Marshall Space Flight Center's role in EASE/ACCESS mission management

The Marshall Space Flight Center (MSFC) Spacelab Payload Project Office was responsible for the mission management and development of several successful payloads. Two recent space construction experiments, the Experimental Assembly of Structures in Extravehicular Activity (EASE) and the Assembly Concept for Construction of Erectable Space Structures (ACCESS), were combined into a payload managed by the center. The Ease/ACCESS was flown aboard the Space Shuttle Mission 61-B. The EASE/ACCESS experiments were the first structures assembled in space, and the method used to manage this successful effort will be useful for future space construction missions. The MSFC mission management responsibilities for the EASE/ACCESS mission are addressed and how the lessons learned from the mission can be applied to future space construction projects are discussed

Catalog of Lunar Craters I

This catalog gives the selenographic coordinates of all craters observable on a selected portion of the moon's surface. The diameter of the crater together with comments on shape are also given. Approximately 25 per cent of the craters have been measured previously by other observers. The catalog gives the position found in the present series of measurements and the name adopted by the International Astronomical Union

The grounded psychometric development and initial validation of the Health Literacy Questionnaire (HLQ)

BACKGROUND: Health literacy has become an increasingly important concept in public health. We sought to develop a comprehensive measure of health literacy capable of diagnosing health literacy needs across individuals and organisations by utilizing perspectives from the general population, patients, practitioners and policymakers. METHODS: Using a validity-driven approach we undertook grounded consultations (workshops and interviews) to identify broad conceptually distinct domains. Questionnaire items were developed directly from the consultation data following a strict process aiming to capture the full range of experiences of people currently engaged in healthcare through to people in the general population. Psychometric analyses included confirmatory factor analysis (CFA) and item response theory. Cognitive interviews were used to ensure questions were understood as intended. Items were initially tested in a calibration sample from community health, home care and hospital settings (N=634) and then in a replication sample (N=405) comprising recent emergency department attendees. RESULTS: Initially 91 items were generated across 6 scales with agree/disagree response options and 5 scales with difficulty in undertaking tasks response options. Cognitive testing revealed that most items were well understood and only some minor re-wording was required. Psychometric testing of the calibration sample identified 34 poorly performing or conceptually redundant items and they were removed resulting in 10 scales. These were then tested in a replication sample and refined to yield 9 final scales comprising 44 items. A 9-factor CFA model was fitted to these items with no cross-loadings or correlated residuals allowed. Given the very restricted nature of the model, the fit was quite satisfactory: χ(2)(WLSMV)(866 d.f.) = 2927, p<0.000, CFI = 0.936, TLI = 0.930, RMSEA = 0.076, and WRMR = 1.698. Final scales included: Feeling understood and supported by healthcare providers; Having sufficient information to manage my health; Actively managing my health; Social support for health; Appraisal of health information; Ability to actively engage with healthcare providers; Navigating the healthcare system; Ability to find good health information; and Understand health information well enough to know what to do. CONCLUSIONS: The HLQ covers 9 conceptually distinct areas of health literacy to assess the needs and challenges of a wide range of people and organisations. Given the validity-driven approach, the HLQ is likely to be useful in surveys, intervention evaluation, and studies of the needs and capabilities of individuals

Different prion disease phenotypes result from inoculation of cattle with two temporally separated sources of sheep scrapie from Great Britain

BACKGROUND: Given the theoretical proposal that bovine spongiform encephalopathy (BSE) could have originated from sheep scrapie, this study investigated the pathogenicity for cattle, by intracerebral (i.c.) inoculation, of two pools of scrapie agents sourced in Great Britain before and during the BSE epidemic. Two groups of ten cattle were each inoculated with pools of brain material from sheep scrapie cases collected prior to 1975 and after 1990. Control groups comprised five cattle inoculated with sheep brain free from scrapie, five cattle inoculated with saline, and for comparison with BSE, naturally infected cattle and cattle i.c. inoculated with BSE brainstem homogenate from a parallel study. Phenotypic characterisation of the disease forms transmitted to cattle was conducted by morphological, immunohistochemical, biochemical and biological methods. RESULTS: Disease occurred in 16 cattle, nine inoculated with the pre-1975 inoculum and seven inoculated with the post-1990 inoculum, with four cattle still alive at 83 months post challenge (as at June 2006). The different inocula produced predominantly two different disease phenotypes as determined by histopathological, immunohistochemical and Western immunoblotting methods and biological characterisation on transmission to mice, neither of which was identical to BSE. Whilst the disease presentation was uniform in all scrapie-affected cattle of the pre-1975 group, the post-1990 inoculum produced a more variable disease, with two animals sharing immunohistochemical and molecular profile characteristics with animals in the pre-1975 group. CONCLUSION: The study has demonstrated that cattle inoculated with different pooled scrapie sources can develop different prion disease phenotypes, which were not consistent with the phenotype of BSE of cattle and whose isolates did not have the strain typing characteristics of the BSE agent on transmission to mice

