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Search Results: 1 - 10 of 1678 matches for " Jill Gould "
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Qualitative studies of obesity: A review of methodology  [PDF]
Ian Brown, Jill Gould
Health (Health) , 2013, DOI: 10.4236/health.2013.58A3010
Abstract:

BACKGROUND: There is a developing interest in qualitative research to understand the perspectives and experiences of people living with obesity. However, obesity is a stigmatised condition associated with negative stereotypes. Social contexts emphasizing large body size as a problem, including research interviews, may amplify obesity stigma. This study reviews the methodology employed by qualitative studies in which study participants were obese and data collection involved face-to-face interviews. METHODS: Database searches identified qualitative studies meeting inclusion criteria from 1995 to 2012. Following screening and appraisal data were systematically extracted and analyzed from 31 studies. RESULTS: The studies included 1206 participants with a mean age of 44 years and mean BMI of37 kg/m2. Women (78.8%) outnumbered men (21.2%) by four to one. Socio-economic background was not consistently reported. The studies employed similar, typically pragmatic, qualitative methodologies, providing rich textual data on the experience of obesity derived from face-to-face interviews. The majority considered quality issues in data collection, analyses and generalizability of findings. However, the studies were weak as regards researcher reflexivity in relation to interviewer characteristics and obesity stigma. CONCLUSIONS: The impact of obesity stigma has not been attended to in the qualitative research. Clear information about study

Chemopreventive effects of celecoxib are limited to hormonally responsive mammary carcinomas in the neu-induced retroviral rat model
Stephan Woditschka, Jill D Haag, Bob Mau, Ronald A Lubet, Michael N Gould
Breast Cancer Research , 2008, DOI: 10.1186/bcr1864
Abstract: The chemopreventive effects of celecoxib were evaluated in the neu-induced retroviral rat mammary carcinogenesis model, to assess the efficacy of celecoxib on hormonally responsive and hormonally nonresponsive mammary carcinomas.Dietary celecoxib at 1,200 mg/kg diet was highly efficacious in the prevention of hormonally responsive mammary carcinomas in intact rats, decreasing tumor multiplicity by 56% (P < 0.0001) and by 74% (P = 0.0002) in two independent experiments. No significant effect was found, however, on hormonally nonresponsive mammary carcinomas of ovariectomized rats. Treatment with a combination diet, consisting of tamoxifen at 2 mg/kg diet and celecoxib at 1,200 mg/kg diet, reduced tumor multiplicity by 72% (P = 0.0002) in intact rats. This reduction was not statistically different from that observed with celecoxib alone. Furthermore, long-term treatment with celecoxib was not associated with reductions in tumor volume in either intact rats or ovariectomized rats. In contrast, tamoxifen treatment and the combination regimen caused significant reductions in tumor volumes in intact rats (P = 0.01 and P = 0.004, respectively). Consistent with these data, decreases in proliferation and increases in apoptosis were detected in tamoxifen-treated and combination diet-treated tumors. No such modulations were observed in celecoxib-treated tumors.The chemopreventive effects of celecoxib appear to be limited to modulations in multiplicity of hormonally responsive mammary carcinomas. The fact that no synergistic or additive effects were observed in combination diet-treated rats raises the question of whether celecoxib is suitable for the prevention of hormonally nonresponsive breast cancer or for use in combination therapy with selective estrogen response modulators or aromatase inhibitors.Although significant advances have been made in the field of breast cancer prevention, the mortality and morbidity rates for this disease remain high. This may in part be due to
The non-protein coding breast cancer susceptibility locus Mcs5a acts in a non-mammary cell-autonomous fashion through the immune system and modulates T-cell homeostasis and functions
Bart MG Smits, Deepak Sharma, David J Samuelson, Stephan Woditschka, Bob Mau, Jill D Haag, Michael N Gould
Breast Cancer Research , 2011, DOI: 10.1186/bcr2933
Abstract: We performed mammary carcinoma multiplicity studies with three mammary carcinoma-inducing treatments, namely 7,12-dimethylbenz(a)anthracene (DMBA) and N-nitroso-N-methylurea (NMU) carcinogenesis, and mammary ductal infusion of retrovirus expressing the activated HER2/neu oncogene. We used mammary gland and bone marrow transplantation assays to assess the target tissue of Mcs5a activity. We used immunophenotyping assays on well-defined congenic rat lines carrying susceptible and resistant Mcs5a alleles to identify changes in T-cell homeostasis and function associated with resistance.We show that Mcs5a acts beyond the initial step of mammary epithelial cell transformation, during early cancer progression. We show that Mcs5a controls susceptibility in a non-mammary cell-autonomous manner through the immune system. The resistant Mcs5a allele was found to be associated with an overabundance