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Search Results: 1 - 10 of 301103 matches for " Deborah J Thompson "
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Assessing Performance of Bayesian State-Space Models Fit to Argos Satellite Telemetry Locations Processed with Kalman Filtering
Mónica A. Silva, Ian Jonsen, Deborah J. F. Russell, Rui Prieto, Dave Thompson, Mark F. Baumgartner
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0092277
Abstract: Argos recently implemented a new algorithm to calculate locations of satellite-tracked animals that uses a Kalman filter (KF). The KF algorithm is reported to increase the number and accuracy of estimated positions over the traditional Least Squares (LS) algorithm, with potential advantages to the application of state-space methods to model animal movement data. We tested the performance of two Bayesian state-space models (SSMs) fitted to satellite tracking data processed with KF algorithm. Tracks from 7 harbour seals (Phoca vitulina) tagged with ARGOS satellite transmitters equipped with Fastloc GPS loggers were used to calculate the error of locations estimated from SSMs fitted to KF and LS data, by comparing those to “true” GPS locations. Data on 6 fin whales (Balaenoptera physalus) were used to investigate consistency in movement parameters, location and behavioural states estimated by switching state-space models (SSSM) fitted to data derived from KF and LS methods. The model fit to KF locations improved the accuracy of seal trips by 27% over the LS model. 82% of locations predicted from the KF model and 73% of locations from the LS model were <5 km from the corresponding interpolated GPS position. Uncertainty in KF model estimates (5.6±5.6 km) was nearly half that of LS estimates (11.6±8.4 km). Accuracy of KF and LS modelled locations was sensitive to precision but not to observation frequency or temporal resolution of raw Argos data. On average, 88% of whale locations estimated by KF models fell within the 95% probability ellipse of paired locations from LS models. Precision of KF locations for whales was generally higher. Whales’ behavioural mode inferred by KF models matched the classification from LS models in 94% of the cases. State-space models fit to KF data can improve spatial accuracy of location estimates over LS models and produce equally reliable behavioural estimates.
Genome-Wide Association Study of Circulating Estradiol, Testosterone, and Sex Hormone-Binding Globulin in Postmenopausal Women
Jennifer Prescott, Deborah J. Thompson, Peter Kraft, Stephen J. Chanock, Tina Audley, Judith Brown, Jean Leyland, Elizabeth Folkerd, Deborah Doody, Susan E. Hankinson, David J. Hunter, Kevin B. Jacobs, Mitch Dowsett, David G. Cox, Douglas F. Easton, Immaculata De Vivo
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0037815
Abstract: Genome-wide association studies (GWAS) have successfully identified common genetic variants that contribute to breast cancer risk. Discovering additional variants has become difficult, as power to detect variants of weaker effect with present sample sizes is limited. An alternative approach is to look for variants associated with quantitative traits that in turn affect disease risk. As exposure to high circulating estradiol and testosterone, and low sex hormone-binding globulin (SHBG) levels is implicated in breast cancer etiology, we conducted GWAS analyses of plasma estradiol, testosterone, and SHBG to identify new susceptibility alleles. Cancer Genetic Markers of Susceptibility (CGEMS) data from the Nurses’ Health Study (NHS), and Sisters in Breast Cancer Screening data were used to carry out primary meta-analyses among ~1600 postmenopausal women who were not taking postmenopausal hormones at blood draw. We observed a genome-wide significant association between SHBG levels and rs727428 (joint β = -0.126; joint P = 2.09×10–16), downstream of the SHBG gene. No genome-wide significant associations were observed with estradiol or testosterone levels. Among variants that were suggestively associated with estradiol (P<10–5), several were located at the CYP19A1 gene locus. Overall results were similar in secondary meta-analyses that included ~900 NHS current postmenopausal hormone users. No variant associated with estradiol, testosterone, or SHBG at P<10–5 was associated with postmenopausal breast cancer risk among CGEMS participants. Our results suggest that the small magnitude of difference in hormone levels associated with common genetic variants is likely insufficient to detectably contribute to breast cancer risk.
