Cryptic female choice favours sperm from major histocompatibility complex-dissimilar males

Cryptic female choice may enable polyandrous females to avoid inbreeding or bias offspring variability at key loci after mating. However, the role of these genetic benefits in cryptic female choice remains poorly understood. Female red junglefowl, Gallus gallus, bias sperm use in favour of unrelated males. Here, we experimentally investigate whether this bias is driven by relatedness per se, or by similarity at the major histocompatibility complex (MHC), genes central to vertebrate acquired immunity, where polymorphism is critical to an individual's ability to combat pathogens. Through experimentally controlled natural matings, we confirm that selection against related males' sperm occurs within the female reproductive tract but demonstrate that this is more accurately predicted by MHC similarity: controlling for relatedness per se, more sperm reached the eggs when partners were MHC-dissimilar. Importantly, this effect appeared largely owing to similarity at a single MHC locus (class I minor). Further, the effect of MHC similarity was lost following artificial insemination, suggesting that male phenotypic cues might be required for females to select sperm differentially. These results indicate that postmating mechanisms that reduce inbreeding may do so as a consequence of more specific strategies of cryptic female choice promoting MHC diversity in offspring

Physics of Ultra-Peripheral Nuclear Collisions

Moving highly-charged ions carry strong electromagnetic fields that act as a field of photons. In collisions at large impact parameters, hadronic interactions are not possible, and the ions interact through photon-ion and photon-photon collisions known as {\it ultra-peripheral collisions} (UPC). Hadron colliders like the Relativistic Heavy Ion Collider (RHIC), the Tevatron and the Large Hadron Collider (LHC) produce photonuclear and two-photon interactions at luminosities and energies beyond that accessible elsewhere; the LHC will reach a $\gamma p$ energy ten times that of the Hadron-Electron Ring Accelerator (HERA). Reactions as diverse as the production of anti-hydrogen, photoproduction of the $\rho^0$, transmutation of lead into bismuth and excitation of collective nuclear resonances have already been studied. At the LHC, UPCs can study many types of `new physics.'Comment: 47 pages, to appear in Annual Review of Nuclear and Particle Scienc

Randomised trial of once-daily vilanterol in children with asthma on inhaled corticosteroid therapy

GSK (ClinicalTrials.gov identifier NCT01573767

Introduction to the Workshop

Public health administrators are forced to consider efficiency as a criterion in their choice of preventive programs because of the numerous programs to choose from, restricted budgets, and declining caries experience in children. Interest in cost effectiveness in dental prevention has risen considerably since the initial conference on this issue at the University of Michigan in 1978. This article introduces the goals of the workshop, the nature of the work groups, and the data they will use.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66042/1/j.1752-7325.1989.tb02083.x.pd

Approximating k-Forest with Resource Augmentation: A Primal-Dual Approach

In this paper, we study the $k$-forest problem in the model of resource augmentation. In the $k$-forest problem, given an edge-weighted graph $G(V,E)$, a parameter $k$, and a set of $m$ demand pairs $\subseteq V \times V$, the objective is to construct a minimum-cost subgraph that connects at least $k$ demands. The problem is hard to approximate---the best-known approximation ratio is $O(\min\{\sqrt{n}, \sqrt{k}\})$. Furthermore, $k$-forest is as hard to approximate as the notoriously-hard densest $k$-subgraph problem. While the $k$-forest problem is hard to approximate in the worst-case, we show that with the use of resource augmentation, we can efficiently approximate it up to a constant factor. First, we restate the problem in terms of the number of demands that are {\em not} connected. In particular, the objective of the $k$-forest problem can be viewed as to remove at most $m-k$ demands and find a minimum-cost subgraph that connects the remaining demands. We use this perspective of the problem to explain the performance of our algorithm (in terms of the augmentation) in a more intuitive way. Specifically, we present a polynomial-time algorithm for the $k$-forest problem that, for every $\epsilon>0$, removes at most $m-k$ demands and has cost no more than $O(1/\epsilon^{2})$ times the cost of an optimal algorithm that removes at most $(1-\epsilon)(m-k)$ demands

Understanding disease control: influence of epidemiological and economic factors

We present a local spread model of disease transmission on a regular network and compare different control options ranging from treating the whole population to local control in a well-defined neighborhood of an infectious individual. Comparison is based on a total cost of epidemic, including cost of palliative treatment of ill individuals and preventive cost aimed at vaccination or culling of susceptible individuals. Disease is characterized by pre- symptomatic phase which makes detection and control difficult. Three general strategies emerge, global preventive treatment, local treatment within a neighborhood of certain size and only palliative treatment with no prevention. The choice between the strategies depends on relative costs of palliative and preventive treatment. The details of the local strategy and in particular the size of the optimal treatment neighborhood weakly depends on disease infectivity but strongly depends on other epidemiological factors. The required extend of prevention is proportional to the size of the infection neighborhood, but this relationship depends on time till detection and time till treatment in a non-nonlinear (power) law. In addition, we show that the optimal size of control neighborhood is highly sensitive to the relative cost, particularly for inefficient detection and control application. These results have important consequences for design of prevention strategies aiming at emerging diseases for which parameters are not known in advance

A 10-Year Retrospective Analysis of Methyl Aminolevulinate Photodynamic Therapy Consultation at the Hospital de Braga

Photodynamic therapy (PDT) is a well-established treatment for actinic keratosis (AK), basal cell carcinoma (BCC), and Bowen's disease (BD). The object of this study was to describe the results of a retrospective analysis of patients treated with methyl aminolevulinate PDT (MAL-PDT) with red light, over the past decade at the Hospital de Braga (Braga, Portugal)

MFGE8 does not influence chorio-retinal homeostasis or choroidal neovascularization in vivo

Purpose: Milk fat globule-epidermal growth factor-factor VIII (MFGE8) is necessary for diurnal outer segment phagocytosis and promotes VEGF-dependent neovascularization. The prevalence of two single nucleotide polymorphisms (SNP) in MFGE8 was studied in two exsudative or “wet” Age-related Macular Degeneration (AMD) groups and two corresponding control groups. We studied the effect of MFGE8 deficiency on retinal homeostasis with age and on choroidal neovascularization (CNV) in mice. Methods: The distribution of the SNP (rs4945 and rs1878326) of MFGE8 was analyzed in two groups of patients with “wet” AMD and their age-matched controls from Germany and France. MFGE8-expressing cells were identified in Mfge8+/− mice expressing ß-galactosidase. Aged Mfge8+/− and Mfge8−/− mice were studied by funduscopy, histology, electron microscopy, scanning electron microscopy of vascular corrosion casts of the choroid, and after laser-induced CNV. Results: rs1878326 was associated with AMD in the French and German group. The Mfge8 promoter is highly active in photoreceptors but not in retinal pigment epithelium cells. Mfge8−/− mice did not differ from controls in terms of fundus appearance, photoreceptor cell layers, choroidal architecture or laser-induced CNV. In contrast, the Bruch's membrane (BM) was slightly but significantly thicker in Mfge8−/− mice as compared to controls. Conclusions: Despite a reproducible minor increase of rs1878326 in AMD patients and a very modest increase in BM in Mfge8−/− mice, our data suggests that MFGE8 dysfunction does not play a critical role in the pathogenesis of AMD