3,417 research outputs found
Health Inequity in the Northern Territory, Australia
INTRODUCTION: Understanding health inequity is necessary for addressing the disparities in health outcomes in many populations, including the health gap between Indigenous and non-Indigenous Australians. This report investigates the links between Indigenous health outcomes and socioeconomic disadvantage in the Northern Territory of Australia (NT).METHODS: Data sources include deaths, public hospital admissions between 2005 and 2007, and Socio-Economic Indexes for Areas from the 2006 Census. Age-sex standardisation, standardised rate ratio, concentration index and Poisson regression model are used for statistical analysis.RESULTS: There was a strong inverse association between socioeconomic status (SES) and both mortality and morbidity rates. Mortality and morbidity rates in the low SES group were approximately twice those in the medium SES group, which were, in turn, 50% higher than those in the high SES group. The gradient was present for most disease categories for both deaths and hospital admissions. Residents in remote and very remote areas experienced higher mortality and hospital morbidity than non-remote areas. Approximately 25-30% of the NT Indigenous health disparity may be explained by socioeconomic disadvantage.CONCLUSIONS: Socioeconomic disadvantage is a shared common denominator for the main causes of deaths and principal diagnoses of hospitalisations for the NT population. Closing the gap in health outcomes between Indigenous and non-Indigenous populations will require improving the socioeconomic conditions of Indigenous Australians
The 492 GHz emission of Sgr A* constrained by ALMA
We report linearly polarized continuum emission properties of Sgr A* at
492 GHz, based on the Atacama Large Millimeter Array (ALMA) observations.
We used the observations of the likely unpolarized continuum emission of Titan,
and the observations of C\textsc{i} line emission, to gauge the degree of
spurious polarization. The Stokes I flux of 3.60.72 Jy during our run is
consistent with extrapolations from the previous, lower frequency observations.
We found that the continuum emission of Sgr A* at 492 GHz shows large
amplitude differences between the XX and the YY correlations. The observed
intensity ratio between the XX and YY correlations as a function of parallactic
angle may be explained by a constant polarization position angle of
1583. The fitted polarization percentage of Sgr
A* during our observational period is 14\%1.2\%. The calibrator quasar
J1744-3116 we observed at the same night can be fitted to Stokes I = 252 mJy,
with 7.9\%0.9\% polarization in position angle P.A. =
4.14.2. The observed polarization percentage and
polarization position angle in the present work appear consistent with those
expected from longer wavelength observations in the period of 1999-2005. In
particular, the polarization position angle at 492 GHz, expected from the
previously fitted 1677 intrinsic polarization position
angle and (-5.60.7)10 rotation measure, is 155,
which is consistent with our new measurement of polarization position angle
within 1. The polarization percentage and the polarization position
angle may be varying over the period of our ALMA 12m Array observations, which
demands further investigation with future polarization observations.Comment: 10 pages, 6 figures, 1st referee report received and revise
Expulsion of Trichuris muris is associated with increased expression of angiogenin 4 in the gut and increased acidity of mucins within the goblet cell
<p>Abstract</p> <p>Background</p> <p><it>Trichuris muris </it>in the mouse is an invaluable model for infection of man with the gastrointestinal nematode <it>Trichuris trichiura</it>. Three <it>T. muris </it>isolates have been studied, the Edinburgh (E), the Japan (J) and the Sobreda (S) isolates. The S isolate survives to chronicity within the C57BL/6 host whereas E and J are expelled prior to reaching fecundity. How the S isolate survives so successfully in its host is unclear.</p> <p>Results</p> <p>Microarray analysis was used as a tool to identify genes whose expression could determine the differences in expulsion kinetics between the E and S <it>T. muris </it>isolates. Clear differences in gene expression profiles were evident as early as day 7 post-infection (p.i.). 43 probe sets associated with immune and defence responses were up-regulated in gut tissue from an E isolate-infected C57BL/6 mouse compared to tissue from an S isolate infection, including the message for the anti-microbial protein, angiogenin 4 (Ang4). This led to the identification of distinct differences in the goblet cell phenotype post-infection with the two isolates.</p> <p>Conclusion</p> <p>Differences in gene expression levels identified between the S and E-infected mice early during infection have furthered our knowledge of how the S isolate persists for longer than the E isolate in the C57BL/6 mouse. Potential new targets for manipulation in order to aid expulsion have been identified. Further we provide evidence for a potential new marker involving the acidity of the mucins within the goblet cell which may predict outcome of infection within days of parasite exposure.</p
