26 resultados para CONTRIBUTE

em Deakin Research Online - Australia


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Background: The Health Promoting School (HPS) is a WHO sponsored framework, compiled to enable education and health sectors to be more effective in school based initiatives.

Aims: This study attempted to test the hypothesis that students from schools that had comprehensively embraced the HPS concept as indicated by the Healthy School Award, were better, in terms of health risk behaviour, self reported health status, and academic results, than students from schools that did not reach the standard of the award.

Methods and Results: The results presented came from nine schools (four primary and five secondary) applying for accreditation of the Healthy Schools Award after adopting the HPS framework for two years. Regular consultancy support and training were available to all schools. Students had completed before and after surveys to assess their health behaviours, self reported health status, and academic standing before the two year intervention, and at its end. Data from the before and after surveys of the students attending schools that reached certain level of HPS standard as indicated by the award, were compared with students whose schools did not receive the award, and the results showed differences. Some differences were found to be more significant among the primary school students than secondary schools students. This illustrated early intervention for lifestyle changes to be more effective. Students’ satisfaction with life also improved if their schools adopted the concept of HPS comprehensively.

Conclusions: The results suggest that comprehensive implementation of HPS would contribute to differences in certain behaviours and self reported health and academic status.

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Mutations in the granulocyte colony-stimulating factor receptor (G-CSF-R) gene leading to a truncated protein have been identified in a cohort of neutropenia patients highly predisposed to acute myeloid leukemia. Such mutations act in a dominant manner resulting in hyperproliferation but impaired differentiation in response to G-CSF. This is due, at least in part, to defective internalization and loss of binding sites for several negative regulators, leading to sustained receptor activation. However, those signaling pathways responsible for mediating the hyperproliferative function have remained unclear. In this study, analysis of an additional G-CSF-R mutant confirmed the importance of residues downstream of Box 2 as important contributors to the sustained proliferation. However, maximal proliferation correlated with the ability to robustly activate signal transducer and activator of transcription (STAT) 5 in a sustained manner, whereas co-expression of dominant-negative STAT5, but not dominant-negative STAT3, was able to inhibit G-CSF-stimulated proliferation from a truncated receptor. Furthermore, a Janus kinase (JAK) inhibitor also strongly reduced the proliferative response, whereas inhibitors of mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK) or phosphatidylinositol (PI) 3-kinase reduced proliferation to a lesser degree. These data suggest that sustained JAK2/STAT5 activation is a major contributor to the hyperproliferative function of truncated G-CSF receptors, with pathways involving MEK and PI 3-kinase playing a reduced role.

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This paper examines the physiological mechanisms responsible for differences in the amplitude of force fluctuations between young and old adults. Because muscle force is a consequence of motor unit activity, the potential mechanisms include both motor unit properties and the behavior of motor unit populations. The force fluctuations, however, depend not only on the age of the individual but also on the muscle group performing the task, the type and intensity of the muscle contraction, and the physical activity status of the individual. Computer simulations and experimental findings performed on tasks that involved single agonist and antagonist muscles suggest that differences in force fluctuations are not attributable to motor unit twitch force, motor unit number, or nonuniform activation of the agonist muscle, but that they are influenced by the variability and common modulation of motor unit discharge in both the agonist and antagonist muscles. Because the amplitude of the force fluctuations does not vary linearly with muscle activation, these results suggest that multiple mechanisms contribute to the differences in force fluctuations between young and old adults, although the boundary conditions for each mechanism remain to be determined.

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Lung transplant recipients (LTx) exhibit marked peripheral limitations to exercise. We investigated whether skeletal muscle Ca2+ and K+ regulation might be abnormal in eight LTx and eight healthy controls. Peak oxygen consumption and arterialized venous plasma [K+] (where brackets denote concentration) were measured during incremental exercise. Vastus lateralis muscle was biopsied at rest and analyzed for sarcoplasmic reticulum Ca2+ release, Ca2+ uptake, and Ca2+-ATPase activity rates; fiber composition; Na+-K+-ATPase (K+-stimulated 3-O-methylfluorescein phosphatase) activity and content ([3H]ouabain binding sites); as well as for [H+] and H+-buffering capacity. Peak oxygen consumption was 47% less in LTx (P < 0.05). LTx had lower Ca2+ release (34%), Ca2+ uptake (31%), and Ca2+-ATPase activity (25%) than controls (P < 0.05), despite their higher type II fiber proportion (LTx, 75.0 ± 5.8%; controls, 43.5 ± 2.1%). Muscle [H+] was elevated in LTx (P < 0.01), but buffering capacity was similar to controls. Muscle 3-O-methylfluorescein phosphatase activity was 31% higher in LTx (P < 0.05), but [3H]ouabain binding content did not differ significantly. However, during exercise, the rise in plasma [K+]-to-work ratio was 2.6-fold greater in LTx (P < 0.05), indicating impaired K+ regulation. Thus grossly subnormal muscle calcium regulation, with impaired potassium regulation, may contribute to poor muscular performance in LTx.