of gd T-cell receptor (TCR)+ T-cells as well as a CD62L (L-selectin)-high population of all T-cell classes. In contrast to in mammary carcinoma, gdTCR+ T-cells are the predominant T-cell type in the mammary gland and were found to be overabundant in the mammary epithelium of Mcs5a resistant congenic rats. Most of them simultaneously expressed the CD4, CD8, and CD161α markers. In cultured T-cells of Mcs5a resistant congenic rats we found increased mitogen-induced proliferation and production of Th1 cytokines IFNg, IL-2, and Tumor Necrosis Factor (TNF), but not Th2 cytokines IL-4 and IL-6, or Th17 cytokine IL-17 when compared with susceptible control rats.These data support a hypothesis that Mcs5a displays a non-mammary cell-autonomous mechanism of action to modulate breast cancer risk through the immune system. The resistant Mcs5a allele is associated with alterations in T-cell homeostasis and functions, and overabundance of γδTCR+ T-cells in carcinogen-exposed mammary epithelium.The genetic component of risk for most common forms of breast cancer defines it as a complex trait consisti
Freund's vaccine adjuvant promotes Her2/Neu breast cancer
Michelle S Cotroneo, Jill D Haag, Nicholas R Stapel, Jordy L Waller, Stephan Woditschka, Michael N Gould
BMC Cancer , 2009, DOI: 10.1186/1471-2407-9-19
Abstract: The effects of FA on hyperplastic mammary lesions and mammary carcinomas were determined in a neu-induced rat model. The inflammatory response to FA treatment was gauged by measuring acute phase serum haptoglobin. In addition, changes in cell proliferation and apoptosis following FA treatment were assessed.Rats receiving FA developed twice the number of mammary carcinomas as controls. Systemic inflammation following FA treatment is chronic, as shown by a doubling of the levels of the serum biomarker, haptoglobin, 15 days following initial treatment. We also show that this systemic inflammation is associated with the increased growth of hyperplastic mammary lesions. This increased growth results from a higher rate of cellular proliferation in the absence of changes in apoptosis.Our data suggests that systemic inflammation induced by Freund's adjuvant (FA) promotes mammary carcinogenesis. It will be important to determine whether adjuvants currently used in human vaccines also promote breast cancer.The etiology of breast cancer involves the interaction of inherited risk with environmental exposure. Approximately 30% of breast cancer risk is inherited [1], the majority of which is controlled by modifier genetic elements individually having low genetic penetrance, but high population frequencies [2]. Our knowledge of environmental factors that modulate breast cancer risk is quite incomplete. The best documented association is for ionizing radiation, which carries the highest risk for breast cancer when exposure occurs prior to adulthood [3]. Other known promoters of breast cancer include exogenously administered hormonal replacement therapies [4].Chronic inflammation arising from a variety of environmental and infectious sources is associated with promotion of many cancer types [5]. Evidence for chronic inflammation in breast cancer etiology is supported by experimental [6] and epidemiological studies suggesting that anti-inflammatory drugs can help prevent breast cance
Characterizing Mutational Heterogeneity in a Glioblastoma Patient with Double Recurrence
Gabrielle C. Nickel, Jill Barnholtz-Sloan, Meetha P. Gould, Sarah McMahon, Andrea Cohen, Mark D. Adams, Kishore Guda, Mark Cohen, Andrew E. Sloan, Thomas LaFramboise
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035262
Abstract: Human cancers are driven by the acquisition of somatic mutations. Separating the driving mutations from those that are random consequences of general genomic instability remains a challenge. New sequencing technology makes it possible to detect mutations that are present in only a minority of cells in a heterogeneous tumor population. We sought to leverage the power of ultra-deep sequencing to study various levels of tumor heterogeneity in the serial recurrences of a single glioblastoma multiforme patient. Our goal was to gain insight into the temporal succession of DNA base-level lesions by querying intra- and inter-tumoral cell populations in the same patient over time. We performed targeted “next-generation" sequencing on seven samples from the same patient: two foci within the primary tumor, two foci within an initial recurrence, two foci within a second recurrence, and normal blood. Our study reveals multiple levels of mutational heterogeneity. We found variable frequencies of specific EGFR, PIK3CA, PTEN, and TP53 base substitutions within individual tumor regions and across distinct regions within the same tumor. In addition, specific mutations emerge and disappear along the temporal spectrum from tumor at the time of diagnosis to second recurrence, demonstrating evolution during tumor progression. Our results shed light on the spatial and temporal complexity of brain tumors. As sequencing costs continue to decline and deep sequencing technology eventually moves into the clinic, this approach may provide guidance for treatment choices as we embark on the path to personalized cancer medicine.