The Goblet Cell Is the Cellular Source of the Anti-Microbial Angiogenin 4 in the Large Intestine Post Trichuris muris Infection
Mouse angiogenin 4 (Ang4) has previously been described as a Paneth cell-derived antimicrobial peptide important in epithelial host defence in the small intestine. However, a source for Ang4 in the large intestine, which is devoid of Paneth cells, has not been defined.Analysis was performed on Ang4 expression in colonic tissue by qPCR and immunohistochemistry following infection with the large intestine dwelling helminth parasite Trichuris muris. This demonstrated an increase in expression of the peptide following infection of resistant BALB/c mice. Further, histological analysis of colonic tissue revealed the cellular source of this Ang4 to be goblet cells. To elucidate the mechanism of Ang4 expression immunohistochemistry and qPCR for Ang4 was performed on colonic tissue from T. muris infected mouse mutants. Experiments comparing C3H/HeN and C3H/HeJ mice, which have a natural inactivating mutation of TLR4, revealed that Ang4 expression is TLR4 independent. Subsequent experiments with IL-13 and IL-4 receptor alpha deficient mice demonstrated that goblet cell expression of Ang4 is controlled either directly or indirectly by IL-13.The cellular source of mouse Ang4 in the colon following T. muris infection is the goblet cell and expression is under the control of IL-13
Expression of Integrin-αE by Mucosal Mast Cells in the Intestinal Epithelium and Its Absence in Nematode-Infected Mice Lacking the Transforming Growth Factor-β1-Activating Integrin αvβ6
Peak intestinal mucosal mast cell (MMC) recruitment coincides with expulsion of Trichinella spiralis, at a time when the majority of the MMCs are located within the epithelium in BALB/c mice. Although expression of integrin-α(E)β(7) by MMCs has not been formally demonstrated, it has been proposed as a potential mechanism to account for the predominantly intraepithelial location of MMCs during nematode infection. Co-expression of integrin-α(E)β(7) and the MMC chymase mouse mast cell protease-1, by mouse bone marrow-derived mast cells, is strictly regulated by transforming growth factor (TGF)-β(1). However, TGF-β(1) is secreted as part of a latent complex in vivo and subsequent extracellular modification is required to render it biologically active. We now show, for the first time, that intraepithelial MMCs express integrin-α(E)β(7) in Trichinella-infected BALB/c and S129 mice. In S129 mice that lack the gene for the integrin-β(6) subunit and, as consequence, do not express the epithelial integrin-α(v)β(6), integrin-α(E) expression is virtually abolished and recruitment of MMCs into the intestinal epithelium is dramatically reduced despite significant overall augmentation of the MMC population. Because a major function of integrin-α(v)β(6) is to activate latent TGF-β(1,) these findings strongly support a role for TGF-β(1) in both the recruitment and differentiation of murine MMCs during nematode infection
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The cost of a primary care-based childhood obesity prevention intervention
Background: United States pediatric guidelines recommend that childhood obesity counseling be conducted in the primary care setting. Primary care-based interventions can be effective in improving health behaviors, but also costly. The purpose of this study was to evaluate the cost of a primary care-based obesity prevention intervention targeting children between the ages of two and six years who are at elevated risk for obesity, measured against usual care. Methods: High Five for Kids was a cluster-randomized controlled clinical trial that aimed to modify children’s nutrition and TV viewing habits through a motivational interviewing intervention. We assessed visit-related costs from a societal perspective, including provider-incurred direct medical costs, provider-incurred equipment costs, parent time costs and parent out-of-pocket costs, in 2011 dollars for the intervention (n = 253) and usual care (n = 192) groups. We conducted a net cost analysis using both societal and health plan costing perspectives and conducted one-way sensitivity and uncertainty analyses on results. Results: The total costs for the intervention group and usual care groups in the first year of the intervention were 64,522, 12,192 (95% CI [13,174]). The mean costs for the intervention and usual care groups were 255, 63 (95% CI [69]) per child, respectively, for a incremental difference of 191, $202]) per child. Children in the intervention group attended a mean of 2.4 of a possible 4 in-person visits and received 0.45 of a possible 2 counseling phone calls. Provider-incurred costs were the primary driver of cost estimates in sensitivity analyses. Conclusions: High Five for Kids was a resource-intensive intervention. Further studies are needed to assess the cost-effectiveness of the intervention relative to other pediatric obesity interventions. Trial registration ClinicalTrials.gov Identifier: NCT00377767
Bostonia: 1993-1994, no. 2-3
Founded in 1900, Bostonia magazine is Boston University's main alumni publication, which covers alumni and student life, as well as university activities, events, and programs
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