Familial relative risks for breast cancer by pathological subtype: a population-based cohort study
Nasim Mavaddat, Paul D Pharoah, Fiona Blows, Kristy E Driver, Elena Provenzano, Deborah Thompson, Robert J MacInnis, Mitul Shah, The SEARCH Team, Douglas F Easton, Antonis C Antoniou
Breast Cancer Research , 2010, DOI: 10.1186/bcr2476
Abstract: We computed breast cancer FRR for subtypes of breast cancer by comparing breast cancer incidence in relatives of breast cancer cases from a population-based series with known estrogen receptor (ER), progesterone receptor (PR) or human epidermal growth factor receptor 2 (HER2) status with that expected from the general population. We estimated the contribution to the FRR of genetic variants associated with breast cancer susceptibility using subtype-specific genotypic relative risks and allele frequencies for each variant.At least one marker was measured for 4,590 breast cancer cases, who reported 9,014 affected and unaffected first-degree female relatives. There was no difference between the breast cancer FRR for relatives of patients with ER-negative (FRR = 1.78, 95% confidence intervals (CI): 1.44 to 2.11) and ER-positive disease (1.82, 95% CI: 1.67 to 1.98), P = 0.99. There was some suggestion that the breast cancer FRR for relatives of patients with ER-negative disease was higher than that for ER-positive disease for ages of the relative less than 50 years old (FRR = 2.96, 95% CI: 2.04 to 3.87; and 2.05, 95% CI: 1.70 to 2.40 respectively; P = 0.07), and that the breast cancer FRR for relatives of patients with ER-positive disease was higher than for ER-negative disease when the age of the relative was greater than 50 years (FRR = 1.76, 95% CI: 1.59 to 1.93; and 1.41, 95% CI: 1.08 to 1.74 respectively, P = 0.06). We estimated that mutations in BRCA1 and BRCA2 explain 32% of breast cancer FRR for relatives of patients with ER-negative and 9.4% of the breast cancer FRR for relatives of patients with ER-positive disease. Twelve recently identified common breast cancer susceptibility variants were estimated to explain 1.9% and 9.6% of the FRR to relatives of patients with ER-negative and ER-positive disease respectively.FRR for breast cancer was significantly increased for both ER-negative and ER-positive disease. Including receptor status in conjunction with genetic
Saving One Smile at a Time: Oral Health Promotion in Pediatric Primary Care Practice  [PDF]
Deborah J. Mattheus, Charl Mattheus
Open Journal of Nursing (OJN) , 2014, DOI: 10.4236/ojn.2014.46046

Oral health continues to be a major issue affecting children these days. Early childhood caries are considered to be the most common chronic childhood disease in the United States. Despite the availability of Medicaid, millions of children can still not access a dental provider to receive proper care. Getting children in for dental care early in their lives saves money. Children that do not receive proper oral health care during their childhood are at higher risk for more complex and restorative care as they age. Plans to reduce childhood caries include more creative interventions such as oral assessment, education and fluoride varnish application in primary care practices. Pediatric primary care providers are trusted by parents to care for their children and have an ideal opportunity to make a lasting impression and create behavioral changes in oral health during their frequent contacts with children and families. Integrating oral health promotion is a simple task with numerous benefits for children and families, as well as primary care doctors’ offices. With proper professional and governmental support oral health promotion programs in primary care practice can further increase in number which can ultimately improve oral health outcomes, save time and prevent costly dental repairs, as well as benefit the practice through proper reimbursement.

Factors and Home- and Community-Based Services (HCBS) that Predict Older Adults’ Residential Transitions  [PDF]
Ya-Mei Chen, Elaine Adams Thompson, Bobbie Berkowitz, Heather M. Young, Deborah Ward
Journal of Service Science and Management (JSSM) , 2011, DOI: 10.4236/jssm.2011.43043
Abstract: Objectives: This study identified specific personal factors and home- and community-based services (HCBS) that predict older adults’ residential transitions between community and institutional settings. Method: Logistic regression of interview data from 5294 participants in the Second Longitudinal Study of Aging identified predictors of three residential transition patterns and of frequency and duration of institutional services use. Results: Different HCBS services differently affected residential transitions. Informal support and paid personal care services (PCS) were the main factors affecting older adults’ ability to reside in community settings or to remain in community longer. Frequency of HCBS use and quantity of paid PCS used indicated direction of transitions: from communities into institutions or vice versa. Discussion: Integration of informal and formal care systems and attention to community-dwelling older adults’ HCBS use and paid PCS use, as a guide for possible future transitions, are tasks for community care professionals.