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CD1d-restricted NKT cells are a novel T cell lineage with unusual features. They co-express some NK cell receptors and recognize glycolipid antigens through an invariant T cell receptor (TCR) in the context of CD1d molecules. Upon activation through the TCR, NKT cells produce large amounts of IFN- and IL-4. It has been proposed that rapid cytokine output by activated NKT cells may induce bystander activation of other lymphoid lineages. The impact of CD1d-restricted NKT cell activation in the induction of B cell-mediated immune responses to infection is still unclear. We show here that CD1-restricted NKT cells contribute to malarial splenomegaly associated with expansion of the splenic B cell pool and enhance parasite-specific antibody formation in response to Plasmodium berghei infection. The increased B cell-mediated response correlates with the ability of NKT cells to promote Th2 immune responses. Additionally, antibody responses against the glycosylphosphatidylinositol (GPI)-anchored protein merozoite surface protein 1 (MSP-1) were found to be significantly lower in CD1-/- mice compared to wild-type animals. P. berghei-infected MHC class II (MHCII)-/- mice also generated antibodies against MSP-1, suggesting that antibody production against GPI-anchored antigens in response to malaria infection can arisefrom both MHCII-dependent and independent pathways.

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Pain in the Achilles tendon commonly affects active individuals but is also seen in sedentary people. This thesis shows that the accumulation of excess body fat, abnormal blood lipids and glucose metabolism were associated with Achilles tendinopathy. Targeting these lifestyle factors may improve treatment outcomes for tendon injury.

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In the face of hybridization, species integrity can only be maintained through post-zygotic isolating barriers (PIBs). PIBs need not only be intrinsic (i.e. hybrid inviability and sterility caused by developmental incompatibilities), but also can be extrinsic due to the hybrid's intermediate phenotype falling between the parental niches. For example, in migratory species, hybrid fitness might be reduced as a result of intermediate migration pathways and reaching suboptimal wintering grounds. Here, we test this idea by comparing the juvenile to adult survival probabilities as well as the wintering grounds of pied flycatchers (Ficedula hypoleuca), collared flycatchers (Ficedula albicollis) and their hybrids using stable isotope ratios of carbon (δ13C) and nitrogen (δ15N) in feathers developed at the wintering site. Our result supports earlier observations of largely segregated wintering grounds of the two parental species. The isotope signature of hybrids clustered with that of pied flycatchers. We argue that this pattern can explain the high annual survival of hybrid flycatchers. Hence, dominant expression of the traits of one of the parental species in hybrids may substantially reduce the ecological costs of hybridization.

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SEM observations of low solid content vitrified clay suspensions reveal that clay platelets build porous three-dimensional networks with platelets contacting each other mostly by their edges. To explain this behaviour, which must require long range edge-to-edge (EE) attractive forces, a hydrophobic-like interaction has been proposed. This interaction may be induced by the presence of nano-bubbles existing on the edges of clay crystals which may cause clay particles to flocculate. The following indirect evidence for such hydrophobic behaviour is presented. First, a clay platelet is shown attached to an oil drop by its edge; second, clay flocs were attracted by a vertically placed Teflon strip but not to the hydrophilic mica basal surface; third, a much thicker porous sediment occurred in CO2-saturated water solution compared with vacuum degassed water.

