Health status of critically ill trauma patients

Aims and objectives: To describe the recovery of trauma intensive care patients up to six months posthospital discharge. Background: Injury is a leading cause of preventable mortality and morbidity worldwide, with approximately 10% of hospitalised trauma patients being admitted to intensive care. Intensive care patients experience significant ongoing physical and psychological burden after discharge; however, the patterns of recovery and the subgroups of intensive care patients who experience the greatest burden are not described. Design: This prospective cohort study was conducted in one tertiary referral hospital in south-east Queensland, Australia. Methods: Following ethics approval, injured patients who required admission to intensive care provided consent. Participants completed questionnaires prior to hospital discharge (n = 123) and one (n = 93) and six months (n = 88) later. Data included demographic and socioeconomic details, pre-injury health, injury characteristics, acute care factors, postacute factors [self-efficacy, illness perception, perceived social support and psychological status as measured by the Kessler Psychological Distress Scale (K10) and the PTSD Civilian Checklist] and health status (SF-36). Results: All participants required ongoing support from healthcare providers in the six months after discharge from hospital, and approximately half required support services such as accommodation and home modifications. Approximately 20% of participants reported post-traumatic stress symptoms, while approximately half the participants reported psychological distress. Average quality of life scores were significantly below the Australian norms both one and six months postdischarge. Conclusions: Trauma intensive care patients rely on ongoing healthcare professional and social support services. Compromised health-related quality of life and psychological health persists at six months. Relevance to clinical practice: Effective discharge planning and communication across the care continuum is essential to facilitate access to healthcare providers and other support services in the community setting

Factors associated with self-efficacy for managing recovery in the trauma intensive care population: A prospective cohort study

Objective: The aim of this paper was to identify factors associated with self-efficacy for managing recovery in the trauma intensive care population. Introduction: Injury accounts for 6.5% of disease burden in Australia, with similar levels being reported in other developed countries. While some studies regarding self-efficacy have identified a relationship to patient recovery post acute injury, others have been inconclusive. This study will identify factors associated with self-efficacy for managing recovery in the trauma intensive care population. Methods: A prospective cohort study of patients aged ≥18 years, admitted to a metropolitan tertiary hospital in South East Queensland between June 2008 and August 2010 for the acute treatment of injury. Demographic, injury, acute care and psychosocial factors were considered. The primary outcome was self-efficacy measured by the 6-item self-efficacy scale (SES) 1 and 6 months post hospital discharge. All factors significant (p < 0.10) on univariate analysis were included in multivariable modelling where p < 0.05 was considered significant. Results: A total of 88 patients were included. The mean self-efficacy score at 1 and 6 months was similar (6.8 vs 6.9 respectively). Self-efficacy at 1 month, psychological distress (K-10) Score and illness perception (K10) Score accounted for 68.4% (adjusted R2) of the variance in 6 month self-efficacy (F3,75) = 57.17, p < 0.001. Illness perception was the strongest contributor to 6 month self-efficacy (beta = −0.516), followed by psychological distress (beta = −0.243) and self-efficacy at 1 month (beta = 0.205). Conclusion: Significant factors associated with self-efficacy for managing recovery at 6 months included 1 month self-efficacy, illness perception and psychological distress. To promote patient recovery, screening patients at 1 month in order to commence relevant interventions could be beneficial

Targeting of proteins and protein analogs to metal-chelating lipid vesicles

NOTE: Text or symbols not renderable in plain ASCII are indicated by [...]. Abstract is included in .pdf document. This investigation demonstrates that new metal-chelating lipids formed into mixed vesicles can bind to a variety histidine-rich ligands through metal coordination. Our results show the feasibility of metal-chelating lipids as a method for targeting histidine-rich compounds to lipid interfaces. Interesting metal chelating lipid materials for protein orientation studies, matching the surface distribution of surface residues, protein drug delivery, and for two-dimensional protein crystallization could be made with chelating-lipids. Engineered proteins containing a histidine "tag" or proteins with natural surface histidine residues are easily targeted to the interface using metal binding. Both metal binding and histidine-rich ligand binding were investigated with mixed metal-chelating lipid vesicles. New metal-chelating lipids containing an iminodiacetate (IDA) chelating-moiety were formed into mixed vesicles and shown to bind transition metal ions through the lipid headgroup. Metal binding was characterized through calorimetry, freeze-etch microscopy, light scattering, ESR, and fluorescence studies. Fluorescently-labeled lipids containing iminodiacetate showed a large change in the fluorescence emission spectra upon metal binding, behavior which has proven useful for a vesicle-based metal sensor. Metal-loaded vesicles bound a model protein specifically through surface-accessible histidines, as shown using ESR studies. Equilibrium binding measurements showed at least an order of magnitude increase in binding affinity of the protein for the membrane when metal was present. The association constants determined through isothermal titration calorimetry for a model bivalent histidine compound binding to metal-chelating lipid bilayers were of the order of [...], while monovalent binding constants were of the order [...]. Lipid re-organization upon ligand binding was probed with model histidine compounds and histidine polymers using fluorescently-labeled metal-chelating lipid vesicles. The ability of lipids to form multivalent ligand-lipid complexes was investigated using the formation of lipid excimers, as demonstrated by fluorescence measurements of the E/M intensity ratio. Histidine content of model compounds determines the magnitude of the effect on the fluorescence emission spectra. Histidine polymers showed a larger increase of the E/M ratio than the smaller bivalent or monovalent compounds. Combining equilibrium binding results obtained with model complexes and results from fluorescence experiments, studies with metal-chelating vesicles support multivalent coordination and reorganization of the lipids by histidine-rich ligands

Metal-Induced Dispersion of Lipid Aggregates: A Simple, Selective, and Sensitive Fluorescent Metal Ion Sensor

A new metal ion sensor capable of detecting nanomolar concentrations (< 1 ppb) of Cu^(2+) is made from mixed vesicles of a novel pyrene‐labeled metal‐chelating ligand and distearoyl phosphatidylcholine. When copper is added, the fluorescence monomer intensity emitted at 377 nm greatly increases, while the intensity of light emitted at 470 nm decreases. This effect is probably due to the dispersal of the fluorescent lipid throughout the matrix upon metal binding and is depicted schematically below

Specific Protein Attachment to Artificial Membranes via Coordination to Lipid-Bound Copper(II)

A versatile and convenient method for targeting proteins to lipid assemblies using metal ion coordination is described. Mixed lipid bilayers and Langmuir monolayers containing a metal-chelating lipid and divalent copper ions are shown to bind protein via surface-accessible histidine residues. Cu^(2+) chelated by iminodiacetate (IDA) in the headgroup serves as an affinity ligand to target the protein to the interface. The compact, uncharged Cu^(2+)-IDA headgroup can be incorporated into lipid assemblies without disrupting the lipid packing. Surface pressure-area isotherms of DSPC monolayers containing 5 mol % of IDA-lipid show that Cu^(2+) enhances the rate and extent of myoglobin association with the interface. Myoglobin binds to small unilamellar vesicles containing 2% Cu^(2+)-IDA lipid (48% DSPC and 50% cholesterol) at least an order of magnitude more tightly than to vesicles without metal or loaded with Ca^(2+). The Cu^(2+)-IDA lipid more than doubles the amount of protein targeted to the interface. Cu^(2+) ESR parameters g_∥ and A_∥, measured for liposomes with native and DEPC-modified myoglobin, support coordination of surface histidine side chains to Cu^(2+) as the binding interaction