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    1. 7.7. Neurologia
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      1. Neurocirurgia
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      1. Cirurgia vascular
    1. 7.15. Urologia
    1. 7.16. Odontologia/cirurgia bucomaxilofacial
Modelos de dados selecionados

Deve ter sessão iniciada para selecionar vários modelos de dados e para os transferir ou analisar.

5 Resultados da pesquisa.
Relevância Avaliação Novos primeiro Antigos primeiro

dbGaP phs001347 Prematurity, Respiratory Outcomes, Immune System, and Microbiome Study (PRISM) - Eligibility

- 11/11/2024 - 5 Formulários, 2 Grupos de itens, 20 Elementos de dados, 1 Idioma
Grupos de itens: IG.0, IG.5
Principal Investigator: Gloria Pryhuber, University of Rochester Rochester, Rochester, NY, USA MeSH: Infant, Premature,Infant, Newborn,Premature Birth,Term Birth,Microbiota,Gastrointestinal Microbiome,T-Lymphocytes,Bronchopulmonary Dysplasia,Respiratory Tract Diseases https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001347 *Public health importance*: Babies born preterm, approximately 1 out of every 9 live births in the United States, have significant respiratory morbidity over the first two years of life, exacerbated by respiratory viral infections. Many (50%) return to pediatricians, emergency rooms and pulmonologists with symptoms of respiratory dysfunction (SRD): intermittent or chronic wheezing, poor growth and an excess of upper and lower respiratory tract infections (LRTI). SRD correlate inversely with gestational age and weight at birth and is more common in those with chronic lung disease of prematurity, yet its incidence and severity varies widely among both the prematurely born and those born at term. There is evidence from clinical studies and animal models that risks of LRTI and recurrent wheezing is influenced by gut and respiratory flora and by T cell responses to infection. Information gained from this study will be used to identify characteristics, risk factors and potential mechanisms for early and persistent lung disease in children born at term and born preterm. This Clinical Research Study will investigate the relationships between sequential respiratory viral infections, patterns of intestinal and respiratory bacterial colonization, and adaptive cellular immune phenotypes which are associated with increased susceptibility to respiratory infections and long term respiratory morbidity in preterm and full term infants. We hypothesize that the timing and acquisition of specific viral infections and bacterial species are directly related to respiratory morbidity in the first year of life as defined by SRD and by measures of pulmonary function. We hypothesize that cellular and molecular immuno-maturity are altered due to factors presented by premature birth in such a way as to promote chronic inflammatory and cytotoxic damage to the lung, with subsequent enhanced, damaging responses to infectious agents and environmental irritants. Our preliminary studies demonstrate both feasibility and expertise in mutiparameter immunophenotyping of small volume peripheral blood samples obtained from premature infants including gene expression arrays of flow cytometry sorted cells. We will use new technologies for known viral identification, as well as high-throughput metagenome sequencing of RNA and DNA virus like particles (VLP) to be used for viral discovery in infant respiratory sample and use of high-throughput pyrosequencing (454T) of bacterial 16S rRNA to determine shifts in bacterial community structure, occurring in pre-term (PT) as compared to full term (FT) infants, over the first year of life. Finally, we present statistical approaches to stratify disease risk predictors using multivariate logistic regression modeling approaches. We propose to evaluate T cell phenotypic and functional profiles relative to viral and predominant bacterial exposures according to highly complementary, but independent, Specific Objectives. *Objective 1*: To determine if viral respiratory infections and patterns of respiratory and gut bacterial community structure (microbiome) in prematurely born babies predict the rate and degree of immunologic maturation, and pulmonary dysfunction, measured from birth to 36 weeks corrected gestational age (CGA). *Objective 2*: To determine the relationship between respiratory viral infections and disease severity up to one year CGA, and the lymphocyte (Lc) phenotypes documented at term gestation (birth for term infants and 36 wks/NICU discharge in preterm infants) and at one year CGA. Three secondary outcomes of this objective will be to a) relate the quantity, type and severity of viral infections with pulmonary function at one and three years of life, b) relate the viral community structure to severity of viral infections and c) to seek evidence of modulation of viral susceptibility by bacterial respiratory and gut community structure (microbiome). The relationship of colonization with known and non-identified bacterial species in both the respiratory tract and the gut will be evaluated. Flow cytometry data corresponding to this study can be found within Immport study SDY1302. Positive and negative controls for microbiome samples are uploaded under SRA bioproject PRJNA474485. Microbiome samples corresponding to PRISM2 are distinguished from PRISM1 via "_PRISM2" appended to the sample name. Within the positive and negative controls, PRISM1 controls are uploaded as bam files and PRISM2 controls are uploaded as paired fastq. Samples ending in -08 correspond to TLDA qPCR results for a given sample. There is a column for each pathogen tested and a column to indicate where that pathogen was bacteria or virus.

