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Introduction: An important impediment to the large-scale adoption of evidence-based school nutrition interventions is the lack of evidence on effective strategies to implement them. This paper describes the protocol for a "Collaborative Network Trial" to support the simultaneous testing of different strategies undertaken by New South Wales Local Health Districts to facilitate the adoption of an effective school-based healthy lunchbox program ('SWAP IT'). The primary objective of this study is to assess the effectiveness of different implementation strategies to increase school adoption of the SWAP across New South Wales Local Health Districts. Methods: Within a Master Protocol framework, a collaborative network trial will be undertaken. Independent randomized controlled trials to test implementation strategies to increase school adoption of SWAP IT within primary schools in 10 different New South Wales Local Health Districts will occur. Schools will be randomly allocated to either the intervention or control condition. Schools allocated to the intervention group will receive a combination of implementation strategies. Across the 10 participating Local Health Districts, six broad strategies were developed and combinations of these strategies will be executed over a 6 month period. In six districts an active comparison group (containing one or more implementation strategies) was selected. The primary outcome of the trial will be adoption of SWAP IT, assessed via electronic registration records captured automatically following online school registration to the program. The primary outcome will be assessed using logistic regression analyses for each trial. Individual participant data component network meta-analysis, under a Bayesian framework, will be used to explore strategy-covariate interactions; to model additive main effects (separate effects for each component of an implementation strategy); two way interactions (synergistic/antagonistic effects of components), and full interactions. Discussion: The study will provide rigorous evidence of the effects of a variety of implementation strategies, employed in different contexts, on the adoption of a school-based healthy lunchbox program at scale. Importantly, it will also provide evidence as to whether health service-centered, collaborative research models can rapidly generate new knowledge and yield health service improvements. Clinical trial registration: This trial is registered prospectively with the Australian New Zealand Clinical Trials Registry (ACTRN12623000558628).
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Servicios de Salud Escolar , Instituciones Académicas , Humanos , Australia , Teorema de Bayes , Nueva Gales del Sur , Metaanálisis como AsuntoRESUMEN
Wildlife living in proximity to people are exposed to both natural and anthropogenic factors that may influence cortisol production associated with stress response. While some species, including coyotes (Canis latrans), have become commonplace in developed areas throughout North America, urban individuals still must navigate ever-changing, novel environments and cope with frequent disturbance. Given that coyotes are relatively large predators compared to most other urban wildlife, they face unique pressures such as crossing roadways to use suitable habitat fragments and are at a greater risk of being detected and experiencing negative human interactions. To assess whether urbanization influences hypothalamic-pituitary-adrenal axis activity in free-ranging coyotes, we analyzed cortisol concentration in hair samples from 97 coyotes residing across the urbanization gradient within the Greater Chicago Metropolitan area. As the proportion of developed landcover within coyote home ranges increased, coyotes experienced more stress. Body condition and social status also had strong relationships with stress. Animals in poorer body condition experienced more stress and subordinate coyotes experienced less stress than alphas. We also found some evidence that stress varied seasonally and among different age classes. Understanding how intrinsic and extrinsic factors influence endocrine activity in urban carnivores is vital for predicting how hormone production and related behavioral patterns may change in future populations as more areas become developed.
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BACKGROUND: Physical Activity 4 Everyone (PA4E1) is an evidence-based program effective at increasing adolescent physical activity (PA) and improving weight status. This study aimed to determine a) the effectiveness of an adapted implementation intervention to scale-up PA4E1 at 24-month follow-up, b) fidelity and reach, and c) the cost and cost-effectiveness of the implementation support intervention. METHODS: A cluster randomised controlled trial using a type III hybrid implementation-effectiveness design in 49 lower socio-economic secondary schools, randomised to a program (n = 24) or control group (n = 25). An adapted implementation intervention consisting of seven strategies was developed to support schools to implement PA4E1 over 24-months. The primary outcome was the proportion of schools implementing at least four of the 7 PA practices, assessed via computer assisted telephone interviews (CATI) with Head Physical Education Teachers. Secondary outcomes included the mean number of PA practices implemented, fidelity and reach, cost and cost-effectiveness. Logistic regression models assessed program effects. RESULTS: At baseline, no schools implemented four of the 7 PA practices. At 24-months, significantly more schools in the program group (16/23, 69.6%) implemented at least four of the 7 PA practices than the control group (0/25, 0%) (p < 0.001). At 24-months, program schools were implementing an average of 3.6 more practices than control schools (4.1 (1.7) vs. 0.5 (0.8), respectively) (P < 0.001). Fidelity and reach of the implementation intervention were high (> 75%). The total cost of the program was $415,112 AUD (2018) ($17,296 per school; $117.30 per student). CONCLUSIONS: The adapted implementation intervention provides policy makers and researchers with an effective and potentially cost-effective model for scaling-up the delivery of PA4E1 in secondary schools. Further assessment of sustainability is warranted. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry ACTRN12617000681358 prospectively registered 12th May 2017.
