278 resultados para CHRONIC NONCOMMUNICABLE DISEASES
Resumo:
Climate change is an urgent global public health issue with substantial predicted impacts in the coming decades. Concurrently, global burden of disease studies highlight problems such as obesity, mental health problems and a range of other chronic diseases, many of which have origins in childhood. There is a unique opportunity to engage children in both health promotion and education for sustainability during their school years to help ameliorate both environmental and health issues. Evidence exists for the most effective ways to do this, through education that is empowering, action orientated and relevant to children’s day to day interests and concerns, and by tailoring such education to different educational sectors. The aim of this discussion paper is to argue the case for sustainability education in schools that links with health promotion and that adopts a practical approach to engaging children in these important public health and environmental issues. We describe two internationally implemented whole-school reform movements, Health Promoting Schools (HPS) and Sustainable Schools (SS) which seek to operationalise transformative educational processes. Drawing on international evidence and Australian case examples, we contend that children’s active involvement in such processes is not only educationally engaging and rewarding, it also contributes to human and environmental resilience and health. Further, school settings can play an important ecological public health role, incubating and amplifying the socially transformative changes urgently required to create pathways to healthy, just and sustainable human futures, on a viable planet.
Resumo:
Background: There is limited information on the effect of isoflavones on homocysteine concentrations, a risk factor for a number of chronic diseases. Methods: Twenty-three premenopausal women participated in a double-blind, randomized, parallel study for four menstrual cycles. Subjects consumed either placebo or purified red clover (Trifolium pratense) isoflavone (86mg/day) tablets. Blood samples were collected weekly during cycles 1, 3, and 4 for determination of serum folate and total homocysteine concentrations. Dietary intake was monitored monthly. Results: Concentrations of folate and homocysteine in serum did not change significantly in either group, and there were no significant differences observed between the follicular and luteal phases of the menstrual cycle. The participants' dietary records indicated that nutrient intake was constant, and compliance was confirmed by analysis of urinary isoflavone concentrations and tablet counts in returned containers. Conclusions: These results suggest that in the absence of any dietary modification, supplementation with purified isoflavones that are predominantly methoxylated has no effect on serum homocysteine or folate in premenopausal women.
Resumo:
Globally, the main contributors to morbidity and mortality are chronic diseases, including cardiovascular disease and diabetes. Chronic diseases are costly and partially avoidable, with around sixty percent of deaths and nearly fifty percent of the global disease burden attributable to these conditions. By 2020, chronic illnesses will likely be the leading cause of disability worldwide. Existing health care systems, both national and international, that focus on acute episodic health conditions, cannot address the worldwide transition to chronic illness; nor are they appropriate for the ongoing care and management of those already afflicted with chronic diseases. International and Australian strategic planning documents articulate similar elements to manage chronic disease; including the need for aligning sectoral policies for health, forming partnerships and engaging communities in decision-making. The Australian National Chronic Disease Strategy focuses on four core areas for managing chronic disease; prevention across the continuum, early detection and treatment, integrated and coordinated care, and self-management. Such a comprehensive approach incorporates the entire population continuum, from the ‘healthy’, to those with risk factors, through to people suffering from chronic conditions and their sequelae. This chapter examines comprehensive approach to the prevention, management and care of the population with non-communicable, chronic diseases and communicable diseases. It analyses models of care in the context of need, service delivery options and the potential to prevent or manage early intervention for chronic and communicable diseases. Approaches to chronic diseases require integrated approaches that incorporate interventions targeted at both individuals and populations, and emphasise the shared risk factors of different conditions. Communicable diseases are a common and significant contributor to ill health throughout the world. In many countries, this impact has been minimised by the combined efforts of preventative health measures and improved treatment of infectious diseases. However in underdeveloped nations, communicable diseases continue to contribute significantly to the burden of disease. The aim of this chapter is to outline the impact that chronic and communicable diseases have on the health of the community, the public health strategies that are used to reduce the burden of those diseases and the old and emerging risks to public health from infectious diseases.
Resumo:
After reading this chapter, you should be able to: • understand the concept of globalisation and appreciate its complexity • identify the significant impacts of globalisation on population health, particularly the incidence of communicable and non-communicable diseases • understand the distribution of the global burden of disease in high-, middle- and low-income countries • critically evaluate the factors contributing to the major causes of death in low-income countries • understand some of the achievements of the global public health community and appreciate the challenges it faces.
