Life History and Multi-Partner Mating: A Novel Explanation for Moral Stigma Against Consensual Non-monogamy.

Life history theory (LHT) predicts that individuals vary in their sexual, reproductive, parental, familial, and social behavior according to the physical and social challenges imposed upon them throughout development. LHT provides a framework for understanding why non-monogamy may be the target of significant moral condemnation: individuals who habitually form multiple romantic or sexual partnerships may pursue riskier, more competitive interpersonal strategies that strain social cooperation. We compared several indices of life history (i.

Jealousy, Consent, and Compersion Within Monogamous and Consensually Non-Monogamous Romantic Relationships.

Evolutionary psychological research has studied romantic jealousy extensively within monogamous relationships, but has largely ignored jealousy among partners who mutually consent to forming extra-pair relationships (i.e., consensual non-monogamy; CNM).

The Drosophila anatomy ontology.

Background: Anatomy ontologies are query-able classifications of anatomical structures. They provide a widely-used means for standardising the annotation of phenotypes and expression in both human-readable and programmatically accessible forms. They are also frequently used to group annotations in biologically meaningful ways.

A strategy for building neuroanatomy ontologies.

Motivation: Advancing our understanding of how nervous systems work will require the ability to store and annotate 3D anatomical datasets, recording morphology, partonomy and connectivity at multiple levels of granularity from subcellular to gross anatomy. It will also require the ability to integrate this data with other data-types including functional, genetic and electrophysiological data. The web ontology language OWL2 provides the means to solve many of these problems.

The Virtual Fly Brain browser and query interface.

Motivation: Sources of neuroscience data in Drosophila are diverse and disparate making integrated search and retrieval difficult. A major obstacle to this is the lack of a comprehensive and logically structured anatomical framework and an intuitive interface.

Results: We present an online resource that provides a convenient way to study and query fly brain anatomy, expression and genetic data.

Expression of the GABAergic system in animal models for fragile X syndrome and fragile X associated tremor/ataxia syndrome (FXTAS).

After our initial discovery of reduced expression of several subunits of the GABA(A) receptor in two different animal models for fragile X syndrome, a frequent form of inherited mental retardation, we analyzed further components of the GABAergic pathway. Interestingly, we found a down regulation of many additional elements of the GABA signalling system, strengthening our hypothesis of involvement of the GABAergic pathway in the pathophysiology of fragile X syndrome. This is of special interest with regard to new therapeutic opportunities for treatment of this disorder.

Mutational analysis establishes a critical role for the N terminus of fragile X mental retardation protein FMRP.

Fragile X syndrome is the most common form of heritable mental retardation caused by the loss of function of the fragile X mental retardation protein FMRP. FMRP is a multidomain, RNA-binding protein involved in RNA transport and/or translational regulation. However, the binding specificity between FMRP and its various partners including interacting proteins and mRNA targets is essentially unknown.

Slowmo is required for Drosophila germline proliferation.

Null mutations in the Drosophila gene, slowmo (slmo), result in reduced mobility and lethality in first-instar larvae. Slowmo encodes a mitochondrial protein of unknown function, as do the two other homologs found in Drosophila. Here, we have studied a hypomorphic P-element allele of slmo demonstrating its effects on germline divisions in both testes and ovaries.

Decreased expression of the GABAA receptor in fragile X syndrome.

After our initial discovery of under expression of the GABA(A) receptor delta subunit in a genome wide screening for differentially expressed mRNAs in brain of fragile X mice, a validated model for fragile X mental retardation syndrome, we analyzed expression of the 17 remaining subunits of the GABA(A) receptor using real-time PCR. We confirmed nearly 50% under expression of the delta subunit and found a significant 35%-50% reduction in expression of 7 additional subunit mRNAs, namely alpha(1), alpha(3), and alpha(4), beta(1) and beta(2) and gamma(1) and gamma(2), in fragile X mice compared to wild-type littermates. In concordance with previous results, under expression was found in cortex, but not in cerebellum.

Amyloid precursor protein promotes post-developmental neurite arborization in the Drosophila brain.

The mechanisms regulating the outgrowth of neurites during development, as well as after injury, are key to the understanding of the wiring and functioning of the brain under normal and pathological conditions. The amyloid precursor protein (APP) is involved in the pathogenesis of Alzheimer's disease (AD). However, its physiological role in the central nervous system is not known.

The Drosophila fragile X mental retardation protein controls actin dynamics by directly regulating profilin in the brain.

Loss of Fragile X mental retardation protein (FMRP) function causes the highly prevalent Fragile X syndrome [1 and 2]. Identifying targets for the RNA binding FMRP is a major challenge and an important goal of research into the pathology of the disease. Perturbations in neuronal development and circadian behavior are seen in Drosophila dfmr1 mutants.

Effective strategy to guide pathology test ordering in surgical patients.

Background: Ordering of pathology testing by junior medical staff is often a haphazard process with little regard to the appropriateness of test ordering. The aim of the present study was to reduce ordering of inappropriate pathology tests in surgical patients attending the pre-admission clinic (PAC) through the introduction of a protocol-based test ordering system and to create an environment where such improvement can be sustained.

Methods: This is a prospective study with a retrospective control group.

Mutation in slowmo causes defects in Drosophila larval locomotor behaviour.

We have identified a mutant slowmotion phenotype in first instar larval peristaltic behaviour of Drosophila. By the end of embryogenesis and during early first instar phases, slowmo mutant animals show a marked decrease in locomotory behaviour, resulting from both a reduction in number and rate of peristaltic contractions. Inhibition of neurotransmitter release, using targeted expression of tetanus toxin light chain (TeTxLC), in the slowmo neurons marked by an enhancer-trap results in a similar phenotype of largely absent or uncoordinated contractions.