pht006796.v3.p2

1 Grupo de itens 32 Elementos de dados

pht006794.v3.p2

1 Grupo de itens 7 Elementos de dados

pht006795.v3.p2

1 Grupo de itens 2 Elementos de dados

pht006797.v3.p2

1 Grupo de itens 94 Elementos de dados

Personal and Family History of Respiratory Symptoms/Diseases - Child Protocol PhenX Toolkit

- 26/04/2016 - 1 Formulário, 1 Grupo de itens, 41 Elementos de dados, 1 Idioma
Grupo de itens: PhenX - respiratory - personal - family hx of respiratory symptoms - diseases - child protocol
Age-specific questions are asked in this protocol to two different age ranges of children. For children ages 13 and 14, a set of questions is asked directly to the child. For children 6 or 7 years old, a set of questions is asked of the parents. ODM derived from: https://cde.nlm.nih.gov Primary source: https://www.phenxtoolkit.org/ Recent publication: Hendershot, T., Pan, H., Haines, J., Harlan, W.R., Marazita, M.L., McCarty, C.A., Ramos, E.M., and Hamilton, C.M. (2015) Using the PhenX toolkit to add standard measures to a study. Curr. Protoc. Hum. Genet. 86:1.21.1-1.21.17. doi: 10.1002/0471142905.hg0121s86 Permission to publish granted by Carol M. Hamilton.

Quality of Life as Affected by Respiratory Disease Protocol PhenX Toolkit

- 29/04/2016 - 1 Formulário, 1 Grupo de itens, 47 Elementos de dados, 1 Idioma
Grupo de itens: PhenX - respiratory - quality of life protocol
Self-administered questionnaire contains 50 items and 76 weighted responses divided into three components: Symptoms (frequency and severity); Activity (activities that cause or are limited by breathlessness); and Impacts (social unctioning, psychological disturbances resulting from airways disease). The protocol is designed to measure health impairment in patients with asthma and chronic obstructive pulmonary disease (COPD). It is also valid for use in bronchiectasis and has been used successfully in patients with kyphoscoliosis and sarcoidosis. ODM derived from: https://cde.nlm.nih.gov Primary source: https://www.phenxtoolkit.org/ Recent publication: Hendershot, T., Pan, H., Haines, J., Harlan, W.R., Marazita, M.L., McCarty, C.A., Ramos, E.M., and Hamilton, C.M. (2015) Using the PhenX toolkit to add standard measures to a study. Curr. Protoc. Hum. Genet. 86:1.21.1-1.21.17. doi: 10.1002/0471142905.hg0121s86 Permission to publish granted by Carol M. Hamilton.

dbGaP phs001073 Epigenetic Analysis of Malnutrition - Eligibility

- 23/06/2023 - 6 Formulários, 1 Grupo de itens, 15 Elementos de dados, 1 Idioma
Grupo de itens: IG.elig
Principal Investigator: MeSH: Stunting,Growth Disorders,Malnutrition,Epigenomics,Virus Diseases,Parasitic Diseases,Digestive System Diseases,Respiratory Tract Diseases,Nervous System Diseases,Nutritional and Metabolic Diseases,Immune System Diseases,Disorders of Environmental Origin https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001073 The PROVIDE study (Dhaka, Bangladesh) is a randomized clinical trial platform which evaluated the efficacy of delayed-dose oral rotavirus vaccine as well as the benefit of an injectable polio vaccine replacing one dose of oral polio vaccine. This rigorous infrastructure supported the additional examination of hypotheses of vaccine underperformance. Primary and secondary efficacy and immunogenicity measures for rotavirus and polio vaccines were measured, as well as the impact of maternal and childhood malnutrition, environmental enteropathy, and additional exploratory variables. This study has been conducted to test the role of epigenetics in malnutrition, specifically the genome-wide role of histone modifications, which are known to provide a precise signature of metabolic state and immune system function.

pht005954.v2.p1

1 Grupo de itens 2 Elementos de dados

pht005955.v2.p1

1 Grupo de itens 23 Elementos de dados

pht005956.v2.p1

1 Grupo de itens 7 Elementos de dados

pht005952.v2.p1

1 Grupo de itens 5 Elementos de dados

pht005953.v2.p1

1 Grupo de itens 5 Elementos de dados

dbGaP phs001297 PROP Functional and Lymphocytic Markers of Respiratory Morbidity in Hyperoxic Preemies - Dataset pht006199