Quantification of Epithelial Cell Differentiation in Mammary Glands and Carcinomas from DMBA- and MNU-Exposed Rats
Deepak Sharma, Bart M. G. Smits, Mark R. Eichelberg, Amanda L. Meilahn, Matthew J. Muelbl, Jill D. Haag, Michael N. Gould
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0026145
Abstract: Rat mammary carcinogenesis models have been used extensively to study breast cancer initiation, progression, prevention, and intervention. Nevertheless, quantitative molecular data on epithelial cell differentiation in mammary glands of untreated and carcinogen-exposed rats is limited. Here, we describe the characterization of rat mammary epithelial cells (RMECs) by multicolor flow cytometry using antibodies against cell surface proteins CD24, CD29, CD31, CD45, CD49f, CD61, Peanut Lectin, and Thy-1, intracellular proteins CK14, CK19, and FAK, along with phalloidin and Hoechst staining. We identified the luminal and basal/myoepithelial populations and actively dividing RMECs. In inbred rats susceptible to mammary carcinoma development, we quantified the changes in differentiation of the RMEC populations at 1, 2, and 4 weeks after exposure to mammary carcinogens DMBA and MNU. DMBA exposure did not alter the percentage of basal or luminal cells, but upregulated CD49f (Integrin α6) expression and increased cell cycle activity. MNU exposure resulted in a temporary disruption of the luminal/basal ratio and no CD49f upregulation. When comparing DMBA- or MNU-induced mammary carcinomas, the RMEC differentiation profiles are indistinguishable. The carcinomas compared with mammary glands from untreated rats, showed upregulation of CD29 (Integrin β1) and CD49f expression, increased FAK (focal adhesion kinase) activation especially in the CD29hi population, and decreased CD61 (Integrin β3) expression. This study provides quantitative insight into the protein expression phenotypes underlying RMEC differentiation. The results highlight distinct RMEC differentiation etiologies of DMBA and MNU exposure, while the resulting carcinomas have similar RMEC differentiation profiles. The methodology and data will enhance rat mammary carcinogenesis models in the study of the role of epithelial cell differentiation in breast cancer.
Team Players and Team Managers: Special Educators Working with Paraeducators to Support Inclusive Classrooms  [PDF]
Betty Y. Ashbaker, Jill Morgan
Creative Education (CE) , 2012, DOI: 10.4236/ce.2012.33051
Abstract: This paper summarizes recommendations from a selection of international research literature urging teachers to take the initiative in their own classrooms to invite paraeducators to participate fully as team players in collaborative work. In US classrooms paraeducators (teacher aides/teacher assistants) have long been making valuable contributions in providing education services to students with a variety of needs. The literature documents change in their roles. Legislation has influenced their required qualifications—although legislation still refers to them as paraprofessionals. While some researchers have cast doubt on whether paraeducators are truly effective in their assigned roles, others have warned that the education system is over-reliant on them. In response to this changing perspective, teacher educators must revise programs to better prepare teacher candidates to effectively team with paraeducators. Personnel developers and school administrators must provide inservice training for a generation of teachers who have received little if any training in this area.