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Promoción de la Salud , Servicios de Salud Escolar , Adolescente , Australia , Ejercicio Físico , Humanos , Instituciones AcadémicasRESUMEN
While the fundamental laws of physics are time-reversal invariant, most macroscopic processes are irreversible. Given that the fundamental laws are taken to underpin all other processes, how can the fundamental time-symmetry be reconciled with the asymmetry manifest elsewhere? In statistical mechanics (SM), progress can be made with this question. What I dub the 'Zwanzig-Zeh-Wallace framework' can be used to construct the irreversible equations of SM from the underlying microdynamics. Yet this framework uses coarse-graining, a procedure that has faced much criticism. I focus on two objections in the literature: claims that coarse-graining makes time-asymmetry (i) 'illusory' and (ii) 'anthropocentric'. I argue that these objections arise from an unsatisfactory justification of coarse-graining prevalent in the literature, rather than from coarse-graining itself. This justification relies on the idea of measurement imprecision. By considering the role that abstraction and autonomy play, I provide an alternative justification and offer replies to the illusory and anthropocentric objections. Finally, I consider the broader consequences of this alternative justification: the connection to debates about inter-theoretic reduction and the implication that the time-asymmetry in SM is weakly emergent. 1Introduction 1.1Prospectus2The Zwanzig-Zeh-Wallace Framework3Why Does This Method Work? 3.1The special conditions account3.2When is a density forwards-compatible?4Anthropocentrism and Illusion: Two Objections 4.1The two objections in more detail4.2Against the justification by measurement imprecision5An Alternative Justification 5.1Abstraction and autonomy5.2An illustration: the Game of Life6Reply to Illusory7Reply to Anthropocentric8The Wider Landscape: Concluding Remarks 8.1Inter-theoretic relations8.2The nature of irreversibility.
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Morgagni hernia is a rare type of congenital diaphragmatic hernia caused by lack of fusion of the pleuroperitoneal membrane anteriorly leading to a defect in the foramen of Morgagni. These are rare hernias and typically present early in life. Those that do not get repaired during infancy or adolescence often present later in life with variable symptoms including obstruction, incarceration, strangulation, pulmonary symptoms, chest pain, etc. Herein we present an adult case that was found incidentally after a screening computerized tomography (CT) chest scan was done for history of smoking. There are two unique aspects to this case: first, given the large size of her hernia, her only complaint was mild shortness of breath and second, the innovative use of mesh as a suture bolster.
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Foundational puzzles surround (Newtonian) gravitational thermal physics-a realm in which stars are treated as akin to molecules in a gas. Whether such an enterprise is successful and the domain of thermal physics extends beyond our terrestrial sphere is disputed. There are successes (such as the collisionless Boltzmann equation) and paradoxical features (such as the 'gravothermal catastrophe'). Callender (Found Phys 41(6):960-981, 2011) advocates reconciling the two sides of the dispute by taking a broader view of thermodynamics. Here I argue for an alternative position: if we are careful in distinguishing statistical mechanics and thermodynamics, then no reconciliation is required. Both sides can live in harmony because whilst statistical mechanics applies, thermodynamics does not. This state of affairs-the applicability of statistical mechanics without the emergence of thermodynamic behaviour-can be explained in terms of an infamous infinite idealisation: the thermodynamic limit.