The rhesus macaque is three times as diverse but more closely equivalent in damaging coding variation as compared to the human
Qiaoping Yuan, Zhifeng Zhou, Stephen G Lindell, J Dee Higley, Betsy Ferguson, Robert C Thompson, Juan F Lopez, Stephen J Suomi, Basel Baghal, Maggie Baker, Deborah C Mash, Christina S Barr, David Goldman
BMC Genetics , 2012, DOI: 10.1186/1471-2156-13-52
Abstract: We sequenced the mRNA transcriptome and H3K4me3-marked DNA regions in hippocampus from 14 humans and 14 rhesus macaques. Using equivalent methodology and sampling spaces, we identified 462,802 macaque SNPs, most of which were novel and disproportionately located in the functionally important genomic regions we had targeted in the sequencing. At least one SNP was identified in each of 16,797 annotated macaque genes. Accuracy of macaque SNP identification was conservatively estimated to be >90%. Comparative analyses using SNPs equivalently identified in the two species revealed that rhesus macaque has approximately three times higher SNP density and average nucleotide diversity as compared to the human. Based on this level of diversity, the effective population size of the rhesus macaque is approximately 80,000 which contrasts with an effective population size of less than 10,000 for humans. Across five categories of genomic regions, intergenic regions had the highest SNP density and average nucleotide diversity and CDS (coding sequences) the lowest, in both humans and macaques. Although there are more coding SNPs (cSNPs) per individual in macaques than in humans, the ratio of dN/dS is significantly lower in the macaque. Furthermore, the number of damaging nonsynonymous cSNPs (have damaging effects on protein functions from PolyPhen-2 prediction) in the macaque is more closely equivalent to that of the human.This large panel of newly identified macaque SNPs enriched for functionally significant regions considerably expands our knowledge of genetic variation in the rhesus macaque. Comparative analysis reveals that this widespread, highly adaptable species is approximately three times as diverse as the human but more closely equivalent in damaging variation.
Analysis of the Lung Microbiome in the “Healthy” Smoker and in COPD
John R. Erb-Downward,Deborah L. Thompson,Meilan K. Han,Christine M. Freeman,Lisa McCloskey,Lindsay A. Schmidt,Vincent B. Young,Galen B. Toews,Jeffrey L. Curtis,Baskaran Sundaram,Fernando J. Martinez,Gary B. Huffnagle
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0016384
Abstract: Although culture-independent techniques have shown that the lungs are not sterile, little is known about the lung microbiome in chronic obstructive pulmonary disease (COPD). We used pyrosequencing of 16S amplicons to analyze the lung microbiome in two ways: first, using bronchoalveolar lavage (BAL) to sample the distal bronchi and air-spaces; and second, by examining multiple discrete tissue sites in the lungs of six subjects removed at the time of transplantation. We performed BAL on three never-smokers (NS) with normal spirometry, seven smokers with normal spirometry (“heathy smokers”, HS), and four subjects with COPD (CS). Bacterial 16 s sequences were found in all subjects, without significant quantitative differences between groups. Both taxonomy-based and taxonomy-independent approaches disclosed heterogeneity in the bacterial communities between HS subjects that was similar to that seen in healthy NS and two mild COPD patients. The moderate and severe COPD patients had very limited community diversity, which was also noted in 28% of the healthy subjects. Both approaches revealed extensive membership overlap between the bacterial communities of the three study groups. No genera were common within a group but unique across groups. Our data suggests the existence of a core pulmonary bacterial microbiome that includes Pseudomonas, Streptococcus, Prevotella, Fusobacterium, Haemophilus, Veillonella, and Porphyromonas. Most strikingly, there were significant micro-anatomic differences in bacterial communities within the same lung of subjects with advanced COPD. These studies are further demonstration of the pulmonary microbiome and highlight global and micro-anatomic changes in these bacterial communities in severe COPD patients.
