Search

Your search keyword '"Bishop, T"' showing total 817 results
Start Over Author "Bishop, T"
817 results on '"Bishop, T"'

5. If your foot is pretty, show it.

Author

Bishop, T. Brigham and Bishop, T. Brigham

Subjects
Broadsides 19th century. United States, Songs Texts. 19th century United States, Popular music Texts. 19th century United States, Foot Songs and music Texts., Flirting Songs and music Texts., Courtship Songs and music Texts., Musique populaire Textes. 19e siècle États-Unis, Broadsides., Courtship., Flirting., Foot., Popular music., Songs., United States.
Published
2024

6. Germline ATM variants predispose to melanoma: a joint analysis across the GenoMEL and MelaNostrum consortia

Author

Dalmasso, B, Pastorino, L, Nathan, V, Shah, NN, Palmer, JM, Howlie, M, Johansson, PA, Freedman, ND, Carter, BD, Beane-Freeman, L, Hicks, B, Molven, A, Helgadottir, H, Sankar, A, Tsao, H, Stratigos, AJ, Helsing, P, Van Doorn, R, Gruis, NA, Visser, M, Wadt, KAW, Mann, G, Holland, EA, Nagore, E, Potrony, M, Puig, S, Menin, C, Peris, K, Fargnoli, MC, Calista, D, Soufir, N, Harland, M, Bishop, T, Kanetsky, PA, Elder, DE, Andreotti, V, Vanni, I, Bruno, W, Höiom, V, Tucker, MA, Yang, XR, Andresen, PA, Adams, DJ, Landi, MT, Hayward, NK, Goldstein, AM, and Ghiorzo, P

Subjects
Genetics, Human Genome, Cancer, 2.1 Biological and endogenous factors, Aetiology, Ataxia Telangiectasia, Ataxia Telangiectasia Mutated Proteins, Australia, Genetic Predisposition to Disease, Germ-Line Mutation, Humans, Melanoma, GenoMEL, MelaNostrum consortia, Clinical Sciences, Genetics & Heredity
Abstract

PurposeAtaxia-Telangiectasia Mutated (ATM) has been implicated in the risk of several cancers, but establishing a causal relationship is often challenging. Although ATM single-nucleotide polymorphisms have been linked to melanoma, few functional alleles have been identified. Therefore, ATM impact on melanoma predisposition is unclear.MethodsFrom 22 American, Australian, and European sites, we collected 2,104 familial, multiple primary (MPM), and sporadic melanoma cases who underwent ATM genotyping via panel, exome, or genome sequencing, and compared the allele frequency (AF) of selected ATM variants classified as loss-of-function (LOF) and variants of uncertain significance (VUS) between this cohort and the gnomAD non-Finnish European (NFE) data set.ResultsLOF variants were more represented in our study cohort than in gnomAD NFE, both in all (AF = 0.005 and 0.002, OR = 2.6, 95% CI = 1.56-4.11, p

Published
2021

7. Feasibility of a text-based smoking cessation intervention in rural older adults.

Author

Noonan, D, Silva, S, Njuru, J, Bishop, T, Fish, LJ, Simmons, LA, Choi, SH, and Pollak, KI

Subjects
Health Services and Systems, Public Health, Health Sciences, Behavioral and Social Science, Rare Diseases, Clinical Trials and Supportive Activities, Prevention, Clinical Research, Tobacco, Tobacco Smoke and Health, Cancer, Rural Health, Prevention of disease and conditions, and promotion of well-being, 3.1 Primary prevention interventions to modify behaviours or promote wellbeing, Cardiovascular, Respiratory, Good Health and Well Being, Aged, Female, Humans, Male, Middle Aged, Rural Population, Smoking Cessation, Socioeconomic Factors, Text Messaging, Time Factors, Public Health and Health Services, Curriculum and Pedagogy, Curriculum and pedagogy, Public health
Abstract

Text-based interventions are effective for smoking cessation, but have not been tested in rural older adults. The purpose of this study was to compare the feasibility, acceptability and preliminary efficacy of a text-based Scheduled Gradual Reduction (SGR) program to a non-SGR text messaging support condition among rural older adults. Adults over 60 years were randomized to either: (i) the SGR program (n = 20), a text-based program to reduce smoking over 4-weeks plus text-based support messages; or (ii) control (n = 20), receipt of text-based support messages only. Participants completed surveys at baseline and end of program to assess feasibility and acceptability of the intervention, and biochemically validated 7-day point prevalence cessation was assessed at end of treatment. Most participants (81%) reported reading all the messages they received. Participants found both interventions useful in quitting smoking (SGR = 57%, Control = 63%) and would recommend it to a friend (SGR = 72%, Control = 79%). Although not statically significant, the SGR group had a higher rate of biochemically validated cessation (SGR = 15%, Control = 5%, Cohen d = 0.67). Among those still smoking, the median percent reduction in cigarettes was 33.3% for both groups. Text-based cessation interventions are feasible, acceptable and can be easily disseminated to rural older adult tobacco users.

Published
2018

8. Sagnac interferometry with a single atomic clock

Author

Stevenson, R., Hush, M., Bishop, T., Lesanovsky, I., and Fernholz, T.

Subjects
Physics - Atomic Physics, Quantum Physics
Abstract

We theoretically discuss an implementation of a Sagnac interferometer with cold atoms. In contrast to currently existing schemes our protocol does not rely on any free propagation of atoms. Instead it is based on superpositions of fully confined atoms and state-dependent transport along a closed path. Using Ramsey sequences for an atomic clock, the accumulated Sagnac phase is encoded in the resulting population imbalance between two internal (clock) states. Using minimal models for the above protocol we analytically quantify limitations arising from atomic dynamics and finite temperature. We discuss an actual implementation of the interferometer with adiabatic radio-frequency potentials that is inherently robust against common mode noise as well as phase noise from the reference oscillator., Comment: 5 pages, 2 figures

Published
2015
Full Text
View/download PDF

11. Pteropox infection in a juvenile grey‐headed flying fox (Pteropus poliocephalus).

Author

Valenza, LD, Bishop, T, Cramieri, S, Wang, J, and Ploeg, RJ

Subjects
*TRANSMISSION electron microscopy, *CELLULAR inclusions, *NUCLEOTIDE sequencing, *VIRUS diseases, *SEQUENCE analysis
Abstract

A juvenile grey‐headed flying fox (GHFF) (Pteropus poliocephalus) presented to the Australia Zoo Wildlife Hospital after a wildlife carer found the animal hanging on the outside of an aviary. On presentation, the animal was emaciated and moribund with disseminated, multifocal, depigmented and proliferative lesions on the wing membranes and skin of the neck. Histopathology revealed multiple, well‐circumscribed proliferative epidermal lesions with intracytoplasmic inclusion bodies. A poxvirus was identified via transmission electron microscopy and next‐generation sequencing (NGS). Analysis of sequences obtained demonstrated 99% nucleotide identity to Pteropox virus strain Australia (GenBank KU980965). To the authors' knowledge, this paper describes the first case of Pteropox virus infection in a GHFF. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

13. Influence of flooding variability on the development of an Amazonian peatland.

Author

Sassoon, D., Fletcher, W. J., Roucoux, K. H., Ryan, P., Lawson, I. T., Honorio Coronado, E. N., Del Aguila Pasquel, J., Bishop, T., Åkesson, C. M., and Hastie, A.