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BACKGROUND: The implementation of school nutrition policies, which govern the provision of food in schools, is recommended as a public health strategy to support the development of healthy dietary behaviours in school-aged children. Despite this, research internationally and in Australia indicates that few schools implement such policies. This study aims to examine whether a theoretically designed, multi-strategy intervention was effective in increasing the implementation of a healthy canteen policy in Australian primary schools. METHODS: A parallel group randomised controlled trial was conducted with all government and Catholic primary schools within one region in New South Wales, Australia who had an operational canteen that provided food to primary school aged children (5-12 years) and were not currently receiving an intervention to change their canteen practices. Schools randomised to the intervention arm received a 9-month multicomponent intervention including ongoing support, provision of resources, performance monitoring and feedback, executive support and recognition. The primary outcomes were the proportion of the schools with a canteen menu that: i) did not include 'red' or 'banned' items according to the healthy canteen policy; and ii) had more than 50 % 'green' items. The primary outcome was assessed via menu audit at baseline and follow up by dietitians blinded to group allocation. RESULTS: Fifty-three eligible schools were randomised to either the intervention or control group (28 intervention; 25 control). Analyses with 51 schools who returned school menus found that intervention schools were significantly more likely relative to control schools to have a menu without 'red' or 'banned' items (RR = 5.78 (1.45-23.05); p = 0.002) and have at least 50 % of menu items classified as green (RR = 2.03 (1.01-4.08); p = 0.03). CONCLUSIONS: This study found that a multi-component intervention was effective in improving primary schools' compliance with a healthy canteen policy. Given the lack of evidence regarding how best to support schools with implementing evidence-based policies to improve child diet, this trial for the first time provides high quality evidence to practitioners and policy makers seeking to improve nutrition policy implementation in schools. TRIAL REGISTRATION: This trial was prospectively registered with the Australian New Zealand Clinical Trials Registry ( ACTRN12614001148662 ) 30th October 2014.
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Dieta , Conducta Alimentaria , Servicios de Alimentación/normas , Promoción de la Salud/métodos , Política Nutricional , Servicios de Salud Escolar , Instituciones Académicas , Australia , Niño , Conducta Infantil , Preescolar , Dieta/normas , Femenino , Alimentos , Conductas Relacionadas con la Salud , Humanos , Masculino , Nueva Gales del Sur , Salud PúblicaAsunto(s)
Conducta Alimentaria , Servicios de Alimentación , Promoción de la Salud/métodos , Evaluación de Programas y Proyectos de Salud , Estudiantes , Verduras , Adolescente , Australia , Niño , Femenino , Servicios de Alimentación/normas , Frutas , Conocimientos, Actitudes y Práctica en Salud , Política de Salud , Humanos , Masculino , Instituciones AcadémicasAsunto(s)
Dolor Abdominal/etiología , Enfermedades Intestinales/complicaciones , Anomalía Torsional/complicaciones , Diverticulitis/complicaciones , Diverticulitis/diagnóstico , Diverticulitis/cirugía , Humanos , Enfermedades Intestinales/diagnóstico , Enfermedades Intestinales/cirugía , Laparoscopía , Masculino , Divertículo Ileal/complicaciones , Divertículo Ileal/diagnóstico , Divertículo Ileal/cirugía , Anomalía Torsional/diagnóstico , Anomalía Torsional/cirugía , Adulto JovenRESUMEN
Although IGF-I was known to stimulate the growth of pancreatic islet cells from early in vitro experiments and in vivo reports on rodents, recent gene targeting experiments have indicated that IGF-I and its receptor do not play a major role in normal islet cell growth. In our previous reports, liver- or pancreatic-specific IGF-I deficiency caused no decrease in ß-cell mass; a general and ß-cell-enriched IGF-I overexpression caused no change in normal islet cell growth. On the other hand, increased metabolic demands (such as in obesity and insulin resistance) result in ß-cell compensation in cell number and insulin secretion. In order to test whether IGF-I could promote islet cell growth and facilitate islet compensation due to obesity-induced insulin resistance, we have challenged MT-IGF mice to a high-fat diet. After 28 weeks, both MT-IGF mice and wild-type littermates gained comparable 40-57% of body weight, with similar increases in fat masses; all mice maintained a normal sensitivity to insulin and did not become severely hyperglycemic. Nevertheless, compared to wild-type littermates, the equally obese MT-IGF mice maintained improved glucose tolerance and a diminished insulin level; similar to when fed a normal chow diet. More importantly, under IGF-I overexpression, there was no further increase in ß-cell mass caused by obesity. Thus, IGF-I overexpression had no significant effect on weight gain and islet cell compensation in response to high-fat diet-induced obesity.
