The cost of treating stroke in urban and rural Tanzania: a 6-month pilot study

Background: Economic evaluations have significant roles in informing funding decisions. They provide the means to choose which programme of care to fund among the many competing for resources. Unlike in higher-income countries, published studies on economic evaluations of stroke in Sub-Saharan Africa are rare.Objective: To pilot a method for estimating the cost of treating stroke in rural and urban Tanzania that will assist with future economic evaluations of stroke.Methods: The pilot study was conducted as part of the Tanzania Stroke Incidence Study. Incident cases were reported by resident community informants. Cost data were summarised from project documents and data on out-ofpocket payments were collected by interviewing patients/carers. Productivity losses relating to post-stroke occupations were also estimated in monetary terms using standard monthly salary estimates by job category and gender.Results: Sixteen incident cases (11 rural and 5 urban) were identified and followed-up for six monthsin 2005/2006. The overall mean cost per case was TZS 256,338 (USD 220) and included diagnostic tests (blood, ECG, echocardiogram, chest X-ray, CT scans), hospitalisation cost (registration, inpatient stay and drugs), transport cost to designated hospitals, physiotherapy and out-of-pocket payments to other points of care. Costs were more than four-fold higher in the urban district than in the rural district. Mean productivity loss per patient was TZS 247,930 (USD 213) and was more than double in the urban district than in the rural district.Conclusion: This is the first published research investigating the cost of treating stroke in Tanzania. A bigger sample, long-term follow up and modeling are required for better estimates of stroke economic burden.Keywords: Cost analysis, Stroke, Tanzania, Sub-Saharan Africa, Populations Rural/Urba

Two Meson Systems with Ginsparg-Wilson Valence Quarks

Unphysical effects associated with finite lattice spacing and partial quenching may lead to the presence of unphysical terms in chiral extrapolation formulae. These unphysical terms must then be removed during data analysis before physical predictions can be made. In this work, we show that through next-to-leading order, there are no unphysical counterterms in the extrapolation formulae, expressed in lattice-physical parameters, for meson scattering lengths in theories with Ginsparg-Wilson valence quarks. Our work applies to most sea quark discretization, provided that chiral perturbation theory is a valid approximation. We demonstrate our results with explicit computations and show that, in favorable circumstances, the extrapolation formulae do not depend on the unknown constant C_Mix appearing at lowest order in the mixed action chiral Lagrangian. We show that the I=1 KK scattering length does not depend on C_Mix in contrast to the I=3/2 K-pi scattering length. In addition, we show that these observables combined with f_K / f_pi and the I=2 pi-pi scattering length share only two linearly independent sets of counterterms, providing a means to test the mixed action theory at one lattice spacing. We therefore make a prediction for the I=1 KK scattering length.Comment: 21 pages, 2 figures, 2 tables. Version to be published in PRD. Improved discussion in Sec. III B. Added reference

Thirty Meter Telescope Site Testing I: Overview

As part of the conceptual and preliminary design processes of the Thirty Meter Telescope (TMT), the TMT site testing team has spent the last five years measuring the atmospheric properties of five candidate mountains in North and South America with an unprecedented array of instrumentation. The site testing period was preceded by several years of analyses selecting the five candidates, Cerros Tolar, Armazones and Tolonchar in northern Chile; San Pedro Martir in Baja California, Mexico and the 13 North (13N) site on Mauna Kea, Hawaii. Site testing was concluded by the selection of two remaining sites for further consideration, Armazones and Mauna Kea 13N. It showed that all five candidates are excellent sites for an extremely large astronomical observatory and that none of the sites stands out as the obvious and only logical choice based on its combined properties. This is the first article in a series discussing the TMT site testing project.Comment: Accepted for publication in PASP, April 2009 issu

Identification of hip fracture patients from radiographs using Fourier analysis of the trabecular structure: a cross-sectional study

Peer reviewedPublisher PD

A T cell-myeloid IL-10 axis regulates pathogenic IFN-γ-dependent immunity in a mouse model of type 2-low asthma

Background Although originally defined as a type 2 (T2) immune-mediated condition, non-T2 cytokines, such as IFN-γ and IL-17A, have been implicated in asthma pathogenesis, particularly severe disease. IL-10 regulates T helper (Th) cell phenotypes and can dampen T2 immunity to allergens, but its functions in controlling non-T2 cytokine responses in asthma are unclear. Objective: Determine how IL-10 regulates the balance of Th cell responses to inhaled allergen. Methods Allergic airway disease (AAD) was induced in wild-type, IL-10 reporter and conditional IL-10 or IL-10 receptor α (IL-10Rα) knockout mice, by repeated intranasal administration of house dust mite (HDM). IL-10 and IFN-γ signalling were disrupted using blocking antibodies. Results Repeated HDM inhalation induced a mixed IL-13/IL-17A response and accumulation of IL-10-producing FoxP3- effector CD4+ T cells in the lungs. Ablation of T cell-derived IL-10 increased the IFN-γ and IL-17A response to HDM, reducing IL-13 levels and airway eosinophilia without affecting IgE or airway hyperresponsiveness. The increased IFN-γ response could be recapitulated by IL-10Rα deletion in CD11c+ myeloid cells or local IL-10Rα blockade. Disruption of the T cell-myeloid IL-10 axis resulted in elevated pulmonary monocyte-derived dendritic cell numbers and increased IFN-γ-dependent expression of CXCR3 ligands by airway macrophages, suggestive of a feedforward loop of Th1 cell recruitment. Augmented IFN-γ responses in the HDM AAD model were accompanied by increased disruption of airway epithelium, which was reversed by therapeutic blockade of IFN-γ. Conclusions IL-10 from effector T cells signals to CD11c+ myeloid cells to suppress an atypical and pathogenic IFN-γ response to inhaled HDM

