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3. Homeostatic IL-13 in healthy skin directs dendritic cell differentiation to promote TH2 and inhibit TH17 cell polarization

Author

Mayer, Johannes U., Hilligan, Kerry L., Chandler, Jodie S., Eccles, David A., Old, Samuel I., Domingues, Rita G., Yang, Jianping, Webb, Greta R., Munoz-Erazo, Luis, Hyde, Evelyn J., Wakelin, Kirsty A., Tang, Shiau-Choot, Chappell, Sally C., von Daake, Sventja, Brombacher, Frank, Mackay, Charles R., Sher, Alan, Tussiwand, Roxane, Connor, Lisa M., Gallego-Ortega, David, Jankovic, Dragana, Le Gros, Graham, Hepworth, Matthew R., Lamiable, Olivier, and Ronchese, Franca

Published
2021
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5. Author Correction: Homeostatic IL-13 in healthy skin directs dendritic cell differentiation to promote TH2 and inhibit TH17 cell polarization

Author

Mayer, Johannes U., Hilligan, Kerry L., Chandler, Jodie S., Eccles, David A., Old, Samuel I., Domingues, Rita G., Yang, Jianping, Webb, Greta R., Munoz-Erazo, Luis, Hyde, Evelyn J., Wakelin, Kirsty A., Tang, Shiau-Choot, Chappell, Sally C., von Daake, Sventja, Brombacher, Frank, Mackay, Charles R., Sher, Alan, Tussiwand, Roxane, Connor, Lisa M., Gallego-Ortega, David, Jankovic, Dragana, Le Gros, Graham, Hepworth, Matthew R., Lamiable, Olivier, and Ronchese, Franca

Published
2022
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6. CHICAGO HOPE

Author

Chappell, Sally A. Kitt

Published
2004

7. letters

Author

Dines, Nicholas T., Sachs, Naomi, Chappell, Sally, Osmundson, Theodore, Horsbrugh, Patrick, Green, William A., Hyler, W. Douglas, McKnight, Ray, Tokmakian, Harold, and Miller, E. Lynn

Published
2003

9. Variants in the fetal genome near FLT1 are associated with risk of preeclampsia

Author

McGinnis, Ralph, Steinthorsdottir, Valgerdur, Williams, Nicholas O, Thorleifsson, Gudmar, Shooter, Scott, Hjartardottir, Sigrun, Bumpstead, Suzannah, Stefansdottir, Lilja, Hildyard, Lucy, Sigurdsson, Jon K, Kemp, John P, Silva, Gabriela B, Thomsen, Liv Cecilie V, Jääskeläinen, Tiina, Kajantie, Eero, Chappell, Sally, Kalsheker, Noor, Moffett, Ashley, Hiby, Susan, Lee, Wai Kwong, Padmanabhan, Sandosh, Simpson, Nigel A B, Dolby, Vivien A, Staines-Urias, Eleonora, Engel, Stephanie M, Haugan, Anita, Trogstad, Lill, Svyatova, Gulnara, Zakhidova, Nodira, Najmutdinova, Dilbar, Dominiczak, Anna F, Gjessing, Håkon K, Casas, Juan P, Dudbridge, Frank, Walker, James J, Pipkin, Fiona Broughton, Thorsteinsdottir, Unnur, Geirsson, Reynir T, Lawlor, Debbie A, Iversen, Ann-Charlotte, Magnus, Per, Laivuori, Hannele, Stefansson, Kari, and Morgan, Linda

Published
2017
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13. Polygenic risk score in postmortem diagnosed sporadic early-onset Alzheimer's disease

Author

Passmore, Peter, Craig, David, Johnston, Janet, McGuinness, Bernadette, Todd, Stephen, Heun, Reinhard, Kölsch, Heike, Kehoe, Patrick G., Vardy, Emma R.L.C., Hooper, Nigel M., Pickering-Brown, Stuart, Snowden, Julie, Richardson, Anna, Jones, Matthew, Neary, David, Harris, Jennifer, Lowe, James, Smith, A. David, Wilcock, Gordon, Warden, Donald, Holmes, Clive, Chaudhury, Sultan, Patel, Tulsi, Barber, Imelda S., Guetta-Baranes, Tamar, Brookes, Keeley J., Chappell, Sally, Turton, James, Guerreiro, Rita, Bras, Jose, Hernandez, Dena, Singleton, Andrew, Hardy, John, Mann, David, and Morgan, Kevin