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Factor I del Crecimiento Similar a la Insulina/metabolismo , Islotes Pancreáticos/patología , Obesidad/metabolismo , Adiposidad , Animales , Glucemia/análisis , Grasas de la Dieta/administración & dosificación , Femenino , Intolerancia a la Glucosa , Humanos , Insulina/sangre , Resistencia a la Insulina , Factor I del Crecimiento Similar a la Insulina/análisis , Factor I del Crecimiento Similar a la Insulina/genética , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Transgénicos , Obesidad/sangre , Obesidad/patología , Tamaño de los Órganos , Factores de TiempoRESUMEN
Insulin-like growth factor I (IGF-I) is normally produced from hepatocytes and various other cells and tissues, including the pancreas, and is known to stimulate islet cell replication in vitro, prevent Fas-mediated beta-cell destruction and delay the onset of diabetes in nonobese diabetic mice. Recently, however, the notion that IGF-I stimulates islet cell growth has been challenged by the results of IGF-I and receptor gene targeting. To test the effects of a general, more profound increase in circulating IGF-I on islet cell growth and glucose homeostasis, we have characterized MT-IGF mice, which overexpress the IGF-I gene under the metallothionein I promoter. In early reports, a 1.5-fold-elevated serum IGF-I level caused accelerated somatic growth and pancreatic enlargement. We demonstrated that the transgene expression, although widespread, was highly concentrated in the beta-cells of the pancreatic islets. Yet, islet cell percent and pancreatic morphology were unaffected. IGF-I overexpression resulted in significant hypoglycemia, hypoinsulinemia, and improved glucose tolerance but normal insulin secretion and sensitivity. Pyruvate tolerance test indicated significantly suppressed hepatic gluconeogenesis, which might explain the severe hypoglycemia after fasting. Finally, due to a partial prevention of beta-cell death against onset of diabetes and/or the insulin-like effects of IGF-I overexpression, MT-IGF mice (which overexpress the IGF-I gene under the metallothionein I promoter) were significantly resistant to streptozotocin-induced diabetes, with diminished hyperglycemia and prevention of weight loss and death. Although IGF-I might not promote islet cell growth, its overexpression is clearly antidiabetic by improving islet cell survival and/or providing insulin-like effects.
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Diabetes Mellitus Experimental/metabolismo , Hipoglucemia/metabolismo , Resistencia a la Insulina/fisiología , Factor I del Crecimiento Similar a la Insulina/biosíntesis , Islotes Pancreáticos/metabolismo , Animales , Northern Blotting , Proliferación Celular , Diabetes Mellitus Experimental/genética , Diabetes Mellitus Experimental/patología , Técnica del Anticuerpo Fluorescente , Gluconeogénesis/genética , Prueba de Tolerancia a la Glucosa , Humanos , Inmunohistoquímica , Insulina/sangre , Factor I del Crecimiento Similar a la Insulina/genética , Islotes Pancreáticos/patología , Metalotioneína/biosíntesis , Metalotioneína/genética , Ratones , Ratones Transgénicos , Piruvatos/metabolismo , ARN/biosíntesis , ARN/aislamiento & purificación , Ratas , Reacción en Cadena de la Polimerasa de Transcriptasa InversaRESUMEN
Growth hormone (GH), acting through its receptor (GHR), is essential for somatic growth and development and maintaining metabolic homeostasis. GHR gene-deficient (GHR(-/-)) mice exhibit drastically diminished insulin-like growth factor-I (IGF-I) levels, proportional growth retardation, elevated insulin sensitivity, and reduced islet beta-cell mass. Unlike the liver, which is mostly unaffected by changes in IGF-I level, skeletal muscles express high levels of IGF-I receptor (IGF-IR). The net result of a concurrent deficiency in the actions of both GH and IGF-I, which exert opposite influences on insulin responsiveness, has not been evaluated. We studied insulin-stimulated early responses in the insulin receptor (IR), insulin receptor substrate-1 (IRS-1), and p85 subunit of phosphatidylinositol 3-kinase. Upon in vivo insulin stimulation, skeletal muscles of GHR(-/-) mice exhibit transient delayed responses in IR and IRS-1 phosphorylation but normal levels of p85 association with IRS-1. This is in contrast to normal/elevated insulin responses in hepatocytes and indicates tissue-specific effects of GHR gene deficiency. In addition to stimulating normal islet cell growth, GH may participate in islet cell overgrowth, which compensates for insulin resistance induced by obesity. To determine whether the islet cell overgrowth is dependent on GH signaling, we studied the response of male GHR(-/-) mice to high-fat diet (HFD)-induced obesity. After 17 wk on a HFD, GHR(-/-) mice became more significantly obese than wild-type mice and exhibited increased beta-cell mass to a slightly higher extent. These data demonstrate that GH signaling is not required for compensatory islet growth. Thus, in both muscle insulin responsiveness and islet growth compensation, normal levels of GH signals do not seem to play a dominant role.