Resumo:
Chlamydia pneumoniae is a common human and animal pathogen associated with a wide range of upper and lower respiratory tract infections. In more recent years there has been increasing evidence to suggest a link between C. pneumoniae and chronic diseases in humans, including atherosclerosis, stroke and Alzheimer’s disease. C. pneumoniae human strains show little genetic variation, indicating that the human-derived strain originated from a common ancestor in the recent past. Despite extensive information on the genetics and morphology processes of the human strain, knowledge concerning many other hosts (including marsupials, amphibians, reptiles and equines) remains virtually unexplored. The koala (Phascolarctos cinereus) is a native Australian marsupial under threat due to habitat loss, predation and disease. Koalas are very susceptible to chlamydial infections, most commonly affecting the conjunctiva, urogenital tract and/or respiratory tract. To address this gap in the literature, the present study (i) provides a detailed description of the morphologic and genomic architecture of the C. pneumoniae koala (and human) strain, and shows that the koala strain is microscopically, developmentally and genetically distinct from the C. pneumoniae human strain, and (ii) examines the genetic relationship of geographically diverse C. pneumoniae isolates from human, marsupial, amphibian, reptilian and equine hosts, and identifies two distinct lineages that have arisen from animal-to-human cross species transmissions. Chapter One of this thesis explores the scientific problem and aims of this study, while Chapter Two provides a detailed literature review of the background in this field of work. Chapter Three, the first results chapter, describes the morphology and developmental stages of C. pneumoniae koala isolate LPCoLN, as revealed by fluorescence and transmission electron microscopy. The profile of this isolate, when cultured in HEp-2 human epithelial cells, was quite different to the human AR39 isolate. Koala LPCoLN inclusions were larger; the elementary bodies did not have the characteristic pear-shaped appearance, and the developmental cycle was completed within a shorter period of time (as confirmed by quantitative real-time PCR). These in vitro findings might reflect biological differences between koala LPCoLN and human AR39 in vivo. Chapter Four describes the complete genome sequence of the koala respiratory pathogen, C. pneumoniae LPCoLN. This is the first animal isolate of C. pneumoniae to be fully-sequenced. The genome sequence provides new insights into genomic ‘plasticity’ (organisation), evolution and biology of koala LPCoLN, relative to four complete C. pneumoniae human genomes (AR39, CWL029, J138 and TW183). Koala LPCoLN contains a plasmid that is not shared with any of the human isolates, there is evidence of gene loss in nucleotide salvage pathways, and there are 10 hot spot genomic regions of variation that were previously not identified in the C. pneumoniae human genomes. Sequence (partial-length) from a second, independent, wild koala isolate (EBB) at several gene loci confirmed that the koala LPCoLN isolate was representative of a koala C. pneumoniae strain. The combined sequence data provides evidence that the C. pneumoniae animal (koala LPCoLN) genome is ancestral to the C. pneumoniae human genomes and that human infections may have originated from zoonotic infections. Chapter Five examines key genome components of the five C. pneumoniae genomes in more detail. This analysis reveals genomic features that are shared by and/or contribute to the broad ecological adaptability and evolution of C. pneumoniae. This analysis resulted in the identification of 65 gene sequences for further analysis of intraspecific variation, and revealed some interesting differences, including fragmentation, truncation and gene decay (loss of redundant ancestral traits). This study provides valuable insights into metabolic diversity, adaptation and evolution of C. pneumoniae. Chapter Six utilises a subset of 23 target genes identified from the previous genomic comparisons and makes a significant contribution to our understanding of genetic variability among C. pneumoniae human (11) and animal (6 amphibian, 5 reptilian, 1 equine and 7 marsupial hosts) isolates. It has been shown that the animal isolates are genetically diverse, unlike the human isolates that are virtually clonal. More convincing evidence that C. pneumoniae originated in animals and recently (in the last few hundred thousand years) crossed host species to infect humans is provided in this study. It is proposed that two animal-to-human cross species events have occurred in the context of the results, one evident by the nearly clonal human genotype circulating in the world today, and the other by a more animal-like genotype apparent in Indigenous Australians. Taken together, these data indicate that the C. pneumoniae koala LPCoLN isolate has morphologic and genomic characteristics that are distinct from the human isolates. These differences may affect the survival and activity of the C. pneumoniae koala pathogen in its natural host, in vivo. This study, by utilising the genetic diversity of C. pneumoniae, identified new genetic markers for distinguishing human and animal isolates. However, not all C. pneumoniae isolates were genetically diverse; in fact, several isolates were highly conserved, if not identical in sequence (i.e. Australian marsupials) emphasising that at some stage in the evolution of this pathogen, there has been an adaptation/s to a particular host, providing some stability in the genome. The outcomes of this study by experimental and bioinformatic approaches have significantly enhanced our knowledge of the biology of this pathogen and will advance opportunities for the investigation of novel vaccine targets, antimicrobial therapy, or blocking of pathogenic pathways.
