Information sharing in interteam responses to disaster

Research demonstrates that information sharing is facilitated by familiarity, and having a common understanding of problems, use of lexicon, and semantic meaning. These factors can be difficult to develop within extreme environments such as disasters as members of the multi‐agency system that responds often have limited experience of working together. Public inquiries repeatedly highlight the impact of information sharing difficulties on public safety, but limited academic research has focused on identifying concrete behaviours that facilitate interteam information sharing within such environments. This paper presents a case study of a national disaster response exercise involving 1,000 emergency responders. Data consist of structured observations, recordings of interteam meetings, and interviews with emergency responders. Results of mixed‐method analysis indicate that interteam information sharing is delayed by limited situation awareness and poor articulation. Conversely, adopting behaviours that promote common frames for understanding interteam capabilities and information requirements improves information sharing and potentially reduces cognitive effort required to process information. Findings contribute to interteam communication theory by highlighting that in complex, time‐constrained environments, having a shared understanding of responsibilities and information requirement is important for minimizing redundant deliberation and improving relevance and speed

Rapid decline of the CO2 buffering capacity in the North Sea and implications for the North Atlantic Ocean

Author Posting. © American Geophysical Union, 2007. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Global Biogeochemical Cycles 21 (2007): GB4001, doi:10.1029/2006GB002825.New observations from the North Sea, a NW European shelf sea, show that between 2001 and 2005 the CO2 partial pressure (pCO2) in surface waters rose by 22 μatm, thus faster than atmospheric pCO2, which in the same period rose approximately 11 μatm. The surprisingly rapid decline in air-sea partial pressure difference (ΔpCO2) is primarily a response to an elevated water column inventory of dissolved inorganic carbon (DIC), which, in turn, reflects mostly anthropogenic CO2 input rather than natural interannual variability. The resulting decline in the buffering capacity of the inorganic carbonate system (increasing Revelle factor) sets up a theoretically predicted feedback loop whereby the invasion of anthropogenic CO2 reduces the ocean's ability to uptake additional CO2. Model simulations for the North Atlantic Ocean and thermodynamic principles reveal that this feedback should be stronger, at present, in colder midlatitude and subpolar waters because of the lower present-day buffer capacity and elevated DIC levels driven either by northward advected surface water and/or excess local air-sea CO2 uptake. This buffer capacity feedback mechanism helps to explain at least part of the observed trend of decreasing air-sea ΔpCO2 over time as reported in several other recent North Atlantic studies.S. Doney and I. Lima were supported by NSF/ONR NOPP (N000140210370) and NASA (NNG05GG30G)

Development of a quality indicator set to measure and improve quality of ICU care for patients with traumatic brain injury.

BACKGROUND: We aimed to develop a set of quality indicators for patients with traumatic brain injury (TBI) in intensive care units (ICUs) across Europe and to explore barriers and facilitators for implementation of these quality indicators. METHODS: A preliminary list of 66 quality indicators was developed, based on current guidelines, existing practice variation, and clinical expertise in TBI management at the ICU. Eight TBI experts of the Advisory Committee preselected the quality indicators during a first Delphi round. A larger Europe-wide expert panel was recruited for the next two Delphi rounds. Quality indicator definitions were evaluated on four criteria: validity (better performance on the indicator reflects better processes of care and leads to better patient outcome), feasibility (data are available or easy to obtain), discriminability (variability in clinical practice), and actionability (professionals can act based on the indicator). Experts scored indicators on a 5-point Likert scale delivered by an electronic survey tool. RESULTS: The expert panel consisted of 50 experts from 18 countries across Europe, mostly intensivists (N = 24, 48%) and neurosurgeons (N = 7, 14%). Experts agreed on a final set of 42 indicators to assess quality of ICU care: 17 structure indicators, 16 process indicators, and 9 outcome indicators. Experts are motivated to implement this finally proposed set (N = 49, 98%) and indicated routine measurement in registries (N = 41, 82%), benchmarking (N = 42, 84%), and quality improvement programs (N = 41, 82%) as future steps. Administrative burden was indicated as the most important barrier for implementation of the indicator set (N = 48, 98%). CONCLUSIONS: This Delphi consensus study gives insight in which quality indicators have the potential to improve quality of TBI care at European ICUs. The proposed quality indicator set is recommended to be used across Europe for registry purposes to gain insight in current ICU practices and outcomes of patients with TBI. This indicator set may become an important tool to support benchmarking and quality improvement programs for patients with TBI in the future

A constitutive framework for predicting weakening and reduced buttressing of ice shelves based on observations of the progressive deterioration of the remnant Larsen B Ice Shelf