Common variants in the ATM, BRCA1, BRCA2, CHEK2 and TP53 cancer susceptibility genes are unlikely to increase breast cancer risk
Caroline Baynes, Catherine S Healey, Karen A Pooley, Serena Scollen, Robert N Luben, Deborah J Thompson, Paul DP Pharoah, Douglas F Easton, Bruce AJ Ponder, Alison M Dunning, the SEARCH breast cancer study
Breast Cancer Research , 2007, DOI: 10.1186/bcr1669
Abstract: We have attempted a comprehensive, single nucleotide polymorphism (SNP)- and haplotype-tagging association study on each of these five genes in up to 4,474 breast cancer cases from the British, East Anglian SEARCH study and 4,560 controls from the EPIC-Norfolk study, using a two-stage study design. Nine tag SNPs were genotyped in ATM, together with five in BRCA1, sixteen in BRCA2, ten in CHEK2 and five in TP53, with the aim of tagging all other known, common variants. SNPs generating the common amino acid substitutions were specifically forced into the tagging set for each gene.No significant breast cancer associations were detected with any individual or combination of tag SNPs.It is unlikely that there are any other common variants in these genes conferring measurably increased risks of breast cancer in our study population.Four of the genes which lie in the DNA damage-recognition and repair pathway, ATM, BRCA1, BRCA2 and TP53, have mutations that are recognised to increase breast cancer susceptibility with moderate to high penetrance. Such mutations are very rare, and most probably of recent origin. A fifth gene, CHEK2, in the same pathway, has a deletion (1100delC) that reaches polymorphic frequencies (>0.01) in some European countries and doubles the risk of breast cancer in female carriers [1]. Together these mutations account for only a small proportion (2% to 5%) of all breast cancer incidences [2,3]. Breast cancer is, however, a common disease and genetic epidemiological data suggest that there is a low-penetrance genetic contribution to most cases [4,5]. It is likely that at least a part of breast cancer aetiology will fit the common disease-common variant hypothesis, which states that patients with a common, complex disease are likely to share some common, low-penetrance alleles that increase their susceptibility to that disease. This raises the question of whether such common, polymorphic susceptibility alleles exist within these five genes in addition t
Telomere Length Shows No Association with BRCA1 and BRCA2 Mutation Status
Emma Killick, Malgorzata Tymrakiewicz, Clara Cieza-Borrella, Paula Smith, Deborah J. Thompson, Karen A. Pooley, Doug F. Easton, Elizabeth Bancroft, Elizabeth Page, Daniel Leongamornlert, The IMPACT collaborators , Zsofia Kote-Jarai, Rosalind A. Eeles
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0086659
Abstract: This study aimed to determine whether telomere length (TL) is a marker of cancer risk or genetic status amongst two cohorts of BRCA1 and BRCA2 mutation carriers and controls. The first group was a prospective set of 665 male BRCA1/2 mutation carriers and controls (mean age 53 years), all healthy at time of enrolment and blood donation, 21 of whom have developed prostate cancer whilst on study. The second group consisted of 283 female BRCA1/2 mutation carriers and controls (mean age 48 years), half of whom had been diagnosed with breast cancer prior to enrolment. TL was quantified by qPCR from DNA extracted from peripheral blood lymphocytes. Weighted and unweighted Cox regressions and linear regression analyses were used to assess whether TL was associated with BRCA1/2 mutation status or cancer risk. We found no evidence for association between developing cancer or being a BRCA1 or BRCA2 mutation carrier and telomere length. It is the first study investigating TL in a cohort of genetically predisposed males and although TL and BRCA status was previously studied in females our results don't support the previous finding of association between hereditary breast cancer and shorter TL.
Preventative tele-health supported services for early stage chronic obstructive pulmonary disease: a protocol for a pragmatic randomized controlled trial pilot
Deborah A Fitzsimmons, Jill Thompson, Mark Hawley, Gail A Mountain
Trials , 2011, DOI: 10.1186/1745-6215-12-6
Abstract: Tele-health monitoring offers potential to reduce the rates of re-hospitalisation and emergency department visits and improve quality of life for people with COPD. However, the current evidence base to support technology adoption and implementation is limited and the resource implications for implementing tele-health in practice can be very high. This trial will employ tele-health monitoring in a preventative capacity for patients diagnosed with early stage COPD following discharge from hospital to determine whether it reduces their need for additional health service support or hospital admission and improves their quality of life.We describe a pilot study for a two arm, one site randomized controlled trial (RCT) to determine the effect of tele-health monitoring on self-management, quality of life and patient satisfaction. Sixty patients who have been discharged from one acute trust with a primary diagnosis of COPD and who have agreed to receive community clinical support following discharge from acute care will be randomly assigned to one of two groups: (a) Tele-health supported Community COPD Service; or (b) Usual Care. The tele-health supported service involves the patient receiving two home visits with a specialist COPD clinician (nurse or physiotherapist) then participating in daily tele-monitoring over an eight week period. Usual care consists of six home visits to the patient by specialist COPD clinicians again over eight successive weeks. Health status and quality of life data for all participants will be measured at baseline, on discharge from the service and at six months post discharge from the service.The tele-health service under study is a complex service delivered through a collaboration between local authority and health care partners. The implementation of this service demanded significant changes to established working patterns and has been a challenging process requiring considerable planning - a challenge that many providers are likely to face in
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