997 resultados para Chronic


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Objectives: To quantify the benefits that people receive from participating in self-management courses and identify subgroups that benefit most.
Research Design: People with a wide range of chronic conditions attending self-management courses (N=1,341 individuals) were administered the generic Health Education Impact Questionnaire (HEI-Q). Data were collected before the first session (baseline) and at the end of courses (follow-up) resulting in 842 complete responses. The median (interquartile range) age was 64 (54 to 73) years and most participants were female (75%). Outcomes were categorized as Substantial improvement (Effect Size, ES ≥ 0.5), Minimal/No change (ES -0.49 to 0.49) and Substantial decline (ES ≤ -0.5).
Results: On average, one third of participants reported substantial benefits after attending a self-management course. Proportions of participants reporting substantial benefits ranged from 49% in Skill and technique acquisition to 27% in Health service navigation. Stratification by gender, age and education showed that younger participants were more likely to benefit, particularly young women. No further subgroup differences were observed.
Conclusions: Given that the health of people with chronic diseases tends to decline, this evaluation is reassuring in that about one third of participants coming from a wide range of backgrounds receive substantial improvements in their self-management skills.

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Aim. This paper reports a study whose purpose was to determine whether there is an increase in the incidence of chronic insomnia following hospitalization and, if so, to identify patients at risk.

Background. The consequences of difficulty sleeping in hospital have received scant attention from clinicians or researchers. Implicit in this lack of interest is the assumption that difficulty in sleeping is a transient reaction to hospitalization that will resolve on discharge, an assumption not empirically supported. It has been argued that in susceptible people this type of temporary disruption to sleep can be the catalyst for the development of chronic insomnia.

Method. Established sleep and depression rating instruments were used to monitor the sleep of 57 cardiac and 29 orthopaedic patients after elective surgery (n = 86), recruited through a hospital preadmission clinic.

Results. Preadmission chronic insomnia of 10% was consistent with general population prevalence estimates of 6–12%. Three months after discharge the incidence had almost doubled to 19%. Sixty-one per cent of this variance could be explained by hyperarousal, sleep hygiene issues, and dysfunctional cognitions about sleep. Depression was found to be a salient predictor but not an independent risk factor. Age, sex, and hospital-related data, such as score for difficulty sleeping in hospital, proved to be statistically insignificant.

Conclusions. The results support the role of hyperarousal and dysfunctional sleep attitudes and behaviours as stronger predictors of chronic insomnia than patient demographics or environmental issues. Given that most of the patients were ambivalent about how they slept in hospital, with high satisfaction (71%) in the presence of significant disruption (63%), preadmission sleep education given to these patients prior to admission potentially contributed to the development of more realistic expectations of the quality of in-hospital sleep.

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Chronic disease self-management emerged as an organised, formal entity in Australia in the 1980s, when a specific group-based program was introduced from the United States. This program, the Stanford Arthritis Self-Management Course, was promulgated in Australia and other countries by its creator, Professor Kate Lorig of Stanford University. The program showed much early promise, particularly with its dissemination and uptake by an enthusiastic non-government sector. Over subsequent years it has matured, and many other programs endeavouring to support patients to engage in self-management have been developed. In some ways, chronic disease self-management has become mainstream.1-3

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This paper reports on the findings of a pilot study that collated and categorised a range of Welsh-medium chronic pain descriptors and their conceptually equivalent English translations in order to provide a preliminary basis for chronic pain assessment amongst patients in the bilingual community of North West Wales. The results demonstrate the unique and complex nature of individual pain experiences and the challenges of meaningful interpretation, particularly when patient and practitioner do not share a common preferred language. Detailed analysis of the descriptors provided valuable insight into the patient's world, revealing cultural patterns of beliefs and behaviours as well as the suffering associated with chronic pain. Implications for improving chronic pain assessment amongst bilingual speakers are explored.