Published
2018
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14. LETTERS

Author

Brittenum, Judy Byrd, Ball, Jocelyn, Beatty, Russ, Chappell, Sally A. Kitt, McGown, Mary, Guenther, Deb, and Drum, R. Gus

Published
2006

15. Exome-wide analysis of rare coding variation identifies novel associations with COPD and airflow limitation in MOCS3, IFIT3 and SERPINA12

Author

Jackson, Victoria E, Ntalla, Ioanna, Sayers, Ian, Morris, Richard, Whincup, Peter, Casas, Juan-Pablo, Amuzu, Antoinette, Choi, Minkyoung, Dale, Caroline, Kumari, Meena, Engmann, Jorgen, Kalsheker, Noor, Chappell, Sally, Guetta-Baranes, Tamar, McKeever, Tricia M, Palmer, Colin N A, Tavendale, Roger, Holloway, John W, Sayer, Avan A, Dennison, Elaine M, Cooper, Cyrus, Bafadhel, Mona, Barker, Bethan, Brightling, Chris, Bolton, Charlotte E, John, Michelle E, Parker, Stuart G, Moffat, Miriam F, Wardlaw, Andrew J, Connolly, Martin J, Porteous, David J, Smith, Blair H, Padmanabhan, Sandosh, Hocking, Lynne, Stirrups, Kathleen E, Deloukas, Panos, Strachan, David P, Hall, Ian P, Tobin, Martin D, and Wain, Louise V

Published
2016
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16. Mutation analysis of sporadic early-onset Alzheimer's disease using the NeuroX array

Author

Passmore, Peter, Craig, David, Johnston, Janet, McGuinness, Bernadette, Todd, Stephen, Heun, Reinhard, Kölsch, Heike, Kehoe, Patrick G., Vardy, Emma R.L.C., Hooper, Nigel M., Pickering-Brown, Stuart, Snowden, Julie, Richardson, Anna, Jones, Matthew, Neary, David, Harris, Jennifer, Lowe, James, Smith, A. David, Wilcock, Gordon, Warden, Donald, Holmes, Clive, Barber, Imelda S., Braae, Anne, Clement, Naomi, Patel, Tulsi, Guetta-Baranes, Tamar, Brookes, Keeley, Medway, Christopher, Chappell, Sally, Guerreiro, Rita, Bras, Jose, Hernandez, Dena, Singleton, Andrew, Hardy, John, Mann, David M., and Morgan, Kevin

Published
2017
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18. Scavenger receptor class B type I genetic variants associated with disease severity in chronic hepatitis C virus infection.

Author

Arandhara, Victoria L., McClure, Charles Patrick, Tarr, Alexander W., Chappell, Sally, Morgan, Kevin, Baumert, Thomas F., Irving, William L., and Ball, Jonathan K.

Subjects
GENETIC variation, CHRONIC hepatitis C, SINGLE nucleotide polymorphisms, NUTRITION surveys, GENE expression, HEPATIC fibrosis, FIBROSIS
Abstract

