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450 results on '"Williams, Frances M. K."'

1. Discovery of circulating blood biomarkers in patients with and without Modic changes of the lumbar spine: a preliminary analysis

Author

Aboushaala, Khaled, Chee, Ana V., Toro, Sheila J., Vucicevic, Rajko, Yuh, Catherine, Dourdourekas, Jake, Patel, Ishani K., Espinoza-Orias, Alejandro, Oh, Chundo, Al-Harthi, Lena, Karppinen, Jaro, Goldberg, Edward J., Phillips, Frank M., Colman, Matthew, Williams, Frances M. K., Borgia, Jeffrey A., Green, Stefan, Forsyth, Christopher, An, Howard S., and Samartzis, Dino

Published
2024
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10. Long COVID burden and risk factors in 10 UK longitudinal studies and electronic health records

Author

Thompson, Ellen J., Williams, Dylan M., Walker, Alex J., Mitchell, Ruth E., Niedzwiedz, Claire L., Yang, Tiffany C., Huggins, Charlotte F., Kwong, Alex S. F., Silverwood, Richard J., Di Gessa, Giorgio, Bowyer, Ruth C. E., Northstone, Kate, Hou, Bo, Green, Michael J., Dodgeon, Brian, Doores, Katie J., Duncan, Emma L., Williams, Frances M. K., Steptoe, Andrew, Porteous, David J., McEachan, Rosemary R. C., Tomlinson, Laurie, Goldacre, Ben, Patalay, Praveetha, Ploubidis, George B., Katikireddi, Srinivasa Vittal, Tilling, Kate, Rentsch, Christopher T., Timpson, Nicholas J., Chaturvedi, Nishi, and Steves, Claire J.

Published
2022
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13. Decomposing the genetic background of chronic back pain

Author

Elgaeva, Elizaveta E., primary, Zorkoltseva, Irina V., additional, Nostaeva, Arina V., additional, Verzun, Dmitrii A., additional, Tiys, Evgeny S., additional, Timoshchuk, Anna N., additional, Kirichenko, Anatoliy V., additional, Svishcheva, Gulnara R., additional, Freidin, Maxim B., additional, Williams, Frances M. K., additional, Suri, Pradeep, additional, Aulchenko, Yurii S., additional, Axenovich, Tatiana I., additional, and Tsepilov, Yakov A., additional

Published
2024
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15. Attributes and predictors of long COVID

Author

Sudre, Carole H., Murray, Benjamin, Varsavsky, Thomas, Graham, Mark S., Penfold, Rose S., Bowyer, Ruth C., Pujol, Joan Capdevila, Klaser, Kerstin, Antonelli, Michela, Canas, Liane S., Molteni, Erika, Modat, Marc, Jorge Cardoso, M., May, Anna, Ganesh, Sajaysurya, Davies, Richard, Nguyen, Long H., Drew, David A., Astley, Christina M., Joshi, Amit D., Merino, Jordi, Tsereteli, Neli, Fall, Tove, Gomez, Maria F., Duncan, Emma L., Menni, Cristina, Williams, Frances M. K., Franks, Paul W., Chan, Andrew T., Wolf, Jonathan, Ourselin, Sebastien, Spector, Tim, and Steves, Claire J.

Published
2021
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16. Glycoprotein Acetyls Is a Novel Biomarker Predicting Cardiovascular Complications in Rheumatoid Arthritis.

Author

Kasher, Melody, Freidin, Maxim B., Williams, Frances M. K., Cherny, Stacey S., Ashkenazi, Shai, and Livshits, Gregory

Subjects
CARDIOLOGICAL manifestations of general diseases, RHEUMATOID arthritis, LOW density lipoproteins, GENOME-wide association studies, CARDIOVASCULAR diseases
Abstract

The relationship between rheumatoid arthritis (RA) and early onset atherosclerosis is well depicted, each with an important inflammatory component. Glycoprotein acetyls (GlycA), a novel biomarker of inflammation, may play a role in the manifestation of these two inflammatory conditions. The present study examined a potential mediating role of GlycA within the RA–atherosclerosis relationship to determine whether it accounts for the excess risk of cardiovascular disease over that posed by lipid risk factors. The UK Biobank dataset was acquired to establish associations among RA, atherosclerosis, GlycA, and major lipid factors: total cholesterol (TC), high- and low-density lipoprotein (HDL, LDL) cholesterol, and triglycerides (TGs). Genome-wide association study summary statistics were collected from various resources to perform genetic analyses. Causality among variables was tested using Mendelian Randomization (MR) analysis. Genes of interest were identified using colocalization analysis and gene enrichment analysis. MR results appeared to indicate that the genetic relationship between GlycA and RA and also between RA and atherosclerosis was explained by horizontal pleiotropy (p-value = 0.001 and <0.001, respectively), while GlycA may causally predict atherosclerosis (p-value = 0.017). Colocalization analysis revealed several functionally relevant genes shared between GlycA and all the variables assessed. Two loci were apparent in all relationships tested and included the HLA region as well as SLC22A1. GlycA appears to mediate the RA–atherosclerosis relationship through several possible pathways. GlycA, although pleiotropically related to RA, appears to causally predict atherosclerosis. Thus, GlycA is suggested as a significant factor in the etiology of atherosclerosis development in RA. [ABSTRACT FROM AUTHOR]

