Knowledge co-production for Indigenous adaptation pathways: transform post-colonial articulation complexes to empower local decision-making

Co-production between scientific and Indigenous knowledge has been identified as useful to generating adaptation pathways with Indigenous peoples, who are attached to their traditional lands and thus highly exposed to the impacts of climate change. However, ignoring the complex and contested histories of nation-state colonisation can result in naïve adaptation plans that increase vulnerability. Here, through a case study in central Australia, we investigate the conditions under which co-production between scientific and Indigenous knowledge can support climate change adaptation pathways among place-attached Indigenous communities. A research team including scientists, Ltyentye Apurte Rangers and other staff from the Central Land Council first undertook activities to co-produce climate change presentations in the local Arrernte language; enable community members to identify potential adaptation actions; and implement one action, erosion control. Second, we reflected on the outcomes of these activities in order to unpack deeper influences. Applying the theory of articulation complexes, we show how ideologies, institutions and economies have linked Indigenous societies and the establishing Australian nation-state since colonisation. The sequence of complexes characterised as frontier, mission, pastoral, land-rights, community-development and re-centralisation, which is current, have both enabled and constrained adaptation options. We found knowledge co-production generates adaptation pathways when: (1) effective methods for knowledge co-production are used, based on deeply respectful partnerships, cultural governance and working together through five co-production tasks—prepare, communicate, discuss, bring together and apply; (2) Indigenous people have ongoing connection to their traditional territories to maintain their Indigenous knowledge; (3) the relationship between the Indigenous people and the nation-state empowers local decision-making and learning, which requires and creates consent, trust, accountability, reciprocity, and resurgence of Indigenous culture, knowledge and practices. These conditions foster the emergence of articulation complexes that enable the necessary transformative change from the colonial legacies. Both these conditions and our approach are likely to be relevant for place-attached Indigenous peoples across the globe in generating climate adaptation pathways

No imminent quantum supremacy by boson sampling

It is predicted that quantum computers will dramatically outperform their conventional counterparts. However, large-scale universal quantum computers are yet to be built. Boson sampling is a rudimentary quantum algorithm tailored to the platform of photons in linear optics, which has sparked interest as a rapid way to demonstrate this quantum supremacy. Photon statistics are governed by intractable matrix functions known as permanents, which suggests that sampling from the distribution obtained by injecting photons into a linear-optical network could be solved more quickly by a photonic experiment than by a classical computer. The contrast between the apparently awesome challenge faced by any classical sampling algorithm and the apparently near-term experimental resources required for a large boson sampling experiment has raised expectations that quantum supremacy by boson sampling is on the horizon. Here we present classical boson sampling algorithms and theoretical analyses of prospects for scaling boson sampling experiments, showing that near-term quantum supremacy via boson sampling is unlikely. While the largest boson sampling experiments reported so far are with 5 photons, our classical algorithm, based on Metropolised independence sampling (MIS), allowed the boson sampling problem to be solved for 30 photons with standard computing hardware. We argue that the impact of experimental photon losses means that demonstrating quantum supremacy by boson sampling would require a step change in technology.Comment: 25 pages, 9 figures. Comments welcom

Genome-wide and Ordered-Subset linkage analyses provide support for autism loci on 17q and 19p with evidence of phenotypic and interlocus genetic correlates

BACKGROUND: Autism is a neurobehavioral spectrum of phenotypes characterized by deficits in the development of language and social relationships and patterns of repetitive, rigid and compulsive behaviors. Twin and family studies point to a significant genetic etiology, and several groups have performed genomic linkage screens to identify susceptibility loci. METHODS: We performed a genome-wide linkage screen in 158 combined Tufts, Vanderbilt and AGRE (Autism Genetics Research Exchange) multiplex autism families using parametric and nonparametric methods with a categorical autism diagnosis to identify loci of main effect. Hypothesizing interdependence of genetic risk factors prompted us to perform exploratory studies applying the Ordered-Subset Analysis (OSA) approach using LOD scores as the trait covariate for ranking families. We employed OSA to test for interlocus correlations between loci with LOD scores ≥1.5, and empirically determined significance of linkage in optimal OSA subsets using permutation testing. Exploring phenotypic correlates as the basis for linkage increases involved comparison of mean scores for quantitative trait-based subsets of autism between optimal subsets and the remaining families. RESULTS: A genome-wide screen for autism loci identified the best evidence for linkage to 17q11.2 and 19p13, with maximum multipoint heterogeneity LOD scores of 2.9 and 2.6, respectively. Suggestive linkage (LOD scores ≥1.5) at other loci included 3p, 6q, 7q, 12p, and 16p. OSA revealed positive correlations of linkage between the 19p locus and 17q, between 19p and 6q, and between 7q and 5p. While potential phenotypic correlates for these findings were not identified for the chromosome 7/5 combination, differences indicating more rapid achievement of "developmental milestones" was apparent in the chromosome 19 OSA-defined subsets for 17q and 6q. OSA was used to test the hypothesis that 19p linkage involved more rapid achievement of these milestones and it revealed significantly increased LOD* scores at 19p13. CONCLUSIONS: Our results further support 19p13 as harboring an autism susceptibility locus, confirm other linkage findings at 17q11.2, and demonstrate the need to analyze more discreet trait-based subsets of complex phenotypes to improve ability to detect genetic effects

