41 research outputs found
Predicting the Importance of Hospital Chaplain Care in a Trauma Population
Background. The purpose of this exploratory study was to determine if the importance of chaplain care is associated with and could be predicted by patient or injury characteristics. Methods. A telephone survey of recently discharged trauma patients was conducted. Logistic regression analyses were conducted to determine what factors are associated with the importance of chaplain care and satisfaction with chaplain care. Results. Self-reported religious affiliation was associated with the importance of chaplain care and importance of chaplain care was associated with satisfaction with chaplain care. Conclusions. The value of chaplain care cannot be measured by patient characteristics, therefore, chaplain care should be offered to all patients and families
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The UNITE Collaborative: Early Experiences of Introducing Collaborative Trainee Research to Interventional Radiology in the United Kingdom.
Praktische Erfahrungen bei der Erfassung der rÀumlichen VariabilitÀt von pH-Werten in Ackerböden durch das Online-Messverfahren Veris MSP
Der pH-Wert ist ein relevanter Parameter fĂŒr die ErtragsfĂ€higkeit, auf dessen rĂ€umliche Variation zu reagieren ist. Der hohe Bodenuntersuchungsaufwand verhindert dies oft in der Praxis. Die mobile Sensorplattform MSP der Firma Veris Technologies Inc. ermöglicht eine rĂ€umlich hoch aufgelöste pH-Kartierung. In diesem Artikel wird die EinsatzfĂ€higkeit dieses Systems fĂŒr den Ăkolandbau unter Praxisbedingungen geprĂŒft. Eine effiziente Erstellung von Boden-pH-Karten ist grundsĂ€tzlich möglich. Allerdings sind weitere Untersuchungen zur Vergleichbarkeit der Ergebnisse mit der in Deutschland ĂŒblichen Methode notwendig und technische Modifikationen erforderlich, um einen störungsfreien Einsatz unter Praxisbedingungen sicherzustellen
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Atomoxetine and citalopram alter brain network organization in Parkinson's disease.
Parkinson's disease has multiple detrimental effects on motor and cognitive systems in the brain. In contrast to motor deficits, cognitive impairments in Parkinson's disease are usually not ameliorated, and can even be worsened, by dopaminergic treatments. Recent evidence has shown potential benefits from restoring other neurotransmitter deficits, including noradrenergic and serotonergic transmission. Here, we study global and regional brain network organization using task-free imaging (also known as resting-state), which minimizes performance confounds and the bias towards predetermined networks. Thirty-three patients with idiopathic Parkinson's disease were studied three times in a double-blinded, placebo-controlled counter-balanced crossover design, following placebo, 40âmg oral atomoxetine (selective noradrenaline reuptake inhibitor) or 30âmg oral citalopram (selective serotonin reuptake inhibitor). Neuropsychological assessments were performed outside the scanner. Seventy-six controls were scanned without medication to provide normative data for comparison to the patient cohort. Graph theoretical analysis of task-free brain connectivity, with a random 500-node parcellation, was used to measure the effect of disease in placebo-treated state (versus unmedicated controls) and pharmacological intervention (drug versus placebo). Relative to controls, patients on placebo had executive impairments (reduced fluency and inhibitory control), which was reflected in dysfunctional network dynamics in terms of reduced clustering coefficient, hub degree and hub centrality. In patients, atomoxetine improved fluency in proportion to plasma concentration (Pâ=â0.006, r 2â=â0.24), and improved response inhibition in proportion to increased hub Eigen centrality (Pâ=â0.044, r 2â=â0.14). Citalopram did not improve fluency or inhibitory control, but its influence on network integration and efficiency depended on disease severity: clustering (Pâ=â0.01, r 2â=â0.22), modularity (Pâ=â0.043, r 2â=â0.14) and path length (Pâ=â0.006, r 2â=â0.25) increased in patients with milder forms of Parkinson's disease, but decreased in patients with more advanced disease (Unified Parkinson's Disease Rating Scale motor subscale part III > 30). This study supports the use of task-free imaging of brain networks in translational pharmacology of neurodegenerative disorders. We propose that hub connectivity contributes to cognitive performance in Parkinson's disease, and that noradrenergic treatment strategies can partially restore the neural systems supporting executive function
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[11C]PK11195 binding in Alzheimer disease and progressive supranuclear palsy.
