900 resultados para Health belief model
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BACKGROUND CONTEXT: The Neck Disability Index frequently is used to measure outcomes of the neck. The statistical rigor of the Neck Disability Index has been assessed with conflicting outcomes. To date, Confirmatory Factor Analysis of the Neck Disability Index has not been reported for a suitably large population study. Because the Neck Disability Index is not a condition-specific measure of neck function, initial Confirmatory Factor Analysis should consider problematic neck patients as a homogenous group. PURPOSE: We sought to analyze the factor structure of the Neck Disability Index through Confirmatory Factor Analysis in a symptomatic, homogeneous, neck population, with respect to pooled populations and gender subgroups. STUDY DESIGN: This was a secondary analysis of pooled data. PATIENT SAMPLE: A total of 1,278 symptomatic neck patients (67.5% female, median age 41 years), 803 nonspecific and 475 with whiplash-associated disorder. OUTCOME MEASURES: The Neck Disability Index was used to measure outcomes. METHODS: We analyzed pooled baseline data from six independent studies of patients with neck problems who completed Neck Disability Index questionnaires at baseline. The Confirmatory Factor Analysis was considered in three scenarios: the full sample and separate sexes. Models were compared empirically for best fit. RESULTS: Two-factor models have good psychometric properties across both the pooled and sex subgroups. However, according to these analyses, the one-factor solution is preferable from both a statistical perspective and parsimony. The two-factor model was close to significant for the male subgroup (p<.07) where questions separated into constructs of mental function (pain, reading headaches and concentration) and physical function (personal care, lifting, work, driving, sleep, and recreation). CONCLUSIONS: The Neck Disability Index demonstrated a one-factor structure when analyzed by Confirmatory Factor Analysis in a pooled, homogenous sample of neck problem patients. However, a two-factor model did approach significance for male subjects where questions separated into constructs of mental and physical function. Further investigations in different conditions, subgroup and sex-specific populations are warranted.
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Cued recall and item recognition are considered the standard episodic memory retrieval tasks. However, only the neural correlates of the latter have been studied in detail with fMRI. Using an event-related fMRI experimental design that permits spoken responses, we tested hypotheses from an auto-associative model of cued recall and item recognition [Chappell, M., & Humphreys, M. S. (1994). An auto-associative neural network for sparse representations: Analysis and application to models of recognition and cued recall. Psychological Review, 101, 103-128]. In brief, the model assumes that cues elicit a network of phonological short term memory (STM) and semantic long term memory (LTM) representations distributed throughout the neocortex as patterns of sparse activations. This information is transferred to the hippocampus which converges upon the item closest to a stored pattern and outputs a response. Word pairs were learned from a study list, with one member of the pair serving as the cue at test. Unstudied words were also intermingled at test in order to provide an analogue of yes/no recognition tasks. Compared to incorrectly rejected studied items (misses) and correctly rejected (CR) unstudied items, correctly recalled items (hits) elicited increased responses in the left hippocampus and neocortical regions including the left inferior prefrontal cortex (LIPC), left mid lateral temporal cortex and inferior parietal cortex, consistent with predictions from the model. This network was very similar to that observed in yes/no recognition studies, supporting proposals that cued recall and item recognition involve common rather than separate mechanisms.
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Large multisite efforts (e.g., the ENIGMA Consortium), have shown that neuroimaging traits including tract integrity (from DTI fractional anisotropy, FA) and subcortical volumes (from T1-weighted scans) are highly heritable and promising phenotypes for discovering genetic variants associated with brain structure. However, genetic correlations (rg) among measures from these different modalities for mapping the human genome to the brain remain unknown. Discovering these correlations can help map genetic and neuroanatomical pathways implicated in development and inherited risk for disease. We use structural equation models and a twin design to find rg between pairs of phenotypes extracted from DTI and MRI scans. When controlling for intracranial volume, the caudate as well as related measures from the limbic system - hippocampal volume - showed high rg with the cingulum FA. Using an unrelated sample and a Seemingly Unrelated Regression model for bivariate analysis of this connection, we show that a multivariate GWAS approach may be more promising for genetic discovery than a univariate approach applied to each trait separately.
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We present a new algorithm to compute the voxel-wise genetic contribution to brain fiber microstructure using diffusion tensor imaging (DTI) in a dataset of 25 monozygotic (MZ) twins and 25 dizygotic (DZ) twin pairs (100 subjects total). First, the structural and DT scans were linearly co-registered. Structural MR scans were nonlinearly mapped via a 3D fluid transformation to a geometrically centered mean template, and the deformation fields were applied to the DTI volumes. After tensor re-orientation to realign them to the anatomy, we computed several scalar and multivariate DT-derived measures including the geodesic anisotropy (GA), the tensor eigenvalues and the full diffusion tensors. A covariance-weighted distance was measured between twins in the Log-Euclidean framework [2], and used as input to a maximum-likelihood based algorithm to compute the contributions from genetics (A), common environmental factors (C) and unique environmental ones (E) to fiber architecture. Quanititative genetic studies can take advantage of the full information in the diffusion tensor, using covariance weighted distances and statistics on the tensor manifold.