HSD3B1 genotype identifies glucocorticoid responsiveness in severe asthma

Asthma resistance to glucocorticoid treatment is a major health problem with unclear etiology. Glucocorticoids inhibit adrenal androgen production. However, androgens have potential benefits in asthma. HSD3B1 encodes for 3β-hydroxysteroid dehydrogenase-1 (3β-HSD1), which catalyzes peripheral conversion from adrenal dehydroepiandrosterone (DHEA) to potent androgens and has a germline missense-encoding polymorphism. The adrenal restrictive HSD3B1(1245A) allele limits conversion, whereas the adrenal permissive HSD3B1(1245C) allele increases DHEA metabolism to potent androgens. In the Severe Asthma Research Program (SARP) III cohort, we determined the association between DHEA-sulfate and percentage predicted forced expiratory volume in 1 s (FEV1PP). HSD3B1(1245) genotypes were assessed, and association between adrenal restrictive and adrenal permissive alleles and FEV1PP in patients with (GC) and without (noGC) daily oral glucocorticoid treatment was determined (n = 318). Validation was performed in a second cohort (SARP I&II; n = 184). DHEA-sulfate is associated with FEV1PP and is suppressed with GC treatment. GC patients homozygous for the adrenal restrictive genotype have lower FEV1PP compared with noGC patients (54.3% vs. 75.1%; P < 0.001). In patients with the homozygous adrenal permissive genotype, there was no FEV1PP difference in GC vs. noGC patients (73.4% vs. 78.9%; P = 0.39). Results were independently confirmed: FEV1PP for homozygous adrenal restrictive genotype in GC vs. noGC is 49.8 vs. 63.4 (P < 0.001), and for homozygous adrenal permissive genotype, it is 66.7 vs. 67.7 (P = 0.92). The adrenal restrictive HSD3B1(1245) genotype is associated with GC resistance. This effect appears to be driven by GC suppression of 3β-HSD1 substrate. Our results suggest opportunities for prediction of GC resistance and pharmacologic intervention

Distribution of health literacy strengths and weaknesses across socio-demographic groups: a cross-sectional survey using the Health Literacy Questionnaire (HLQ)

BACKGROUND: Recent advances in the measurement of health literacy allow description of a broad range of personal and social dimensions of the concept. Identifying differences in patterns of health literacy between population sub-groups will increase understanding of how health literacy contributes to health inequities and inform intervention development. The aim of this study was to use a multi-dimensional measurement tool to describe the health literacy of adults in urban and rural Victoria, Australia. METHODS: Data were collected from clients (n = 813) of 8 health and community care organisations, using the Health Literacy Questionnaire (HLQ). Demographic and health service data were also collected. Data were analysed using descriptive statistics. Effect sizes (ES) for standardised differences in means were used to describe the magnitude of difference between demographic sub-groups. RESULTS: Mean age of respondents was 72.1 (range 19-99) years. Females comprised 63% of the sample, 48% had not completed secondary education, and 96% reported at least one existing health condition. Small to large ES were seen for mean differences in HLQ scales between most demographic groups. Compared with participants who spoke English at home, those not speaking English at home had much lower scores for most HLQ scales including the scales 'Understanding health information well enough to know what to do' (ES -1.09 [95% confidence interval (CI) -1.33 to -0.84]), 'Ability to actively engage with healthcare providers' (ES -1.00 [95% CI -1.24, -0.75]), and 'Navigating the healthcare system' (ES -0.72 [95% CI -0.97, -0.48]). Similar patterns and ES were seen for participants born overseas compared with those born in Australia. Smaller ES were seen for sex, age group, private health insurance status, number of chronic conditions, and living alone. CONCLUSIONS: This study has revealed some large health literacy differences across nine domains of health literacy in adults using health services in Victoria. These findings provide insights into the relationship between health literacy and socioeconomic position in vulnerable groups and, given the focus of the HLQ, provide guidance for the development of equitable interventions

Studies of the transmissibility of the agent of bovine spongiform encephalopathy to the domestic chicken

<p>Abstract</p> <p>Background</p> <p>Transmission of the prion disease bovine spongiform encephalopathy (BSE) occurred accidentally to cattle and several other mammalian species via feed supplemented with meat and bone meal contaminated with infected bovine tissue. Prior to United Kingdom controls in 1996 on the feeding of mammalian meat and bone meal to farmed animals, the domestic chicken was potentially exposed to feed contaminated with the causal agent of BSE. Although confirmed prion diseases are unrecorded in avian species a study was undertaken to transmit BSE to the domestic chicken by parenteral and oral inoculations. Transmissibility was assessed by clinical monitoring, histopathological examinations, detection of a putative disease form of an avian prion protein (PrP) in recipient tissues and by mouse bioassay of tissues. Occurrence of a progressive neurological syndrome in the primary transmission study was investigated by sub-passage experiments.</p> <p>Results</p> <p>No clinical, pathological or bioassay evidence of transmission of BSE to the chicken was obtained in the primary or sub-passage experiments. Survival data showed no significant differences between control and treatment groups. Neurological signs observed, not previously described in the domestic chicken, were not associated with significant pathology. The diagnostic techniques applied failed to detect a disease associated form of PrP.</p> <p>Conclusion</p> <p>Important from a risk assessment perspective, the present study has established that the domestic chicken does not develop a prion disease after large parenteral exposures to the BSE agent or after oral exposures equivalent to previous exposures via commercial diets. Future investigations into the potential susceptibility of avian species to mammalian prion diseases require species-specific immunochemical techniques and more refined experimental models.</p