Subjects
PALMS, ECOSYSTEM services, PALEOECOLOGY, ENVIRONMENTAL protection, FLOODS, PEATLANDS, VEGETATION dynamics, PEAT
Abstract

Peat in the Pastaza–Marañón Foreland Basin (PMFB), northern Peru, forms beneath open wetlands, palm swamps, pole forests and seasonally flooded forests. These vegetation communities may represent different successional stages of peatlands, but the spatiotemporal patterns of peatland development in Amazonia are still poorly understood. We present a new geochemical and palaeoecological record spanning the last c. 4330 years from an open peatland (San Roque, core SAR_T3_03_B). Our results suggest the persistence of predominantly herbaceous vegetation communities at the core site since the start of peat accumulation (c. 3180 cal a bp). Micro‐X‐ray fluorescence core scanning provides evidence for episodes of fluvially derived minerogenic input and simultaneous increases in flood‐tolerant taxa relating to intervals of increased frequency and depth of riverine flooding. The establishment of Mauritia flexuosa palms from around 440 cal a bp coincided with a shift to lower flooding depth and frequency which continues to the present day. This study reveals the role of flooding variability in shaping peatland development and influencing vegetation succession in the PMFB, underlining the need to understand natural environmental variability for the conservation of these ecosystems due to their vital contributions to ecosystem services and carbon storage. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

14. Living at a snail's pace : the cellular basis of metabolic depression

Author

Bishop, T.

Subjects
571.6
Abstract

The garden snail Helix aspersa depresses its metabolic rate in response to desiccation (termed aestivation), as well as in response to reduced oxygen tension (termed oxygen conformation). This depression persists in cells isolated from the hepatopancreas of snails, thereby providing a good model system for analysing the cellular basis of metabolic depression. Isolated hepatopancreas cells were used to assess the contributions of various cellular processes (non-mitochondrial and mitochondrial respiration, and, within mitochondrial respiration, substrate oxidation and respiration to drive proton leak and ATP turnover) to metabolic depression seen during oxygen conformation and aestivation. Non-mitochondrial respiration accounts for a large proportion (~50%) of metabolic rate at physiological oxygen tensions, and it is solely responsible for the oxygen conforming behaviour of the cells. Both non-mitochondrial and mitochondrial respiration, however, decrease in aestivation. This decrease in mitochondrial respiration is not caused by differences in mitochondrial volume or inner membrane surface density but is associated with other intrinsic changes in the mitochondria (decrease in the activities of the mitochondrial enzymes citrate synthase and cytochrome c oxidase). Within mitochondrial respiration, the activity of substrate oxidation and probably ATP turnover, but not the activity of proton leak, decrease during aestivation. At least 75% of the total response of mitochondrial respiration to aestivation is due to primary changes in the kinetics of substrate oxidation, with only 25% or less of the response occurring through primary effects on ATP turnover. The primary change in the activity of substrate oxidation resulted in a lower mitochondrial membrane potential in hepatopancreas cells from aestivating compared to active snails, leading to secondary decreases in respiration to drive ATP turnover and proton leak.

Published
2002

15. Genome-wide Association Study of Bladder Cancer Reveals New Biological and Translational Insights

Author

Koutros, S, Kiemeney, LA, Choudhury, PP, Milne, RL, de Maturana, EL, Ye, Y, Joseph, V, Florez-Vargas, O, Dyrskjot, L, Figueroa, J, Dutta, D, Giles, GG, Hildebrandt, MAT, Offit, K, Kogevinas, M, Weiderpass, E, McCullough, ML, Freedman, ND, Albanes, D, Kooperberg, C, Cortessis, VK, Karagas, MR, Johnson, A, Schwenn, MR, Baris, D, Furberg, H, Bajorin, DF, Cussenot, O, Cancel-Tassin, G, Benhamou, S, Kraft, P, Porru, S, Carta, A, Bishop, T, Southey, MC, Matullo, G, Fletcher, T, Kumar, R, Taylor, JA, Lamy, P, Prip, F, Kalisz, M, Weinstein, SJ, Hengstler, JG, Selinski, S, Harland, M, Teo, M, Kiltie, AE, Tardon, A, Serra, C, Carrato, A, Garcia-Closas, R, Lloreta, J, Schned, A, Lenz, P, Riboli, E, Brennan, P, Tjonneland, A, Otto, T, Ovsiannikov, D, Volkert, F, Vermeulen, SH, Aben, KK, Galesloot, TE, Turman, C, De Vivo, I, Giovannucci, E, Hunter, DJ, Hohensee, C, Hunt, R, V. Patel, A, Huang, W-Y, Thorleifsson, G, Gago-Dominguez, M, Amiano, P, Golka, K, Stern, MC, Yan, W, Liu, J, Alfred, S, Katta, S, Hutchinson, A, Hicks, B, Wheeler, WA, Purdue, MP, McGlynn, KA, Kitahara, CM, Haiman, CA, Greene, MH, Rafnar, T, Chatterjee, N, Chanock, SJ, Wu, X, Real, FX, Silverman, DT, Garcia-Closas, M, Stefansson, K, Prokunina-Olsson, L, Malats, N, Rothman, N, Koutros, S, Kiemeney, LA, Choudhury, PP, Milne, RL, de Maturana, EL, Ye, Y, Joseph, V, Florez-Vargas, O, Dyrskjot, L, Figueroa, J, Dutta, D, Giles, GG, Hildebrandt, MAT, Offit, K, Kogevinas, M, Weiderpass, E, McCullough, ML, Freedman, ND, Albanes, D, Kooperberg, C, Cortessis, VK, Karagas, MR, Johnson, A, Schwenn, MR, Baris, D, Furberg, H, Bajorin, DF, Cussenot, O, Cancel-Tassin, G, Benhamou, S, Kraft, P, Porru, S, Carta, A, Bishop, T, Southey, MC, Matullo, G, Fletcher, T, Kumar, R, Taylor, JA, Lamy, P, Prip, F, Kalisz, M, Weinstein, SJ, Hengstler, JG, Selinski, S, Harland, M, Teo, M, Kiltie, AE, Tardon, A, Serra, C, Carrato, A, Garcia-Closas, R, Lloreta, J, Schned, A, Lenz, P, Riboli, E, Brennan, P, Tjonneland, A, Otto, T, Ovsiannikov, D, Volkert, F, Vermeulen, SH, Aben, KK, Galesloot, TE, Turman, C, De Vivo, I, Giovannucci, E, Hunter, DJ, Hohensee, C, Hunt, R, V. Patel, A, Huang, W-Y, Thorleifsson, G, Gago-Dominguez, M, Amiano, P, Golka, K, Stern, MC, Yan, W, Liu, J, Alfred, S, Katta, S, Hutchinson, A, Hicks, B, Wheeler, WA, Purdue, MP, McGlynn, KA, Kitahara, CM, Haiman, CA, Greene, MH, Rafnar, T, Chatterjee, N, Chanock, SJ, Wu, X, Real, FX, Silverman, DT, Garcia-Closas, M, Stefansson, K, Prokunina-Olsson, L, Malats, N, and Rothman, N

