Mate-Finding as an Overlooked Critical Determinant of Dispersal Variation in Sexually-Reproducing Animals

Dispersal is a critically important process in ecology, but robust predictive models of animal dispersal remain elusive. We identify a potentially ubiquitous component of variation in animal dispersal that has been largely overlooked until now: the influence of mate encounters on settlement probability. We use an individual-based model to simulate dispersal in sexually-reproducing organisms that follow a simple set of movement rules based on conspecific encounters, within an environment lacking spatial habitat heterogeneity. We show that dispersal distances vary dramatically with fluctuations in population density in such a model, even in the absence of variation in dispersive traits between individuals. In a simple random-walk model with promiscuous mating, dispersal distributions become increasingly ‘fat-tailed’ at low population densities due to the increasing scarcity of mates. Similar variation arises in models incorporating territoriality. In a model with polygynous mating, we show that patterns of sex-biased dispersal can even be reversed across a gradient of population density, despite underlying dispersal mechanisms remaining unchanged. We show that some widespread dispersal patterns found in nature (e.g. fat tailed distributions) can arise as a result of demographic variability in the absence of heterogeneity in dispersive traits across the population. This implies that models in which individual dispersal distances are considered to be fixed traits might be unrealistic, as dispersal distances vary widely under a single dispersal mechanism when settlement is influenced by mate encounters. Mechanistic models offer a promising means of advancing our understanding of dispersal in sexually-reproducing organisms

Using systems science to understand the determinants of inequities in healthy eating

Introduction: Systems thinking has emerged in recent years as a promising approach to understanding and acting on the prevention and amelioration of non-communicable disease. However, the evidence on inequities in non-communicable diseases and their risks factors, particularly diet, has not been examined from a systems perspective. We report on an approach to developing a system oriented policy actor perspective on the multiple causes of inequities in healthy eating. Methods: Collaborative conceptual modelling workshops were held in 2015 with an expert group of representatives from government, non-government health organisations and academia in Australia. The expert group built a systems model using a system dynamics theoretical perspective. The model developed from individual mind maps to pair blended maps, before being finalised as a causal loop diagram. Results: The work of the expert stakeholders generated a comprehensive causal loop diagram of the determinants of inequity in healthy eating (the HE2Diagram). This complex dynamic system has seven sub-systems: (1) food supply and environment; (2) transport; (3) housing and the built environment; (4) employment; (5) social protection; (6) health literacy; and (7) food preferences. Discussion: The HE2causal loop diagram illustrates the complexity of determinants of inequities in healthy eating. This approach, both the process of construction and the final visualisation, can provide the basis for planning the prevention and amelioration of inequities in healthy eating that engages with multiple levels of causes and existing policies and programs

Diagnosis and Management of Infected Total Knee Arthroplasty§

Infection following total knee arthroplasty can be difficult to diagnose and treat. Diagnosis is multifactorial and relies on the clinical picture, radiographs, bone scans, serologic tests, synovial fluid examination, intra-operative culture and histology. Newer techniques including ultrasonication and molecular diagnostic studies are playing an expanded role. Two-stage exchange arthroplasty with antibiotic cement and 4-6 weeks of intravenous antibiotic treatment remains the most successful intervention for infection eradication. There is no consensus on the optimum type of interval antibiotic cement spacer. There is a limited role for irrigation and debridement, direct one-stage exchange, chronic antibiotic suppression and salvage procedures like arthrodesis and amputation. We examine the literature on each of the diagnostic modalities and treatment options in brief and explain their current significance

Human malarial disease: a consequence of inflammatory cytokine release

Malaria causes an acute systemic human disease that bears many similarities, both clinically and mechanistically, to those caused by bacteria, rickettsia, and viruses. Over the past few decades, a literature has emerged that argues for most of the pathology seen in all of these infectious diseases being explained by activation of the inflammatory system, with the balance between the pro and anti-inflammatory cytokines being tipped towards the onset of systemic inflammation. Although not often expressed in energy terms, there is, when reduced to biochemical essentials, wide agreement that infection with falciparum malaria is often fatal because mitochondria are unable to generate enough ATP to maintain normal cellular function. Most, however, would contend that this largely occurs because sequestered parasitized red cells prevent sufficient oxygen getting to where it is needed. This review considers the evidence that an equally or more important way ATP deficency arises in malaria, as well as these other infectious diseases, is an inability of mitochondria, through the effects of inflammatory cytokines on their function, to utilise available oxygen. This activity of these cytokines, plus their capacity to control the pathways through which oxygen supply to mitochondria are restricted (particularly through directing sequestration and driving anaemia), combine to make falciparum malaria primarily an inflammatory cytokine-driven disease