Pulmonary ORMDL3 is critical for induction of Alternaria -induced allergic airways disease

Genome-wide association studies have identified the ORM (yeast)-like protein isoform 3 (ORMDL3) gene locus on human chromosome 17q to be a highly significant risk factor for childhood-onset asthma. Objective We sought to investigate in vivo the functional role of ORMDL3 in disease inception. Methods An Ormdl3-deficient mouse was generated and the role of ORMDL3 in the generation of allergic airways disease to the fungal aeroallergen Alternaria alternata was determined. An adeno-associated viral vector was also used to reconstitute ORMDL3 expression in airway epithelial cells of Ormdl3 knockout mice. Results Ormdl3 knockout mice were found to be protected from developing allergic airways disease and showed a marked decrease in pathophysiology, including lung function and airway eosinophilia induced by Alternaria. Alternaria is a potent inducer of cellular stress and the unfolded protein response, and ORMDL3 was found to play a critical role in driving the activating transcription factor 6–mediated arm of this response through Xbp1 and downstream activation of the endoplasmic reticulum–associated degradation pathway. In addition, ORMDL3 mediated uric acid release, another marker of cellular stress. In the knockout mice, reconstitution of Ormdl3 transcript levels specifically in the bronchial epithelium resulted in reinstatement of susceptibility to fungal allergen–induced allergic airways disease. Conclusions This study demonstrates that ORMDL3, an asthma susceptibility gene identified by genome-wide association studies, contributes to key pathways that promote changes in airway physiology during allergic immune responses

Pathways into services for offenders with intellectual disabilities : childhood experience, diagnostic information and offence variables

The patterns and pathways into intellectual disability (ID) offender services were studied through case file review for 477 participants referred in one calendar year to community generic, community forensic, and low, medium, and maximum secure services. Data were gathered on referral source, demographic information, index behavior, prior problem behaviors, diagnostic information, and abuse or deprivation. Community referrers tended to refer to community services and secure service referrers to secure services. Physical and verbal violence were the most frequent index behaviors, whereas contact sexual offenses were more prominent in maximum security. Age at first incident varied with security, with the youngest in maximum secure services. Attention-deficit/hyperactivity disorder or conduct disorder was the most frequently recorded diagnosis, and severe deprivation was the most frequent adverse developmental experience. Fire starting, theft, and road traffic offenses did not feature prominently. Generic community services accepted a number of referrals with forensic-type behavior and had higher proportions of both women and people with moderate or severe ID

Pediatric severe asthma with fungal sensitization is mediated by steroid-resistant IL-33

Background: The mechanism underlying severe asthma with fungal sensitization (SAFS) is unknown. IL-33 is important in fungus-induced asthma exacerbations, but its role in fungal sensitization is unexplored. Objective: We sought to determine whether fungal sensitization in children with severe therapy-resistant asthma is mediated by IL-33. Methods: Eighty-two children (median age, 11.7 years; 63% male) with severe therapy-resistant asthma were included. SAFS (n= 38) was defined as specific IgE or skin prick test response positivity to Aspergillus fumigatus, Alternaria alternata, or Cladosporium herbarum. Clinical features and airway immunopathology were assessed. Chronic exposure to house dust mite and A alternata were compared in a neonatal mouse model. Results: Children with SAFS had earlier symptom onset (0.5 vs 1.5 years, P= .006), higher total IgE levels (637 vs 177 IU/mL, P= .002), and nonfungal inhalant allergen-specific IgE. Significantly more children with SAFS were prescribed maintenance oral steroids (42% vs 14%, P= .02). SAFS was associated with higher airway IL-33 levels. In neonatal mice A alternata exposure induced higher serum IgE levels, pulmonary IL-33 levels, and IL-13+ innate lymphoid cell (ILC) and TH2 cell numbers but similar airway hyperresponsiveness (AHR) compared with those after house dust mite exposure. Lung IL-33 levels, IL-13+ ILC numbers, TH2 cell numbers, IL-13 levels, and AHR remained increased with inhaled budesonide during A alternata exposure, but all features were significantly reduced in ST2-/- mice lacking a functional receptor for IL-33. Conclusion: Pediatric SAFS was associated with more oral steroid therapy and higher IL-33 levels. A alternata exposure resulted in increased IL-33-mediated ILC2 numbers, TH2 cell numbers, and steroid-resistant AHR. IL-33 might be a novel therapeutic target for SAFS