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Insulina/farmacología , Islotes Pancreáticos/crecimiento & desarrollo , Músculo Esquelético/metabolismo , Obesidad/metabolismo , Receptores de Somatotropina/genética , Tejido Adiposo/efectos de los fármacos , Tejido Adiposo/patología , Animales , Peso Corporal , Dieta , Hiperplasia , Insulina/sangre , Proteínas Sustrato del Receptor de Insulina , Islotes Pancreáticos/efectos de los fármacos , Hígado/efectos de los fármacos , Hígado/metabolismo , Masculino , Ratones , Ratones Endogámicos BALB C , Ratones Endogámicos C57BL , Ratones Noqueados , Músculo Esquelético/efectos de los fármacos , Obesidad/patología , Fosfatidilinositol 3-Quinasas/metabolismo , Fosfoproteínas/metabolismo , Fosforilación/efectos de los fármacos , Receptor de Insulina/metabolismo , Receptores de Somatotropina/deficienciaRESUMEN
Both GH and IGF-I stimulate islet cell growth, inhibit cell apoptosis, and regulate insulin biosynthesis and secretion. GH receptor gene deficiency (GHR(-/-)) caused diminished pancreatic islet cell mass and serum insulin level and elevated insulin sensitivity. Because IGF-I gene expression was nearly abolished in these mice, we sought to determine whether that had caused the islet defects. To restore IGF-I level, we have generated transgenic mice that express rat IGF-I cDNA under the direction of rat insulin promoter 1 (RIP-IGF). Using RNase protection assay and immunohistochemistry, the IGF-I transgene expression was revealed specifically in pancreatic islets of the RIP-IGF mice, which exhibited normal growth and development and possess no abnormalities in glucose homeostasis, insulin production, and islet cell mass. GHR(-/-) mice exhibited 50% reduction in the ratio of islet cell mass to body weight and increased insulin sensitivity but impaired glucose tolerance. Compared with GHR(-/-) alone, IGF-I overexpression on a GHR(-/-) background caused no change in the diminished blood glucose and serum insulin levels, pancreatic insulin contents, and insulin tolerance but improved glucose tolerance and insulin secretion. Remarkably, islet-specific overexpression of IGF-I gene in GHR(-/-) mice restored islet cell mass, at least partially through cell hypertrophy. Interestingly, double-transgenic male mice demonstrated a transient rescue in growth rates vs. GHR(-/-) alone, at 2-3 months of age. Our results suggest that IGF-I deficiency is part of the underlying mechanism of diminished islet growth in GHR(-/-) mice and are consistent with the notion that IGF-I mediates GH-induced islet cell growth.
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Proteínas de Homeodominio/genética , Factor I del Crecimiento Similar a la Insulina/genética , Islotes Pancreáticos/citología , Islotes Pancreáticos/fisiología , Receptores de Somatotropina/genética , Transactivadores/genética , Animales , Glucemia/metabolismo , División Celular/fisiología , Expresión Génica/fisiología , Glucagón/sangre , Glucagón/metabolismo , Intolerancia a la Glucosa/fisiopatología , Insulina/sangre , Insulina/metabolismo , Secreción de Insulina , Factor I del Crecimiento Similar a la Insulina/fisiología , Islotes Pancreáticos/metabolismo , Ratones , Ratones Endogámicos C3H , Ratones Endogámicos C57BL , Ratones Transgénicos , Transgenes/fisiologíaRESUMEN
Growth hormone, acting through its receptor (GHR), plays an important role in carbohydrate metabolism and in promoting postnatal growth. GHR gene-deficient (GHR(-/-)) mice exhibit severe growth retardation and proportionate dwarfism. To assess the physiological relevance of growth hormone actions, GHR(-/-) mice were used to investigate their phenotype in glucose metabolism and pancreatic islet function. Adult GHR(-/-) mice exhibited significant reductions in the levels of blood glucose and insulin, as well as insulin mRNA accumulation. Immunohistochemical analysis of pancreatic sections revealed normal distribution of the islets despite a significantly smaller size. The average size of the islets found in GHR(-/-) mice was only one-third of that in wild-type littermates. Total beta-cell mass was reduced 4.5-fold in GHR(-/-) mice, significantly more than their body size reduction. This reduction in pancreatic islet mass appears to be related to decreases in proliferation and cell growth. GHR(-/-) mice were different from the human Laron syndrome in serum insulin level, insulin responsiveness, and obesity. We conclude that growth hormone signaling is essential for maintaining pancreatic islet size, stimulating islet hormone production, and maintaining normal insulin sensitivity and glucose homeostasis.