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Sökning: WFRF:(Bodin L)

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  • Bodin, Örjan, et al. (författare)
  • Improving network approaches to the study of complex social–ecological interdependencies
  • 2019
  • Ingår i: Nature Sustainability. - : Springer Science and Business Media LLC. - 2398-9629. ; 2:7, s. 551-559
  • Tidskriftsartikel (refereegranskat)abstract
    • Achieving effective, sustainable environmental governance requires a better understanding of the causes and consequences of the complex patterns of interdependencies connecting people and ecosystems within and across scales. Network approaches for conceptualizing and analysing these interdependencies offer one promising solution. Here, we present two advances we argue are needed to further this area of research: (i) a typology of causal assumptions explicating the causal aims of any given network-centric study of social–ecological interdependencies; (ii) unifying research design considerations that facilitate conceptualizing exactly what is interdependent, through what types of relationships and in relation to what kinds of environmental problems. The latter builds on the appreciation that many environmental problems draw from a set of core challenges that re-occur across contexts. We demonstrate how these advances combine into a comparative heuristic that facilitates leveraging case-specific findings of social–ecological interdependencies to generalizable, yet context-sensitive, theories based on explicit assumptions of causal relationships.
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  • Franzen, L., et al. (författare)
  • Letter to the editor (multiple letter)
  • 2005
  • Ingår i: Clinical Transplantation. - : Wiley. - 0902-0063 .- 1399-0012. ; 19:4, s. 571-
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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16.
  • Glendor, Ulf, et al. (författare)
  • Direct and indirect time spent on care of dental trauma : a 2-year prospective study of children and adolescents
  • 2000
  • Ingår i: Endodontics and dental traumatology. - : Wiley. - 0109-2502 .- 1600-4469 .- 1600-9657. ; 16:1, s. 16-23
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim was to account for the total time spent by professional care-givers (direct time) and by patients and companions engaged as support and help (indirect time) to treat and otherwise attend to children and adolescents with dental trauma to primary and permanent teeth. The study was based on a random sample of 192 children and adolescents with dental traumas reported to an insurance company and prospectively followed up by telephone interviews over a period of 2 years after the trauma episode. On average, direct time represented 16% of total time for all visits for dental trauma to permanent teeth and 11% for trauma to primary teeth. The most extensive type of indirect time was transport time, which took up 30% of the total time spent on injuries to permanent teeth and 36% for injuries to primary teeth. Multiple regression analysis of the impact of dental and demographic injury variables on the time variables showed that complicated trauma was associated with extended time, direct as well as indirect, for permanent and primary teeth injuries. Our estimate of the average relative increase in total time spent by patients and companions in cases of complicated injury to permanent teeth was 117% (95% confidence interval [CI], 52-211) for patients and 112% (95% CI, 42-217) for companions. For transport time a strong predictor was access to a dental clinic near the place of residence. Lack of access could extend the average transport time by 180% (95% CI, 80-335) for patients and 163% (95% CI, 67-317) for their companions in cases of injuries to primary teeth.
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17.
  • Hosie, S., et al. (författare)
  • Gastrointestinal dysfunction in patients and mice expressing the autism-associated R451C mutation in neuroligin-3
  • 2019
  • Ingår i: Autism Research. - : Wiley. - 1939-3792 .- 1939-3806. ; 12:7, s. 1043-1056
  • Tidskriftsartikel (refereegranskat)abstract
    • Gastrointestinal (GI) problems constitute an important comorbidity in many patients with autism. Multiple mutations in the neuroligin family of synaptic adhesion molecules are implicated in autism, however whether they are expressed and impact GI function via changes in the enteric nervous system is unknown. We report the GI symptoms of two brothers with autism and an R451C mutation in Nlgn3 encoding the synaptic adhesion protein, neuroligin-3. We confirm the presence of an array of synaptic genes in the murine GI tract and investigate the impact of impaired synaptic protein expression in mice carrying the human neuroligin-3 R451C missense mutation (NL3(R451C)). Assessing in vivo gut dysfunction, we report faster small intestinal transit in NL3(R451C) compared to wild-type mice. Using an ex vivo colonic motility assay, we show increased sensitivity to GABA(A) receptor modulation in NL3(R451C) mice, a well-established Central Nervous System (CNS) feature associated with this mutation. We further show increased numbers of small intestine myenteric neurons in NL3(R451C) mice. Although we observed altered sensitivity to GABA(A) receptor modulators in the colon, there was no change in colonic neuronal numbers including the number of GABA-immunoreactive myenteric neurons. We further identified altered fecal microbial communities in NL3(R451C) mice. These results suggest that the R451C mutation affects small intestinal and colonic function and alter neuronal numbers in the small intestine as well as impact fecal microbes. Our findings identify a novel GI phenotype associated with the R451C mutation and highlight NL3(R451C) mice as a useful preclinical model of GI dysfunction in autism. Autism Res 2019, 12: 1043-1056. (c) 2019 International Society for Autism Research, Wiley Periodicals, Inc. Lay Summary People with autism commonly experience gastrointestinal problems, however the cause is unknown. We report gut symptoms in patients with the autism-associated R451C mutation encoding the neuroligin-3 protein. We show that many of the genes implicated in autism are expressed in mouse gut. The neuroligin-3 R451C mutation alters the enteric nervous system, causes gastrointestinal dysfunction, and disrupts gut microbe populations in mice. Gut dysfunction in autism could be due to mutations that affect neuronal communication.
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