Abstract

BACKGROUND: Genomic regions identified by genome-wide association studies (GWAS) for bladder cancer risk provide new insights into etiology. OBJECTIVE: To identify new susceptibility variants for bladder cancer in a meta-analysis of new and existing genome-wide genotype data. DESIGN, SETTING, AND PARTICIPANTS: Data from 32 studies that includes 13,790 bladder cancer cases and 343,502 controls of European ancestry were used for meta-analysis. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSES: Log-additive associations of genetic variants were assessed using logistic regression models. A fixed-effects model was used for meta-analysis of the results. Stratified analyses were conducted to evaluate effect modification by sex and smoking status. A polygenic risk score (PRS) was generated on the basis of known and novel susceptibility variants and tested for interaction with smoking. RESULTS AND LIMITATIONS: Multiple novel bladder cancer susceptibility loci (6p.22.3, 7q36.3, 8q21.13, 9p21.3, 10q22.1, 19q13.33) as well as improved signals in three known regions (4p16.3, 5p15.33, 11p15.5) were identified, bringing the number of independent markers at genome-wide significance (p < 5 × 10-8) to 24. The 4p16.3 (FGFR3/TACC3) locus was associated with a stronger risk for women than for men (p-interaction = 0.002). Bladder cancer risk was increased by interactions between smoking status and genetic variants at 8p22 (NAT2; multiplicative p value for interaction [pM-I] = 0.004), 8q21.13 (PAG1; pM-I = 0.01), and 9p21.3 (LOC107987026/MTAP/CDKN2A; pM-I = 0.02). The PRS based on the 24 independent GWAS markers (odds ratio per standard deviation increase 1.49, 95% confidence interval 1.44-1.53), which also showed comparable results in two prospective cohorts (UK Biobank, PLCO trial), revealed an approximately fourfold difference in the lifetime risk of bladder cancer according to the PRS (e.g., 1st vs 10th decile) for both smokers and nonsmokers. CONCLUSIONS: We report novel loci associated

Published
2023

16. Deciphering colorectal cancer genetics through multi-omic analysis of 100,204 cases and 154,587 controls of European and east Asian ancestries

Author

Fernandez-Rozadilla, C, Timofeeva, M, Chen, Z, Law, P, Thomas, M, Bien, S, Diez-Obrero, V, Li, L, Fernandez-Tajes, J, Palles, C, Sherwood, K, Harris, S, Svinti, V, McDonnell, K, Farrington, S, Studd, J, Vaughan-Shaw, P, Shu, X-O, Long, J, Cai, Q, Guo, X, Lu, Y, Scacheri, P, Huyghe, J, Harrison, T, Shibata, D, Haiman, C, Devall, M, Schumacher, F, Melas, M, Rennert, G, Obon-Santacana, M, Martin-Sanchez, V, Moratalla-Navarro, F, Oh, JH, Kim, J, Jee, SH, Jung, KJ, Kweon, S-S, Shin, M-H, Shin, A, Ahn, Y-O, Kim, D-H, Oze, I, Wen, W, Matsuo, K, Matsuda, K, Tanikawa, C, Ren, Z, Gao, Y-T, Jia, W-H, Potter, J, Jenkins, M, Win, AK, Pai, R, Figueiredo, J, Haile, R, Gallinger, S, Woods, M, Newcomb, P, Cheadle, J, Kaplan, R, Maughan, T, Kerr, R, Kerr, D, Kirac, I, Boehm, J, Mecklin, L-P, Jousilahti, P, Knekt, P, Aaltonen, L, Rissanen, H, Pukkala, E, Eriksson, J, Cajuso, T, Hanninen, U, Kondelin, J, Palin, K, Tanskanen, T, Renkonen-Sinisalo, L, Zanke, B, Mannisto, S, Albanes, D, Weinstein, S, Ruiz-Narvaez, E, Palmer, J, Buchanan, D, Platz, E, Visvanathan, K, Ulrich, C, Siegel, E, Brezina, S, Gsur, A, Campbell, P, Chang-Claude, J, Hoffmeister, M, Brenner, H, Slattery, M, Tsilidis, K, Schulze, M, Gunter, M, Murphy, N, Castells, A, Castellvi-Bel, S, Moreira, L, Arndt, V, Shcherbina, A, Stern, M, Pardamean, B, Bishop, T, Giles, G, Southey, M, Idos, G, Abu-Ful, Z, Greenson, J, Shulman, K, Lejbkowicz, F, Offit, K, Su, Y-R, Steinfelder, R, Keku, T, van Guelpen, B, Hudson, T, Hampel, H, Pearlman, R, Berndt, S, Hayes, R, Martinez, ME, Thomas, S, Corley, D, Pharoah, P, Larsson, S, Yen, Y, Lenz, H-J, White, E, Doheny, K, Pugh, E, Shelford, T, Chan, A, Cruz-Correa, M, Lindblom, A, Joshi, A, Schafmayer, C, Kundaje, A, Nickerson, D, Schoen, R, Hampe, J, Stadler, Z, Vodicka, P, Vodickova, L, Vymetalkova, V, Papadopoulos, N, Edlund, C, Gauderman, W, Thomas, D, Toland, A, Markowitz, S, Kim, A, Gruber, S, van Duijnhoven, F, Feskens, E, Sakoda, L, Gago-Dominguez, M, Wolk, A, Naccarati, A, Pardini, B, FitzGerald, L, Lee, SC, Ogino, S, Kooperberg, C, Li, C, Lin, Y, Prentice, R, Qu, C, Bezieau, S, Tangen, C, Mardis, E, Yamaji, T, Sawada, N, Iwasaki, M, Le Marchand, L, Wu, A, McNeil, C, Coetzee, G, Hayward, C, Deary, I, Theodoratou, E, Reid, S, Walker, M, Ooi, LY, Moreno, V, Casey, G, Tomlinson, I, Zheng, W, Dunlop, M, Houlston, R, Peters, U, Fernandez-Rozadilla, C, Timofeeva, M, Chen, Z, Law, P, Thomas, M, Bien, S, Diez-Obrero, V, Li, L, Fernandez-Tajes, J, Palles, C, Sherwood, K, Harris, S, Svinti, V, McDonnell, K, Farrington, S, Studd, J, Vaughan-Shaw, P, Shu, X-O, Long, J, Cai, Q, Guo, X, Lu, Y, Scacheri, P, Huyghe, J, Harrison, T, Shibata, D, Haiman, C, Devall, M, Schumacher, F, Melas, M, Rennert, G, Obon-Santacana, M, Martin-Sanchez, V, Moratalla-Navarro, F, Oh, JH, Kim, J, Jee, SH, Jung, KJ, Kweon, S-S, Shin, M-H, Shin, A, Ahn, Y-O, Kim, D-H, Oze, I, Wen, W, Matsuo, K, Matsuda, K, Tanikawa, C, Ren, Z, Gao, Y-T, Jia, W-H, Potter, J, Jenkins, M, Win, AK, Pai, R, Figueiredo, J, Haile, R, Gallinger, S, Woods, M, Newcomb, P, Cheadle, J, Kaplan, R, Maughan, T, Kerr, R, Kerr, D, Kirac, I, Boehm, J, Mecklin, L-P, Jousilahti, P, Knekt, P, Aaltonen, L, Rissanen, H, Pukkala, E, Eriksson, J, Cajuso, T, Hanninen, U, Kondelin, J, Palin, K, Tanskanen, T, Renkonen-Sinisalo, L, Zanke, B, Mannisto, S, Albanes, D, Weinstein, S, Ruiz-Narvaez, E, Palmer, J, Buchanan, D, Platz, E, Visvanathan, K, Ulrich, C, Siegel, E, Brezina, S, Gsur, A, Campbell, P, Chang-Claude, J, Hoffmeister, M, Brenner, H, Slattery, M, Tsilidis, K, Schulze, M, Gunter, M, Murphy, N, Castells, A, Castellvi-Bel, S, Moreira, L, Arndt, V, Shcherbina, A, Stern, M, Pardamean, B, Bishop, T, Giles, G, Southey, M, Idos, G, Abu-Ful, Z, Greenson, J, Shulman, K, Lejbkowicz, F, Offit, K, Su, Y-R, Steinfelder, R, Keku, T, van Guelpen, B, Hudson, T, Hampel, H, Pearlman, R, Berndt, S, Hayes, R, Martinez, ME, Thomas, S, Corley, D, Pharoah, P, Larsson, S, Yen, Y, Lenz, H-J, White, E, Doheny, K, Pugh, E, Shelford, T, Chan, A, Cruz-Correa, M, Lindblom, A, Joshi, A, Schafmayer, C, Kundaje, A, Nickerson, D, Schoen, R, Hampe, J, Stadler, Z, Vodicka, P, Vodickova, L, Vymetalkova, V, Papadopoulos, N, Edlund, C, Gauderman, W, Thomas, D, Toland, A, Markowitz, S, Kim, A, Gruber, S, van Duijnhoven, F, Feskens, E, Sakoda, L, Gago-Dominguez, M, Wolk, A, Naccarati, A, Pardini, B, FitzGerald, L, Lee, SC, Ogino, S, Kooperberg, C, Li, C, Lin, Y, Prentice, R, Qu, C, Bezieau, S, Tangen, C, Mardis, E, Yamaji, T, Sawada, N, Iwasaki, M, Le Marchand, L, Wu, A, McNeil, C, Coetzee, G, Hayward, C, Deary, I, Theodoratou, E, Reid, S, Walker, M, Ooi, LY, Moreno, V, Casey, G, Tomlinson, I, Zheng, W, Dunlop, M, Houlston, R, and Peters, U

