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AIMS: Unintentional injuries in the home contribute substantially to preschool child morbidity and mortality. Practitioners such as health visitors, family mentors and children's centre staff are well-positioned to facilitate child injury prevention by providing home safety advice to families, and training may enhance their ability to do so. We aimed to assess the impact of child home safety training for these practitioners. METHODS: An explanatory mixed-methods design was used. Practitioners completed questionnaires before, and up to 7 months after, receiving child home safety training and took part in interviews. Seventy-eight health visitors, 72 family mentors and 11 children's centre staff members completed questionnaires. Items were used to calculate scores on home safety knowledge, confidence to provide home safety advice and belief that child home safety promotion is important. Thematic analysis of interviews with seven health visitors and nine family mentors, open-ended responses to the questionnaires and an additional evaluation form was conducted to explore attendees' perceptions of the training and its impact. In addition, seven health visitors and six children's centre staff who had received no training were interviewed. RESULTS: Knowledge was greater post-training than pre-training across all participants (p < .001). When practitioner groups were analysed separately, there were significant increases in family mentors' knowledge (p < .001) and belief (p = .016), and health visitors' confidence (p = .0036). Qualitative findings indicated that most training session attendees valued the training, believed their practice relating to child home safety had improved as a result, and felt further similar training sessions would be beneficial. Those who had not attended the sessions described a need for more child home safety training. CONCLUSIONS: Delivering training to practitioners providing child home safety promotion to families with preschool children can enhance injury prevention knowledge, beliefs and confidence and positively impact on home safety promotion by practitioners.
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OBJECTIVES: Falls in older adults cause significant morbidity and mortality and incur cost to health and care services. The Falls Management Exercise (FaME) programme is a 24-week intervention for older adults that, in clinical trials, improves balance and functional strength and leads to fewer falls. Similar but more modest outcomes have been found when FaME is delivered in routine practice. Understanding the degree to which the programme is delivered with fidelity is important if 'real-world' delivery of FaME is to achieve the same magnitude of outcome as in clinical trials. The objective of this study was to examine the implementation fidelity of FaME when delivered in the community to inform quality improvement strategies that maximise programme effectiveness. STUDY DESIGN: A mixed methods implementation study of FaME programme delivery. METHODS: Data from programme registers, expert observations of FaME classes, and semistructured interviews with FaME instructors were triangulated using a conceptual framework for implementation fidelity. Quantitative data were analysed using descriptive statistics. Interviews were transcribed verbatim and analysed using thematic analysis. RESULTS: In total, 356 participants enrolled on 29 FaME programmes, and 143 (40%) participants completed at least 75% of the classes within a programme. Observations showed that 72%-78% of programme content was delivered, and 80%-84% quality criteria were met. Important content that was most often left out included home exercises, Tai Chi moves, and floor work, whereas quality items most frequently missed out included asking about falls in the previous week, following up attendance absence and explaining the purpose of exercises. Only 24% of class participants made the expected strength training progression. Interviews with FaME instructors helped explain why elements of programme content and quality were not delivered. Strategies for improving FaME delivery were established and helped to maintain quality and fidelity. CONCLUSIONS: FaME programmes delivered in the 'real world' can be implemented with a high degree of fidelity, although important deviations were found. Facilitation strategies could be used to further improve programme fidelity and maximise participant outcomes.
Assuntos
Exercício Físico , Treinamento Resistido , Idoso , Terapia por Exercício , Humanos , Avaliação de Programas e Projetos de SaúdeRESUMO
BACKGROUND: Childhood falls, poisonings and scalds, occurring predominantly in the home, are an important public health problem, yet there is limited evidence on the costs of these injuries to individuals and society. OBJECTIVES: To estimate National Health Service (NHS) and child and family costs of falls, poisonings and scalds. METHODS: We undertook a multicentre longitudinal study of falls, poisonings and scalds in children under 5â years old, set in acute NHS Trusts across four UK study centres. Data from parental self-reported questionnaires on health service resource use, family costs and expenditure were combined with unit cost data from published sources to calculate average cost for participants and injury mechanism. RESULTS: 344 parents completed resource use questionnaires until their child recovered from their injury or until 12â months, whichever came soonest. Most injuries were minor, with >95% recovering within 2â weeks, and 99% within 1â month of the injury. 61% emergency department (ED) attendees were not admitted, 35% admitted for ≤1â day and 4% admitted for ≥2 days. The typical healthcare cost of an admission for ≥2 days was estimated at £2000-3000, for an admission for ≤1â day was £700-1000 and for an ED attendance without admission was £100-180. Family costs were considerable and varied across injury mechanisms. Of all injuries, scalds accrued highest healthcare and family costs. CONCLUSIONS: Falls, poisonings and scalds incur considerable short-term healthcare and family costs. These data can inform injury prevention policy and commissioning of preventive services.