The increasing contribution of the Antarctic Ice Sheet to sea level rise is linked to reductions in ice shelf buttressing, driven in large part by basal melting of ice shelves. These ocean-driven buttressing losses are being compounded as ice shelves weaken and fracture. To date, model projections of ice sheet evolution have not accounted for weakening ice shelves. Here we present the first constitutive framework for ice deformation that explicitly includes mechanical weakening, based on observations of the progressive degradation of the remnant Larsen B Ice Shelf from 2000 to 2015. We implement this framework in an ice sheet model and are able to reproduce most of the observed weakening of the ice shelf. In addition to predicting ice shelf weakening and reduced buttressing, this new framework opens the door for improved understanding and predictions of iceberg calving, meltwater routing and hydrofracture, and ice shelf collapse

Can social dancing prevent falls in older adults? a protocol of the Dance, Aging, Cognition,Economics (DAnCE) fall prevention randomised controlled trial

Background:  Falls are one of the most common health problems among older people and pose a major economic burden on health care systems. Exercise is an accepted stand-alone fall prevention strategy particularly if it is balance training or regular participation in Tai chi. Dance shares the ‘holistic’ approach of practices such as Tai chi. It is a complex sensorimotor rhythmic activity integrating multiple physical, cognitive and social elements. Small-scale randomised controlled trials have indicated that diverse dance styles can improve measures of balance and mobility in older people, but none of these studies has examined the effect of dance on falls or cognition. This study aims to determine whether participation in social dancing: i) reduces the number of falls; and ii) improves cognitive functions associated with fall risk in older people. Methods/design: A single-blind, cluster randomised controlled trial of 12 months duration will be conducted. Approximately 450 participants will be recruited from 24 self-care retirement villages that house at least 60 residents each in Sydney, Australia. Village residents without cognitive impairment and obtain medical clearance will be eligible. After comprehensive baseline measurements including physiological and cognitive tests and self-completed questionnaires, villages will be randomised to intervention sites (ballroom or folk dance) or to a wait-listed control using a computer randomisation method that minimises imbalances between villages based on two baseline fall risk measures. Main outcome measures are falls, prospectively measured, and the Trail Making cognitive function test. Cost-effectiveness and cost-utility analyses will be performed. Discussion: This study offers a novel approach to balance training for older people. As a community-based approach to fall prevention, dance offers older people an opportunity for greater social engagement, thereby making a major contribution to healthy ageing. Providing diversity in exercise programs targeting seniors recognises the heterogeneity of multicultural populations and may further increase the number of taking part in exercise

Impact of Systemic Inflammation and Autoimmune Diseases on apoA-I and HDL Plasma Levels and Functions

The cholesterol of high-density lipoproteins (HDLs) and its major proteic component, apoA-I, have been widely investigated as potential predictors of acute cardiovascular (CV) events. In particular, HDL cholesterol levels were shown to be inversely and independently associated with the risk of acute CV diseases in different patient populations, including autoimmune and chronic inflammatory disorders. Some relevant and direct anti-inflammatory activities of HDL have been also recently identified targeting both immune and vascular cell subsets. These studies recently highlighted the improvement of HDL function (instead of circulating levels) as a promising treatment strategy to reduce inflammation and associated CV risk in several diseases, such as systemic lupus erythematosus and rheumatoid arthritis. In these diseases, anti-inflammatory treatments targeting HDL function might improve both disease activity and CV risk. In this narrative review, we will focus on the pathophysiological relevance of HDL and apoA-I levels/functions in different acute and chronic inflammatory pathophysiological conditions

Effect of new cyclophilin D ligands on mitochondrial permeability transition pore opening