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Purpose Health service quality is an important determinant for health service satisfaction and behavioral intentions. The purpose of this paper is to investigate requirements of e‐health services and to develop a measurement model to analyze the construct of “perceived e‐health service quality.” Design/methodology/approach The paper adapts the C‐OAR‐SE procedure for scale development by Rossiter. The focal aspect is the “physician‐patient relationship” which forms the core dyad in the healthcare service provision. Several in‐depth interviews were conducted in Switzerland; first with six patients (as raters), followed by two experts of the healthcare system (as judges). Based on the results and an extensive literature research, the classification of object and attributes is developed for this model. Findings The construct e‐health service quality can be described as an abstract formative object and is operationalized with 13 items: accessibility, competence, information, usability/user friendliness, security, system integration, trust, individualization, empathy, ethical conduct, degree of performance, reliability, and ability to respond. Research limitations/implications Limitations include the number of interviews with patients and experts as well as critical issues associated with C‐OAR‐SE. More empirical research is needed to confirm the quality indicators of e‐health services. Practical implications Health care providers can utilize the results for the evaluation of their service quality. Practitioners can use the hierarchical structure to measure service quality at different levels. The model provides a diagnostic tool to identify poor and/or excellent performance with regard to the e‐service delivery. Originality/value The paper contributes to knowledge with regard to the measurement of e‐health quality and improves the understanding of how customers evaluate the quality of e‐health services.
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When working with the world’s most vulnerable populations there are questions surrounding the salience of physical activity promotion programs given the multitude of basic needs that must first be met. Indeed, physical activity may be a low priority for individuals seeking safety, reunification with loved ones, and food for their families, as a subsistence lifestyle makes excess weight gain, diabetes, and cardiovascular disease irrelevant. Yet, when working with people from a refugee background for whom these challenges all too frequently apply, opportunities for sport and activity have repeatedly surfaced as desirable and needed, yet are utterly deficient. If we conceptualize physical activity purely as a chronic disease prevention tool, its significance within under-resourced communities is most assuredly lost; however, if we harness the power of physical activity to serve as an agent of positive social change, then it instantly becomes more meaningful and necessary.
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Issue addressed The paper examines the meanings of food safety among food businesses deemed non-compliant and considers the need for an ‘insider perspective’ to inform a more nuanced health promotion practice. Methods In-depth interviews were conducted with 29 food business operators who had been recently deemed ‘non-compliant’ through Council inspection. Result Paradoxically, these ‘non-compliers’ revealed a strong belief in the importance of food safety as well as a desire to comply with the regulations as communicated to them by Environmental Health Officers (EHOs). Conclusions The evidence base of food safety is largely informed by the science of food hazards, yet there is a very important need to illuminate the ‘insider’ experience of food businesses doing food safety on a daily basis. This requires a more socially nuanced appreciation of food businesses beyond the simple dichotomy of compliant/ non-compliant. So what? Armed with a deeper understanding of the social context surrounding food safety practice, it is anticipated that a more balanced, collaborative mode of food safety health promotion could develop which could add to the current signature model of regulation.
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Aerosol deposition in cylindrical tubes is a subject of interest to researchers and engineers in many applications of aerosol physics and metrology. Investigation of nano-particles in different aspects such as lungs, upper airways, batteries and vehicle exhaust gases is vital due the smaller size, adverse health effect and higher trouble for trapping than the micro-particles. The Lagrangian particle tracking provides an effective method for simulating the deposition of nano-particles as well as micro-particles as it accounts for the particle inertia effect as well as the Brownian excitation. However, using the Lagrangian approach for simulating ultrafine particles has been limited due to computational cost and numerical difficulties. In this paper, the deposition of nano-particles in cylindrical tubes under laminar condition is studied using the Lagrangian particle tracking method. The commercial Fluent software is used to simulate the fluid flow in the pipes and to study the deposition and dispersion of nano-particles. Different particle diameters as well as different flow rates are examined. The point analysis in a uniform flow is performed for validating the Brownian motion. The results show good agreement between the calculated deposition efficiency and the analytic correlations in the literature. Furthermore, for the nano-particles with the diameter more than 40 nm, the calculated deposition efficiency by the Lagrangian method is less than the analytic correlations based on Eulerian method due to statistical error or the inertia effect.
