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2,968 results on '"Borja, A."'

1. Population genomics of post-glacial western Eurasia

Author

Allentoft, Morten E, Sikora, Martin, Refoyo-Martínez, Alba, Irving-Pease, Evan K, Fischer, Anders, Barrie, William, Ingason, Andrés, Stenderup, Jesper, Sjögren, Karl-Göran, Pearson, Alice, Sousa da Mota, Bárbara, Schulz Paulsson, Bettina, Halgren, Alma, Macleod, Ruairidh, Jørkov, Marie Louise Schjellerup, Demeter, Fabrice, Sørensen, Lasse, Nielsen, Poul Otto, Henriksen, Rasmus A, Vimala, Tharsika, McColl, Hugh, Margaryan, Ashot, Ilardo, Melissa, Vaughn, Andrew, Fischer Mortensen, Morten, Nielsen, Anne Birgitte, Ulfeldt Hede, Mikkel, Johannsen, Niels Nørkjær, Rasmussen, Peter, Vinner, Lasse, Renaud, Gabriel, Stern, Aaron, Jensen, Theis Zetner Trolle, Scorrano, Gabriele, Schroeder, Hannes, Lysdahl, Per, Ramsøe, Abigail Daisy, Skorobogatov, Andrei, Schork, Andrew Joseph, Rosengren, Anders, Ruter, Anthony, Outram, Alan, Timoshenko, Aleksey A, Buzhilova, Alexandra, Coppa, Alfredo, Zubova, Alisa, Silva, Ana Maria, Hansen, Anders J, Gromov, Andrey, Logvin, Andrey, Gotfredsen, Anne Birgitte, Henning Nielsen, Bjarne, González-Rabanal, Borja, Lalueza-Fox, Carles, McKenzie, Catriona J, Gaunitz, Charleen, Blasco, Concepción, Liesau, Corina, Martinez-Labarga, Cristina, Pozdnyakov, Dmitri V, Cuenca-Solana, David, Lordkipanidze, David O, En’shin, Dmitri, Salazar-García, Domingo C, Price, T Douglas, Borić, Dušan, Kostyleva, Elena, Veselovskaya, Elizaveta V, Usmanova, Emma R, Cappellini, Enrico, Brinch Petersen, Erik, Kannegaard, Esben, Radina, Francesca, Eylem Yediay, Fulya, Duday, Henri, Gutiérrez-Zugasti, Igor, Merts, Ilya, Potekhina, Inna, Shevnina, Irina, Altinkaya, Isin, Guilaine, Jean, Hansen, Jesper, Aura Tortosa, Joan Emili, Zilhão, João, Vega, Jorge, Buck Pedersen, Kristoffer, Tunia, Krzysztof, Zhao, Lei, Mylnikova, Liudmila N, Larsson, Lars, Metz, Laure, Yepiskoposyan, Levon, Pedersen, Lisbeth, Sarti, Lucia, Orlando, Ludovic, Slimak, Ludovic, Klassen, Lutz, Blank, Malou, González-Morales, Manuel, and Silvestrini, Mara

Subjects
Biological Sciences, Genetics, History, Heritage and Archaeology, Human Society, Historical Studies, Anthropology, Biotechnology, Humans, Genomics, Diploidy, Agriculture, Europe, Metagenomics, General Science & Technology
Abstract

Western Eurasia witnessed several large-scale human migrations during the Holocene1-5. Here, to investigate the cross-continental effects of these migrations, we shotgun-sequenced 317 genomes-mainly from the Mesolithic and Neolithic periods-from across northern and western Eurasia. These were imputed alongside published data to obtain diploid genotypes from more than 1,600 ancient humans. Our analyses revealed a 'great divide' genomic boundary extending from the Black Sea to the Baltic. Mesolithic hunter-gatherers were highly genetically differentiated east and west of this zone, and the effect of the neolithization was equally disparate. Large-scale ancestry shifts occurred in the west as farming was introduced, including near-total replacement of hunter-gatherers in many areas, whereas no substantial ancestry shifts happened east of the zone during the same period. Similarly, relatedness decreased in the west from the Neolithic transition onwards, whereas, east of the Urals, relatedness remained high until around 4,000 BP, consistent with the persistence of localized groups of hunter-gatherers. The boundary dissolved when Yamnaya-related ancestry spread across western Eurasia around 5,000 BP, resulting in a second major turnover that reached most parts of Europe within a 1,000-year span. The genetic origin and fate of the Yamnaya have remained elusive, but we show that hunter-gatherers from the Middle Don region contributed ancestry to them. Yamnaya groups later admixed with individuals associated with the Globular Amphora culture before expanding into Europe. Similar turnovers occurred in western Siberia, where we report new genomic data from a 'Neolithic steppe' cline spanning the Siberian forest steppe to Lake Baikal. These prehistoric migrations had profound and lasting effects on the genetic diversity of Eurasian populations.