Analysis of host genetic polymorphisms is an increasingly important tool for understanding and predicting pathogenesis and treatment response of viral diseases. The gene locus of scavenger receptor class B type I (SR‐BI), encoding a cell entry factor and receptor for hepatitis C virus (HCV), contains several genetic polymorphisms. We applied a probe extension assay to determine the frequency of six single nucleotide polymorphisms (SNPs) within the SR‐BI gene locus in 374 individuals with history of HCV infection. In addition, SR‐BI messenger RNA (mRNA) levels were analyzed in liver biopsy specimens of chronically infected HCV subjects. The rs5888 variant allele T was present at a higher frequency in subjects with advanced fibrosis (χ2, p = 0.016) and after adjusting for age, duration of infection and alcohol intake as confounding factors. Haplotype analysis of SNP frequencies showed that a haplotype consisting of rs61932577 variant allele C and rs5888 variant allele T was associated with an increased risk of advanced liver fibrosis (defined by an Ishak score 4−6) (adjusted odds ratio 2.81; 95% confidence interval 1.06−7.46. p = 0.038). Carriers of the rs5888 variant allele T displayed reduced SR‐BI mRNA expression in liver biopsy specimens. In conclusion the rs5888 polymorphism variant is associated with decreased SR‐BI expression and an increased risk of development of advanced fibrosis in chronic HCV infection. These findings provide further evidence for a role of SR‐BI in HCV pathogenesis and provides a genetic marker for prediction of those infected individuals at greater risk of developing severe disease. [ABSTRACT FROM AUTHOR]

Published
2023
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19. Screening exons 16 and 17 of the amyloid precursor protein gene in sporadic early-onset Alzheimer's disease

Author

Passmore, Peter, Craig, David, Johnston, Janet, McGuinness, Bernadette, Todd, Stephen, Heun, Reinhard, Kölsch, Heike, Kehoe, Patrick G., Vardy, Emma R.L.C., Hooper, Nigel M., Pickering-Brown, Stuart, Snowden, Julie, Richardson, Anna, Jones, Matt, Neary, David, Harris, Jenny, Medway, Christopher, Lowe, James, Smith, A. David, Wilcock, Gordon, Warden, Donald, Holmes, Clive, Barber, Imelda S., García-Cárdenas, Jennyfer M., Sakdapanichkul, Chidchanok, Deacon, Christopher, Zapata Erazo, Gabriela, Guerreiro, Rita, Bras, Jose, Hernandez, Dena, Singleton, Andrew, Guetta-Baranes, Tamar, Braae, Anne, Clement, Naomi, Patel, Tulsi, Brookes, Keeley, Chappell, Sally, Mann, David M., and Morgan, Kevin

Published
2016
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22. The skin environment controls local dendritic cell differentiation and function through innate IL-13

Author

Mayer, Johannes U, primary, Lamiable, Olivier, additional, Hilligan, Kerry L, additional, Chandler, Jodie S, additional, Old, Samuel I, additional, Eccles, David A, additional, Yang, Jianping, additional, Webb, Greta R, additional, Domingues, Rita G, additional, Munoz-Erazo, Luis, additional, Wakelin, Kirsty A, additional, Hyde, Evelyn J, additional, Tang, Shiau-Choot, additional, Chappell, Sally C, additional, Mackay, Charles R, additional, Brombacher, Frank, additional, Sher, Alan, additional, Tussiwand, Roxane, additional, Connor, Lisa M, additional, Jankovic, Dragana, additional, Hepworth, Matthew R, additional, Le Gros, Graham, additional, and Ronchese, Franca, additional

Published
2021
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33. The role of IREB2 and transforming growth factor beta-1 genetic variants in COPD: a replication case-control study

Author

Stolk Jan, MacNee William, Keatings Vera, Donnelly Seamas C, Millar Ann B, Morgan Kevin, Rabinovich Roberto, Roca Josep, Guetta-Baranes Tamar, Alsaegh Aiman, Lotya Juzer, Daly Leslie, Chappell Sally L, Hiemstra Pieter S, Miniati Massimo, Monti Simonetta, O'Connor Clare M, and Kalsheker Noor