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This paper describes the development of Pictorial Conceptual Metaphors, created out of a literature review on gendered Indigenous health and wellbeing that depicts the inherited effects of the ‘system’ past, present and future. The Pictorial Conceptual Metaphors are pictures that were created to tell the story of colonisation and its inherited and ongoing impacts on Indigenous people’s health and wellbeing. Aboriginal historical experiences, past, present and future are briefly overviewed in order to unpack and communicate to readers the significance and impact of these experiences on Aboriginal health, and ultimately, to bring about understanding to initiate change within the Australian health system. Systemic racism, embedded in the Australian health system, excludes and discriminates against Indigenous peoples through a lack of cultural consideration resulting in a cumulative and ongoing negative effect on Indigenous people’s health (Dudgeon et al. 2014; Fredericks 2008; Marmot 2011; Queensland Government 2012). Systemic action research identifies actions and processes in large systems such as health and education in order to bring about systemic change. Our intention to highlight the systemic changes needed in the Australian health system to improve Indigenous people’s health and wellbeing require us to understand the processes involved in bringing about systemic change. For this to occur, we needed to ‘see the system’ in order to identify the system dynamics in operation. The Pictorial Conceptual Metaphors are the first step in ‘seeing the system’; they illustrate the past and the present, and identify the preferred future for Indigenous health and wellbeing outcomes
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The transfusion of platelet concentrates (PCs) is widely used to treat thrombocytopenia and severe trauma. Ex vivo storage of PCs is associated with a storage lesion characterized by partial platelet activation and the release of soluble mediators, such as soluble CD40 ligand (sCD40L), RANTES, and interleukin (IL)-8. An in vitro whole blood culture transfusion model was employed to assess whether mediators present in PC supernatants (PC-SNs) modulated dendritic cell (DC)-specific inflammatory responses (intracellular staining) and the overall inflammatory response (cytometric bead array). Lipopolysaccharide (LPS) was included in parallel cultures to model the impact of PC-SNs on cell responses following toll-like receptor-mediated pathogen recognition. The impact of both the PC dose (10%, 25%) and ex vivo storage period was investigated [day 2 (D2), day 5 (D5), day 7 (D7)]. PC-SNs alone had minimal impact on DC-specific inflammatory responses and the overall inflammatory response. However, in the presence of LPS, exposure to PC-SNs resulted in a significant dose associated suppression of the production of DC IL-12, IL-6, IL-1a, tumor necrosis factor-a (TNF-a), and macrophage inflammatory protein (MIP)-1b and storage-associated suppression of the production of DC IL-10, TNF-a, and IL-8. For the overall inflammatory response, IL-6, TNF-a, MIP-1a, MIP-1b, and inflammatory protein (IP)-10 were significantly suppressed and IL-8, IL-10, and IL-1b significantly increased following exposure to PC-SNs in the presence of LPS. These data suggest that soluble mediators present in PCs significantly suppress DC function and modulate the overall inflammatory response, particularly in the presence of an infectious stimulus. Given the central role of DCs in the initiation and regulation of the immune response, these results suggest that modulation of the DC inflammatory profile is a probable mechanism contributing to transfusion-related complications.
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Mutations of UDP-N-acetyl-alpha-D-galactosamine polypeptide N-acetyl galactosaminyl transferase 3 (GALNT3) result in familial tumoural calcinosis (FTC) and the hyperostosis-hyperphosphataemia syndrome (HHS), which are autosomal recessive disorders characterised by soft-tissue calcification and hyperphosphataemia. To facilitate in vivo studies of these heritable disorders of phosphate homeostasis, we embarked on establishing a mouse model by assessing progeny of mice treated with the chemical mutagen N-ethyl-N-nitrosourea (ENU), and identified a mutant mouse, TCAL, with autosomal recessive inheritance of ectopic calcification, which involved multiple tissues, and hyperphosphataemia; the phenotype was designated TCAL and the locus, Tcal. TCAL males were infertile with loss of Sertoli cells and spermatozoa, and increased testicular apoptosis. Genetic mapping localized Tcal to chromosome 2 (62.64-71.11 Mb) which contained the Galnt3. DNA sequence analysis identified a Galnt3 missense mutation (Trp589Arg) in TCAL mice. Transient transfection of wild-type and mutant Galnt3-enhanced green fluorescent protein (EGFP) constructs in COS-7 cells revealed endoplasmic reticulum retention of the Trp589Arg mutant and Western blot analysis of kidney homogenates demonstrated defective glycosylation of Galnt3 in Tcal/Tcal mice. Tcal/Tcal mice had normal plasma calcium and parathyroid hormone concentrations; decreased alkaline phosphatase activity and intact Fgf23 concentrations; and elevation of circulating 1,25-dihydroxyvitamin D. Quantitative reverse transcriptase-PCR (qRT-PCR) revealed that Tcal/Tcal mice had increased expression of Galnt3 and Fgf23 in bone, but that renal expression of Klotho, 25-hydroxyvitamin D-1α-hydroxylase (Cyp27b1), and the sodium-phosphate co-transporters type-IIa and -IIc was similar to that in wild-type mice. Thus, TCAL mice have the phenotypic features of FTC and HHS, and provide a model for these disorders of phosphate metabolism. © 2012 Esapa et al.