Published
2024

2. Subcortical Brain Alterations in Carriers of Genomic Copy Number Variants.

Author

Kumar, Kuldeep, Modenato, Claudia, Moreau, Clara, Ching, Christopher, Harvey, Annabelle, Martin-Brevet, Sandra, Huguet, Guillaume, Jean-Louis, Martineau, Douard, Elise, Martin, Charles-Olivier, Younis, Nadine, Tamer, Petra, Maillard, Anne, Rodriguez-Herreros, Borja, Pain, Aurélie, Kushan, Leila, Isaev, Dmitry, Alpert, Kathryn, Ragothaman, Anjani, Turner, Jessica, Wang, Lei, Ho, Tiffany, Schmaal, Lianne, Silva, Ana, van den Bree, Marianne, Linden, David, Owen, Michael, Hall, Jeremy, Lippé, Sarah, Dumas, Guillaume, Draganski, Bogdan, Gutman, Boris, Sønderby, Ida, Andreassen, Ole, Schultz, Laura, Almasy, Laura, Glahn, David, Bearden, Carrie, Thompson, Paul, and Jacquemont, Sébastien

Subjects
Depressive Disorders, Genetics/Genomics, Neurodevelopmental Disorders, Neuroimaging, Schizophrenia Spectrum and Other Psychotic Disorders, Male, Adult, Humans, Child, Adolescent, Young Adult, Middle Aged, Aged, Aged, 80 and over, DNA Copy Number Variations, Schizophrenia, Brain, Attention Deficit Disorder with Hyperactivity, Genomics
Abstract

OBJECTIVE: Copy number variants (CNVs) are well-known genetic pleiotropic risk factors for multiple neurodevelopmental and psychiatric disorders (NPDs), including autism (ASD) and schizophrenia. Little is known about how different CNVs conferring risk for the same condition may affect subcortical brain structures and how these alterations relate to the level of disease risk conferred by CNVs. To fill this gap, the authors investigated gross volume, vertex-level thickness, and surface maps of subcortical structures in 11 CNVs and six NPDs. METHODS: Subcortical structures were characterized using harmonized ENIGMA protocols in 675 CNV carriers (CNVs at 1q21.1, TAR, 13q12.12, 15q11.2, 16p11.2, 16p13.11, and 22q11.2; age range, 6-80 years; 340 males) and 782 control subjects (age range, 6-80 years; 387 males) as well as ENIGMA summary statistics for ASD, schizophrenia, attention deficit hyperactivity disorder, obsessive-compulsive disorder, bipolar disorder, and major depression. RESULTS: All CNVs showed alterations in at least one subcortical measure. Each structure was affected by at least two CNVs, and the hippocampus and amygdala were affected by five. Shape analyses detected subregional alterations that were averaged out in volume analyses. A common latent dimension was identified, characterized by opposing effects on the hippocampus/amygdala and putamen/pallidum, across CNVs and across NPDs. Effect sizes of CNVs on subcortical volume, thickness, and local surface area were correlated with their previously reported effect sizes on cognition and risk for ASD and schizophrenia. CONCLUSIONS: The findings demonstrate that subcortical alterations associated with CNVs show varying levels of similarities with those associated with neuropsychiatric conditions, as well distinct effects, with some CNVs clustering with adult-onset conditions and others with ASD. These findings provide insight into the long-standing questions of why CNVs at different genomic loci increase the risk for the same NPD and why a single CNV increases the risk for a diverse set of NPDs.