When Children Draw vs When Children Don’t: Exploring the Effects of Observational Drawing in Science  [PDF]
Jill E. Fox, Joohi Lee
Creative Education (CE) , 2013, DOI: 10.4236/ce.2013.47A1002
Abstract:

The purpose of this study was to investigate how kindergarten children’s observational drawings impact their information retention. This research was conducted in an urban school in a large metropolitan area in the southwestern United States. Forty-two kindergarten children participated in this study; approximately 97% of them qualified for free and/or reduced lunch. For this study, children’s retention of factual information was compared using a paired t-test of when they drew and when they didn’t. Children scored higher on all 7 items—descriptions of observation, location, action, color, size, shape, and sound—when they drew than when they didn’t. Findings were statistically significant for descriptions of observation (t = 3.08, p = .00) and location (t = 2.36, p = .02).

Occupational Noise Levels in Two Fish Rearing Buildings at an Aquaculture Facility  [PDF]
Jill Voorhees, Michael E. Barnes
Occupational Diseases and Environmental Medicine (ODEM) , 2017, DOI: 10.4236/odem.2017.52006
Abstract: Occupational noise is commonly encountered during aquaculture. This study documented noise levels in two buildings at a production fish hatchery, a tank room with 32, 1.8-m diameter tanks, and a rearing pavilion with 32, 6.1-m diameter tanks. With water flowing to all of the tanks in the tank room, mean noise levels were 68.4 dB, and significantly increased to 73.0 dB during tank cleaning and 73.2 dB when intermittent automatic feeders were running. The highest tank room values of 77.1 dB were recorded directly next to individual tanks during cleaning. With water flowing to all of the tanks in the rearing pavilion, mean noise levels were 70.2 dB. A significant increase to 76.1 dB was observed when the pavilion tanks were being power washed, with the highest value of 83.2 dB recorded immediately adjacent to the power washer. Although none of the noise levels exceeded regulatory limits, the use of techniques to reduce occupational noise in aquaculture environments is recommended.
Resisting Postmodernity: Swedish social policy in the 1990s
Gould, Arthur
Social Work and Society , 2005,
Abstract: The purpose of this paper is to introduce ideas that have emerged during the course of writing a book on Swedish welfare in the 1990s. The book is the result of many years of writing about two subjects: Swedish drug policy and the Swedish welfare state. The one very specialised, the other, more general. I first became interested in Swedish drug policy on a research visit to rebro L n in 1986. A social worker showed me a copy of the county's drug policy programme and explained the significance of the 'restrictive line'. I have spent the years since that visit, trying to understand and explain the Swedish goal of a drug-free society (Gould 1988, 1994, 1996b). I only began to write about the welfare state in Sweden in the early 1990s, just as things were beginning to go wrong for the economy (Gould 1993a, 1993b, 1996a, 1999). For the last few years I have intended to write a book on the events covered by the period 1991-1998 - the years of a Bourgeois and a Social Democratic Government -which would bring the two halves of my work together. Material for this study has been accumulated over many years. A number of research visits have been made; large numbers of academics, politicians, civil servants, journalists, unemployed people, social workers and their clients have been interviewed; and extensive use has been made of academic, administrative and public libraries. Since September 1991 I have systematically collected articles from Dagens Nyheter about social services, social insurance, health care, employment, social issues and problems, the economy and politics. The journal Riksdag och Departement (Parliament and Ministry), which summarises a wide range of public documents, has been invaluable. Friends and informal contacts have also given me insights into the Swedish way of life. The new book is based upon all of these experiences. This paper will begin with a brief account of major global social and economic changes that have occurred in the last twenty years. This is intended to provide a background to the more recent changes that have occurred in Swedish society in the last decade. It will be suggested that the changes in Sweden, particularly in the field of welfare, have been less severe than elsewhere and that this is due to political, institutional and cultural resistance. The paper will conclude by arguing that Sweden, as an exemplar of an Apollonian modern society, has had much to fear from the Dionysian characteristics of postmodernity.
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