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It is now widely accepted that there are important links between inactivity and lifestyle-related chronic diseases, and that exercise can bring tangible therapeutic benefits to people with long-term chronic conditions. Exercise and Chronic Disease: An Evidence-Based Approach offers the most up-to-date survey currently available of the scientific and clinical evidence underlying the effects of exercise in relation to functional outcomes, disease-specific health-related outcomes and quality of life in patients with chronic disease conditions. Drawing on data from randomized controlled trials and observational evidence, and written by a team of leading international researchers and medical and health practitioners, the book explores the evidence across a wide range of chronic diseases, including:
Resumo:
Introduction: Floods are the most common hazard to cause disasters and have led to extensive morbidity and mortality throughout the world. The impact of floods on the human community is related directly to the location and topography of the area, as well as human demographics and characteristics of the built environment. Objectives: The aim of this study is to identify the health impacts of disasters and the underlying causes of health impacts associated with floods. A conceptual framework is developed that may assist with the development of a rational and comprehensive approach to prevention, mitigation, and management. Methods: This study involved an extensive literature review that located >500 references, which were analyzed to identify common themes, findings, and expert views. The findings then were distilled into common themes. Results: The health impacts of floods are wide ranging, and depend on a number of factors. However, the health impacts of a particular flood are specific to the particular context. The immediate health impacts of floods include drowning, injuries, hypothermia, and animal bites. Health risks also are associated with the evacuation of patients, loss of health workers, and loss of health infrastructure including essential drugs and supplies. In the mediumterm, infected wounds, complications of injury, poisoning, poor mental health, communicable diseases, and starvation are indirect effects of flooding. In the long-term, chronic disease, disability, poor mental health, and poverty-related diseases including malnutrition are the potential legacy. Conclusions: This article proposes a structured approach to the classification of the health impacts of floods and a conceptual framework that demonstrates the relationships between floods and the direct and indirect health consequences.
Resumo:
Objective: With growing recognition of the role of inflammation in the development of chronic and acute disease, fish oil is increasingly used as a therapeutic agent, but the nature of the intervention may pose barriers to adherence in clinical populations. Our objective was to investigate the feasibility of using a fish oil supplement in hemodialysis patients. ---------- Design: This was a nonrandomized intervention study.---------- Setting: Eligible patients were recruited at the Hemodialysis Unit of Wesley Hospital, Brisbane, Queensland, Australia. Patients The sample included 28 maintenance hemodialysis patients out of 43 eligible patients in the unit. Exclusion criteria included patients regularly taking a fish oil supplement at baseline, receiving hemodialysis for less than 3 months, or being unable to give informed consent.---------- Intervention: Eicosapentaenoic acid (EPA) was administered at 2000 mg/day (4 capsules) for 12 weeks. Adherence was measured at baseline and weekly throughout the study according to changes in plasma EPA, and was further measured subjectively by self-report.---------- Results: Twenty patients (74%) adhered to the prescription based on changes in plasma EPA, whereas an additional two patients self-reported good adherence. There was a positive relationship between fish oil intake and change in plasma EPA. Most patients did not report problems with taking the fish oil. Using the baseline data, it was not possible to characterize adherent patients.---------- Conclusions: Despite potential barriers, including the need to take a large number of prescribed medications already, 74% of hemodialysis patients adhered to the intervention. This study demonstrated the feasibility of using fish oil in a clinical population.
