 cm−3. For electron densities n0\u3c1018 cm−3, the lifetime is found to be controlled by radiative recombination and photon recycling with no evidence of Shockley–Read–Hall recombination. For higher electron densities, samples show evidence of Shockley–Read–Hall recombination as reflected in the intensity dependence of the photoluminescence decay. Still, we find that radiative recombination and photon recycling are important for all electron concentrations studied, and no evidence for Auger recombination was observed

Lacosamide add-on therapy for focal epilepsy

BACKGROUND: This is an updated version of the Cochrane review published in 2015. Around half of people with epilepsy will not achieve seizure freedom on their first antiepileptic drug; many will require add‐on therapy. Around a third of people fail to achieve complete seizure freedom despite multiple antiepileptic drugs. Lacosamide has been licenced as an add‐on therapy for drug‐resistant focal epilepsy. OBJECTIVES: To evaluate the efficacy and tolerability of lacosamide as an add‐on therapy for children and adults with drug‐resistant focal epilepsy. SEARCH METHODS: We searched the following databases (22 August 2019): the Cochrane Register of Studies (CRS Web), including the Cochrane Epilepsy Group Specialized Register and the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE (Ovid, 1946 to 20 August 2019), ClinicalTrials.gov, and the WHO International Clinical Trials Registry Platform (ICTRP), with no language restrictions. We contacted UCB Pharma (sponsors of lacosamide). SELECTION CRITERIA: Randomised controlled trials of add‐on lacosamide in people with drug‐resistant focal epilepsy. DATA COLLECTION AND ANALYSIS: We used standard Cochrane methodology, assessing the following outcomes: 50% or greater reduction in seizure frequency; seizure freedom; treatment withdrawal; adverse events; quality of life; and cognitive changes. The primary analyses were intention‐to‐treat. We estimated summary risk ratios (RR) for each outcome presented with 99% confidence intervals (CI), except for 50% or greater seizure reduction, seizure freedom and treatment withdrawal which were presented with 95% CIs. We performed subgroup analyses according to lacosamide dose and sensitivity analyses according to population age, whereby data from children were excluded from the meta‐analysis. MAIN RESULTS: We included five trials (2199 participants). The risk of bias for all studies was low to unclear. All studies were placebo‐controlled and assessed doses from 200 mg to 600 mg per day. One study evaluated lacosamide in children; all other studies were in adults. Trial duration ranged from 24 to 26 weeks. All studies used adequate methods of randomisation and were double‐blind. Overall, the certainty of the evidence for the outcomes was judged as moderate to high, with the exception of seizure freedom which was low. The RR for a 50% or greater reduction in seizure frequency for all doses of lacosamide compared with placebo was 1.79 (95% CI 1.55 to 2.08; 5 studies; 2199 participants; high‐certainty evidence). The RR for seizure freedom for all doses of lacosamide compared with placebo was 2.27 (95% CI 1.35 to 3.83; 5 studies; 2199 participants; low‐certainty evidence). The RR for treatment withdrawal for all doses of lacosamide compared with placebo was 1.57 (95% CI 1.24 to 1.98; 5 studies; 2199 participants; moderate‐certainty evidence). The estimated effect size for most outcomes did not change considerably following sensitivity analysis. For seizure freedom, however, the RR nearly doubled upon the exclusion of data from children (RR 4.04, 95% CI 1.52 to 10.73). Adverse events associated with lacosamide included: abnormal co‐ordination (RR 6.12, 99% CI 1.35 to 27.77), blurred vision (RR 4.65, 99% CI 1.24 to 17.37), diplopia (RR 5.59, 99% CI 2.27 to 13.79), dizziness (RR 2.96, 99% CI 2.09 to 4.20), nausea (RR 2.35, 99% CI 1.37 to 4.02), somnolence (RR 2.04, 99% CI 1.22 to 3.41), vomiting (RR 2.94, 99% CI 1.54 to 5.64), and number of participants experiencing one or more adverse events (RR 1.12, 99% CI 1.01 to 1.24). Adverse events that were not significant were: vertigo (RR 3.71, 99% CI 0.86 to 15.95), rash (RR 0.58, 99% CI 0.17 to 1.89), nasopharyngitis (RR 1.41, 99% CI 0.87 to 2.28), headache (RR 1.34, 99% CI 0.90 to 1.98), fatigue (RR 2.11, 99% CI 0.92 to 4.85), nystagmus (RR 1.47, 99% CI 0.61 to 3.52), and upper respiratory tract infection (RR 0.70, 99% CI 0.43 to 1.15). AUTHORS' CONCLUSIONS: Lacosamide is effective and well‐tolerated in the short term when used as add‐on treatment for drug‐resistant focal epilepsy. Lacosamide increases the number of people with 50% or greater reduction in seizure frequency and may increase seizure freedom, compared to placebo. Higher doses of lacosamide may be associated with higher rates of adverse events and treatment withdrawal. Additional evidence is required assessing the use of lacosamide in children and on longer‐term efficacy and tolerability

Central amygdala metabotropic glutamate receptor 5 in the modulation of visceral pain

Painful bladder syndrome is a debilitating condition that affects 3–6% of women in the United States. Multiple lines of evidence suggest that changes in central nervous system processing are key to the development of chronic bladder pain conditions, but little is known regarding the underlying cellular, molecular, and neuronal mechanisms. Using a mouse model of distension-induced bladder pain, we found that the central nucleus of the amygdala (CeA) is a critical site of neuromodulation for processing of bladder nociception. Furthermore, we demonstrate that metabotropic glutamate receptor 5 (mGluR5) activation in the CeA induces bladder pain sensitization by increasing CeA output. Thus, pharmacological activation of mGluR5 in the CeA is sufficient to increase the response to bladder distension. Additionally, pharmacological blockade or virally-mediated conditional deletion of mGluR5 in the CeA reduced responses to bladder distention suggesting that mGluR5 in the CeA is also necessary for these responses. Finally, we used optogenetic activation of the CeA and demonstrated that this caused a robust increase in the visceral pain response. The CeA localized effects on responses to bladder distention are associated with changes in extracellular signal regulated kinases 1/2 phosphorylation in the spinal cord. Overall, these data demonstrate that mGluR5 activation leads to increased CeA output that drives bladder pain sensitization