How many stars form in galaxy mergers?

We forward model the difference in stellar age between post-coalescence mergers and a control sample with the same stellar mass, environmental density, and redshift. In particular, we use a pure sample of 445 post-coalescence mergers from the recent visually-confirmed post-coalescence merger sample identified by Bickley et al. and find that post-coalescence mergers are on average younger than control galaxies for $10<\log (M_\star/\mathrm{M}_\odot)<11$. The difference in age from matched controls is up to 1.5 Gyr, highest for lower stellar mass galaxies. We forward model this difference using parametric star formation histories, accounting for the pre-coalescence inspiral phase of enhanced star formation using close pair data, and a final additive burst of star formation at coalescence. We find a best-fitting stellar mass burst fraction of $f_\mathrm{burst}=\Delta M_\star/M_{\star,\mathrm{merger}}=0.18 \pm 0.02$ for $10<\log (M_\star/\mathrm{M}_\odot)<11$ galaxies, with no evidence of a trend in stellar mass. The modeled burst fraction is robust to choice of parametric star formation history, as well as differences in burst duration. The result appears consistent with some prior observationally-derived values, but is significantly higher than that found in hydrodynamical simulations. Using published Luminous InfraRed Galaxy (LIRG) star formation rates, we find a burst duration increasing with stellar mass, from $120-250$ Myr. A comparison to published cold gas measurements indicates there is enough molecular gas available in very close pairs to fuel the burst. Additionally, given our stellar mass burst estimate, the predicted cold gas fraction remaining after the burst is consistent with observed post-coalescence mergers.Comment: Accepted for publication in MNRAS; 12 pages, 9 figure

Scientific Standards and the Regulation of Genetically Modified Insects

Experimental releases of genetically modified (GM) insects are reportedly being evaluated in various countries, including Brazil, the Cayman Islands (United Kingdom), France, Guatemala, India, Malaysia, Mexico, Panama, Philippines, Singapore, Thailand, the United States of America, and Vietnam. GM mosquitoes (Aedes aegypti) have already been released for field trials into inhabited areas in the Cayman Islands (2009–?), Malaysia (2010–2011), and Brazil (2011–2012). Here, we assess the regulatory process in the first three countries permitting releases (Malaysia, US, and the Cayman Islands) in terms of pre-release transparency and scientific quality. We find that, despite 14 US government–funded field trials over the last 9 years (on a moth pest of cotton), there has been no scientific publication of experimental data, and in only two instances have permit applications been published. The world's first environmental impact statement (EIS) on GM insects, produced by US authorities in 2008, is found to be scientifically deficient on the basis that (1) most consideration of environmental risk is too generic to be scientifically meaningful; (2) it relies on unpublished data to establish central scientific points; and (3) of the approximately 170 scientific publications cited, the endorsement of the majority of novel transgenic approaches is based on just two laboratory studies in only one of the four species covered by the document. We find that it is not possible to determine from documents publically available prior to the start of releases if obvious hazards of the particular GM mosquitoes released in Malaysia, the Cayman Islands, and Brazil received expert examination. Simple regulatory measures are proposed that would build public confidence and stimulate the independent experimental studies that environmental risk assessments require. Finally, a checklist is provided to assist the general public, journalists, and lawmakers in determining, from documents issued by regulators prior to the start of releases, whether permit approval is likely to have a scientifically high quality basi

Successful Desensitization to Docetaxel after Severe Hypersensitivity Reactions in Two Patients

