Disparate MgII Absorption Statistics towards Quasars and Gamma-Ray Bursts : A Possible Explanation

We examine the recent report by Prochter et al. (2006) that gamma-ray burst (GRB) sight lines have a much higher incidence of strong MgII absorption than quasar sight lines. We propose that the discrepancy is due to the different beam sizes of GRBs and quasars, and that the intervening MgII systems are clumpy with the dense part of each cloudlet of a similar size as the quasars, i.e. < 10^16 cm, but bigger than GRBs. We also discuss observational predictions of our proposed model. Most notably, in some cases the intervening MgII absorbers in GRB spectra should be seen varying, and quasars with smaller sizes should show an increased rate of strong MgII absorbers. In fact, our prediction of variable MgII lines in the GRB spectra has been now confirmed by Hao et al. (2007), who observed intervening FeII and MgII lines at z=1.48 to be strongly variable in the multi-epoch spectra of z=4.05 GRB060206.Comment: 12 pages, 2 figures; substantially revised model calculation; accepted for publication in Astrophysics & Space Science as a Lette

Clinical mastitis in cows treated with sometribove (recombinant bovine somatotropin) and its relationship to milk yield.

Effect of sometribove (methionyl bovine somatotropin) on mastitis in 15 full lactation trials (914 cows) in Europe and the US and 70 short-term studies (2697 cows) in eight countries was investigated. In full lactation studies, sometribove (500 mg/2 wk) was given for 252 d, commencing 60 d postpartum. Although herds varied considerably, incidence of clinical mastitis within a herd was similar for cows receiving control and sometribove treatments. Relative risk analyses indicated no treatment effect, and percentage of mastitis during treatment was similar for control and sometribove groups. A positive linear relationship existed between peak milk yield and mastitis incidence (percentage of cows contracting mastitis or cases per 100 cow days); sometribove treatment did not alter this relationship. Increases in mastitis related to milk yield increase from sometribove or related to genetic selection were similar. When expressed per unit of milk, mastitis incidence declined slightly as milk yield increased; this relationship was not altered by sometribove. No effect on clinical mastitis was observed in 70 commercial herds utilizing sometribove for 84 d. However, effects were significant for stage of lactation and milk yield. Overall, studies represented a wide range of research and commercial situations demonstrating that sometribove had no effect on incidence of clinical mastitis during the lactation of treatment. Furthermore, sometribove did not alter typical relationships between milk yield or herd factors and incidence of clinical mastitis

Parting with illusions in evolutionary ethics

I offer a critical analysis of a view that has become a dominant aspect of recent thought on the relationship between evolution and morality, and propose an alternative. An ingredient in Michael Ruse's 'error theory' (Ruse 1995) is that belief in moral (prescriptive, universal, and nonsubjective) guidelines arose in humans because such belief results in the performance of adaptive cooperative behaviors. This statement relies on two particular connections: between ostensible and intentional types of altruism, and between intentional altruism and morality. The latter connection is problematic because it makes morality redundant, its role having already been fulfilled by the psychological dispositions that constitute intentional altruism. Both behavioral ecology and moral psychology support this criticism, and neither human behavioral flexibility nor the self-regard / other-regard distinction can provide a defense of the error theory. I conclude that morality did not evolve to curb rampant selfishness; instead, the evolutionarily recent 'universal law' aspect of morality may function to update behavioral strategies which were adaptive in the paleolithic environment of our ancestors (to which our psychological dispositions are best adapted), by means of norms more appropriate to our novel social environment.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42482/1/10539_2004_Article_5102509.pd

Efficacy and Safety of Three Antiretroviral Regimens for Initial Treatment of HIV-1: A Randomized Clinical Trial in Diverse Multinational Settings

Background:Antiretroviral regimens with simplified dosing and better safety are needed to maximize the efficiency of antiretroviral delivery in resource-limited settings. We investigated the efficacy and safety of antiretroviral regimens with once-daily compared to twice-daily dosing in diverse areas of the world.Methods and Findings:1,571 HIV-1-infected persons (47% women) from nine countries in four continents were assigned with equal probability to open-label antiretroviral therapy with efavirenz plus lamivudine-zidovudine (EFV+3TC-ZDV), atazanavir plus didanosine-EC plus emtricitabine (ATV+DDI+FTC), or efavirenz plus emtricitabine-tenofovir-disoproxil fumarate (DF) (EFV+FTC-TDF). ATV+DDI+FTC and EFV+FTC-TDF were hypothesized to be non-inferior to EFV+3TC-ZDV if the upper one-sided 95% confidence bound for the hazard ratio (HR) was ≤1.35 when 30% of participants had treatment failure.An independent monitoring board recommended stopping study follow-up prior to accumulation of 472 treatment failures. Comparing EFV+FTC-TDF to EFV+3TC-ZDV, during a median 184 wk of follow-up there were 95 treatment failures (18%) among 526 participants versus 98 failures among 519 participants (19%; HR 0.95, 95% CI 0.72-1.27; p = 0.74). Safety endpoints occurred in 243 (46%) participants assigned to EFV+FTC-TDF versus 313 (60%) assigned to EFV+3TC-ZDV (HR 0.64, CI 0.54-0.76; p<0.001) and there was a significant interaction between sex and regimen safety (HR 0.50, CI 0.39-0.64 for women; HR 0.79, CI 0.62-1.00 for men; p = 0.01). Comparing ATV+DDI+FTC to EFV+3TC-ZDV, during a median follow-up of 81 wk there were 108 failures (21%) among 526 participants assigned to ATV+DDI+FTC and 76 (15%) among 519 participants assigned to EFV+3TC-ZDV (HR 1.51, CI 1.12-2.04; p = 0.007).Conclusion: EFV+FTC-TDF had similar high efficacy compared to EFV+3TC-ZDV in this trial population, recruited in diverse multinational settings. Superior safety, especially in HIV-1-infected women, and once-daily dosing of EFV+FTC-TDF are advantageous for use of this regimen for initial treatment of HIV-1 infection in resource-limited countries. ATV+DDI+FTC had inferior efficacy and is not recommended as an initial antiretroviral regimen.Trial Registration:http://www.ClinicalTrials.gov NCT00084136

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease