Are physical education policies working? A snapshot from San Francisco, 2011.

IntroductionSchool physical education (PE) has been identified as a critical public health tool to increase physical activity among youths. We sought to objectively assess compliance with PE quantity mandates and quality recommendations in a large urban California school district.MethodsWe collected PE schedules and systematically observed PE lessons (n=154) in 20 elementary, 4 middle, and 4 high schools from February through May 2011.ResultsOn the basis of schools' master schedules, 83% of elementary schools met the California state mandate of 100 PE minutes per week. Teachers' actual schedules indicated that 20% of schools met the mandate, and observation showed that only 5% were in compliance. All middle and high schools met the mandated 200 minutes per week. On average, classes at all school levels met the recommended 50% of PE lesson time in moderate-to-vigorous physical activity. No teacher- or school-level factors significantly predicted PE quantity, but credentialed elementary PE teachers spent more time building students' motor skills.ConclusionsOur results suggest that current national estimates of PE, which are based on schools' self-report, overestimate the amount of PE provided in elementary schools. Although more than half of PE class time was spent in moderate-to-vigorous physical activity, total physical activity in elementary schools from PE is minimal and may do little to contribute to students' overall health

The Vascular Link Between Intrauterine Hypoxia and Postnatal Cardiovascular Pathology

The effect of intrauterine hypoxia on arterial development was evaluated with use of large and small animal models. Analyses included expression and deposition of extracellular matrix (ECM) proteins, differentiation and proliferation of vascular smooth muscle cells (VSMCs), intima formation and wall thickening. A comprehensive investigation of possible molecular, mechanical and hormonal mediators of altered arterial development was afforded by a sheep model with both acute and chronic hypoxemia studies, whereas a guinea pig model allowed for long-term study. Our findings show that chronically hypoxic fetal sheep and intrauterine growth restricted (IUGR) guinea pigs exhibit a reduction in elastic fibre content of the aorta. In adulthood, the deficiency in aortic elastic fibre content in growth restricted guinea pig offspring was amplified compared to the subtle changes observed in late fetal life. In severely hypoxic fetal sheep, more marked reduction in elastin content occurred with increases in wall thickness and VSMC content. Increased collagen paralleled elevated mRNA levels of procollagen I and transforming growth factor beta (TGF-β 1). Matrix metalloproteinase-2 (MMP-2) mRNA levels were inversely correlated with fetal arterial oxygen saturation and expression of its activator, membrane-type MMP (MTI-MMP), was elevated in severely hypoxic sheep. Marked neointima formation was also apparent in severely hypoxic fetuses concomitant with increased mRNA levels of E-selectin, indicating endothelial inflammation. These structural and molecular changes of the aorta in chronically hypoxic ovine fetuses occurred without changes in pressure or circulating cortisol levels. Further, while the hypoxic sheep showed no change in VSMC maturation, aortae of IUGR guinea pig fetuses and offspring had increased content of myosin heavy chain B (MHC-B), a marker iv of undifferentiated VSMCs. Aortae of growth impaired guinea pig offspring exhibited a left shift in the length-tension curve as measured ex vivo. Thus altered aortic development in association with chronic hypoxia or IUGR leads to persistent structural abnormalities and reduced compliance in later life. In contrast, acute hypoxic study in fetal sheep demonstrated increased elastin content of the carotid artery in association with intermittent hemodynamic changes and elevated cortisol and thus highlight that beneficial adaptations are possible under certain intrauterine insults

The role of \u3cem\u3ePax7\u3c/em\u3e in the formation of the superior colliculus and the vertebrate visual system

This thesis has explored the role of Pax7 in formation and maturation of the mouse superior colliculus, an important brain region associated with topographic visual input and the capacity to evoke appropriate visuomotor responses to environmental stimuli. The research performed was explicitly targeted at understanding the relationship between Pax7 expression and the formation of the topography of the superior colliculus, including neuron specification and differentiation, boundary formation, polarisation and retinocollicular mapping. By employing histochemical, immunohistochemical and immunofluorescent techniques, together with quantification utilising Optimas Digital Image Analysis, this project assessed Pax7 expression in diverse mutant and wildtype mice throughout a variety of developmental timepoints. Quantification revealed dynamic Pax7 expression patterns consisting of gradients of both cellular distribution and cellular protein levels, which act in summation to polarise the superior colliculus. Graded Pax7 cellular distribution and protein levels are optimal during retinal innervation and axon arborisation in wildtype mice. This contrasts with that of Pax6 mutant mice which demonstrate reduced Pax7 protein levels as a result of optic nerve hypoplasia. These results demonstrate a responsive role for Pax7 in retinocollicular mapping, and therefore visual system development. Examination of Pax7 mutant mice divulged a greater understanding of the role of Pax7 during superior collicular development, and provided the first determination of central nervous system defects in Pax7 mutant animals. Results indicate that Pax7 is redundant for neuronal specification and differentiation, but is requisite, in a dosage-dependent manner, for maintenance of a subpopulation of dorsal superior collicular neurons and subsequently superior collicular polarity. The paralogue Pax3 is thought responsible for sustaining embryonic development in Pax7 mutant mice, resulting in a less severe phenotype. Therefore, this project explored temporospatial patterns of Pax3 expression relative to Pax7 expression during all embryonic stages examined. Findings detail a diverging expression pattern between paralogues that is spatially and temporally associated with neuronal differentiation and maturation within the superior colliculus. Moreover, Pax3 expression is spatially perturbed within the central nervous system of Pax7 mutant mice, exhibiting changes in the time at which Pax3-expressing cells exit from the germinal region. The results of the research undertaken in this thesis have significantly contributed to the understanding of developmental mechanisms occurring within the superior colliculus, and the contribution of Pax7 to these processes. Findings delineate that the functional repertoire of Pax7 within the superior colliculus embraces neuronal maturation and maintenance, determination of polarity and participation in retinocollicular mapping

Pax genes during neural development and their potential role in neuroregeneration

Pax genes encode a family of transcription factors that have long been recognised as obligate contributors to embryonic development of the CNS, with evidence obtained from various animal models illustrating phylogenetically conserved functions. Within the CNS, Pax genes play substantial roles in cellular and regional specification, proliferation, progenitor cell maintenance, anti-apoptosis and neural differentiation. This comprehensive review details the critical functions of those Pax genes involved in pre- and post-natal CNS development, provides possible molecular mechanisms by which Pax genes contribute to proliferation and differentiation of neuronal cells, and explains observed changes in Pax gene expression in response to neurotrauma in the mature animal. Knowledge of the ability of individual Pax genes to specify precise lineages within the CNS is beneficial for cell replacement strategies, particularly in the production of ‘‘designer’’ cells for the treatment of neurodegenerative disorders. The manipulation of stem or committed cells so that they express definitive Pax genes may indeed assist in the pursuit of the holy grail of regenerative medicine – that of CNS cell replacement therapies leading to functional repair. We explain here, however, that only the sophisticated and precise use of Pax genes will lead to a successful outcome

Health and Physical Education and the Online Tertiary Environment at Two Universities: Pre-service Teachers’ Perceived ‘Readiness’ to Teach HPE

In recent years in tertiary institutions in Australia, there has been a large increase of enrolments in Education courses delivered via an online/external mode. This has raised a number of concerns around the nexus of theory and practice and whether pre-service teachers feel ready to teach after completing Education study online. The purpose of this study is to examine pre-service teachers’ perceived readiness to teach Health and Physical Education (HPE) after engaging with the subject fully in an online tertiary environment. 26 pre-service teachers studying education online from two separate were involved in this study. Upon completion of the University semester and also after a practicum placement, qualitative data was collected detailing the pre-service teachers’ perceptions in regard to their readiness to teach HPE. Pre-service teachers’ perceptions are used as the primary data highlighting the varying levels of readiness to teach HPE

