135 research outputs found

    Perceived fairness as main determinant of patients' satisfaction with care during psychiatric hospitalisation: An observational study.

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    Patient satisfaction with care is widely recognized as one of the most important indicator of quality in mental health care. It can impact several treatment outcomes, such as treatment adherence and engagement with services. At the same time, as an outcome in itself, satisfaction with care is also affected by several factors, first and foremost by being coerced. The main aim of this study was to test if perceiving treatment pressures as fair and effective could positively impact patient satisfaction, even more than formal coercive measures. Globally, 133 voluntary and involuntary inpatients were interviewed. Socio-demographic and clinical characteristics, including history of previous experiences of formal coercion and legal status of the hospitalisation, were collected through a structured questionnaire and medical charts. The participants were also asked to complete the Index of Fairness and Index of Effectiveness tools as well as a structured questionnaire on satisfaction with care. Simple and multiple linear regressions were performed. Although several factors were found to affect satisfaction with care when taken independently, perceived fairness was the stronger predictor of both satisfaction with treatment (β =.234; p = .022) and satisfaction with decision-making involvement (β =.360; p < .001) when controlling for confounders. Our results point to the paramount importance of developing and implementing interventions that promote procedural fairness in psychiatric treatment and thereby improve patient satisfaction while reducing the risk of disengagement with care

    Poor Correlation Between Perihematomal MRI Hyperintensity and Brain Swelling After Intracerebral Hemorrhage

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    The perihematomal hyperintensity is commonly interpreted to represent cerebral edema following ICH, but the accuracy of this interpretation is unknown. We therefore investigated the relationship between changes in PHH and changes in hemispheric brain volume as a measure of edema during the first week after ICH

    Autoregulation after ischaemic stroke

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    Absent outcome data from randomized clinical trials, management of hypertension in acute ischaemic stroke remains controversial. Data from human participants have failed to resolve the question whether cerebral blood flow (CBF) in the peri-infarct region will decrease due to impaired autoregulation when systemic mean arterial pressure (MAP) is rapidly reduced

    Diagnóstico biomolecular de anomalías genéticas asociadas a Fibrosis Quística usando indicadores mutagénicos.

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    Pacientes diagnosticados con Fibrosis Quística provenientes del Instituto de Salud del Niño del Ministerio de Salud del Perú y del Hospital IV E. Rebagliatti Martins (Seguridad Social), fueron evaluados durante el segundó semestre del 2013 con la finalidad de detectar mutaciones del Gen C.F.T.R. (Regulador de la Conductancia Transmembrana de la Fibrosis Quística). Mediante el método de la A.R.M.S-P.C.R (Reacción en Cadena de la Polimerasa- Sistema de amplificación de la Mutación Refractaria), se analizaron 28 muestras, encontrándose que en el 21,42% estaban presente dos mutaciones y el 32,21% una mutación. La prevalencia de DF508 en Perú, es relativamente baja (31,30%) en comparación con el promedio latinoamericano (43,54%). Al contrario los pacientes peruanos presentan una tasa importante de G542X (7,40%) en comparación con los de Latinoamérica (5,10%)

    Sphingomyelin Synthases Regulate Protein Trafficking and Secretion

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    Sphingomyelin synthases (SMS1 and 2) represent a class of enzymes that transfer a phosphocholine moiety from phosphatidylcholine onto ceramide thus producing sphingomyelin and diacylglycerol (DAG). SMS1 localizes at the Golgi while SMS2 localizes both at the Golgi and the plasma membrane. Previous studies from our laboratory showed that modulation of SMS1 and, to a lesser extent, of SMS2 affected the formation of DAG at the Golgi apparatus. As a consequence, down-regulation of SMS1 and SMS2 reduced the localization of the DAG-binding protein, protein kinase D (PKD), to the Golgi. Since PKD recruitment to the Golgi has been implicated in cellular secretion through the trans golgi network (TGN), the effect of down-regulation of SMSs on TGN-to-plasma membrane trafficking was studied. Down regulation of either SMS1 or SMS2 significantly retarded trafficking of the reporter protein vesicular stomatitis virus G protein tagged with GFP (VSVG-GFP) from the TGN to the cell surface. Inhibition of SMSs also induced tubular protrusions from the trans Golgi network reminiscent of inhibited TGN membrane fission. Since a recent study demonstrated the requirement of PKD activity for insulin secretion in beta cells, we tested the function of SMS in this model. Inhibition of SMS significantly reduced insulin secretion in rat INS-1 cells. Taken together these results provide the first direct evidence that both enzymes (SMS1 and 2) are capable of regulating TGN-mediated protein trafficking and secretion, functions that are compatible with PKD being a down-stream target for SMSs in the Golgi

    Calcineurin Inhibition at the Clinical Phase of Prion Disease Reduces Neurodegeneration, Improves Behavioral Alterations and Increases Animal Survival