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Nitric oxide (NO) is a short-life molecule produced by the enzyme known as the nitric oxide synthase (NOS), in a reaction that converts arginine and oxygen into citrulline and NO. There are three isoforms of the enzyme: neuronal NOS (nNOS, also called NOS1), inducible NOS (iNOS or NOS2), and endothelial NOS (eNOS or NOS3). It is now known that each of these isoforms may be expressed in a variety of tissues and cell types. This paper is a review of the current knowledge of various functions of NO in diseases. We discuss in more detail its role in Cancer, the role of NO in myocardial pathophysiology, in central nervous system (CNS) pathologies. Other diseases such as inflammation, asthma, in chronic liver diseases, inflammatory bowel disease (IBD), arthritis, are also discussed. This review also covers the role of NO in cardiovascular, central nervous, pancreas, lung, gut, kidney, myoskeletal and chronic liver diseases (CLD). The ubiquitous role that the simple gas nitric oxide plays in the body, from maintaining vascular homeostasis and fighting infections to acting as a neurotransmitter and its role in cancer, has spurred a lot of interest among researchers all over the world. Nitric oxide plays an important role in the physiologic modulation of coronary artery tone and myocardial function. Nitric oxide from iNOS appears to be a key mediator of such glial-induced neuronal death. The high sensitivity of neurons to NO is partly due to NO causing inhibition of respiration, rapid glutamate release from both astrocytes and neurons, and subsequent excitotoxic death of the neurons.

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A role for α4 and β7 integrins in mediating leucocyte entry into the central nervous system in the multiple sclerosis (MS)-like disease experimental autoimmune encephalomyelitis (EAE) has been demonstrated. However, the individual contributions of their respective ligands mucosal addressin cell adhesion molecule-1 (MAdCAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-cadherin expressed on the blood-brain barrier has not been determined. In the present paper, it is shown that an antibody directed against MAdCAM-1, the preferential ligand for α4β7, effectively prevented the development of a progressive, non-remitting, form of EAE, actively induced by injection of myelin oligodendrocyte glycoprotein peptide (MOG(35-55)) autoantigen. Combinational treatment with both anti-MAdCAM-1, VCAM-1, and intercellular adhesion molecule-1 (ICAM-1) (ligand for integrin lymphocyte function-associated antigen (LFA)-1) mAbs led to more rapid remission than that obtained with anti-MAdCAM-1 antibody alone. However, neither MAdCAM-1 monotherapy, nor combinational antibody blockade was preventative when administered late in the course of disease progression. In conclusion, MAdCAM-1 plays a major contributory role in the progression of chronic EAE and is a potential therapeutic target for the treatment of MS. Critically, antivascular addressin therapy must be given eaA role for alpha4 and beta7 integrins in mediating leucocyte entry into the central nervous system in the multiple sclerosis (MS)-like disease experimental autoimmune encephalomyelitis (EAE) has been demonstrated. However, the individual contributions of their respective ligands mucosal addressin cell adhesion molecule-1 (MAdCAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-cadherin expressed on the blood-brain barrier has not been determined. In the present paper, it is shown that an antibody directed against MAdCAM-1, the preferential ligand for alpha4beta7, effectively prevented the development of a progressive, non-remitting, form of EAE, actively induced by injection of myelin oligodendrocyte glycoprotein peptide (MOG(35-55)) autoantigen. Combinational treatment with both anti-MAdCAM-1, VCAM-1, and intercellular adhesion molecule-1 (ICAM-1) (ligand for integrin lymphocyte function-associated antigen (LFA)-1) mAbs led to more rapid remission than that obtained with anti-MAdCAM-1 antibody alone. However, neither MAdCAM-1 monotherapy, nor combinational antibody blockade was preventative when administered late in the course of disease progression. In conclusion, MAdCAM-1 plays a major contributory role in the progression of chronic EAE and is a potential therapeutic target for the treatment of MS. Critically, antivascular addressin therapy must be given early in the course of disease prior to the establishment of irreversible damage if it is to be effective, as a single treatment modality.

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The prevalence, course and predictors of chronic child maltreatment were investigated. The majority of children referred experienced chronic child maltreatment. The characteristics of families and maltreatment were more similar than different for chronic and isolated child maltreatment. The type of response provided by child protection services differentiated chronic and isolated maltreatment.

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The national multi-centre study (49 programs, 1158 patients) developed a quality score (HF-IS) and the national benchmarks for heart programs. The higher a program scored on the HF-IS the greater the reduction in hospital admissions and mortality. This score has the potential to change national nursing practice and improve health outcomes of patients.