Compassionate versus consequentialist conservation

Ethical treatment of wildlife and consideration of animal welfare have become important themes in conservation, but ethical perspectives on how best to protect wild animals and promote their welfare are diverse. There are advantages to the consequentialist harms ethical framework applied in managing wild herbivores for conservation purposes. To minimize harms while achieving conservation goals, we argue that overabundant wild herbivores should in many cases be managed through consumptive in situ killing. Advantages of this policy are that the negative welfare states imposed on animals last only a short time; remaining animals are not deprived of positive welfare states (e.g., linked to rearing offspring); poor welfare states of animals in overabundant populations are avoided (e.g., starvation); negative welfare impacts on heterospecifics through resource depletion (i.e., competition) are prevented; harvesting meat reduces the number of (agricultural) animals raised to supply meat; and minimal costs maximize funding for other wildlife management and conservation priorities. Alternative ethical approaches to our consequentialist framework include deontology (containing animal rights) and virtue ethics, some of which underpin compassionate conservation. These alternative ethical approaches emphasize the importance of avoiding intentional killing of animals but, if no population reduction occurs, are likely to impose considerable unintentional harms on overabundant wildlife and indirectly harm heterospecifics through ineffective population reduction. If nonlethal control is used, it is likely that overabundant animals would be deprived of positive welfare states and economic costs would be prohibitive. We encourage conservation stakeholders to consider animal-welfare consequentialism as an ethical approach to minimize harms to the animals under their care as well as other animals that policies may affect while at the same time pursuing conservation goals

The Microbiome in Pediatric Cystic Fibrosis Patients: The Role of Shared Environment Suggests a Window of Intervention

Cystic fibrosis (CF) is caused by mutations in the CFTR gene that predispose the airway to infection. Chronic infection by pathogens such as Pseudomonas aeruginosa leads to inflammation that gradually degrades lung function, resulting in morbidity and early mortality. In a previous study of CF monozygotic twins, we demonstrate that genetic modifiers significantly affect the establishment of persistent P. aeruginosa colonization in CF. Recognizing that bacteria other than P. aeruginosa contribute to the CF microbiome and associated pathology, we used deep sequencing of sputum from pediatric monozygotic twins and nontwin siblings with CF to characterize pediatric bacterial communities and the role that genetics plays in their evolution. We found that the microbial communities in sputum from pediatric patients living together were much more alike than those from pediatric individuals living apart, regardless of whether samples were taken from monozygous twins or from nontwin CF siblings living together, which we used as a proxy for dizygous twins. In contrast, adult communities were comparatively monolithic and much less diverse than the microbiome of pediatric patients

Evaluation of alternative intersection treatments at rural crossroads using simulation software

Objective: Rural roads are characterised by hazardous roadsides and suboptimal geometry, yet allow for high travel speeds and unfavourable impact angles. In Victoria, 25% of persons seriously injured and 52% of fatalities occur on rural roads, with 30% occurring at intersections (Transport Accident Commision, 2016; Victorian Parliament Road Safety Committee 2002). In the USA, almost twice the number of traffic fatalities occur in rural areas than in urban areas, whilst accounting for less than half of all vehicle miles travelled and 21% of the population (NHTSA 2002). The choice of safety countermeasure is therefore paramount. Simulation software provides a cost-effective means of analysing alternative intersection treatments with a view to identifying their effectiveness in mitigating crashes. The aim of this research was to assess the safety benefits of four alternative intersection treatments using in-depth crash data with an advanced crash reconstruction process. Method: Using a single serious injury real-world crash from the MUARC Enhanced Crash Investigation Study (ECIS, Fitzharris et al., 2015) and crash reconstruction software, an exemplar rural crash was reconstructed and validated against real-world data. The crash involved a passenger vehicle (EuroNCAP 5*) approaching from a minor road and failing to yield at a ‘give-way’ sign; the posted speed limit was 80 km/h. The vehicle was struck on the right/driver side by a rigid truck (B-vehicle; 1990) travelling on the major approach (100 km/h). The driver of the case vehicle was seriously injured. Four alternative intersection treatments appropriate for the crash site were constructed in CAD software (Rhinoceros V5): roundabout; rumble strips; a reduced speed limit and the combination of lower speed limit and rumbles to determine the reduction in crash forces in the presence of the countermeasures. Results: The hypothetical scenarios demonstrate substantial reductions in impact force and different points of impact, resulting in a significantly lower injury severity for the struck driver. Speed limit reduction to 80 km/h on the main approach (from 100 km/h) in combination with rumble strips on both intersection approaches had the most favorable outcome with the crash avoided entirely, assuming speed compliance. Discussion: The findings have implications for understanding the role of speed in crashes, and hence the design of effective countermeasures. Simulation software, validated using real-world data, provides a cost effective means of evaluating alternative intersection treatments for rural intersections. Scaled up, implementing these treatments would have significant safety benefits and reduce the road trauma currently associated with rural roads