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    Prion diseases are fatal neurodegenerative disorders characterized by a long pre-symptomatic phase followed by rapid and progressive clinical phase. Although rare in humans, the unconventional infectious nature of the disease raises the potential for an epidemic. Unfortunately, no treatment is currently available. The hallmark event in prion diseases is the accumulation of a misfolded and infectious form of the prion protein (PrPSc). Previous reports have shown that PrPSc induces endoplasmic reticulum stress and changes in calcium homeostasis in the brain of affected individuals. In this study we show that the calcium-dependent phosphatase Calcineurin (CaN) is hyperactivated both in vitro and in vivo as a result of PrPSc formation. CaN activation mediates prion-induced neurodegeneration, suggesting that inhibition of this phosphatase could be a target for therapy. To test this hypothesis, prion infected wild type mice were treated intra-peritoneally with the CaN inhibitor FK506 at the clinical phase of the disease. Treated animals exhibited reduced severity of the clinical abnormalities and increased survival time compared to vehicle treated controls. Treatment also led to a significant increase in the brain levels of the CaN downstream targets pCREB and pBAD, which paralleled the decrease of CaN activity. Importantly, we observed a lower degree of neurodegeneration in animals treated with the drug as revealed by a higher number of neurons and a lower quantity of degenerating nerve cells. These changes were not dependent on PrPSc formation, since the protein accumulated in the brain to the same levels as in the untreated mice. Our findings contribute to an understanding of the mechanism of neurodegeneration in prion diseases and more importantly may provide a novel strategy for therapy that is beneficial at the clinical phase of the disease

    Cerebrovascular Autoregulation Monitoring in the Management of Adult Severe Traumatic Brain Injury: A Delphi Consensus of Clinicians

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    Abstract: Background: Several methods have been proposed to measure cerebrovascular autoregulation (CA) in traumatic brain injury (TBI), but the lack of a gold standard and the absence of prospective clinical data on risks, impact on care and outcomes of implementation of CA-guided management lead to uncertainty. Aim: To formulate statements using a Delphi consensus approach employing a group of expert clinicians, that reflect current knowledge of CA, aspects that can be implemented in TBI management and CA research priorities. Methods: A group of 25 international academic experts with clinical expertise in the management of adult severe TBI patients participated in this consensus process. Seventy-seven statements and multiple-choice questions were submitted to the group in two online surveys, followed by a face-to-face meeting and a third online survey. Participants received feedback on average scores and the rationale for resubmission or rephrasing of statements. Consensus on a statement was defined as agreement of more than 75% of participants. Results: Consensus amongst participants was achieved on the importance of CA status in adult severe TBI pathophysiology, the dynamic non-binary nature of CA impairment, its association with outcome and the inadvisability of employing universal and absolute cerebral perfusion pressure targets. Consensus could not be reached on the accuracy, reliability and validation of any current CA assessment method. There was also no consensus on how to implement CA information in clinical management protocols, reflecting insufficient clinical evidence. Conclusion: The Delphi process resulted in 25 consensus statements addressing the pathophysiology of impaired CA, and its impact on cerebral perfusion pressure targets and outcome. A research agenda was proposed emphasizing the need for better validated CA assessment methods as well as the focused investigation of the application of CA-guided management in clinical care using prospective safety, feasibility and efficacy studies

    An economic model of long-term use of celecoxib in patients with osteoarthritis

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    <p>Abstract</p> <p>Background</p> <p>Previous evaluations of the cost-effectiveness of the cyclooxygenase-2 selective inhibitor celecoxib (Celebrex, Pfizer Inc, USA) have produced conflicting results. The recent controversy over the cardiovascular (CV) risks of rofecoxib and other coxibs has renewed interest in the economic profile of celecoxib, the only coxib now available in the United States. The objective of our study was to evaluate the long-term cost-effectiveness of celecoxib compared with nonselective nonsteroidal anti-inflammatory drugs (nsNSAIDs) in a population of 60-year-old osteoarthritis (OA) patients with average risks of upper gastrointestinal (UGI) complications who require chronic daily NSAID therapy.</p> <p>Methods</p> <p>We used decision analysis based on data from the literature to evaluate cost-effectiveness from a modified societal perspective over patients' lifetimes, with outcomes expressed as incremental costs per quality-adjusted life-year (QALY) gained. Sensitivity tests were performed to evaluate the impacts of advancing age, CV thromboembolic event risk, different analytic horizons and alternate treatment strategies after UGI adverse events.</p> <p>Results</p> <p>Our main findings were: 1) the base model incremental cost-effectiveness ratio (ICER) for celecoxib versus nsNSAIDs was 31,097perQALY;2)theICERperQALYwas31,097 per QALY; 2) the ICER per QALY was 19,309 for a model in which UGI ulcer and ulcer complication event risks increased with advancing age; 3) the ICER per QALY was $17,120 in sensitivity analyses combining serious CV thromboembolic event (myocardial infarction, stroke, CV death) risks with base model assumptions.</p> <p>Conclusion</p> <p>Our model suggests that chronic celecoxib is cost-effective versus nsNSAIDs in a population of 60-year-old OA patients with average risks of UGI events.</p
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