Abstract

Colorectal cancer (CRC) is a leading cause of mortality worldwide. We conducted a genome-wide association study meta-analysis of 100,204 CRC cases and 154,587 controls of European and east Asian ancestry, identifying 205 independent risk associations, of which 50 were unreported. We performed integrative genomic, transcriptomic and methylomic analyses across large bowel mucosa and other tissues. Transcriptome- and methylome-wide association studies revealed an additional 53 risk associations. We identified 155 high-confidence effector genes functionally linked to CRC risk, many of which had no previously established role in CRC. These have multiple different functions and specifically indicate that variation in normal colorectal homeostasis, proliferation, cell adhesion, migration, immunity and microbial interactions determines CRC risk. Crosstissue analyses indicated that over a third of effector genes most probably act outside the colonic mucosa. Our findings provide insights into colorectal oncogenesis and highlight potential targets across tissues for new CRC treatment and chemoprevention strategies.

Published
2023

17. Genome-wide Association Study of Bladder Cancer Reveals New Biological and Translational Insights.

Author

Koutros, S., Kiemeney, L.A., Pal Choudhury, P., Milne, R.L., Lopez de Maturana, E., Ye, Y., Joseph, V., Florez-Vargas, O., Dyrskjøt, L., Figueroa, J., Dutta, D., Giles, G.G., Hildebrandt, M.A.T., Offit, K., Kogevinas, M., Weiderpass, E., McCullough, M.L., Freedman, N.D., Albanes, D., Kooperberg, C., Cortessis, V.K., Karagas, M.R., Johnson, A., Schwenn, M.R., Baris, D., Furberg, H., Bajorin, D.F., Cussenot, O., Cancel-Tassin, G., Benhamou, S., Kraft, P., Porru, S., Carta, A., Bishop, T., Southey, M.C., Matullo, G., Fletcher, T., Kumar, R., Taylor, J.A., Lamy, P., Prip, F., Kalisz, M., Weinstein, S.J., Hengstler, J.G., Selinski, S., Harland, M., Teo, M., Kiltie, A.E., Tardón, A., Serra, C., Carrato, A., García-Closas, R., Lloreta, J., Schned, A., Lenz, P., Riboli, E., Brennan, P., Tjønneland, A., Otto, T., Ovsiannikov, D., Volkert, F., Vermeulen, S.H., Aben, K.K.H., Galesloot, T.E., Turman, C., Vivo, I. De, Giovannucci, E., Hunter, D.J., Hohensee, C., Hunt, R., Patel, A.V., Huang, W.Y., Thorleifsson, G., Gago-Dominguez, M., Amiano, P., Golka, K., Stern, M.C., Yan, W., Liu, J., Li, S.A., Katta, S., Hutchinson, A., Hicks, B., Wheeler, W.A., Purdue, M.P., McGlynn, K.A., Kitahara, C.M., Haiman, C.A., Greene, M.H., Rafnar, T., Chatterjee, N., Chanock, S.J., Wu, X., Real, F.X., Silverman, D.T., Garcia-Closas, M., Stefansson, K., Prokunina-Olsson, L., Malats, N., Rothman, N., Koutros, S., Kiemeney, L.A., Pal Choudhury, P., Milne, R.L., Lopez de Maturana, E., Ye, Y., Joseph, V., Florez-Vargas, O., Dyrskjøt, L., Figueroa, J., Dutta, D., Giles, G.G., Hildebrandt, M.A.T., Offit, K., Kogevinas, M., Weiderpass, E., McCullough, M.L., Freedman, N.D., Albanes, D., Kooperberg, C., Cortessis, V.K., Karagas, M.R., Johnson, A., Schwenn, M.R., Baris, D., Furberg, H., Bajorin, D.F., Cussenot, O., Cancel-Tassin, G., Benhamou, S., Kraft, P., Porru, S., Carta, A., Bishop, T., Southey, M.C., Matullo, G., Fletcher, T., Kumar, R., Taylor, J.A., Lamy, P., Prip, F., Kalisz, M., Weinstein, S.J., Hengstler, J.G., Selinski, S., Harland, M., Teo, M., Kiltie, A.E., Tardón, A., Serra, C., Carrato, A., García-Closas, R., Lloreta, J., Schned, A., Lenz, P., Riboli, E., Brennan, P., Tjønneland, A., Otto, T., Ovsiannikov, D., Volkert, F., Vermeulen, S.H., Aben, K.K.H., Galesloot, T.E., Turman, C., Vivo, I. De, Giovannucci, E., Hunter, D.J., Hohensee, C., Hunt, R., Patel, A.V., Huang, W.Y., Thorleifsson, G., Gago-Dominguez, M., Amiano, P., Golka, K., Stern, M.C., Yan, W., Liu, J., Li, S.A., Katta, S., Hutchinson, A., Hicks, B., Wheeler, W.A., Purdue, M.P., McGlynn, K.A., Kitahara, C.M., Haiman, C.A., Greene, M.H., Rafnar, T., Chatterjee, N., Chanock, S.J., Wu, X., Real, F.X., Silverman, D.T., Garcia-Closas, M., Stefansson, K., Prokunina-Olsson, L., Malats, N., and Rothman, N.