Anr and Its Activation by PlcH Activity in Pseudomonas aeruginosa Host Colonization and Virulence

Pseudomonas aeruginosa hemolytic phospholipase C (PlcH) degrades phosphatidylcholine (PC), an abundant lipid in cell membranes and lung surfactant. A ΔplcHR mutant, known to be defective in virulence in animal models, was less able to colonize epithelial cell monolayers and was defective in biofilm formation on plastic when grown in lung surfactant. Microarray analyses found that strains defective in PlcH production had lower levels of Anr-regulated transcripts than the wild type. PC degradation stimulated the Anr regulon in an Anr-dependent manner under conditions where Anr activity was submaximal because of the presence of oxygen. Two PC catabolites, choline and glycine betaine (GB), were sufficient to stimulate Anr activity, and their catabolism was required for Anr activation. The addition of choline or GB to glucose-containing medium did not alter Anr protein levels, growth rates, or respiratory activity, and Anr activation could not be attributed to the osmoprotectant functions of GB. The Δanr mutant was defective in virulence in a mouse pneumonia model. Several lines of evidence indicate that Anr is important for the colonization of biotic and abiotic surfaces in both P. aeruginosa PAO1 and PA14 and that increases in Anr activity resulted in enhanced biofilm formation. Our data suggest that PlcH activity promotes Anr activity in oxic environments and that Anr activity contributes to virulence, even in the acute infection phase, where low oxygen tensions are not expected. This finding highlights the relationships among in vivo bacterial metabolism, the activity of the oxygen-sensitive regulator Anr, and virulence

Neurodegeneration progresses despite complete elimination of clinical relapses in a mouse model of multiple sclerosis.

BACKGROUND: [corrected] Multiple Sclerosis has two clinical phases reflecting distinct but inter-related pathological processes: focal inflammation drives the relapse-remitting stage and neurodegeneration represents the principal substrate of secondary progression. In contrast to the increasing number of effective anti-inflammatory disease modifying treatments for relapse-remitting disease, the absence of therapies for progressive disease represents a major unmet clinical need. This raises the unanswered question of whether elimination of clinical relapses will prevent subsequent progression and if so how early in the disease course should treatment be initiated. Experimental autoimmune encephalomyelitis in the Biozzi ABH mouse recapitulates the clinical and pathological features of multiple sclerosis including relapse-remitting episodes with inflammatory mediated demyelination and progressive disability with neurodegeneration. To address the relationship between inflammation and neurodegeneration we used an auto-immune tolerance strategy to eliminate clinical relapses in EAE in a manner analogous to the clinical effect of disease modifying treatments. RESULTS: By arresting clinical relapses in EAE at two distinct stages, early and late disease, we demonstrate that halting immune driven demyelination even after the first major clinical event is insufficient to prevent long-term neurodegeneration and associated gliosis. Nonetheless, early intervention is partially neuroprotective, whereas later interventions are not. Furthermore early tolerisation is also associated with increased remyelination. CONCLUSIONS: These findings are consistent with both a partial uncoupling of inflammation and neurodegeneration and that the regenerative response of remyelination is negatively correlated with inflammation. These findings strongly support the need for early combinatorial treatment of immunomodulatory therapies and neuroprotective treatments to prevent long-term neurodegeneration in multiple sclerosis

Mild Cystic Fibrosis Lung Disease Is Associated with Bacterial Community Stability

While much research supports a polymicrobial view of the CF airway, one in which the community is seen as the pathogenic unit, only controlled experiments using model bacterial communities can unravel the mechanistic role played by different communities. This report uses a large data set to identify a small number of communities as a starting point in the development of tractable model systems