Resumo:
Adherence to medicines is a major determinant of the effectiveness of medicines. However, estimates of non-adherence in the older-aged with chronic conditions vary from 40 to 75%. The problems caused by non-adherence in the older-aged include residential care and hospital admissions, progression of the disease, and increased costs to society. The reasons for non-adherence in the older-aged include items related to the medicine (e.g. cost, number of medicines, adverse effects) and those related to person (e.g. cognition, vision, depression). It is also known that there are many ways adherence can be increased (e.g. use of blister packs, cues). It is assumed that interventions by allied health professions, including a discussion of adherence, will improve adherence to medicines in the older aged but the evidence for this has not been reviewed. There is some evidence that telephone counselling about adherence by a nurse or pharmacist does improve adherence, short- and long-term. However, face-to-face intervention counselling at the pharmacy, or during a home visit by a pharmacist, has shown variable results with some studies showing improved adherence and some not. Education programs during hospital stays have not been shown to improve adherence on discharge, but education programs for subjects with hypertension have been shown to improve adherence. In combination with an education program, both counselling and a medicine review program have been shown to improve adherence short-term in the older-aged. Thus, there are many unanswered questions about the most effective interventions to promote adherence. More studies are needed to determine the most appropriate interventions by allied health professions, and these need to consider the disease state, demographics, and socio-economic status of the older-aged subject, and the intensity and duration of intervention needed.
Resumo:
Poor patient compliance with peritoneal dialysis (PD) has significant adverse effects on morbidity and mortality rates in individuals with chronic kidney disease (CKD). It also adds to the resource burdens of healthcare services and providers. This paper explores the notion of PD compliance in patients with CKD with reference to the relevant published literature. The analysis of the literature reveals that ‘PD compliance’ is a complex and challenging construct for both patients and health professionals. There is no universal definition of compliance that is widely adopted in practice and research, and therefore a lack of consensus on how to determine ‘compliant’ patient outcomes. There are also multiple and interconnected determinants of PD compliance that are context-bound, which healthcare professionals must be aware of, and which makes producing consensus of measuring PD compliance difficult. The complexity of the interventions required to produce even a modest improvement in PD compliance, which are described in this paper, are significant. Compliance with PD and other treatments for CKD is a multidimensional, context-bound concept, that to date has tended to efface the role and needs of the renal patient. We conclude the paper with the implications for contemporary practice.
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Background: Palliative care should be provided according to the individual needs of the patient, caregiver and family, so that the type and level of care provided, as well as the setting in which it is delivered, are dependent on the complexity and severity of individual needs, rather than prognosis or diagnosis. This paper presents a study designed to assess the feasibility and efficacy of an intervention to assist in the allocation of palliative care resources according to need, within the context of a population of people with advanced cancer. ---------- Methods/design: People with advanced cancer and their caregivers completed bi-monthly telephone interviews over a period of up to 18 months to assess unmet needs, anxiety and depression, quality of life, satisfaction with care and service utilisation. The intervention, introduced after at least two baseline phone interviews, involved a) training medical, nursing and allied health professionals at each recruitment site on the use of the Palliative Care Needs Assessment Guidelines and the Needs Assessment Tool: Progressive Disease - Cancer (NAT: PD-C); b) health professionals completing the NAT: PD-C with participating patients approximately monthly for the rest of the study period. Changes in outcomes will be compared pre-and post-intervention.---------- Discussion: The study will determine whether the routine, systematic and regular use of the Guidelines and NAT: PD-C in a range of clinical settings is a feasible and effective strategy for facilitating the timely provision of needs based care.
Resumo:
Objective--To determine whether heart failure with preserved systolic function (HFPSF) has different natural history from left ventricular systolic dysfunction (LVSD). Design and setting--A retrospective analysis of 10 years of data (for patients admitted between 1 July 1994 and 30 June 2004, and with a study census date of 30 June 2005) routinely collected as part of clinical practice in a large tertiary referral hospital.Main outcome measures-- Sociodemographic characteristics, diagnostic features, comorbid conditions, pharmacotherapies, readmission rates and survival.Results--Of the 2961 patients admitted with chronic heart failure, 753 had echocardiograms available for this analysis. Of these, 189 (25%) had normal left ventricular size and systolic function. In comparison to patients with LVSD, those with HFPSF were more often female (62.4% v 38.5%; P = 0.001), had less social support, and were more likely to live in nursing homes (17.9% v 7.6%; P < 0.001), and had a greater prevalence of renal impairment (86.7% v 6.2%; P = 0.004), anaemia (34.3% v 6.3%; P = 0.013) and atrial fibrillation (51.3% v 47.1%; P = 0.008), but significantly less ischaemic heart disease (53.4% v 81.2%; P = 0.001). Patients with HFPSF were less likely to be prescribed an angiotensin-converting enzyme inhibitor (61.9% v 72.5%; P = 0.008); carvedilol was used more frequently in LVSD (1.5% v 8.8%; P < 0.001). Readmission rates were higher in the HFPSF group (median, 2 v 1.5 admissions; P = 0.032), particularly for malignancy (4.2% v 1.8%; P < 0.001) and anaemia (3.9% v 2.3%; P < 0.001). Both groups had the same poor survival rate (P = 0.912). Conclusions--Patients with HFPSF were predominantly older women with less social support and higher readmission rates for associated comorbid illnesses. We therefore propose that reduced survival in HFPSF may relate more to comorbid conditions than suboptimal cardiac management.