Abstract

01 juli 2023, Item does not contain fulltext, BACKGROUND: Genomic regions identified by genome-wide association studies (GWAS) for bladder cancer risk provide new insights into etiology. OBJECTIVE: To identify new susceptibility variants for bladder cancer in a meta-analysis of new and existing genome-wide genotype data. DESIGN, SETTING, AND PARTICIPANTS: Data from 32 studies that includes 13,790 bladder cancer cases and 343,502 controls of European ancestry were used for meta-analysis. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSES: Log-additive associations of genetic variants were assessed using logistic regression models. A fixed-effects model was used for meta-analysis of the results. Stratified analyses were conducted to evaluate effect modification by sex and smoking status. A polygenic risk score (PRS) was generated on the basis of known and novel susceptibility variants and tested for interaction with smoking. RESULTS AND LIMITATIONS: Multiple novel bladder cancer susceptibility loci (6p.22.3, 7q36.3, 8q21.13, 9p21.3, 10q22.1, 19q13.33) as well as improved signals in three known regions (4p16.3, 5p15.33, 11p15.5) were identified, bringing the number of independent markers at genome-wide significance (p < 5 × 10(-8)) to 24. The 4p16.3 (FGFR3/TACC3) locus was associated with a stronger risk for women than for men (p-interaction = 0.002). Bladder cancer risk was increased by interactions between smoking status and genetic variants at 8p22 (NAT2; multiplicative p value for interaction [p(M-I)] = 0.004), 8q21.13 (PAG1; p(M-I) = 0.01), and 9p21.3 (LOC107987026/MTAP/CDKN2A; p(M-I) = 0.02). The PRS based on the 24 independent GWAS markers (odds ratio per standard deviation increase 1.49, 95% confidence interval 1.44-1.53), which also showed comparable results in two prospective cohorts (UK Biobank, PLCO trial), revealed an approximately fourfold difference in the lifetime risk of bladder cancer according to the PRS (e.g., 1st vs 10th decile) for both smokers and nonsmokers. CONCLUSIONS: We report novel loci ass

Published
2023

21. Analysis of rare disruptive germline mutations in 2135 enriched BRCA-negative breast cancers excludes additional high-impact susceptibility genes

Author

Loveday, C., primary, Garrett, A., additional, Law, P., additional, Hanks, S., additional, Poyastro-Pearson, E., additional, Adlard, J.W., additional, Barwell, J., additional, Berg, J., additional, Brady, A.F., additional, Brewer, C., additional, Chapman, C., additional, Cook, J., additional, Davidson, R., additional, Donaldson, A., additional, Douglas, F., additional, Greenhalgh, L., additional, Henderson, A., additional, Izatt, L., additional, Kumar, A., additional, Lalloo, F., additional, Miedzybrodzka, Z., additional, Morrison, P.J., additional, Paterson, J., additional, Porteous, M., additional, Rogers, M.T., additional, Walker, L., additional, Eccles, D., additional, Evans, D.G., additional, Snape, K., additional, Hanson, H., additional, Houlston, R.S., additional, Turnbull, C., additional, Ardern-Jones, A., additional, Adlard, J., additional, Ahmed, M., additional, Attard, G., additional, Bailey, K., additional, Bancroft, E., additional, Bardsley, C., additional, Barton, D., additional, Bartlett, M., additional, Baxter, L., additional, Belk, R., additional, Bernhard, B., additional, Bishop, T., additional, Boyes, L., additional, Bradshaw, N., additional, Brant, S., additional, Brice, G., additional, Bromilow, G., additional, Brooks, C., additional, Bruce, A., additional, Bulman, B., additional, Burgess, L., additional, Campbell, J., additional, Canham, N., additional, Castle, B., additional, Cetnarskyj, R., additional, Claber, O., additional, Coates, N., additional, Cole, T., additional, Collins, A., additional, Coulson, S., additional, Crawford, G., additional, Cruger, D., additional, Cummings, C., additional, D’Mello, L., additional, Day, L., additional, Dell, B., additional, Dolling, C., additional, Dorkins, H., additional, Downing, S., additional, Drummond, S., additional, Dubras, C., additional, Dunlop, J., additional, Durrell, S., additional, Eddy, C., additional, Edwards, M., additional, Edwards, E., additional, Edwardson, J., additional, Eeles, R., additional, Ellis, I., additional, Elmslie, F., additional, Evans, G., additional, Gibbons, B., additional, Gardiner, C., additional, Ghali, N., additional, Giblin, C., additional, Gibson, S., additional, Goff, S., additional, Goodman, S., additional, Goudie, D., additional, Grier, J., additional, Gregory, H., additional, Halliday, S., additional, Hardy, R., additional, Hartigan, C., additional, Heaton, T., additional, Higgins, C., additional, Hodgson, S., additional, Homfray, T., additional, Horrigan, D., additional, Houghton, C., additional, Hughes, L., additional, Hunt, V., additional, Irvine, L., additional, Jacobs, C., additional, James, S., additional, James, M., additional, Jeffers, L., additional, Jobson, I., additional, Jones, W., additional, Kennedy, M.J., additional, Kenwrick, S., additional, Kightley, C., additional, Kirk, C., additional, Kirk, E., additional, Kivuva, E., additional, Kohut, K., additional, Kosicka-Slawinska, M., additional, Kulkarni, A., additional, Lambord, N., additional, Langman, C., additional, Leonard, P., additional, Levene, S., additional, Locker, S., additional, Logan, P., additional, Longmuir, M., additional, Lucassen, A., additional, Lyus, V., additional, Magee, A., additional, Male, A., additional, Mansour, S., additional, McBride, D., additional, McCann, E., additional, McConnell, V., additional, McEntagart, M., additional, McKeown, C., additional, McLeish, L., additional, McLeod, D., additional, Melville, A., additional, Mercer, L., additional, Mercer, C., additional, Mitra, A., additional, Murday, V., additional, Murray, A., additional, Myhill, K., additional, Myring, J., additional, O'Hara, E., additional, Pearson, P., additional, Pichert, G., additional, Platt, K., additional, Pottinger, C., additional, Price, S., additional, Protheroe, L., additional, Pugh, S., additional, Quarrell, O., additional, Randhawa, K., additional, Riddick, C., additional, Robertson, L., additional, Robinson, A., additional, Roffey-Johnson, V., additional, Rogers, M., additional, Rose, S., additional, Rowe, S., additional, Schofield, A., additional, Rahman, N., additional, Saya, S., additional, Scott, G., additional, Scott, J., additional, Searle, A., additional, Shanley, S., additional, Sharif, S., additional, Shaw, A., additional, Shaw, J., additional, Shea-Simonds, J., additional, Side, L., additional, Sillibourne, J., additional, Simon, K., additional, Simpson, S., additional, Slater, S., additional, Smalley, S., additional, Smith, K., additional, Snadden, L., additional, Soloway, J., additional, Stait, Y., additional, Stayner, B., additional, Steel, M., additional, Steel, C., additional, Stewart, H., additional, Stirling, D., additional, Thomas, M., additional, Thomas, S., additional, Tomkins, S., additional, Turner, H., additional, Vandersteen, A., additional, Wakeling, E., additional, Waldrup, F., additional, Watt, C., additional, Watts, S., additional, Webber, A., additional, Whyte, C., additional, Wiggins, J., additional, Williams, E., additional, and Winchester, L., additional