Subjects
Internal medicine, RC31-1245, Genetics, QH426-470
Abstract

Abstract Background Genetic factors are known to contribute to COPD susceptibility and these factors are not fully understood. Conflicting results have been reported for many genetic studies of candidate genes based on their role in the disease. Genome-wide association studies in combination with expression profiling have identified a number of new candidates including IREB2. A meta-analysis has implicated transforming growth factor beta-1 (TGFbeta1) as a contributor to disease susceptibility. Methods We have examined previously reported associations in both genes in a collection of 1017 white COPD patients and 912 non-diseased smoking controls. Genotype information was obtained for seven SNPs in the IREB2 gene, and for four SNPs in the TGFbeta1 gene. Allele and genotype frequencies were compared between COPD cases and controls, and odds ratios were calculated. The analysis was adjusted for age, sex, smoking and centre, including interactions of age, sex and smoking with centre. Results Our data replicate the association of IREB2 SNPs in association with COPD for SNP rs2568494, rs2656069 and rs12593229 with respective adjusted p-values of 0.0018, 0.0039 and 0.0053. No significant associations were identified for TGFbeta1. Conclusions These studies have therefore confirmed that the IREB2 locus is a contributor to COPD susceptibility and suggests a new pathway in COPD pathogenesis invoking iron homeostasis.

Published
2011
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34. Association of MMP - 12 polymorphisms with severe and very severe COPD: A case control study of MMPs - 1, 9 and 12 in a European population

Author

Keatings Vera, Donnelly Seamas C, Millar Ann B, Rabinovich Roberto, Roca Josep, Guetta-Baranes Tamar, Morgan Kevin, Daly Leslie, Lotya Juzer, Johnson Simon R, Chappell Sally, Haq Imran, MacNee William, Stolk Jan, Hiemstra Pieter S, Miniati Massimo, Monti Simonetta, O'Connor Clare M, and Kalsheker Noor

Subjects
Internal medicine, RC31-1245, Genetics, QH426-470
Abstract

Abstract Background Genetic factors play a role in chronic obstructive pulmonary disease (COPD) but are poorly understood. A number of candidate genes have been proposed on the basis of the pathogenesis of COPD. These include the matrix metalloproteinase (MMP) genes which play a role in tissue remodelling and fit in with the protease - antiprotease imbalance theory for the cause of COPD. Previous genetic studies of MMPs in COPD have had inadequate coverage of the genes, and have reported conflicting associations of both single nucleotide polymorphisms (SNPs) and SNP haplotypes, plausibly due to under-powered studies. Methods To address these issues we genotyped 26 SNPs, providing comprehensive coverage of reported SNP variation, in MMPs- 1, 9 and 12 from 977 COPD patients and 876 non-diseased smokers of European descent and evaluated their association with disease singly and in haplotype combinations. We used logistic regression to adjust for age, gender, centre and smoking history. Results Haplotypes of two SNPs in MMP-12 (rs652438 and rs2276109), showed an association with severe/very severe disease, corresponding to GOLD Stages III and IV. Conclusions Those with the common A-A haplotype for these two SNPs were at greater risk of developing severe/very severe disease (p = 0.0039) while possession of the minor G variants at either SNP locus had a protective effect (adjusted odds ratio of 0.76; 95% CI 0.61 - 0.94). The A-A haplotype was also associated with significantly lower predicted FEV1 (42.62% versus 44.79%; p = 0.0129). This implicates haplotypes of MMP-12 as modifiers of disease severity.

Published
2010
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37. Screening exons 16 and 17 of the amyloid precursor protein gene in sporadic early-onset Alzheimer’s disease

Author

Barber, Imelda S., Sakdapanichkul, Chidchanok, Deacon, Christopher, Zapata Erazo, Gabriela, Guerreiro, Rita, Bras, Jose, Hernandez, Dena, Singleton, Andrew, Guetta-Baranes, Tamar, Braae, Anne, Clement, Naomi, Patel, Tulsi, Brookes, Keeley, Medway, Christopher, Chappell, Sally, and Mann, David M.