Published
2023

3. Rare CNVs and phenome-wide profiling highlight brain structural divergence and phenotypical convergence.

Author

Kopal, Jakub, Kumar, Kuldeep, Saltoun, Karin, Modenato, Claudia, Moreau, Clara, Martin-Brevet, Sandra, Huguet, Guillaume, Jean-Louis, Martineau, Martin, Charles-Olivier, Saci, Zohra, Younis, Nadine, Tamer, Petra, Douard, Elise, Maillard, Anne, Rodriguez-Herreros, Borja, Pain, Aurèlie, Richetin, Sonia, Kushan, Leila, Silva, Ana, van den Bree, Marianne, Linden, David, Owen, Michael, Hall, Jeremy, Lippé, Sarah, Draganski, Bogdan, Sønderby, Ida, Andreassen, Ole, Glahn, David, Thompson, Paul, Jacquemont, Sébastien, Bzdok, Danilo, and Bearden, Carrie

Subjects
Humans, DNA Copy Number Variations, Brain
Abstract

Copy number variations (CNVs) are rare genomic deletions and duplications that can affect brain and behaviour. Previous reports of CNV pleiotropy imply that they converge on shared mechanisms at some level of pathway cascades, from genes to large-scale neural circuits to the phenome. However, existing studies have primarily examined single CNV loci in small clinical cohorts. It remains unknown, for example, how distinct CNVs escalate vulnerability for the same developmental and psychiatric disorders. Here we quantitatively dissect the associations between brain organization and behavioural differentiation across 8 key CNVs. In 534 CNV carriers, we explored CNV-specific brain morphology patterns. CNVs were characteristic of disparate morphological changes involving multiple large-scale networks. We extensively annotated these CNV-associated patterns with ~1,000 lifestyle indicators through the UK Biobank resource. The resulting phenotypic profiles largely overlap and have body-wide implications, including the cardiovascular, endocrine, skeletal and nervous systems. Our population-level investigation established brain structural divergences and phenotypical convergences of CNVs, with direct relevance to major brain disorders.

Published
2023

4. The earliest Ethiopian wolf: implications for the species evolution and its future survival.

Author

Martínez-Navarro, Bienvenido, Gossa, Tegenu, Carotenuto, Francesco, Bartolini-Lucenti, Saverio, Palmqvist, Paul, Asrat, Asfawossen, Figueirido, Borja, Rook, Lorenzo, Niespolo, Elizabeth M, Renne, Paul R, Herzlinger, Gadi, and Hovers, Erella

Subjects
Animals, Wolves, Humans, Biodiversity, Phylogeny, Africa, Endangered Species, Life on Land
Abstract

In 2017, a hemimandible (MW5-B208), corresponding to the Ethiopian wolf (Canis simensis), was found in a stratigraphically-controlled and radio-isotopically-dated sequence of the Melka Wakena paleoanthropological site-complex, on the Southeastern Ethiopian Highlands, ~ 2300 m above sea level. The specimen is the first and unique Pleistocene fossil of this species. Our data provide an unambiguous minimum age of 1.6-1.4 Ma for the species' presence in Africa and constitutes the first empirical evidence that supports molecular interpretations. Currently, C. simensis is one of the most endangered carnivore species of Africa. Bioclimate niche modeling applied to the time frame indicated by the fossil suggests that the lineage of the Ethiopian wolf faced severe survival challenges in the past, with consecutive drastic geographic range contractions during warmer periods. These models help to describe future scenarios for the survival of the species. Projections ranging from most pessimistic to most optimistic future climatic scenarios indicate significant reduction of the already-deteriorating territories suitable for the Ethiopian Wolf, increasing the threat to the specie's future survival. Additionally, the recovery of the Melka Wakena fossil underscores the importance of work outside the East African Rift System in research of early human origins and associated biodiversity on the African continent.

Published
2023

5. Personality Traits in Patients With Cirrhosis Are Different From Those of the General Population and Impact Likelihood of Liver Transplantation.

Author

Thuluvath, Avesh, Siddiqui, Osama, Peipert, John, Levitsky, Josh, Daud, Amna, Mazumder, Nikhilesh, Flores, Anne-Marie, Borja-Cacho, Daniel, Caicedo, Juan, Loftus, Corinne, Wong, Randi, Mroczek, Dan, Ladner, Daniela, and Lai, Jennifer

Subjects
Adult, Humans, Frailty, Liver Transplantation, Prospective Studies, End Stage Liver Disease, Personality Inventory, Severity of Illness Index, Personality, Liver Cirrhosis
Abstract