The effect of BPIFA1/SPLUNC1 genetic variation on its expression and function in asthmatic airway epithelium

Bacterial permeability family member A1 (BPIFA1), also known as short palate, lung, and nasal epithelium clone 1 (SPLUNC1), is a protein involved in the antiinflammatory response. The goal of this study was to determine whether BPIFA1 expression in asthmatic airways is regulated by genetic variations, altering epithelial responses to type 2 cytokines (e.g., IL-13). Nasal epithelial cells from patients with mild to severe asthma were collected from the National Heart, Lung. and Blood Institute Severe Asthma Research Program centers, genotyped for rs750064, and measured for BPIFA1. To determine the function of rs750064, cells were cultured at air-liquid interface and treated with 11-13 with or without recombinant human BPIFA1 (rhBPIFA1). Noncultured nasal cells with the rs750064 CC genotype had significantly less BPIFA1 mRNA expression than the CT and TT genotypes. Cultured CC versus CT and TT cells without stimulation maintained less BPIFA1 expression. With IL-13 treatment, CC genotype cells secreted more eotaxin-3 than CT and TT genotype cells. Also, rhBPIFA1 reduced IL-13-mediated eotaxin-3. BPIFA1 mRNA levels negatively correlated with serum IgE and fractional exhaled nitric oxide. Baseline FEV1% levels were lower in the asthma patients with the CC genotype (n = 1,016). Our data suggest that less BPIFA1 in asthma patients with the CC allele may predispose them to greater eosinophilic inflammation, which could be attenuated by rhBPIFA1 protein therapy.NIH/NHLBI [R01HL125128, U10HL109257, UL1TR00448, U10HL109168]This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk.

Blood pressure is a heritable trait influenced by several biological pathways and responsive to environmental stimuli. Over one billion people worldwide have hypertension (≥140 mm Hg systolic blood pressure or  ≥90 mm Hg diastolic blood pressure). Even small increments in blood pressure are associated with an increased risk of cardiovascular events. This genome-wide association study of systolic and diastolic blood pressure, which used a multi-stage design in 200,000 individuals of European descent, identified sixteen novel loci: six of these loci contain genes previously known or suspected to regulate blood pressure (GUCY1A3-GUCY1B3, NPR3-C5orf23, ADM, FURIN-FES, GOSR2, GNAS-EDN3); the other ten provide new clues to blood pressure physiology. A genetic risk score based on 29 genome-wide significant variants was associated with hypertension, left ventricular wall thickness, stroke and coronary artery disease, but not kidney disease or kidney function. We also observed associations with blood pressure in East Asian, South Asian and African ancestry individuals. Our findings provide new insights into the genetics and biology of blood pressure, and suggest potential novel therapeutic pathways for cardiovascular disease prevention

Association of genetic variation with systolic and diastolic blood pressure among African Americans: the Candidate Gene Association Resource study

The prevalence of hypertension in African Americans (AAs) is higher than in other US groups; yet, few have performed genome-wide association studies (GWASs) in AA. Among people of European descent, GWASs have identified genetic variants at 13 loci that are associated with blood pressure. It is unknown if these variants confer susceptibility in people of African ancestry. Here, we examined genome-wide and candidate gene associations with systolic blood pressure (SBP) and diastolic blood pressure (DBP) using the Candidate Gene Association Resource (CARe) consortium consisting of 8591 AAs. Genotypes included genome-wide single-nucleotide polymorphism (SNP) data utilizing the Affymetrix 6.0 array with imputation to 2.5 million HapMap SNPs and candidate gene SNP data utilizing a 50K cardiovascular gene-centric array (ITMAT-Broad-CARe [IBC] array). For Affymetrix data, the strongest signal for DBP was rs10474346 (P= 3.6 × 10−8) located near GPR98 and ARRDC3. For SBP, the strongest signal was rs2258119 in C21orf91 (P= 4.7 × 10−8). The top IBC association for SBP was rs2012318 (P= 6.4 × 10−6) near SLC25A42 and for DBP was rs2523586 (P= 1.3 × 10−6) near HLA-B. None of the top variants replicated in additional AA (n = 11 882) or European-American (n = 69 899) cohorts. We replicated previously reported European-American blood pressure SNPs in our AA samples (SH2B3, P= 0.009; TBX3-TBX5, P= 0.03; and CSK-ULK3, P= 0.0004). These genetic loci represent the best evidence of genetic influences on SBP and DBP in AAs to date. More broadly, this work supports that notion that blood pressure among AAs is a trait with genetic underpinnings but also with significant complexit