Les phénomènes d’ischémie-reperfusion sont rencontrés dans plusieurs situations physiopathologiques. Le seul traitement de l’ischémie repose sur une restauration précoce du flux sanguin. Paradoxalement, la reperfusion génère des lésions supplémentaires, appelées « lésions de reperfusion », dont la mitochondrie est un acteur majeur via l’ouverture du pore de transition de perméabilité mitochondrial (mPTP). L’ouverture du mPTP est principalement modulée par la cyclophiline D (CypD), une protéine de la matrice mitochondriale, dont l’inhibition pharmacologique par la cyclosporine A (CsA) permet de limiter l’ouverture du pore. Cette inhibition, obtenue in vitro et in vivo, permet de réduire les lésions de reperfusion. Néanmoins, de récents essais cliniques n’ont pas permis de confirmer ce bénéfice dans le cadre de l’infarctus du myocarde, soulignant la nécessité de développer de nouveaux inhibiteurs du mPTP. Dans ce travail, nous avons étudié l’effet de nouveaux ligands de la CypD sur l’ouverture du mPTP. Ces petites molécules innovantes, de structure radicalement différente de la CsA inhibent l’ouverture du mPTP de mitochondries isolées et le dérivé le plus actif, le C31, permet une inhibition plus efficace du mPTP que la CsA. Le C31 inhibe également le mPTP au niveau cellulaire, dans des hépatocytes primaires et dans des cardiomyocytes isolés. In vivo, le C31 atteint les mitochondries hépatiques et protège le foie dans un modèle d’ischémie-reperfusion hépatique. Cependant, la stabilité métabolique du C31 ne lui permet pas d’atteindre le cœur. La poursuite du développement de ces inhibiteurs pourrait aboutir à de nouveaux candidats pour protéger les organes des lésions de reperfusion.Ischemia-reperfusion can occur in various pathophysiological situations such as myocardial infarction or organ transplantation. The only available treatment of ischemia relies on a timely reperfusion which paradoxically causes additional damage, so-called « reperfusion injury ». Mitochondria play a central role in this phenomenon through the opening of the mitochondrial permeability transition pore (mPTP) which extends cell death. mPTP opening is modulated by the matrix protein cyclophilin D (CypD). CypD inhibition by cyclosporin A (CsA), the most described CypD inhibitor, limits reperfusion injury in vivo. Nevertheless, recent clinical trials failed to recapitulate such protection in the context of myocardial infarction, emphasizing the urge to develop new mPTP inhibitors. Here, we investigated the effects of new CypD ligands on mPTP opening. We demonstrated that these small molecules unrelated to CsA are potent mPTP inhibitors and that the most active compound, C31, exhibited stronger mPTP-inhibiting properties as compared to CsA. C31 also inhibited mPTP opening in primary hepatocytes and isolated cardiomyocytes. In vivo, C31 reaches liver mitochondria and protects mitochondrial function in a hepatic ischemia-reperfusion model. Nevertheless, C31 metabolic stability hampers cardiac uptake of the compound. Further development of these new inhibitors might lead to interesting candidates to protect organs against ischemia-reperfusion injury

Étude de l'effet de nouveaux ligands de la cyclophiline D sur le pore de transition de perméabilité mitochondrial et de leur effet protecteur

Ischemia-reperfusion can occur in various pathophysiological situations such as myocardial infarction or organ transplantation. The only available treatment of ischemia relies on a timely reperfusion which paradoxically causes additional damage, so-called « reperfusion injury ». Mitochondria play a central role in this phenomenon through the opening of the mitochondrial permeability transition pore (mPTP) which extends cell death. mPTP opening is modulated by the matrix protein cyclophilin D (CypD). CypD inhibition by cyclosporin A (CsA), the most described CypD inhibitor, limits reperfusion injury in vivo. Nevertheless, recent clinical trials failed to recapitulate such protection in the context of myocardial infarction,emphasizing the urge to develop new mPTP inhibitors. Here, we investigated the effects of new CypD ligands on mPTP opening. We demonstrated that these small molecules unrelated to CsA are potent mPTP inhibitors and that the most active compound, C31, exhibited stronger mPTP-inhibiting properties as compared to CsA. C31 also inhibited mPTP opening in primary hepatocytes and isolated cardiomyocytes. In vivo, C31 reaches liver mitochondria and protects mitochondrial function in a hepatic ischemia-reperfusion model. Nevertheless, C31 metabolic stability hampers cardiac uptake of the compound. Further development of these new inhibitors might lead to interesting candidates to protect organs against ischemia-reperfusion injury.Les phénomènes d’ischémie-reperfusion sont rencontrés dans plusieurs situations physiopathologiques. Le seul traitement de l’ischémie repose sur une restauration précoce du flux sanguin. Paradoxalement, la reperfusion génère des lésions supplémentaires, appelées « lésions de reperfusion », dont la mitochondrie est un acteur majeur via l’ouverture du pore de transition de perméabilité mitochondrial (mPTP). L’ouverture du mPTP est principalement modulée par la cyclophiline D (CypD), une protéine de la matrice mitochondriale, dont l’inhibition pharmacologique par la cyclosporine A (CsA) permet de limiter l’ouverture du pore. Cette inhibition, obtenue in vitro et in vivo, permet de réduire les lésions de reperfusion. Néanmoins, de récents essais cliniques n’ont pas permis de confirmer ce bénéfice dans le cadre de l’infarctus du myocarde, soulignant la nécessité de développer de nouveaux inhibiteurs du mPTP. Dans ce travail, nous avons étudié l’effet de nouveaux ligands de la CypD sur l’ouverture du mPTP. Ces petites molécules innovantes, de structure radicalement différente de la CsA inhibent l’ouverture du mPTP de mitochondries isolées et le dérivé le plus actif, le C31, permet une inhibition plus efficace du mPTP que la CsA. Le C31 inhibe également le mPTP au niveau cellulaire, dans des hépatocytes primaires et dans des cardiomyocytes isolés. In vivo, le C31 atteint les mitochondries hépatiques et protège le foie dans un modèle d’ischémie-reperfusion hépatique. Cependant, la stabilité métabolique du C31 ne lui permet pas d’atteindre le cœur. La poursuite du développement de ces inhibiteurs pourrait aboutir à de nouveaux candidats pour protéger les organes des lésions de reperfusion