The MUARC-TAC enhanced crash investigation study: study update, analysis of crash types and contributing factors [Abstract]

This paper presents an update of the Monash University Accident Research Centre (MUARC) – Transport Accident Commission (TAC) Enhanced Crash Investigation Study (ECIS) as well as an exploration of the characteristics of injured drivers, crash types and factors implicated in crash occurrence. Three configurations are of particularly high frequency and severity, whilst crashes involving young and older drivers are different in nature and have different contributing factors. Fatigue, driver error, and pre-crash driver blackouts due to medical conditions were prominent contributing factors. Injury severity would be significantly lower in 32% of cases if either front or side airbags were fitted. The findings point to key risk factors that can be addressed in road safety strategies

The MUARC-TAC enhanced crash investigation study: a platform to understand the causes and consequences of serious injury crashes.

Background: In recognising the consequences of serious injury crashes, the Transport Accident Commission (TAC) commissioned Monash University Accident Research Centre (MUARC) to undertake the Enhanced Crash Investigation Study (ECIS). This paper describes the program components, seven key research questions and technical innovations used in the study. We describe the information collected and outline a ‘Safe Systems Failure Analysis’ used for each case. Project Method: Participants in ECIS include drivers aged 18 years and older seriously injured in crashes on public Victorian roads. Drivers are recruited whilst inpatients at a major trauma hospital and where possible interviews conducted. The ECIS team inspects their crashed vehicle and critically analyses the crash environment. Event Data Recorder (EDR, black-box) data is acquired from vehicles where possible and crash reconstructions are undertaken. Each case is submitted to an internal panel review with a sub-sample of cases presented to external panels throughout Victoria. This process leads to each case being submitted to a Safe Systems Failure Analysis where contributing factors and countermeasures are identified by a broad group of stakeholders. The ECIS control arm permits examination of the relationship between certain factors, such as speed and crash occurrence. Results and Discussion: In addition to describing the study, we provide an example of how the identification of crash factors, using a Safe Systems paradigm based on real-world serious injury crashes, can lead to the identification of targeted countermeasures, each with an identified policy action. Implications: This paper will demonstrate a method for creating a robust evidence base upon which government road safety policy can be built. By scaling up individual crash findings to the broader crash population, countermeasures and associated policy actions can be appropriately prioritised

What drivers do while speeding: examining the associations between speeding and driver distraction through the Enhanced Crash Investigation Study protocol [Abstract]

This paper represents an exploratory analysis to assess the feasibility of assessing the relationship between driver speed and engagement in potentially distracting behaviours. Control data from the ECIS project are examined. These data include both objective speed measurements recorded via laser camera positioned at ECIS case-vehicle crash locations as well as retrospective self-reported driving behaviours from drivers recorded at these sites. Exploratory analysis suggests that the activities reported by drivers with recorded speeds above the limit may differ from the activities reported by those recorded on or below the limit

Caloric Restriction Suppresses Microglial Activation and Prevents Neuroapoptosis Following Cortical Injury in Rats

Traumatic brain injury (TBI) is a widespread cause of death and a major source of adult disability. Subsequent pathological events occurring in the brain after TBI, referred to as secondary injury, continue to damage surrounding tissue resulting in substantial neuronal loss. One of the hallmarks of the secondary injury process is microglial activation resulting in increased cytokine production. Notwithstanding that recent studies demonstrated that caloric restriction (CR) lasting several months prior to an acute TBI exhibits neuroprotective properties, understanding how exactly CR influences secondary injury is still unclear. The goal of the present study was to examine whether CR (50% of daily food intake for 3 months) alleviates the effects of secondary injury on neuronal loss following cortical stab injury (CSI). To this end, we examined the effects of CR on the microglial activation, tumor necrosis factor-α (TNF-α) and caspase-3 expression in the ipsilateral (injured) cortex of the adult rats during the recovery period (from 2 to 28 days) after injury. Our results demonstrate that CR prior to CSI suppresses microglial activation, induction of TNF-α and caspase-3, as well as neurodegeneration following injury. These results indicate that CR strongly attenuates the effects of secondary injury, thus suggesting that CR may increase the successful outcome following TBI