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Acidentes por Quedas/economia , Acidentes Domésticos/economia , Queimaduras/economia , Hospitalização/economia , Tempo de Internação/economia , Intoxicação/economia , Medicina Preventiva , Acidentes por Quedas/prevenção & controle , Acidentes por Quedas/estatística & dados numéricos , Acidentes Domésticos/prevenção & controle , Queimaduras/prevenção & controle , Queimaduras/reabilitação , Pré-Escolar , Inglaterra/epidemiologia , Feminino , Custos de Cuidados de Saúde , Hospitalização/estatística & dados numéricos , Humanos , Lactente , Recém-Nascido , Tempo de Internação/estatística & dados numéricos , Estudos Longitudinais , Masculino , Pais , Intoxicação/prevenção & controle , Intoxicação/reabilitação , Formulação de Políticas , Medicina Preventiva/economia , Medicina Preventiva/métodos , Inquéritos e QuestionáriosRESUMO
Old age is associated with a higher prevalence of cardiovascular disease and diabetes mellitus. Vascular smooth muscle cells (VSMC) play a role in the pathogenesis of vascular diseases, often a complication of diabetes mellitus. We examined in explanted aortic VSMC from young vs. older rats glucose-related activation of nuclear factor kappaB (NF-kappaB), a transcription factor induced by many oxidants. Data demonstrate that old age is associated with enhanced NF-kappaB activity in unstimulated VSMC that is further increased after exposure to high glucose medium. Furthermore, VSMC from old animals exhibit increased levels of protein carbonyls, an indicator of oxidative stress, and less apoptosis in response to glucose than VSMC isolated from young animals. These changes are accompanied by increased expression of NF-kappaB-related genes, gamma-glutamylcysteine synthetase, inhibitor of apoptosis protein-1 (IAP-1), and inducible nitric oxide synthase (iNOS). Results suggest that high glucose, a putative oxidative stress, causes apoptosis in VSMC from young animals and is associated with greater induction of NF-kappaB in VSMC from older animals. Increases in IAP-1 and decreased apoptosis implicate NF-kappaB as a survival factor in VSMC.
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Apoptose , Senescência Celular/fisiologia , Glucose/farmacologia , Músculo Liso Vascular/efeitos dos fármacos , Animais , Aorta/citologia , Glutamato-Cisteína Ligase/biossíntese , Glutamato-Cisteína Ligase/genética , Proteínas Inibidoras de Apoptose , Masculino , Músculo Liso Vascular/citologia , Músculo Liso Vascular/metabolismo , NF-kappa B/metabolismo , Óxido Nítrico Sintase/biossíntese , Óxido Nítrico Sintase/genética , Óxido Nítrico Sintase Tipo II , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/fisiologia , Biossíntese de Proteínas , Proteínas/genética , RatosRESUMO
Crystalline silica has been classified as a group 1 human carcinogen in the lung. However, its mechanisms of action on pulmonary epithelial cells which give rise to lung cancers are unclear. Using a nontransformed alveolar type II epithelial cell line (C10), we show that alpha-quartz silica causes persistent dose-related increases in phosphorylation of c-Jun-NH2-terminal amino kinases (JNKs) that are inhibited by antioxidants (P < or = 0.05). Increases in activator protein-1 (AP-1) binding to DNA and transactivation of AP-1-dependent gene expression by silica were accompanied by increases in steady-state mRNA levels of the AP-1 family members, c-jun, junB, fra-1, and c-fos at 8 h and elevated mRNA levels of fra-1 at 24 h (P < or = 0.05). Addition of tetramethylthiourea inhibited silica-associated increases infra-1 and proportions of cells in S-phase (P < or = .05). Our findings indicate that silica induces JNK activity, AP-1-dependent gene expression, ie., fra-1, and DNA synthesis via oxidative stress. Moreover, they suggest that silica may act mechanistically as a mitogen or tumor promoter, rather than a genotoxic carcinogen, in the development of lung cancers.