Purpose Two cases of successful desensitization to docetaxel after severe hypersensitivity reactions are reported. Summary Two patients with gynecological malignancies (uterine leiomyosarcoma and ovarian adenocarcinoma) experienced severe hypersensitivity reactions with docetaxel, including flushing, numbness, sharp radiating pain, severe nausea and vomiting, apnea, and unresponsiveness. Both patients received ondansetron before docetaxel. One patient received dexamethasone, diphenhydramine, and famotidine premedication before docetaxel, as she had previously reacted to paclitaxel. Docetaxel infusions were stopped, and the reactions were treated with diphenhydramine and dexamethasone (one patient also received famotidine). After resolution of symptoms, the docetaxel was not reinitiated due to the nature of the reactions. For the next cycle, both patients received a graded drug challenge or desensitization. Both were pre-medicated with dexamethasone, diphenhydramine, and famotidine. The docetaxel was given as infusions of 0.1%, 1%, and 10% of the dose, with each infusion given over one hour. After this, the remainder of the dose was infused over one hour. Both patients tolerated this desensitization well and completed a total of three and four cycles each. The first patient to receive the desensitization did complain of chest pain during the first desensitization, and the infusion rate was decreased to administer the drug over two hours. After she tolerated two cycles of two-hour infusions, the infusion rate was increased to administer each docetaxel infusion over one hour. Conclusion Two patients who had severe hypersensitivity reactions to docetaxel successfully received further docetaxel doses via a desensitization procedure that involved the sequential administration of solutions containing increasing concentrations of the drug

Genes of the serotonergic and dopaminergic pathways and their interaction affect the expression of Behavioural and Psychological Symptoms in Dementia (BPSD).

Although there is evidence for the involvement of genes of serotonergic and dopaminergic systems in the manifestation of the Behavioural and Psychological Symptoms in Dementia (BPSD), genetic association studies are contradictory. We used 1008 probable AD patients from the UK and applied a Multiple Indicators Multiple Causes (MIMIC) approach to investigate the effect of 11 polymorphisms in the serotonergic and dopaminergic systems, on four behavioural sub-phenotypes, namely &#x22;psychosis&#x22;,&#x22; moods&#x22;, &#x22;agitation&#x22; and &#x22;behavioural dyscontrol&#x22;, as well as on 12 NPI items. Significant findings included the association of DRD1 A48G with &#x22;psychosis&#x22; (p=0.037), the association of DAT1 VNTR with &#x22;agitation&#x22; (p=0.006) and the association of DRD4 with &#x22;moods&#x22; sub-phenotype (p=0.008). In addition, associations were identified between DRD1 A48G and DAT1 VNTR with aberrant motor behaviour (AMB) symptoms (p=0.001 and p=0.015 respectively), between DRD4 and sleep disturbances (p=0.018) and between 5HTTLPR and apathy (p=0.033). Finally, significant interactions were observed between COMT Val158Met and 5HTTLPR with &#x22;psychosis&#x22; (p=0.026), between HTTLPR and STin2 with &#x22;psychosis&#x22; (p=0.005), between DAT1 3&#x27;UTR VNTR and COMT Val158Met with &#x22;agitation&#x22; (p=0.0001) and between DAT1 3&#x27;UTR VNTR and 5HTTLPR with the &#x22;moods&#x22; factor (p=0.0027). The complexity of the interrelations between genetic variation, behavioural symptoms and clinical variables was efficiently captured by this MIMIC model

Constraining quenching timescales in galaxy clusters by forward-modelling stellar ages and quiescent fractions in projected phase space

We forward-model mass-weighted stellar ages (MWAs) and quiescent fractions in projected phase space (PPS), using data from the Sloan Digital Sky Survey, to jointly constrain an infall quenching model for galaxies in $\log(M_{\mathrm{vir}}/\mathrm{M}_{\odot})>14$ galaxy clusters at $z\sim 0$. We find the average deviation in MWA from the MWA-$M_\star$ relation depends on position in PPS, with a maximum difference between the inner cluster and infalling interloper galaxies of $\sim 1$ Gyr. Our model employs infall information from N-body simulations and stochastic star-formation histories from the UniverseMachine model. We find total quenching times of $t_\mathrm{Q}=3.7\pm 0.4$ Gyr and $t_\mathrm{Q}=4.0\pm 0.2$ Gyr after first pericentre, for $9<\log(M_{\star}/\mathrm{M}_{\odot})<10$ and $10<\log(M_{\star}/\mathrm{M}_{\odot})<10.5$ galaxies, respectively. By using MWAs, we break the degeneracy in time of quenching onset and timescale of star formation rate (SFR) decline. We find that time of quenching onset relative to pericentre is $t_{\mathrm{delay}}=3.5^{+0.6}_{-0.9}$ Gyr and $t_{\mathrm{delay}}=-0.3^{+0.8}_{-1.0}$ Gyr for our lower and higher stellar mass bins, respectively, and exponential SFR suppression timescales are $\tau_{\mathrm{env}}\leq 1.0$ Gyr and $\tau_{\mathrm{env}}\sim 2.3$ Gyr for our lower and higher stellar mass bins, respectively. Stochastic star formation histories remove the need for rapid infall quenching to maintain the bimodality in the SFR of cluster galaxies; the depth of the green valley prefers quenching onsets close to first pericentre and a longer quenching envelope, in slight tension with the MWA-driven results. Taken together these results suggest that quenching begins close to, or just after pericentre, but the timescale for quenching to be fully complete is much longer and therefore ram-pressure stripping is not complete on first pericentric passage.Comment: 21 pages, 13 figures, submitted to MNRA