Published
2022
Full Text
View/download PDF

25. How has Computer-Navigation changed TKR?

Author

Lucas, D., Bishop, T., Chauhan, S. K., Hozack, William J., editor, Krismer, Martin, editor, Nogler, Michael, editor, Bonutti, Peter M., editor, Rachbauer, Franz, editor, Schaffer, Jonathan L., editor, and Donnelly, William J., editor

Published
2004
Full Text
View/download PDF

26. Life course of retrospective harmonization initiatives:key elements to consider

Author

Fortier, I. (Isabel), Wey, T. W. (Tina W.), Bergeron, J. (Julie), de Moira, A. P. (Angela Pinot), Nybo-Andersen, A.-M. (Anne-Marie), Bishop, T. (Tom), Murtagh, M. J. (Madeleine J.), Miočević, M. (Milica), Swertz, M. A. (Morris A.), van Enckevort, E. (Esther), Marcon, Y. (Yannick), Mayrhofer, M. T. (Michaela. Th.), Ornelas, J. P. (Jos Pedro), Sebert, S. (Sylvain), Santos, A. C. (Ana Cristina), Rocha, A. (Artur), Wilson, R. C. (Rebecca C.), Griffith, L. E. (Lauren E.), Burton, P. (Paul), Fortier, I. (Isabel), Wey, T. W. (Tina W.), Bergeron, J. (Julie), de Moira, A. P. (Angela Pinot), Nybo-Andersen, A.-M. (Anne-Marie), Bishop, T. (Tom), Murtagh, M. J. (Madeleine J.), Miočević, M. (Milica), Swertz, M. A. (Morris A.), van Enckevort, E. (Esther), Marcon, Y. (Yannick), Mayrhofer, M. T. (Michaela. Th.), Ornelas, J. P. (Jos Pedro), Sebert, S. (Sylvain), Santos, A. C. (Ana Cristina), Rocha, A. (Artur), Wilson, R. C. (Rebecca C.), Griffith, L. E. (Lauren E.), and Burton, P. (Paul)

Abstract

Optimizing research on the developmental origins of health and disease (DOHaD) involves implementing initiatives maximizing the use of the available cohort study data; achieving sufficient statistical power to support subgroup analysis; and using participant data presenting adequate follow-up and exposure heterogeneity. It also involves being able to undertake comparison, cross-validation, or replication across data sets. To answer these requirements, cohort study data need to be findable, accessible, interoperable, and reusable (FAIR), and more particularly, it often needs to be harmonized. Harmonization is required to achieve or improve comparability of the putatively equivalent measures collected by different studies on different individuals. Although the characteristics of the research initiatives generating and using harmonized data vary extensively, all are confronted by similar issues. Having to collate, understand, process, host, and co-analyze data from individual cohort studies is particularly challenging. The scientific success and timely management of projects can be facilitated by an ensemble of factors. The current document provides an overview of the ‘life course’ of research projects requiring harmonization of existing data and highlights key elements to be considered from the inception to the end of the project.

Published
2022

33. Germline ATM variants predispose to melanoma: a joint analysis across the GenoMEL and MelaNostrum consortia

Author

Dalmasso, B., Pastorino, L., Nathan, V., Shah, N.N., Palmer, J.M., Howlie, M., Johansson, P.A., Freedman, N.D., Carter, B.D., Beane-Freeman, L., Hicks, B., Molven, A., Helgadottir, H., Sankar, A., Tsao, H., Stratigos, A.J., Helsing, P., Doorn, R. van, Gruis, N.A., Visser, M., Wadt, K.A.W., Mann, G., Holland, E.A., Nagore, E., Potrony, M., Puig, S., Menin, C., Peris, K., Fargnoli, M.C., Calista, D., Soufir, N., Harland, M., Bishop, T., Kanetsky, P.A., Elder, D.E., Andreotti, V., Vanni, I., Bruno, W., Hoiom, V., Tucker, M.A., Yang, X.R., Andresen, P.A., Adams, D.J., Landi, M.T., Hayward, N.K., Goldstein, A.M., Ghiorzo, P., GenoMEL, and MelaNostrum Consortia

Subjects
0301 basic medicine, Oncology, medicine.medical_specialty, Clinical Sciences, Ataxia Telangiectasia Mutated Proteins, MelaNostrum consortia, Article, Germline, Ataxia Telangiectasia, 03 medical and health sciences, 0302 clinical medicine, Germline mutation, Internal medicine, Genetics, medicine, 2.1 Biological and endogenous factors, Humans, Genetic Predisposition to Disease, Aetiology, Allele, Melanoma, Allele frequency, Exome, Genotyping, Germ-Line Mutation, Genetics (clinical), Cancer, Genetics & Heredity, business.industry, Human Genome, Australia, GenoMEL, medicine.disease, 030104 developmental biology, 030220 oncology & carcinogenesis, Ataxia-telangiectasia, Cohort, Settore MED/35 - MALATTIE CUTANEE E VENEREE, business
Abstract