- 26/06/2023 - 4 Formulários, 1 Grupo de itens, 4 Elementos de dados, 1 Idioma
Grupo de itens: pht006199
dbGaP Study Accession: phs001297.v1.p1 NCT01607216 Approximately 550,000 babies born prematurely each year in the United States suffer from birth at a time in development when the respiratory tract and immune system would normally be protected and maintained in a naïve state. This project is a component of the NIH Prematurity and Respiratory Outcomes Program (PROP) whose goals are the identification of disease mechanisms and biomarkers to stratify premature infants, at the time of discharge, for their risk of subsequent pulmonary morbidity. This Clinical Research Center (CRC) project will investigate prematurity-dependent alterations in cellular innate and adaptive immune systems resulting in increased susceptibility to respiratory infections and environmental irritants, and leading to respiratory morbidity in the first year of life. Prior studies have established developmental (maturity) and disease-related changes in circulating and pulmonary lymphocyte populations, but a comprehensive assessment of their relationship to disease risk/outcome has not been undertaken. We hypothesize that cellular and molecular immuno-maturity is altered due to intrinsic and extrinsic factors presented by premature birth in such a way as to reduce resistance to viral infections and to promote cytotoxic damage to the lung. We will evaluate immunologic maturity by comprehensively phenotyping lymphocyte populations in peripheral blood sampled at premature delivery, at the time of discharge from the hospital and at twelve months corrected age. The lymphocytic phenotype will be analyzed particularly in the context of gestational age and maternal-fetal stressors capable of modulating oxidative stress (oxygen exposure, infection and environmental tobacco smoke exposure). Additionally, we will assess changes in the molecular phenotype of isolated CD8 lymphocytes, a cell type preferentially recruited to the lungs of premature infants and capable of contributing to disease pathogenesis, by genome-wide expression profiling, in order to uncover novel disease pathways and define a gene expression signature associated with disease risk. We propose to build a statistical model, using cellular and molecular phenotypes and additional clinical variables, for stratifying risk of lung morbidity within the first year of life. Finally, we will assess the development of the gut microbiome in the preterm subjects to correlate with the observation of development of the adaptive immune system. Study Design: Prospective Longitudinal Cohort Study Type: Observational Longitudinal Prospective Cohort Total number of consented subjects: 277 Acknowledgement Statement: Please cite/reference the use of dbGaP data by including the dbGaP accession phs001297.v1.p1. Additionally, use the following statement to acknowledge the submitter(s) of this study: The datasets used for the analyses described in this manuscript were obtained from dbGaP ( https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001297.v1.p1 ) through dbGaP study accession numbers phs001297.v1.p1 . The data for the study Functional and Lymphocytic Markers of Respiratory Morbidity in Hyperoxic Preemies were provided by Drs. Gloria Pryhuber, Tom Mariani, Steven Gill, Rita Ryan, and Anne Marie Reynolds, University of Rochester and University at Buffalo Center for the Prematurity and Respiratory Outcomes Program (PROP). This study was supported by the U.S. National Institutes of Health (NIH), National Heart, Lung, and Blood Institute (NHLBI) grants U01 HL101813 and U01 HL101794, NHLBI and National Institute of Child Health and Human Development (NICHD) supplement grant R01 HL101794-01S1, National Institute of Allergy and Infectious Diseases (NIAID) contract HHSN272201200005C, and National Center for Advancing Translational Sciences (NCATS) grant UL1 TR000042. Dr. Pryhuber and her collaborators request that publications resulting from these data cite their original publications: Misra RS, Bhattacharya S, Huyck HL, Wang J-C E, Slaunwhite CG, Slaunwhite SL, Wightman TR, Secor- Soch S, Misra SK, Bushnell TP, Reynolds A-M, Ryan RM, Quataert SA, Pryhuber GS, Mariani TJ. Flow-Based Sorting of Neonatal Lymphocyte Populations for Transcriptomics Analysis. J Immunol Methods 2016; 437: 13-20. PMID: 27438473. PMCID in process. (And original microbiome publication to follow, after submission).

Dataset pht006201

1 Grupo de itens 10 Elementos de dados

Dataset pht006202

1 Grupo de itens 27 Elementos de dados

Dataset pht006200

1 Grupo de itens 5 Elementos de dados

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