Role of metal-dependent regulation of ESX-3 secretion in intracellular survival of Mycobacterium tuberculosis

More people die every year from Mycobacterium tuberculosis infection than from infection by any other bacterial pathogen. Type VII secretion systems (T7SS) are used by both environmental and pathogenic mycobacteria to secrete proteins across their complex cell envelope. In the nonpathogen Mycobacterium smegmatis, the ESX-1 T7SS plays a role in conjugation, and the ESX-3 T7SS is involved in metal homeostasis. In M. tuberculosis, these secretion systems have taken on roles in virulence, and they also are targets of the host immune response. ESX-3 secretes a heterodimer composed of EsxG (TB9.8) and EsxH (TB10.4), which impairs phagosome maturation in macrophages and is essential for virulence in mice. Given the importance of EsxG and EsxH during infection, we examined their regulation. With M. tuberculosis, the secretion of EsxG and EsxH was regulated in response to iron and zinc, in accordance with the previously described transcriptional response of the esx-3 locus to these metals. While iron regulated the esx-3 expression in both M. tuberculosis and M. smegmatis, there is a significant difference in the dynamics of this regulation. In M. smegmatis, the esx-3 locus behaved like other iron-regulated genes such as mbtB. In M. tuberculosis, both iron and zinc modestly repressed esx-3 expression. Diminished secretion of EsxG and EsxH in response to these metals altered the interaction of M. tuberculosis with macrophages, leading to impaired intracellular M. tuberculosis survival. Our findings detail the regulatory differences of esx-3 in M. tuberculosis and M. smegmatis and demonstrate the importance of metal-dependent regulation of ESX-3 for virulence in M. tuberculosis

Evaluation of the Induction of Immune Memory following Infant Immunisation with Serogroup C Neisseria meningitidis Conjugate Vaccines - Exploratory Analyses within a Randomised Controlled Trial

Aim: We measured meningococcal serogroup C (MenC)-specific memory B-cell responses in infants by Enzyme-Linked Immunospot (ELISpot) following different MenC conjugate vaccine schedules to investigate the impact of priming on immune memory. Methods: Infants aged 2 months were randomised to receive 1 or 2 doses of MenC-CRM197 at 3 or 3 and 4 months, 1 dose of MenC-TT at 3 months, or no primary MenC doses. All children received a Haemophilus influenzae type b (Hib)-MenC booster at 12 months. Blood was drawn at 5, 12, 12 months +6 days and 13 months of age. Results: Results were available for 110, 103, 76 and 44 children from each group respectively. Following primary immunisations, and prior to the 12-month booster, there were no significant differences between 1- or 2-dose primed children in the number of MenC memory B-cells detected. One month following the booster, children primed with 1 dose MenC-TT had more memory B-cells than children primed with either 1-dose (p = 0.001) or 2-dose (p<0.0001) MenC-CRM197. There were no differences in MenC memory B-cells detected in children who received 1 or 2 doses of MenC-CRM197 in infancy and un-primed children. Conclusions: MenC-specific memory B-cell production may be more dependent on the type of primary vaccine used than the number of doses administered. Although the mechanistic differences between MenC-CRM197 and MenC-TT priming are unclear, it is possible that structural differences, including the carrier proteins, may underlie differential interactions with B- and T-cell populations, and thus different effects on various memory B-cell subsets. A MenC-TT/Hib-MenC-TT combination for priming/boosting may offer an advantage in inducing more persistent antibody.peer-reviewe

The optimal design of stepped wedge trials with equal allocation to sequences and a comparison to other trial designs.