Purpose Ataxia–Telangiectasia Mutated (ATM) has been implicated in the risk of several cancers, but establishing a causal relationship is often challenging. Although ATM single-nucleotide polymorphisms have been linked to melanoma, few functional alleles have been identified. Therefore, ATM impact on melanoma predisposition is unclear. Methods From 22 American, Australian, and European sites, we collected 2,104 familial, multiple primary (MPM), and sporadic melanoma cases who underwent ATM genotyping via panel, exome, or genome sequencing, and compared the allele frequency (AF) of selected ATM variants classified as loss-of-function (LOF) and variants of uncertain significance (VUS) between this cohort and the gnomAD non-Finnish European (NFE) data set. Results LOF variants were more represented in our study cohort than in gnomAD NFE, both in all (AF = 0.005 and 0.002, OR = 2.6, 95% CI = 1.56–4.11, p

Published
2021

34. Large-scale cross-cancer fine-mapping of the 5p15.33 region reveals multiple independent signals

Author

Chen, H, Majumdar, A, Wang, L, Kar, S, Brown, KM, Feng, H, Turman, C, Dennis, J, Easton, D, Michailidou, K, Simard, J, Breast Cancer Association Consortium (BCAC), Bishop, T, Cheng, IC, Huyghe, JR, Schmit, SL, Colorectal Transdisciplinary Study (CORECT), Colon Cancer Family Registry Study (CCFR), Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO, O'Mara, TA, Spurdle, AB, Endometrial Cancer Association Consortium (ECAC), Gharahkhani, P, Schumacher, J, Jankowski, J, Gockel, I, Esophageal Cancer GWAS Consortium, Bondy, ML, Houlston, RS, Jenkins, RB, Melin, B, Glioma International Case Control Consortium (GICC), Lesseur, C, Ness, AR, Diergaarde, B, Olshan, AF, Head-Neck Cancer GWAS Consortium, Amos, CI, Christiani, DC, Landi, MT, McKay, JD, International Lung Cancer Consortium (ILCCO), Brossard, M, Iles, MM, Law, MH, MacGregor, S, Melanoma GWAS Consortium, Beesley, J, Jones, MR, Tyrer, J, Winham, SJ, Ovarian Cancer Association Consortium (OCAC), Klein, AP, Petersen, G, Li, D, Wolpin, BM, Pancreatic Cancer Case-Control Consortium (PANC4), Pancreatic Cancer Cohort Consortium (PanScan), Eeles, RA, Haiman, CA, Kote-Jarai, Z, Schumacher, FR, PRACTICAL consortium, CRUK, BPC3, CAPS, PEGASUS, Brennan, P, Chanock, SJ, Gaborieau, V, Purdue, MP, Renal Cancer GWAS Consortium, Pharoah, P, Hung, RJ, Amundadottir, LT, Kraft, P, Pasaniuc, B, and Lindström, S

Abstract

Genome-wide association studies (GWASs) have identified thousands of cancer risk loci revealing many risk regions shared across multiple cancers. Characterizing the cross-cancer shared genetic basis can increase our understanding of global mechanisms of cancer development. In this study, we collected GWAS summary statistics based on up to 375,468 cancer cases and 530,521 controls for fourteen types of cancer, including breast (overall, estrogen receptor [ER]-positive, and ER-negative), colorectal, endometrial, esophageal, glioma, head/neck, lung, melanoma, ovarian, pancreatic, prostate, and renal cancer, to characterize the shared genetic basis of cancer risk. We identified thirteen pairs of cancers with statistically significant local genetic correlations across eight distinct genomic regions. Specifically, the 5p15.33 region, harboring the TERT and CLPTM1L genes, showed statistically significant local genetic correlations for multiple cancer pairs. We conducted a cross-cancer fine-mapping of the 5p15.33 region based on eight cancers that showed genome-wide significant associations in this region (ER-negative breast, colorectal, glioma, lung, melanoma, ovarian, pancreatic, and prostate cancer). We used an iterative analysis pipeline implementing a subset-based meta-analysis approach based on cancer-specific conditional analyses and identified ten independent cross-cancer associations within this region. For each signal, we conducted cross-cancer fine-mapping to prioritize the most plausible causal variants. Our findings provide a more in-depth understanding of the shared inherited basis across human cancers and expand our knowledge of the 5p15.33 region in carcinogenesis.

Published
2021

37. Hypoxia compromises the mitochondrial metabolism of Alzheimer's disease microglia via HIF1

Author

March-Diaz, R., Lara-Ureña, N, Romero-Molina, C., Heras-Garvin, A., Ortega-de San Luis, C., Alvarez-Vergara, M.I., Sanchez-Garcia, M.A., Sanchez-Mejias, E., Davila, J.C., Rosales-Nieves, A.E., Forja, C., Navarro, V., Gomez-Arboledas, A., Sanchez-Mico, M.V., Viehweger, A., Gerpe, A., Hodson, E.J., Vizuete, M., Bishop, T., Serrano-Pozo, A., Lopez-Barneo, J., Berra, E., Gutierrez, A., Vitorica, J., and Pascual, A.

Subjects
aerobic respiration, HIF1, anaerobic glycolysis, microglia, Alzheimer's disease, Hypoxia
Abstract

Genetic Alzheimer’s disease (AD) risk factors associate with reduced defensive amyloid β plaque-associated microglia (AβAM), but the contribution of modifiable AD risk factors to microglial dysfunction is unknown. In AD mouse models, we observe concomitant activation of the hypoxia-inducible factor 1 (HIF1) pathway and transcription of mitochondrial-related genes in AβAM, and elongation of mitochondria, a cellular response to maintain aerobic respiration under low nutrient and oxygen conditions. Overactivation of HIF1 induces microglial quiescence in cellulo, with lower mitochondrial respiration and proliferation. In vivo, overstabilization of HIF1, either genetically or by exposure to systemic hypoxia, reduces AβAM clustering and proliferation and increases Aβ neuropathology. In the human AD hippocampus, upregulation of HIF1α and HIF1 target genes correlates with reduced Aβ plaque microglial coverage and an increase of Aβ plaque-associated neuropathology. Thus, hypoxia (a modifiable AD risk factor) hijacks microglial mitochondrial metabolism and converges with genetic susceptibility to cause AD microglial dysfunction.