Systematic review of the evidence relating FEV1 decline to giving up smoking

<p>Abstract</p> <p>Background</p> <p>The rate of forced expiratory volume in 1 second (FEV₁) decline ("beta") is a marker of chronic obstructive pulmonary disease risk. The reduction in beta after quitting smoking is an upper limit for the reduction achievable from switching to novel nicotine delivery products. We review available evidence to estimate this reduction and quantify the relationship of smoking to beta.</p> <p>Methods</p> <p>Studies were identified, in healthy individuals or patients with respiratory disease, that provided data on beta over at least 2 years of follow-up, separately for those who gave up smoking and other smoking groups. Publications to June 2010 were considered. Independent beta estimates were derived for four main smoking groups: never smokers, ex-smokers (before baseline), quitters (during follow-up) and continuing smokers. Unweighted and inverse variance-weighted regression analyses compared betas in the smoking groups, and in continuing smokers by amount smoked, and estimated whether beta or beta differences between smoking groups varied by age, sex and other factors.</p> <p>Results</p> <p>Forty-seven studies had relevant data, 28 for both sexes and 19 for males. Sixteen studies started before 1970. Mean follow-up was 11 years. On the basis of weighted analysis of 303 betas for the four smoking groups, never smokers had a beta 10.8 mL/yr (95% confidence interval (CI), 8.9 to 12.8) less than continuing smokers. Betas for ex-smokers were 12.4 mL/yr (95% CI, 10.1 to 14.7) less than for continuing smokers, and for quitters, 8.5 mL/yr (95% CI, 5.6 to 11.4) less. These betas were similar to that for never smokers. In continuing smokers, beta increased 0.33 mL/yr per cigarette/day. Beta differences between continuing smokers and those who gave up were greater in patients with respiratory disease or with reduced baseline lung function, but were not clearly related to age or sex.</p> <p>Conclusion</p> <p>The available data have numerous limitations, but clearly show that continuing smokers have a beta that is dose-related and over 10 mL/yr greater than in never smokers, ex-smokers or quitters. The greater decline in those with respiratory disease or reduced lung function is consistent with some smokers having a more rapid rate of FEV₁decline. These results help in designing studies comparing continuing smokers of conventional cigarettes and switchers to novel products.</p

Affect and subjectivity

Editoria

A geobotanical study of the remnant natural vegetation of temperate South Australia / Ashley Dean Sparrow

Bibliography: leaves 187-2052 v. (various foliations) : ill. (some col.), maps ; 30 cm.Thesis (Ph.D.) -- University of Adelaide, Dept. of Botany, 199

Competitive exclusion after invasion?

The ‘Competitive Exclusion Principle’ is a foundation stone in the understanding of interspecific competition and niche relationships between species. In spite of having the status of a biological law, the principle has limited empirical support. In this study, we document strong effects of competition from the invading fish species vendace Coregonus albula over a 14-year period in the sub-arctic Pasvik watercourse. The native d.r. whitefish, that shared food and habitat niche with the invader, was displaced from its original niche and showed a more than 90% decline in population density over the study period. The study thus provides a unique record of how an exotic fish species excludes a native species from its original niche. Our data support the competitive exclusion principle, but also indicate that the vulnerability of the inferior competitor depends on a lack of alternative resources and on indirect ecological interactions