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Hypothalamic nuclei, particularly the paraventricular nuclei (PVN), are important brain sites responsible for central nervous system responses during an immune challenge. The brainstem catecholamine cells of the nucleus tractus solitarius (NTS) and ventrolateral medulla (VLM) have been shown to play critical roles in relaying systemic immune signals to the PVN. However, whilst it is well recognised that PVN divisions also innervate the NTS and VLM, it is not known whether descending PVN pathways can modulate the recruitment of brainstem cells during an immune challenge. Using systemic administration of the proinflammatory cytokine interleukin-1β, in combination with Fos immunolabelling, we firstly investigated the effect of PVN lesions on NTS and VLM catecholamine and non-catecholamine cell responses. We found that ibotenic acid lesions of the PVN significantly reduced numbers of Fos-positive non-catecholamine, noradrenergic and adrenergic cells observable in the VLM and NTS after interleukin-1β administration. We then investigated the origins of descending inputs to the VLM and NTS, activated by systemic interleukin-1β, by mapping the distribution of Fos-positive retrogradely-labelled cells in divisions of the PVN after iontophoretically depositing choleratoxin-b subunit into the NTS or VLM one week prior to interleukin-1β administration. We found that, after either NTS or VLM deposits, the majority of retrogradely-labelled Fos-positive cells activated by interleukin-1β were localised in the medial and lateral parvocellular PVN divisions. Retrogradely-labelled Fos-positive cells were also observed in the NTS after VLM deposits, and in the VLM after NTS tracer deposits, suggesting reciprocal communication between these two nuclei after systemic interleukin-1β. Thus the present study shows that the PVN has the capacity to modulate NTS and VLM responses after an immune challenge and that these may result from descending projections arising in the medial and lateral PVN divisions. These findings suggest that central nervous system responses to an immune challenge are likely to involve complex reciprocal connections between the PVN and the brainstem as well as between brainstem nuclei themselves.

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Medial parvocellular paraventricular corticotropin-releasing hormone (mPVN CRH) cells are critical in generating hypothalamic-pituitary-adrenal (HPA) axis responses to systemic interleukin-1beta (IL-1beta). However, although it is understood that catecholamine inputs are important in initiating mPVN CRH cell responses to IL-1beta, the contributions of distinct brainstem catecholamine cell groups are not known. We examined the role of nucleus tractus solitarius (NTS) and ventrolateral medulla (VLM) catecholamine cells in the activation of mPVN CRH, hypothalamic oxytocin (OT) and central amygdala cells in response to IL-1beta (1 microg/kg, i.a.). Immunolabelling for the expression of c-fos was used as a marker of neuronal activation in combination with appropriate cytoplasmic phenotypic markers. First we confirmed that PVN 6-hydroxydopamine lesions, which selectively depleted catecholaminergic terminals, significantly reduced IL-1beta-induced mPVN CRH cell activation. The contribution of VLM (A1/C1 cells) versus NTS (A2 cells) catecholamine cells to mPVN CRH cell responses was then examined by placing ibotenic acid lesions in either the VLM or NTS. The precise positioning of these lesions was guided by prior retrograde tracing studies in which we mapped the location of IL-1beta-activated VLM and NTS cells that project to the mPVN. Both VLM and NTS lesions reduced the mPVN CRH and OT cell responses to IL-1beta. Unlike VLM lesions, NTS lesions also suppressed the recruitment of central amygdala neurons. These studies provide novel evidence that both the NTS and VLM catecholamine cells have important, but differential, contributions to the generation of IL-1beta-induced HPA axis responses.

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Large surveys of library user service quality perception are common. However, student evaluation of teaching (SET) data often show a disparity between ratings of library service quality and library resource quality. In this situation, perhaps SET data can also provide insights into what contributes to the perception of library resource quality, and hence identify leverage points for quality improvement interventions. This paper documents an analysis of available Deakin University SET data relating to student interaction with, and evaluation of, library resources. It highlights significant correlations associated with library-related SET items, and from them infers actions that the library could undertake to improve the value and perception of the quality of library resources. The following results were observed. High ratings for library resources were likely to be associated with high general ratings of teaching and unit quality. Postgraduate coursework students rated library resources significantly higher than students in the first three years of undergraduate programs. Students in one faculty (Health) rated library resources significantly higher than students in all other faculties. There was a strong correlation observed in Australasian Survey of Student Engagement data for both 2009 and 2010 between the two items “Used library resources on campus or online” and “Worked on an essay or assignment that required integrating ideas or information from various sources”. These findings suggest the following conclusions. Well-planned learning environments are likely to integrate meaningful student interaction with the library. Initiatives to improve the value and perception of the quality of library resources should be focussed on the specific characteristics and needs of particular student cohorts to have maximum impact. More sophisticated assessment tasks that require students to interact with the library have the potential to result in higher student ratings of the value of library resources.