Published
2024
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17. GlycA and CRP Are Genetically Correlated: Insight into the Genetic Architecture of Inflammageing.

Author

Kasher, Melody, Freidin, Maxim B., Williams, Frances M. K., and Livshits, Gregory

Subjects
C-reactive protein, GENOME-wide association studies, INFLAMMATORY mediators, GENETIC correlations, STATISTICAL association, GENETIC variation
Abstract

Inflammageing is a condition of perpetual low-grade inflammation induced by ageing. Inflammageing may be predicted by the C-reactive protein (CRP) or by a recently described biomarker which measures N-glycosylated side chains of the carbohydrate component of several acute-phase proteins known as GlycA. The objective of this study was to examine in depth the genetic relationships between CRP and GlycA as well as between each of them and other selected cytokines, which may shed light on the mechanisms of inflammageing. Using the Olink 96 Inflammation panel, data on inflammatory mediators for 1518 twins from the TwinsUK dataset were acquired. Summary statistics for genome-wide association studies for several cytokines as well as CRP and GlycA were collected from public sources. Extensive genetic correlation analyses, colocalization and genetic enrichment analyses were carried out to detect the shared genetic architecture between GlycA and CRP. Mendelian randomization was carried out to assess potential causal relationships. GlycA predicted examined cytokines with a magnitude twice as great as that of CRP. GlycA and CRP were significantly genetically correlated (Rg = 0.4397 ± 0.0854, p-value = 2.60 × 10−7). No evidence of a causal relationship between GlycA and CRP, or between these two biomarkers and the cytokines assessed was obtained. However, the aforementioned relationships were explained well by horizontal pleiotropy. Five exonic genetic variants annotated to five genes explain the shared genetic architecture observed between GlycA and CRP: IL6R, GCKR, MLXIPL, SERPINA1, and MAP1A. GlycA and CRP possess a shared genetic architecture, but the relationship between them appears to be modest, which may imply the promotion of differing inflammatory pathways. GlycA appears to be a more robust predictor of cytokines compared to CRP. [ABSTRACT FROM AUTHOR]

Published
2024
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26. Multi-Trait Exome-Wide Association Study of Back Pain-Related Phenotypes

Author

Zorkoltseva, Irina V., primary, Elgaeva, Elizaveta E., additional, Belonogova, Nadezhda M., additional, Kirichenko, Anatoliy V., additional, Svishcheva, Gulnara R., additional, Freidin, Maxim B., additional, Williams, Frances M. K., additional, Suri, Pradeep, additional, Tsepilov, Yakov A., additional, and Axenovich, Tatiana I., additional

Published
2023
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27. The Human Microbiome and Its Role in Musculoskeletal Disorders

Author

Aboushaala, Khaled, primary, Wong, Arnold Y. L., additional, Barajas, Juan Nicolas, additional, Lim, Perry, additional, Al-Harthi, Lena, additional, Chee, Ana, additional, Forsyth, Christopher B., additional, Oh, Chun-do, additional, Toro, Sheila J., additional, Williams, Frances M. K., additional, An, Howard S., additional, and Samartzis, Dino, additional

Published
2023
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30. Author Correction: Attributes and predictors of long COVID

Author

Sudre, Carole H., Murray, Benjamin, Varsavsky, Thomas, Graham, Mark S., Penfold, Rose S., Bowyer, Ruth C., Pujol, Joan Capdevila, Klaser, Kerstin, Antonelli, Michela, Canas, Liane S., Molteni, Erika, Modat, Marc, Jorge Cardoso, M., May, Anna, Ganesh, Sajaysurya, Davies, Richard, Nguyen, Long H., Drew, David A., Astley, Christina M., Joshi, Amit D., Merino, Jordi, Tsereteli, Neli, Fall, Tove, Gomez, Maria F., Duncan, Emma L., Menni, Cristina, Williams, Frances M. K., Franks, Paul W., Chan, Andrew T., Wolf, Jonathan, Ourselin, Sebastien, Spector, Tim, and Steves, Claire J.

Published
2021
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32. Genome-wide association meta-analysis identifies five novel loci for age-related hearing impairment

Author

Nagtegaal, Andries Paul, Broer, Linda, Zilhao, Nuno R., Jakobsdottir, Johanna, Bishop, Charles E., Brumat, Marco, Christiansen, Mark W., Cocca, Massimiliano, Gao, Yan, Heard-Costa, Nancy L., Evans, Daniel S., Pankratz, Nathan, Pratt, Sheila R., Price, T. Ryan, Spankovich, Christopher, Stimson, Mary R., Valle, Karen, Vuckovic, Dragana, Wells, Helena, Eiriksdottir, Gudny, Fransen, Erik, Ikram, Mohammad Arfan, Li, Chuang-Ming, Longstreth, Jr, W. T., Steves, Claire, Van Camp, Guy, Correa, Adolfo, Cruickshanks, Karen J., Gasparini, Paolo, Girotto, Giorgia, Kaplan, Robert C., Nalls, Michael, Schweinfurth, John M., Seshadri, Sudha, Sotoodehnia, Nona, Tranah, Gregory J., Uitterlinden, André G., Wilson, James G., Gudnason, Vilmundur, Hoffman, Howard J., Williams, Frances M. K., and Goedegebure, André

Published
2019
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37. Development and Replication of a Genome-Wide Polygenic Risk Score for Chronic Back Pain.

Author

Tsepilov, Yakov A., Elgaeva, Elizaveta E., Nostaeva, Arina V., Compte, Roger, Kuznetsov, Ivan A., Karssen, Lennart C., Freidin, Maxim B., Suri, Pradeep, Williams, Frances M. K., and Aulchenko, Yurii S.

Subjects
DISEASE risk factors, MONOGENIC & polygenic inheritance (Genetics), BACKACHE, CHRONIC pain, MYOCARDIAL ischemia
Abstract

Chronic back pain (CBP) is a complex heritable trait and a major cause of disability worldwide. We developed and validated a genome-wide polygenic risk score (PRS) for CBP using a large-scale GWAS based on UK Biobank participants of European ancestry (N = 265,000). The PRS showed poor overall predictive ability (AUC = 0.56 and OR = 1.24 per SD, 95% CI: 1.22–1.26), but individuals from the 99th percentile of PRS distribution had a nearly two-fold increased risk of CBP (OR = 1.82, 95% CI: 1.60–2.06). We validated the PRS on an independent TwinsUK sample, obtaining a similar magnitude of effect. The PRS was significantly associated with various ICD-10 and OPCS-4 diagnostic codes, including chronic ischemic heart disease (OR = 1.1, p-value = 4.8 × 10−15), obesity, metabolism-related traits, spine disorders, disc degeneration, and arthritis-related disorders. PRS and environment interaction analysis with twelve known CBP risk factors revealed no significant results, suggesting that the magnitude of G × E interactions with studied factors is small. The limited predictive ability of the PRS that we developed is likely explained by the complexity, heterogeneity, and polygenicity of CBP, for which sample sizes of a few hundred thousand are insufficient to estimate small genetic effects robustly. [ABSTRACT FROM AUTHOR]

Published
2023
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43. Large meta-analysis of genome-wide association studies identifies five loci for lean body mass