OBJECTIVE: We tested whether in vivo neuroinflammation relates to the distinctive distributions of pathology in Alzheimer disease (AD) and progressive supranuclear palsy (PSP). METHODS: Sixteen patients with symptomatic AD (including amnestic mild cognitive impairment with amyloid-positive PET scan), 16 patients with PSP-Richardson syndrome, and 13 age-, sex-, and education-matched healthy controls were included in this case-control study. Participants underwent [11C]PK11195 PET scanning, which was used as an in vivo index of neuroinflammation. RESULTS: [11C]PK11195 binding in the medial temporal lobe and occipital, temporal, and parietal cortices was increased in patients with AD, relative both to patients with PSP and to controls. Compared to controls, patients with PSP showed elevated [11C]PK11195 binding in the thalamus, putamen, and pallidum. [11C]PK11195 binding in the cuneus/precuneus correlated with episodic memory impairment in AD, while [11C]PK11195 binding in the pallidum, midbrain, and pons correlated with disease severity in PSP. CONCLUSIONS: Together, our results suggest that neuroinflammation has an important pathogenic role in the 2 very different human neurodegenerative disorders of AD and PSP. The increase and distribution of microglial activation suggest that immunotherapeutic strategies may be useful in slowing the progression of both diseases
Functional network resilience to pathology in presymptomatic genetic frontotemporal dementia.
The presymptomatic phase of neurodegenerative diseases are characterized by structural brain changes without significant clinical features. We set out to investigate the contribution of functional network resilience to preserved cognition in presymptomatic genetic frontotemporal dementia. We studied 172 people from families carrying genetic abnormalities in C9orf72, MAPT, or PGRN. Networks were extracted from functional MRI data and assessed using graph theoretical analysis. We found that despite loss of both brain volume and functional connections, there is maintenance of an efficient topological organization of the brain's functional network in the years leading up to the estimated age of frontotemporal dementia symptom onset. After this point, functional network efficiency declines markedly. Reduction in connectedness was most marked in highly connected hub regions. Measures of topological efficiency of the brain's functional network and organization predicted cognitive dysfunction in domains related to symptomatic frontotemporal dementia and connectivity correlated with brain volume loss in frontotemporal dementia. We propose that maintaining the efficient organization of the brain's functional network supports cognitive health even as atrophy and connectivity decline presymptomatically.The Italian Ministry of Health
The Canadian Institutes of Health Research as part of a Centres of Excellence in Neurodegeneration grant [grant number CoEN01
18F-AV-1451 positron emission tomography in Alzheimer's disease and progressive supranuclear palsy.
The ability to assess the distribution and extent of tau pathology in Alzheimer's disease and progressive supranuclear palsy in vivo would help to develop biomarkers for these tauopathies and clinical trials of disease-modifying therapies. New radioligands for positron emission tomography have generated considerable interest, and controversy, in their potential as tau biomarkers. We assessed the radiotracer 18F-AV-1451 with positron emission tomography imaging to compare the distribution and intensity of tau pathology in 15 patients with Alzheimer's pathology (including amyloid-positive mild cognitive impairment), 19 patients with progressive supranuclear palsy, and 13 age- and sex-matched controls. Regional analysis of variance and a support vector machine were used to compare and discriminate the clinical groups, respectively. We also examined the 18F-AV-1451 autoradiographic binding in post-mortem tissue from patients with Alzheimer's disease, progressive supranuclear palsy, and a control case to assess the 18F-AV-1451 binding specificity to Alzheimer's and non-Alzheimer's tau pathology. There was increased 18F-AV-1451 binding in multiple regions in living patients with Alzheimer's disease and progressive supranuclear palsy relative to controls [main effect of group, F(2,41) = 17.5, P 2.2, P's 2.7, P's < 0.02). The support vector machine assigned patients' diagnoses with 94% accuracy. The post-mortem autoradiographic data showed that 18F-AV-1451 strongly bound to Alzheimer-related tau pathology, but less specifically in progressive supranuclear palsy. 