Subjects
Alzheimer's disease, early-onset, sporadic, screening, APP, rs367709245
Abstract

Early-onset Alzheimer’s disease (EOAD) can be familial (FAD) or sporadic (sEOAD); both have a disease onset ≤ 65 years of age. 451 sEOAD samples were screened for known causative mutations in exon 16 and 17 of the Amyloid Precursor Protein gene (APP). Four samples were shown to be heterozygous for one of three known causative mutations: p.A713T, p.V717I and p.V717G, this highlights the importance of screening EOAD patients for causative mutations. Additionally, we document an intronic 6 base pair (bp) deletion located 83 bp downstream of exon 17 (rs367709245, IVS17 83-88delAAGTAT), which has a nonsignificantly increased minor allele frequency in our sEOAD cohort (0.006) compared to LOAD (0.002) and controls (0.002). To assess the effect of the 6 bp deletion on splicing, COS-7 and BE(2)-C cells were transfected with a minigene vector encompassing exon 17. There was no change in splicing of exon 17 from constructs containing either wild type or deletion inserts. Sequencing of cDNA generated from cerebellum and temporal cortex of a patient harbouring the deletion found no evidence of transcripts with exon 17 removed.

Published
2016

38. Polygenic risk score in postmortem diagnosed sporadic early-onset Alzheimer's disease

Author

Chaudhury, Sultan, primary, Patel, Tulsi, additional, Barber, Imelda S., additional, Guetta-Baranes, Tamar, additional, Brookes, Keeley J., additional, Chappell, Sally, additional, Turton, James, additional, Guerreiro, Rita, additional, Bras, Jose, additional, Hernandez, Dena, additional, Singleton, Andrew, additional, Hardy, John, additional, Mann, David, additional, Morgan, Kevin, additional, Passmore, Peter, additional, Craig, David, additional, Johnston, Janet, additional, McGuinness, Bernadette, additional, Todd, Stephen, additional, Heun, Reinhard, additional, Kölsch, Heike, additional, Kehoe, Patrick G., additional, Vardy, Emma R.L.C., additional, Hooper, Nigel M., additional, Pickering-Brown, Stuart, additional, Snowden, Julie, additional, Richardson, Anna, additional, Jones, Matthew, additional, Neary, David, additional, Harris, Jennifer, additional, Lowe, James, additional, Smith, A. David, additional, Wilcock, Gordon, additional, Warden, Donald, additional, and Holmes, Clive, additional

Published
2018
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41. [P3-110]: CALCULATING POLYGENIC RISK FOR INDIVIDUALS WITH SPORADIC EARLY ONSET ALZHEIMER's DISEASE

Author

Chaudhury, Sultan Raja, primary, Patel, Tulsi, additional, Barber, Imelda, additional, Guetta-Baranes, Tamar, additional, Brookes, Keeley J., additional, Chappell, Sally, additional, Guerreiro, Rita, additional, Bras, Jose T., additional, Hernandez, Dena, additional, Singleton, Andrew, additional, Hardy, John, additional, Mann, David M.A., additional, and Morgan, Kevin, additional

Published
2017
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42. Mutation analysis of sporadic early-onset Alzheimer's disease using the NeuroX array

Author

Barber, Imelda S., primary, Braae, Anne, additional, Clement, Naomi, additional, Patel, Tulsi, additional, Guetta-Baranes, Tamar, additional, Brookes, Keeley, additional, Medway, Christopher, additional, Chappell, Sally, additional, Guerreiro, Rita, additional, Bras, Jose, additional, Hernandez, Dena, additional, Singleton, Andrew, additional, Hardy, John, additional, Mann, David M., additional, Morgan, Kevin, additional, Passmore, Peter, additional, Craig, David, additional, Johnston, Janet, additional, McGuinness, Bernadette, additional, Todd, Stephen, additional, Heun, Reinhard, additional, Kölsch, Heike, additional, Kehoe, Patrick G., additional, Vardy, Emma R.L.C., additional, Hooper, Nigel M., additional, Pickering-Brown, Stuart, additional, Snowden, Julie, additional, Richardson, Anna, additional, Jones, Matthew, additional, Neary, David, additional, Harris, Jennifer, additional, Lowe, James, additional, Smith, A. David, additional, Wilcock, Gordon, additional, Warden, Donald, additional, and Holmes, Clive, additional

Published
2017
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44. P3-091: Investigating SARM1 Variants in Alzheimer’s Disease Cohorts

Author

Patel, Tulsi, primary, Clement, Naomi S., additional, Barber, Imelda, additional, Braae, Anne, additional, Brookes, Keeley J., additional, Guetta-Baranes, Tamar, additional, Chappell, Sally, additional, Guerreiro, Rita, additional, Bras, Jose T., additional, Singleton, Andrew, additional, Hardy, John, additional, and Morgan, Kevin, additional

Published
2016
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45. P3-092: Mapping Regulatory Variants in the Alzheimer's Disease Candidate Gene ABCA7

Author

Clement, Naomi S., primary, Medway, Christopher, additional, Ertekin-Taner, Nilufer, additional, Carrasquillo, Minerva M., additional, Younkin, Steven G., additional, Guetta-Baranes, Tamar, additional, Burgess, Jeremy D., additional, Allen, Mariet, additional, Tam, Tammie, additional, Dickson, Dennis W., additional, Petersen, Ronald C., additional, Graff-Radford, Neill R., additional, Chappell, Sally, additional, and Morgan, Kevin, additional

Published
2016
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46. Copy number variation of the beta-defensin genes in Europeans: no supporting evidence for association with lung function, chronic obstructive pulmonary disease or asthma

Author

Ahuja, Sunil K., Wain, Louise V., Odenthal-Hesse, Linda, Abujaber, Razan, Sayers, Ian, Beardsmore, Caroline, Gaillard, Erol A., Chappell, Sally, Dogaru, Cristian M., McKeever, Tricia M., Guetta-Baranes, Tamar, Kalsheker, Noor, Kuehni, Claudia E., Hall, Ian P., Tobin, Martin D., and Hollox, Edward J.

Subjects
Male, beta-Defensins, Pulmonology, Chronic Obstructive Pulmonary Diseases, Epidemiology, Genome-wide association study, Pulmonary Disease, Chronic Obstructive, Missing heritability problem, Gene Duplication, Copy-number variation, Child, Aged, 80 and over, Genetics, education.field_of_study, COPD, Multidisciplinary, Middle Aged, 3. Good health, Genetic Epidemiology, Medicine, Female, Research Article, Adult, Adolescent, DNA Copy Number Variations, Science, Population, 610 Medicine & health, Single-nucleotide polymorphism, White People, Molecular Genetics, 360 Social problems & social services, medicine, Humans, Genetic Predisposition to Disease, education, Biology, Genetic Association Studies, Aged, Asthma, Population Biology, business.industry, Case-control study, Human Genetics, medicine.disease, respiratory tract diseases, Case-Control Studies, Genetics of Disease, Immunology, Genetic Polymorphism, business, Population Genetics
Abstract

Lung function measures are heritable, predict mortality and are relevant in diagnosis of chronic obstructive pulmonary disease (COPD). COPD and asthma are diseases of the airways with major public health impacts and each have a heritable component. Genome-wide association studies of SNPs have revealed novel genetic associations with both diseases but only account for a small proportion of the heritability. Complex copy number variation may account for some of the missing heritability. A well-characterised genomic region of complex copy number variation contains beta-defensin genes (DEFB103, DEFB104 and DEFB4), which have a role in the innate immune response. Previous studies have implicated these and related genes as being associated with asthma or COPD. We hypothesised that copy number variation of these genes may play a role in lung function in the general population and in COPD and asthma risk. We undertook copy number typing of this locus in 1149 adult and 689 children using a paralogue ratio test and investigated association with COPD, asthma and lung function. Replication of findings was assessed in a larger independent sample of COPD cases and smoking controls. We found evidence for an association of beta-defensin copy number with COPD in the adult cohort (OR = 1.4, 95%CI:1.02–1.92, P = 0.039) but this finding, and findings from a previous study, were not replicated in a larger follow-up sample(OR = 0.89, 95%CI:0.72–1.07, P = 0.217). No robust evidence of association with asthma in children was observed. We found no evidence for association between beta-defensin copy number and lung function in the general populations. Our findings suggest that previous reports of association of beta-defensin copy number with COPD should be viewed with caution. Suboptimal measurement of copy number can lead to spurious associations. Further beta-defensin copy number measurement in larger sample sizes of COPD cases and children with asthma are needed.

Published
2014
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