Electroencephalographic correlates of Chronic Fatigue Syndrome

<p>Abstract</p> <p>Background</p> <p>Unremitting fatigue and unrefreshing sleep, hallmark traits of Chronic Fatigue Syndrome (CFS), are also pathognomonic of sleep disorders. Yet, no reproducible perturbations of sleep architecture, multiple sleep latency times or Epworth Sleepiness Scores are found to be associated consistently with CFS. This led us to hypothesize that sleep homeostasis, rather than sleep architecture, may be perturbed in CFS. To probe this hypothesis, we measured and compared EEG frequencies associated with restorative sleep between persons with CFS and matched controls, both derived from a population-based sample.</p> <p>Methods</p> <p>We evaluated overnight polysomnography (PSG) in 35 CFS and 40 control subjects. PSG records were manually scored and epochs containing artifact removed. Fast Fourier Transformation was utilized to deconstruct individual EEG signals into primary frequency bands of alpha, delta, theta, sigma, and beta frequency domains. The spectral power of each frequency domain for each sleep state was compared between persons with CFS and matched controls.</p> <p>Results</p> <p>In persons with CFS, delta power was diminished during slow wave sleep, but elevated during both stage 1 and REM. Alpha power was reduced during stage 2, slow wave, and REM sleep. Those with CFS also had significantly lower theta, sigma, and beta spectral power during stage 2, Slow Wave Sleep, and REM.</p> <p>Discussion</p> <p>Employing quantitative EEG analysis we demonstrate reduced spectral power of cortical delta activity during SWS. We also establish reduced spectral power of cortical alpha activity, with the greatest reduction occurring during REM sleep. Reductions in theta, beta, and sigma spectral power were also apparent.</p> <p>Conclusion</p> <p>Unremitting fatigue and unrefreshing sleep, the waking manifestations of CFS, may be the consequence of impaired sleep homeostasis rather than a primary sleep disorder.</p

Reciprocal and dynamic polarization of planar cell polarity core components and myosin

Citation: Newman-Smith, E., Kourakis, M. J., Reeves, W., Veeman, M., & Smith, W. C. (2015). Reciprocal and dynamic polarization of planar cell polarity core components and myosin. eLife, 2015(4). doi:10.7554/eLife.05361The Ciona notochord displays PCP-dependent polarity, with anterior localization of Prickle (Pk) and Strabismus (Stbm). We report that a myosin is polarized anteriorly in these cells and strongly colocalize with Stbm. Disruption of the actin/myosin machinery with cytochalasin or blebbistatin disrupts polarization of Pk and Stbm, but not of myosin complexes, suggesting a PCP-independent aspect of myosin localization. Washout of cytochalasin restored Pk polarization, but not if done in the presence of blebbistatin, suggesting an active role for myosin in core PCP protein localization. On the other hand, in the pk mutant line aimless myosin polarization in approximately one third of the cells, indicating a reciprocal action of core PCP signaling on myosin localization. Our results indicate a complex relationship between the actomyosin cytoskeleton and core PCP components in which myosin is not simply a downstream target of PCP signaling, but also required for PCP protein localization. © 2015, eLife. All rights reserved

Processes of Care Associated With Risk of Mortality and Recurrent Stroke Among Patients With Transient Ischemic Attack and Nonsevere Ischemic Stroke