BACKGROUND: Personality traits influence clinical outcomes in chronic diseases, but their impact in cirrhosis is unknown. We studied the personality of patients with cirrhosis undergoing liver transplant (LT) evaluation and determined their correlation to clinical outcomes. METHODS: A multicenter prospective study of adult patients undergoing LT evaluation was performed from January 2018 to October 2019. The Big Five personality traits of conscientiousness, extraversion, openness, neuroticism, and agreeableness plus agency were assessed with the Midlife Development Inventory Personality Scale and compared with the general population. Frailty was assessed with the Liver Frailty Index. RESULTS: Two hundred sixty-three LT candidates were enrolled. Twenty-four percent had hepatitis C virus, 25% nonalcoholic steatohepatitis, and 25% ethyl alcohol (mean model for end-stage liver disease = 15.7). Compared with the general population, LT candidates had higher openness (3.1 versus 2.9; P < 0.001), extraversion (3.2 versus 3.1; P < 0.001), agreeableness (3.5 versus 3.4; P = 0.04), agency (2.9 versus 2.6; P < 0.001), neuroticism (2.2 versus 2.1; P = 0.001), and lower conscientiousness (3.3 versus 3.4; P = 0.007). Patients with higher conscientiousness were more likely to receive an LT (HR = 2.76; P = 0.003). CONCLUSIONS: Personality traits in LT candidates differ significantly from the general population, with higher conscientiousness associated with a higher likelihood of receiving a transplant.

Published
2023

6. How predictive of SARS-CoV-2 infection are clinical characteristics at presentation among individuals with COVID-like symptoms treated at the Mexican Institute of Social Security.

Author

Gutierrez, Juan, Olaiz, Gustavo, Juárez-Flores, Arturo, Borja-Aburto, Víctor, Ascencio-Montiel, Iván, and Bertozzi, Stefano

Subjects
Humans, COVID-19, SARS-CoV-2, Pandemics, Retrospective Studies, Mexico, Social Security
Abstract

BACKGROUND: The COVID-19 pandemic has progressed rapidly, with the emergence of new virus variants that pose challenges in treating infected individuals. In Mexico, four epidemic waves have been recorded with varying disease severity. To understand the heterogeneity in clinical presentation over time and the sensitivity and specificity of signs and symptoms in identifying COVID-19 cases, an analysis of the changes in the clinical presentation of the disease was conducted. AIM: To analyze the changes in the clinical presentation of COVID-19 among 3.38 million individuals tested for SARS-CoV-2 at the Mexican Social Security Institute (IMSS) from March 2020 to October 2021 and evaluate the predictivity of signs and symptoms in identifying COVID-19 cases. METHODS: A retrospective analysis of clinical presentation patterns of COVID-19 among individuals treated at IMSS was performed, contrasting the signs and symptoms among SARS-CoV-2-positive individuals with those who tested negative for the virus but had respiratory infection symptoms. The sensitivity and specificity of each sign and symptom in identifying SARS-CoV-2 infection were estimated. RESULTS: The set of signs and symptoms reported for COVID-19-suspected patients treated at IMSS were not highly specific for SARS-CoV-2 positivity. The signs and symptoms exhibited variability based on age and epidemic wave. The area under the receiver operating characteristic (ROC) curve was 0.62 when grouping the five main symptoms (headache, dyspnea, fever, arthralgia, and cough). Most of the individual symptoms had ROC values close to 0.5 (16 out of 22 between 0.48 and 0.52), indicating non-specificity. CONCLUSIONS: The results highlight the difficulty in making a clinical diagnosis of COVID-19 due to the lack of specificity of signs and symptoms. The variability of clinical presentation over time and among age groups highlights the need for further research to differentiate whether the changes are due to changes in the virus, who is becoming infected, or the population, particularly with respect to prior infection and vaccination status.

Published
2023

7. Evolution of differences in clinical presentation across epidemic waves among patients with COVID-like-symptoms who received care at the Mexican Social Security Institute

Author

Olaiz, Gustavo, Bertozzi, Stefano M, Juárez-Flores, Arturo, Borja-Aburto, Víctor H, Vicuña, Félix, Ascencio-Montiel, Iván J, and Gutiérrez, Juan Pablo

Subjects
Health Services and Systems, Public Health, Health Sciences, Infectious Diseases, Prevention, Clinical Research, Infection, Good Health and Well Being, Humans, SARS-CoV-2, COVID-19, Mexico, Social Security, symptoms and signs, social security, big data, Public Health and Health Services, Health services and systems, Public health
Abstract