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Chronic kidney disease (CKD) is characterized by renal fibrosis that can lead to end-stage renal failure, and studies have supported a strong genetic influence on the risk of developing CKD. However, investigations of the underlying molecular mechanisms are hampered by the lack of suitable hereditary models in animals. We therefore sought to establish hereditary mouse models for CKD and renal fibrosis by investigating mice treated with the chemical mutagen N-ethyl-N-nitrosourea, and identified a mouse with autosomal recessive renal failure, designated RENF. Three-week old RENF mice were smaller than their littermates, whereas at birth they had been of similar size. RENF mice, at 4-weeks of age, had elevated concentrations of plasma urea and creatinine, indicating renal failure, which was associated with small and irregularly shaped kidneys. Genetic studies using DNA from 10 affected mice and 91 single nucleotide polymorphisms mapped the Renf locus to a 5.8Mbp region on chromosome 17E1.3. DNA sequencing of the xanthine dehydrogenase (Xdh) gene revealed a nonsense mutation at codon 26 that co-segregated with affected RENF mice. The Xdh mutation resulted in loss of hepatic XDH and renal Cyclooxygenase-2 (COX-2) expression. XDH mutations in man cause xanthinuria with undetectable plasma uric acid levels and three RENF mice had plasma uric acid levels below the limit of detection. Histological analysis of RENF kidney sections revealed abnormal arrangement of glomeruli, intratubular casts, cellular infiltration in the interstitial space, and interstitial fibrosis. TUNEL analysis of RENF kidney sections showed extensive apoptosis predominantly affecting the tubules. Thus, we have established a mouse model for autosomal recessive early-onset renal failure due to a nonsense mutation in Xdh that is a model for xanthinuria in man. This mouse model could help to increase our understanding of the molecular mechanisms associated with renal fibrosis and the specific roles of XDH and uric acid. © 2012 Piret et al.
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Objectives Mental health workers are constantly exposed to their clients’ stories of distress and trauma. While listening to these stories can be emotionally draining, professionals in this field still derive pleasure from their work. This study examined the role of personality and workplace belongingness in predicting compassion satisfaction, secondary traumatic stress, and burnout in mental health professionals. Methods Mental health staff (N = 156) working in a counselling service completed a questionnaire that included measures relating to professional quality of life, the Five-Factor Model of personality, workplace belongingness, as well as questions relating to the participants’ demographic profile, work roles and trauma history. Results The results indicated that, high levels of emotional stability (low neuroticism), extraversion, agreeableness, conscientiousness, and being connected at work, are essential factors that promote the professional quality of life of mental health workers. Specifically, workplace belongingness was the strongest predictor of compassion satisfaction and low levels of burnout, while neuroticism was the strongest predictor of secondary traumatic stress. Conclusions Important implications from this study include: (1) encouraging mental health staff to increase self-awareness of their dispositional characteristics and how their personalities affect their wellbeing at work, and; (2) encouraging management to facilitate practices where mental health workers feel connected, respected, and supported in their organisation.
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Introduction: Ankylosing spondylitis (AS) is unique in its pathology where inflammation commences at the entheses before progressing to an osteoproliferative phenotype generating excessive bone formation that can result in joint fusion. The underlying mechanisms of this progression are poorly understood. Recent work has suggested that changes in Wnt signalling, a key bone regulatory pathway, may contribute to joint ankylosis in AS. Using the proteoglycan-induced spondylitis (PGISp) mouse model which displays spondylitis and eventual joint fusion following an initial inflammatory stimulus, we have characterised the structural and molecular changes that underlie disease progression. Methods: PGISp mice were characterised 12 weeks after initiation of inflammation using histology, immunohistochemistry (IHC) and expression profiling. Results: Inflammation initiated at the periphery of the intervertebral discs progressing to disc destruction followed by massively excessive cartilage and bone matrix formation, as demonstrated by toluidine blue staining and IHC for collagen type I and osteocalcin, leading to syndesmophyte formation. Expression levels of DKK1 and SOST, Wnt signalling inhibitors highly expressed in joints, were reduced by 49% and 63% respectively in the spine PGISp compared with control mice (P < 0.05) with SOST inhibition confirmed by IHC. Microarray profiling showed genes involved in inflammation and immune-regulation were altered. Further, a number of genes specifically involved in bone regulation including other members of the Wnt pathway were also dysregulated. Conclusions: This study implicates the Wnt pathway as a likely mediator of the mechanism by which inflammation induces bony ankylosis in spondyloarthritis, raising the potential that therapies targeting this pathway may be effective in preventing this process.