Importance: Early evaluation and management of patients with transient ischemic attack (TIA) and nonsevere ischemic stroke improves outcomes. Objective: To identify processes of care associated with reduced risk of death or recurrent stroke among patients with TIA or nonsevere ischemic stroke. Design, Setting, and Participants: This cohort study included all patients with TIA or nonsevere ischemic stroke at Department of Veterans Affairs emergency department or inpatient settings from October 2010 to September 2011. Multivariable logistic regression was used to model associations of processes of care and without-fail care, defined as receiving all guideline-concordant processes of care for which patients are eligible, with risk of death and recurrent stroke. Data were analyzed from March 2018 to April 2019. Main Outcomes and Measures: Risk of all-cause mortality and recurrent ischemic stroke at 90 days and 1 year was calculated. Overall, 28 processes of care were examined. Without-fail care was assessed for 6 processes: brain imaging, carotid artery imaging, hypertension medication intensification, high- or moderate-potency statin therapy, antithrombotics, and anticoagulation for atrial fibrillation. Results: Among 8076 patients, the mean (SD) age was 67.8 (11.6) years, 7752 patients (96.0%) were men, 5929 (73.4%) were white, 474 (6.1%) had a recurrent ischemic stroke within 90 days, 793 (10.7%) had a recurrent ischemic stroke within 1 year, 320 (4.0%) died within 90 days, and 814 (10.1%) died within 1 year. Overall, 9 processes were independently associated with lower odds of both 90-day and 1-year mortality after adjustment for multiple comparisons: carotid artery imaging (90-day adjusted odds ratio [aOR], 0.49; 95% CI, 0.38-0.63; 1-year aOR, 0.61; 95% CI, 0.52-0.72), antihypertensive medication class (90-day aOR, 0.58; 95% CI, 0.45-0.74; 1-year aOR, 0.70; 95% CI, 0.60-0.83), lipid measurement (90-day aOR, 0.68; 95% CI, 0.51-0.90; 1-year aOR, 0.64; 95% CI, 0.53-0.78), lipid management (90-day aOR, 0.46; 95% CI, 0.33-0.65; 1-year aOR, 0.67; 95% CI, 0.53-0.85), discharged receiving statin medication (90-day aOR, 0.51; 95% CI, 0.36-0.73; 1-year aOR, 0.70; 95% CI, 0.55-0.88), cholesterol-lowering medication intensification (90-day aOR, 0.47; 95% CI, 0.26-0.83; 1-year aOR, 0.56; 95% CI, 0.41-0.77), antithrombotics by day 2 (90-day aOR, 0.56; 95% CI, 0.40-0.79; 1-year aOR, 0.69; 95% CI, 0.55-0.87) or at discharge (90-day aOR, 0.59; 95% CI, 0.41-0.86; 1-year aOR, 0.69; 95% CI, 0.54-0.88), and neurology consultation (90-day aOR, 0.67; 95% CI, 0.52-0.87; 1-year aOR, 0.74; 95% CI, 0.63-0.87). Anticoagulation for atrial fibrillation was associated with lower odds of 1-year mortality only (aOR, 0.59; 95% CI, 0.40-0.85). No processes were associated with reduced risk of recurrent stroke after adjustment for multiple comparisons. The rate of without-fail care was 15.3%; 1216 patients received all guideline-concordant processes of care for which they were eligible. Without-fail care was associated with a 31.2% lower odds of 1-year mortality (aOR, 0.69; 95% CI, 0.55-0.87) but was not independently associated with stroke risk. Conclusions and Relevance: Patients who received 6 readily available processes of care had lower adjusted mortality 1 year after TIA or nonsevere ischemic stroke. Clinicians caring for patients with TIA and nonsevere ischemic stroke should seek to ensure that patients receive all guideline-concordant processes of care for which they are eligible

Short-range ordering in a battery electrode, the 'cation-disordered' rocksalt Li1.25Nb0.25Mn0.5O2.

Cation order, with a local structure related to γ-LiFeO2, is observed in the nominally cation-disordered Li-excess rocksalt Li1.25Nb0.25Mn0.5O2via X-ray diffraction, neutron pair distribution function analysis, magnetic susceptibility and NMR spectroscopy. The correlation length of ordering depends on synthesis conditions and has implications for the electrochemistry of these phases.EPSRC: EP/L015978/1 Basic Energy Science, US Department of Energy: DE-SC001258