Background/Aims We sought to optimise the design of stepped wedge trials with an equal allocation of clusters to sequences and explored sample size comparisons with alternative trial designs. Methods We developed a new expression for the design effect for a stepped wedge trial, assuming that observations are equally correlated within clusters and an equal number of observations in each period between sequences switching to the intervention. We minimised the design effect with respect to (1) the fraction of observations before the first and after the final sequence switches (the periods with all clusters in the control or intervention condition, respectively) and (2) the number of sequences. We compared the design effect of this optimised stepped wedge trial to the design effects of a parallel cluster-randomised trial, a cluster-randomised trial with baseline observations, and a hybrid trial design (a mixture of cluster-randomised trial and stepped wedge trial) with the same total cluster size for all designs. Results We found that a stepped wedge trial with an equal allocation to sequences is optimised by obtaining all observations after the first sequence switches and before the final sequence switches to the intervention; this means that the first sequence remains in the control condition and the last sequence remains in the intervention condition for the duration of the trial. With this design, the optimal number of sequences is [Formula: see text], where [Formula: see text] is the cluster-mean correlation, [Formula: see text] is the intracluster correlation coefficient, and m is the total cluster size. The optimal number of sequences is small when the intracluster correlation coefficient and cluster size are small and large when the intracluster correlation coefficient or cluster size is large. A cluster-randomised trial remains more efficient than the optimised stepped wedge trial when the intracluster correlation coefficient or cluster size is small. A cluster-randomised trial with baseline observations always requires a larger sample size than the optimised stepped wedge trial. The hybrid design can always give an equally or more efficient design, but will be at most 5% more efficient. We provide a strategy for selecting a design if the optimal number of sequences is unfeasible. For a non-optimal number of sequences, the sample size may be reduced by allowing a proportion of observations before the first or after the final sequence has switched. Conclusion The standard stepped wedge trial is inefficient. To reduce sample sizes when a hybrid design is unfeasible, stepped wedge trial designs should have no observations before the first sequence switches or after the final sequence switches

It Takes a Library to Support Distance Learners

Wallace Library\u27s philosophy is to create and provide resources and services that will support all users. Consequently, distance learners and distance faculty have a plethora of online resources available to them, some of which is pushed out, saving time and effort for the library user. The evolvement of Wallace\u27s online resources is continuous, focused on the student or professor\u27s research need from a geographic distance

Brain putamen volume changes in newly-diagnosed patients with obstructive sleep apnea.

Obstructive sleep apnea (OSA) is accompanied by cognitive, motor, autonomic, learning, and affective abnormalities. The putamen serves several of these functions, especially motor and autonomic behaviors, but whether global and specific sub-regions of that structure are damaged is unclear. We assessed global and regional putamen volumes in 43 recently-diagnosed, treatment-naïve OSA (age, 46.4&nbsp;±&nbsp;8.8&nbsp;years; 31 male) and 61 control subjects (47.6&nbsp;±&nbsp;8.8&nbsp;years; 39 male) using high-resolution T1-weighted images collected with a 3.0-Tesla MRI scanner. Global putamen volumes were calculated, and group differences evaluated with independent samples t-tests, as well as with analysis of covariance (covariates; age, gender, and total intracranial volume). Regional differences between groups were visualized with 3D surface morphometry-based group ratio maps. OSA subjects showed significantly higher global putamen volumes, relative to controls. Regional analyses showed putamen areas with increased and decreased tissue volumes in OSA relative to control subjects, including increases in caudal, mid-dorsal, mid-ventral portions, and ventral regions, while areas with decreased volumes appeared in rostral, mid-dorsal, medial-caudal, and mid-ventral sites. Global putamen volumes were significantly higher in the OSA subjects, but local sites showed both higher and lower volumes. The appearance of localized volume alterations points to differential hypoxic or perfusion action on glia and other tissues within the structure, and may reflect a stage in progression of injury in these newly-diagnosed patients toward the overall volume loss found in patients with chronic OSA. The regional changes may underlie some of the specific deficits in motor, autonomic, and neuropsychologic functions in OSA