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Regulação da Expressão Gênica/efeitos dos fármacos , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Estresse Oxidativo/fisiologia , Proteínas Proto-Oncogênicas c-fos/biossíntese , Alvéolos Pulmonares/efeitos dos fármacos , Fase S/efeitos dos fármacos , Dióxido de Silício/toxicidade , Tioureia/análogos & derivados , Animais , Linhagem Celular , DNA/metabolismo , Relação Dose-Resposta a Droga , Ativação Enzimática/efeitos dos fármacos , Células Epiteliais/citologia , Células Epiteliais/efeitos dos fármacos , Células Epiteliais/metabolismo , Sequestradores de Radicais Livres/farmacologia , Radical Hidroxila/metabolismo , Proteínas Quinases JNK Ativadas por Mitógeno , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Camundongos , Fosforilação/efeitos dos fármacos , Proto-Oncogene Mas , Proteínas Proto-Oncogênicas c-fos/genética , Alvéolos Pulmonares/citologia , Alvéolos Pulmonares/metabolismo , RNA Mensageiro/biossíntese , RNA Mensageiro/genética , Dióxido de Silício/antagonistas & inibidores , Tioureia/farmacologia , Fator de Transcrição AP-1/metabolismoRESUMO
High levels of ambient air pollution are associated with exacerbation of asthma and respiratory morbidity, yet little is known concerning the mechanisms of inflammation and toxicity by components of inhaled particulate matter (PM). Brief inhalation of PM(2.5) (particles of an aerodynamic diameter of < 2.5 microns) (300 microg/m(3) air for 6 h followed by a period of 24 h in clean air) by either C3H/HeJ or C57/BL6 mice caused significant (P = 0.05) increases in steady-state messenger RNA (mRNA) levels of a number of nuclear factor (NF)-kappaB-associated and/ or -regulated genes, including tumor necrosis factor-alpha and -beta, interleukin-6, interferon-gamma, and transforming growth factor-beta. Lung mRNA levels of lymphotoxin-beta and macrophage migration inhibitory factor were unchanged. In murine C10 alveolar cells and an NF-kappaB-luciferase reporter cell line, exposure to PM(2.5) at noncytotoxic concentrations resulted in increases in transcriptional activation of NF-kappaB-dependent gene expression which were inhibited in the presence of catalase. Early and persistent increases in intracellular oxidants, as measured by flow cytometry and cell imaging using the oxidant probe 2'-7'-dichlorofluoroscin diacetate, were observed in epithelial cells exposed to PM(2.5) and ultrafine carbon black particles. Studies here are the first to show NF-kappaB-related inflammatory and cytokine gene expression after inhalation of PM(2.5) and oxidant-dependent induction of NF-kappaB activity by PM(2.5) in pulmonary epithelial cells.
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Poluentes Atmosféricos/farmacologia , Regulação da Expressão Gênica/efeitos dos fármacos , NF-kappa B/efeitos dos fármacos , Oxidantes/fisiologia , Animais , Carbono/farmacologia , Linhagem Celular , DNA/metabolismo , Células Epiteliais/efeitos dos fármacos , Células Epiteliais/metabolismo , Fluoresceínas/metabolismo , Exposição por Inalação , Interferon gama/genética , Interleucina-6/genética , Pulmão/citologia , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Linfotoxina-alfa/genética , Masculino , Camundongos , Camundongos Endogâmicos C3H , Camundongos Endogâmicos C57BL , NF-kappa B/metabolismo , Oxidantes/metabolismo , Tamanho da Partícula , Ligação Proteica/efeitos dos fármacos , RNA Mensageiro/efeitos dos fármacos , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Ativação Transcricional/efeitos dos fármacos , Fator de Crescimento Transformador beta/genética , Fator de Necrose Tumoral alfa/genéticaRESUMO
Cell signaling by pathogenic minerals may initiate the transactivation of genes that are critical to carcinogenesis and fibroproliferative diseases of the lung and pleura. We have shown previously that stimulation of the mitogen-activated protein kinase (MAPK) cascade by asbestos fibers leads to phosphorylation events involved in transactivation of lun and Fos proteins that comprise the activator protein-1 (AP-1) transcription factor. Recently, we have also used AP-1 luciferase reporter transgenic mice and immunocytochemistry to show that transactivation of AP-1 occurs in bronchiolar and alveolar epithelial cells after inhalation of asbestos fibers. After inhalation of asbestos, epithelial cells of the lung also show increased immunoreactivity of pliosphorylated extracellular signal regulated kinases (ERKs 1/2) at sites of fibrogenesis. The availability of lung epithelial cell-specific promoters has allowed the creation of transgenic mice with mutations in the transactivation domains of key receptors and protein intermediates that comprise the MAPK signaling cascade. These rodent models may reveal whether cell signaling events initiated by mineral dusts in epithelial cells are critical to the development of cell proliferation, apoptosis, and lung disease.
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Aging is characterized by an accumulation of oxidative injury to DNA, RNA, proteins, lipids, and carbohydrates. In addition to damage, oxidative stress can initiate cell signaling cascades that modulate cell function, growth, and death. Aging and two common age-related diseases, diabetes mellitus and atherosclerosis, may share common oxidant-related signaling pathways that lead to abnormal transcription factor activation and ultimately to cellular dysfunction, degeneration, or death. This review will focus on approaches to evaluate key redox-sensitive signaling pathways and the transcription factors altered by diabetes, atherosclerosis, and aging.