Published
2021

48. Germline ATM variants predispose to melanoma: a joint analysis across the GenoMEL and MelaNostrum consortia

Author

Dalmasso, B. Pastorino, L. Nathan, V Shah, N. N. Palmer, J. M. Howlie, M. Johansson, P. A. Freedman, N. D. and Carter, B. D. Beane-Freeman, L. Hicks, B. Molven, A. and Helgadottir, H. Sankar, A. Tsao, H. Stratigos, A. J. and Helsing, P. Van Doorn, R. Gruis, N. A. Visser, M. Wadt, K. A. W. Mann, G. Holland, E. A. Nagore, E. Potrony, M. and Puig, S. Menin, C. Peris, K. Fargnoli, M. C. and Calista, D. Soufir, N. Harland, M. Bishop, T. Kanetsky, P. A. Elder, D. E. Andreotti, V Vanni, I Bruno, W. and Hoiom, V Tucker, M. A. Yang, X. R. Andresen, P. A. and Adams, D. J. Landi, M. T. Hayward, N. K. Goldstein, A. M. and Ghiorzo, P. GenoMEL MelaNostrum Consortia

Abstract

Purpose Ataxia-Telangiectasia Mutated (ATM) has been implicated in the risk of several cancers, but establishing a causal relationship is often challenging. Although ATM single-nucleotide polymorphisms have been linked to melanoma, few functional alleles have been identified. Therefore, ATM impact on melanoma predisposition is unclear. Methods From 22 American, Australian, and European sites, we collected 2,104 familial, multiple primary (MPM), and sporadic melanoma cases who underwent ATM genotyping via panel, exome, or genome sequencing, and compared the allele frequency (AF) of selected ATM variants classified as loss-of-function (LOF) and variants of uncertain significance (VUS) between this cohort and the gnomAD non-Finnish European (NFE) data set. Results LOF variants were more represented in our study cohort than in gnomAD NFE, both in all (AF = 0.005 and 0.002, OR = 2.6, 95% CI = 1.56-4.11, p < 0.01), and familial + MPM cases (AF = 0.0054 and 0.002, OR = 2.97, p < 0.01). Similarly, VUS were enriched in all (AF = 0.046 and 0.033, OR = 1.41, 95% CI = 1.6-5.09, p < 0.01) and familial + MPM cases (AF = 0.053 and 0.033, OR = 1.63, p < 0.01). In a case-control comparison of two centers that provided 1,446 controls, LOF and VUS were enriched in familial + MPM cases (p = 0.027, p = 0.018). Conclusion This study, describing the largest multicenter melanoma cohort investigated for ATM germline variants, supports the role of ATM as a melanoma predisposition gene, with LOF variants suggesting a moderate-risk.

Published
2021

49. Heterogeneity of Associations between Total and Types of Fish Intake and the Incidence of Type 2 Diabetes: Federated Meta-Analysis of 28 Prospective Studies Including 956,122 Participants

Author

Pastorino, S, Bishop, T, Sharp, SJ, Pearce, M, Akbaraly, T, Barbieri, NB, Bes-Rastrollo, M, Beulens, JWJ, Chen, Z, Du, H, Duncan, BB, Goto, A, Harkanen, T, Hashemian, M, Kromhout, D, Jarvinen, R, Kivimaki, M, Knekt, P, Lin, X, Lund, E, Magliano, DJ, Malekzadeh, R, Angel Martinez-Gonzalez, M, O'Donoghue, G, O'Gorman, D, Poustchi, H, Rylander, C, Sawada, N, Shaw, JE, Schmidt, M, Soedamah-Muthu, SS, Sun, L, Wen, W, Wolk, A, Shu, X-O, Zheng, W, Wareham, NJ, Forouhi, NG, Pastorino, S, Bishop, T, Sharp, SJ, Pearce, M, Akbaraly, T, Barbieri, NB, Bes-Rastrollo, M, Beulens, JWJ, Chen, Z, Du, H, Duncan, BB, Goto, A, Harkanen, T, Hashemian, M, Kromhout, D, Jarvinen, R, Kivimaki, M, Knekt, P, Lin, X, Lund, E, Magliano, DJ, Malekzadeh, R, Angel Martinez-Gonzalez, M, O'Donoghue, G, O'Gorman, D, Poustchi, H, Rylander, C, Sawada, N, Shaw, JE, Schmidt, M, Soedamah-Muthu, SS, Sun, L, Wen, W, Wolk, A, Shu, X-O, Zheng, W, Wareham, NJ, and Forouhi, NG

Abstract

The association between fish consumption and new-onset type 2 diabetes is inconsistent and differs according to geographical location. We examined the association between the total and types of fish consumption and type 2 diabetes using individual participant data from 28 prospective cohort studies from the Americas (6), Europe (15), the Western Pacific (6), and the Eastern Mediterranean (1) comprising 956,122 participants and 48,084 cases of incident type 2 diabetes. Incidence rate ratios (IRRs) for associations of total fish, shellfish, fatty, lean, fried, freshwater, and saltwater fish intake and type 2 diabetes were derived for each study, adjusting for a consistent set of confounders and combined across studies using random-effects meta-analysis. We stratified all analyses by sex due to observed interaction (p = 0.002) on the association between fish and type 2 diabetes. In women, for each 100 g/week higher intake the IRRs (95% CIs) of type 2 diabetes were 1.02 (1.01-1.03, I2 = 61%) for total fish, 1.04 (1.01-1.07, I2 = 46%) for fatty fish, and 1.02 (1.00-1.04, I2 = 33%) for lean fish. In men, all associations were null. In women, we observed variation by geographical location: IRRs for total fish were 1.03 (1.02-1.04, I2 = 0%) in the Americas and null in other regions. In conclusion, we found evidence of a neutral association between total fish intake and type 2 diabetes in men, but there was a modest positive association among women with heterogeneity across studies, which was partly explained by geographical location and types of fish intake. Future research should investigate the role of cooking methods, accompanying foods and environmental pollutants, but meanwhile, existing dietary regional, national, or international guidelines should continue to guide fish consumption within overall healthy dietary patterns.

Published
2021

50. Automatic classification of takeaway food outlet cuisine type using machine (deep) learning

Author

Bishop, T, von Hinke, Stephanie, Hollingsworth, B, Lake, A, Brown, H, Burgoine, T, Bishop, T, von Hinke, Stephanie, Hollingsworth, B, Lake, A, Brown, H, and Burgoine, T

Abstract

Background and purpose: Researchers have not disaggregated neighbourhood exposure to takeaway (‘fast-’) food outlets by cuisine type sold, which would otherwise permit examination of differential impacts on diet, obesity and related disease. This is partly due to the substantial resource challenge of manual classification of unclassified takeaway outlets at scale. We describe the development of a new model to automatically classify takeaway food outlets, by 10 major cuisine types, based on business name alone. Material and methods: We used machine (deep) learning, and specifically a Long Short Term Memory variant of a Recurrent Neural Network, to develop a predictive model trained on labelled outlets (n14,145), from an online takeaway food ordering platform. We validated the accuracy of predictions on unseen labelled outlets (n4,000) from the same source. Results: Although accuracy of prediction varied by cuisine type, overall the model (or ‘classifier’) made a correct prediction approximately three out of four times. We demonstrated the potential of the classifier to public health researchers and for surveillance to support decision-making, through using it to characterise nearly 55,000 takeaway food outlets in England by cuisine type, for the first time. Conclusions: Although imperfect, we successfully developed a model to classify takeaway food outlets, by 10 major cuisine types, from business name alone, using innovative data science methods. We have made the model available for use elsewhere by others, including in other contexts and to characterise other types of food outlets, and for further development.

Published
2021

Catalog

Books, media, physical & digital resources
See catalog results