Author

Zillikens, M. Carola, Demissie, Serkalem, Hsu, Yi-Hsiang, Yerges-Armstrong, Laura M., Chou, Wen-Chi, Stolk, Lisette, Livshits, Gregory, Broer, Linda, Johnson, Toby, Koller, Daniel L., Kutalik, Zoltán, Luan, Jian’an, Malkin, Ida, Ried, Janina S., Smith, Albert V., Thorleifsson, Gudmar, Vandenput, Liesbeth, Hua Zhao, Jing, Zhang, Weihua, Aghdassi, Ali, Åkesson, Kristina, Amin, Najaf, Baier, Leslie J., Barroso, Inês, Bennett, David A., Bertram, Lars, Biffar, Rainer, Bochud, Murielle, Boehnke, Michael, Borecki, Ingrid B., Buchman, Aron S., Byberg, Liisa, Campbell, Harry, Campos Obanda, Natalia, Cauley, Jane A., Cawthon, Peggy M., Cederberg, Henna, Chen, Zhao, Cho, Nam H., Jin Choi, Hyung, Claussnitzer, Melina, Collins, Francis, Cummings, Steven R., De Jager, Philip L., Demuth, Ilja, Dhonukshe-Rutten, Rosalie A. M., Diatchenko, Luda, Eiriksdottir, Gudny, Enneman, Anke W., Erdos, Mike, Eriksson, Johan G., Eriksson, Joel, Estrada, Karol, Evans, Daniel S., Feitosa, Mary F., Fu, Mao, Garcia, Melissa, Gieger, Christian, Girke, Thomas, Glazer, Nicole L., Grallert, Harald, Grewal, Jagvir, Han, Bok-Ghee, Hanson, Robert L., Hayward, Caroline, Hofman, Albert, Hoffman, Eric P., Homuth, Georg, Hsueh, Wen-Chi, Hubal, Monica J., Hubbard, Alan, Huffman, Kim M., Husted, Lise B., Illig, Thomas, Ingelsson, Erik, Ittermann, Till, Jansson, John-Olov, Jordan, Joanne M., Jula, Antti, Karlsson, Magnus, Khaw, Kay-Tee, Kilpeläinen, Tuomas O., Klopp, Norman, Kloth, Jacqueline S. L., Koistinen, Heikki A., Kraus, William E., Kritchevsky, Stephen, Kuulasmaa, Teemu, Kuusisto, Johanna, Laakso, Markku, Lahti, Jari, Lang, Thomas, Langdahl, Bente L., Launer, Lenore J., Lee, Jong-Young, Lerch, Markus M., Lewis, Joshua R., Lind, Lars, Lindgren, Cecilia, Liu, Yongmei, Liu, Tian, Liu, Youfang, Ljunggren, Östen, Lorentzon, Mattias, Luben, Robert N., Maixner, William, McGuigan, Fiona E., Medina-Gomez, Carolina, Meitinger, Thomas, Melhus, Håkan, Mellström, Dan, Melov, Simon, Michaëlsson, Karl, Mitchell, Braxton D., Morris, Andrew P., Mosekilde, Leif, Newman, Anne, Nielson, Carrie M., O’Connell, Jeffrey R., Oostra, Ben A., Orwoll, Eric S., Palotie, Aarno, Parker, Stephen C. J., Peacock, Munro, Perola, Markus, Peters, Annette, Polasek, Ozren, Prince, Richard L., Räikkönen, Katri, Ralston, Stuart H., Ripatti, Samuli, Robbins, John A., Rotter, Jerome I., Rudan, Igor, Salomaa, Veikko, Satterfield, Suzanne, Schadt, Eric E., Schipf, Sabine, Scott, Laura, Sehmi, Joban, Shen, Jian, Soo Shin, Chan, Sigurdsson, Gunnar, Smith, Shad, Soranzo, Nicole, Stančáková, Alena, Steinhagen-Thiessen, Elisabeth, Streeten, Elizabeth A., Styrkarsdottir, Unnur, Swart, Karin M. A., Tan, Sian-Tsung, Tarnopolsky, Mark A., Thompson, Patricia, Thomson, Cynthia A., Thorsteinsdottir, Unnur, Tikkanen, Emmi, Tranah, Gregory J., Tuomilehto, Jaakko, van Schoor, Natasja M., Verma, Arjun, Vollenweider, Peter, Völzke, Henry, Wactawski-Wende, Jean, Walker, Mark, Weedon, Michael N., Welch, Ryan, Wichmann, H.-Erich, Widen, Elisabeth, Williams, Frances M. K., Wilson, James F., Wright, Nicole C., Xie, Weijia, Yu, Lei, Zhou, Yanhua, Chambers, John C., Döring, Angela, van Duijn, Cornelia M., Econs, Michael J., Gudnason, Vilmundur, Kooner, Jaspal S., Psaty, Bruce M., Spector, Timothy D., Stefansson, Kari, Rivadeneira, Fernando, Uitterlinden, André G., Wareham, Nicholas J., Ossowski, Vicky, Waterworth, Dawn, Loos, Ruth J. F., Karasik, David, Harris, Tamara B., Ohlsson, Claes, and Kiel, Douglas P.

Published
2017
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48. Additional file 1 of Baseline predictors of remission, pain and fatigue in rheumatoid arthritis: the TITRATE trial

Author

Lee, Sook Yan, Ibrahim, Fowzia, Tom, Brian D. M., Nikiphorou, Elena, Williams, Frances M. K., Lempp, Heidi, and Scott, David L.

Subjects
skin and connective tissue diseases
Abstract

Additional file 1: Supplementary Table 1: Characteristics of the TITRATE trial patients (N=335). Supplementary Table 2: Baseline characteristics of patients who achieved remission at 12 months. Supplementary Table 3: Baseline characteristics of patients who achieved minimal clinical change in Pain at 12 months. Supplementary Table 4: Baseline characteristics of patients who achieved minimal clinical change in Fatigue at 12 months. Supplementary Table 5: Impact of Obesity on Components of DAS28-ESR at 12 Months.

Published
2021
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