18F-AV-1451 binding to the basal ganglia was strong in all groups in vivo. Postmortem histochemical staining showed absence of neuromelanin-containing cells in the basal ganglia, indicating that off-target binding to neuromelanin is an insufficient explanation of 18F-AV-1451 positron emission tomography data in vivo, at least in the basal ganglia. Overall, we confirm the potential of 18F-AV-1451 as a heuristic biomarker, but caution is indicated in the neuropathological interpretation of its binding. Off-target binding may contribute to disease profiles of 18F-AV-1451 positron emission tomography, especially in primary tauopathies such as progressive supranuclear palsy. We suggest that 18F-AV-1451 positron emission tomography is a useful biomarker to assess tau pathology in Alzheimer's disease and to distinguish it from other tauopathies with distinct clinical and pathological characteristics such as progressive supranuclear palsy.This study was funded by the National Institute for Health Research (NIHR, RG64473) Cambridge Biomedical Research Centre and Biomedical Research Unit in Dementia, PSP Association, the Wellcome Trust (JBR 103838), the Medical Research Council of Cognition and Brain Sciences Unit, Cambridge (MC-A060-5PQ30), and partially by a Medical Research Council grant (MR/K02308X/1) held by J.T.O., J.B.R., and F.I.A. The Human Research Tissue Bank is supported by the NIHR Cambridge Biomedical Research Centre
A novel causal mechanism for grey squirrel bark stripping: The Calcium Hypothesis
AbstractGrey squirrels, Sciurus carolinensis, damage trees in the UK by stripping bark and eating the underlying phloem; squirrel motivation for damage is, however, unknown. Damage can result in deterioration of timber quality and a significant economic toll on the forestry industry. Prediction of severe damage followed by targeted killing of squirrels is the current recommended management option. However, the use of warfarin (an anticoagulant poison) is now restricted in the UK and other more humane methods of killing are labour-intensive, so an alternative solution is needed. A better understanding of what motivates grey squirrels to strip bark may enable a preventive approach to be developed. Whilst the bark stripping literature has explored predictive factors affecting the likelihood of damage, causal understanding is lacking. The aim of this review is to introduce the Calcium Hypothesis as a possible explanation for bark stripping, with a view to informing the prevention of damage. The Calcium Hypothesis states that grey squirrels damage trees to ameliorate a calcium deficiency. The main predictive factors of bark stripping behaviour each inform and lend support to the Calcium Hypothesis. Calcium is stored in tree phloem, and damage increases with phloem width, providing squirrels with more calcium per unit area ingested. Calcium levels increase in trees as active growth resumes after winter dormancy, this occurs immediately prior to the main bark stripping season of MayâJuly, and trees growing most vigorously are at increased risk of damage. It is likely grey squirrels also have a requirement for calcium during the bark stripping season. Adult females will be under post-parturition pressures such as lactation, and juveniles will be going through their main period of bone growth, both of which likely represent a requirement for calcium â which supports an observed positive correlation between juvenile abundance and bark stripping. A high autumnal seed crop increases juvenile recruitment the following spring, and could also induce a requirement for calcium to a population due to the high phosphorus to calcium ratio of seeds. To further investigate the hypothesis, the extent to which grey squirrels can utilise calcium oxalate, as calcium occurs in bark, should be determined, and also the extent to which grey squirrels undergo seasonal periods of calcium deficiency. Increasing our causal understanding of bark stripping could inform the future development of preventive measures to aid forest management
P2Y12 inhibitors for the neurointerventionalist.
The use of antiplatelets is widespread in clinical practice. However, for neurointerventional procedures, protocols for antiplatelet use are scarce and practice varies between individuals and institutions. This is further complicated by the quantity of antiplatelet agents which differ in route of administration, dosage, onset of action, efficacy and ischemic and hemorrhagic complications. Clarifying the individual characteristics for each antiplatelet agent, and their associated risks, will increasingly become relevant as the practice of mechanical thrombectomy, stenting, coiling and flow diversion procedures grows. The aim of this review is to summarize the existing literature for the use of P2Y12 inhibitors in neurointerventional procedures, examine the quality of the evidence, and highlight areas in need of further research