Resumo:
Heart failure is a complex disorder, characterized by activation of the sympathetic nervous system, leading to dysregulated Ca2+ homeostasis in cardiac myocytes and tissue remodeling. In a variety of diseases, cardiac malfunction is associated with aberrant fluxes of Ca2+ across both the surface membrane and the internal Ca2+ store, the sarcoplasmic reticulum (SR). One prominent hypothesis residues is that in heart failure, the activity of the ryanodine receptor (RyR2) Ca2+ release channel in the SR is increased due to excess phosphorylation and that this contributes to excess SR Ca2+ leak in diastole, reduced SR Ca2+ load and decreased contractility (Huke & Bers, 2008). There is controversy over which serine residues in RyR2 are hyperphosphorylated in animal models of heart failure and whether this is via the CaMKII or the PKA-linked signaling pathway. S2808, S2814 and S2030 in RyR2 have been variously claimed to be hyperphosphorylated. Our aim was to examine the degree of phosphorylation of these residues in RyR2 from failing human hearts. The use of human tissue was approved by the Human Research Ethics Committee, The Prince Charles Hospital, EC28114. Left ventricular tissue samples were obtained from an explanted heart of a patient with endstage heart failure (Emery Dreifuss Muscular Dystrophy with cardiomyopathy) and non-failing tissue was from a patient with cystic fibrosis undergoing heart-lung transplantation with no history of heart disease. SR vesicles were prepared as described by Laver et al. (1995) and examined with SDS-Page and Western Blot. Transferred proteins were probed with antibodies to detect total protein phosphorylation, phosphorylation of RyR2 serine residues S2808, S2814, S2030 and for the key proteins calsequestrin, triadin, junctin and FKBP12.6. To avoid membrane stripping artifact, each membrane was exposed to one phosphorylation-specific antibody and signal densities quantified using Bio-Rad Quantity One software. We found no distinguishable difference between failing and healthy hearts in the protein expression levels of RyR2, triadin, junctin or calsequestrin. We found an expected upregulation of total RyR2 phosphorylation in the failing heart sample, compared to a matched amount of RyR2 (quantified using densiometry) in healthy heart. Probing with antibodies detecting only the phosphorylated form of the specific RyR2 residues showed that the increase in total RyR2 phosphorylation in the failing heart was due to hyperphosphorylation of S2808 and S2814. We found that S2030 phosphorylation levels were unchanged in human heart failure. Interestingly, we found that S2030 has a basal level of phosphorylation in the healthy human heart, different from the absence of basal phosphorylation recently reported in rodent heart (Huke & Bers, 2008). Finally, preliminary results indicate that less FKBP 12.6 is associated with RyR2 in the failing heart, possibly as a consequence of PKA activation. In conclusion, residues S2808 and S2814 are hyperphosphorylated in human heart failure, presumably due to upregulation of the CaMKII and/or PKA signaling pathway as a result of chronic activation of the sympathetic nervous system. Such changes in RyR2 phosphorylation are believed to contribute to the leaky RyR2 phenotype associated with heart failure, which increases the incidence of arrhythmia and contributes to the severely impaired contractile performance of the failing heart. Huke S & Bers DM. (2008). Ryanodine receptor phosphorylation at serine 2030, 2808 and 2814 in rat cardiomyocytes. Biochemical and Biophysical Research Communications 376, 80-85. Laver DR, Roden LD, Ahern GP, Eager KR, Junankar PR & Dulhunty AF. (1995). Cytoplasmic Ca2+ inhibits the ryanodine receptor from cardiac muscle. Journal of Membrane Biology 147, 7-22. Proceedings