BackgroundTimely monitoring of SARS-CoV-2 variants is crucial to effectively managing both prevention and treatment efforts. In this paper, we aim to describe demographic and clinical patterns of individuals with COVID-19-like symptoms during the first three epidemic waves in Mexico to identify changes in those patterns that may reflect differences determined by virus variants.MethodsWe conducted a descriptive analysis of a large database containing records for all individuals who sought care at the Mexican Social Security Institute (IMSS) due to COVID-19-like symptoms from March 2020 to October 2021 (4.48 million records). We described the clinical and demographic profile of individuals tested (3.38 million, 32% with PCR and 68% with rapid test) by test result (positives and negatives) and untested, and among those tested, and the changes in those profiles across the first three epidemic waves.ResultsIndividuals with COVID-19-like symptoms were older in the first wave and younger in the third one (the mean age for those positive was 46.6 in the first wave and 36.1 in the third wave; for negatives and not-tested, the mean age was 41 and 38.5 in the first wave and 34.3 and 33.5 in the third wave). As the pandemic progressed, an increasing number of individuals sought care for suspected COVID-19. The positivity rate decreased over time but remained well over the recommended 5%. The pattern of presenting symptoms changed over time, with some of those symptoms decreasing over time (dyspnea 40.6 to 14.0%, cough 80.4 to 76.2%, fever 77.5 to 65.2%, headache 80.3 to 78.5%), and some increasing (odynophagia 48.7 to 58.5%, rhinorrhea 28.6 to 47.5%, anosmia 11.8 to 23.2%, dysgeusia 11.2 to 23.2%).ConclusionDuring epidemic surges, the general consensus was that any individual presenting with respiratory symptoms was a suspected COVID-19 case. However, symptoms and signs are dynamic, with clinical patterns changing not only with the evolution of the virus but also with demographic changes in the affected population. A better understanding of these changing patterns is needed to improve preparedness for future surges and pandemics.

Published
2023

8. Effects of copy number variations on brain structure and risk for psychiatric illness: Large‐scale studies from the ENIGMA working groups on CNVs

Author

Sønderby, Ida E, Ching, Christopher RK, Thomopoulos, Sophia I, van der Meer, Dennis, Sun, Daqiang, Villalon‐Reina, Julio E, Agartz, Ingrid, Amunts, Katrin, Arango, Celso, Armstrong, Nicola J, Ayesa‐Arriola, Rosa, Bakker, Geor, Bassett, Anne S, Boomsma, Dorret I, Bülow, Robin, Butcher, Nancy J, Calhoun, Vince D, Caspers, Svenja, Chow, Eva WC, Cichon, Sven, Ciufolini, Simone, Craig, Michael C, Crespo‐Facorro, Benedicto, Cunningham, Adam C, Dale, Anders M, Dazzan, Paola, de Zubicaray, Greig I, Djurovic, Srdjan, Doherty, Joanne L, Donohoe, Gary, Draganski, Bogdan, Durdle, Courtney A, Ehrlich, Stefan, Emanuel, Beverly S, Espeseth, Thomas, Fisher, Simon E, Ge, Tian, Glahn, David C, Grabe, Hans J, Gur, Raquel E, Gutman, Boris A, Haavik, Jan, Håberg, Asta K, Hansen, Laura A, Hashimoto, Ryota, Hibar, Derrek P, Holmes, Avram J, Hottenga, Jouke‐Jan, Pol, Hilleke E Hulshoff, Jalbrzikowski, Maria, Knowles, Emma EM, Kushan, Leila, Linden, David EJ, Liu, Jingyu, Lundervold, Astri J, Martin‐Brevet, Sandra, Martínez, Kenia, Mather, Karen A, Mathias, Samuel R, McDonald‐McGinn, Donna M, McRae, Allan F, Medland, Sarah E, Moberget, Torgeir, Modenato, Claudia, Sánchez, Jennifer Monereo, Moreau, Clara A, Mühleisen, Thomas W, Paus, Tomas, Pausova, Zdenka, Prieto, Carlos, Ragothaman, Anjanibhargavi, Reinbold, Céline S, Marques, Tiago Reis, Repetto, Gabriela M, Reymond, Alexandre, Roalf, David R, Rodriguez‐Herreros, Borja, Rucker, James J, Sachdev, Perminder S, Schmitt, James E, Schofield, Peter R, Silva, Ana I, Stefansson, Hreinn, Stein, Dan J, Tamnes, Christian K, Tordesillas‐Gutiérrez, Diana, Ulfarsson, Magnus O, Vajdi, Ariana, van 't Ent, Dennis, van den Bree, Marianne BM, Vassos, Evangelos, Vázquez‐Bourgon, Javier, Vila‐Rodriguez, Fidel, Walters, G Bragi, Wen, Wei, Westlye, Lars T, Wittfeld, Katharina, Zackai, Elaine H, Stefánsson, Kári, and Jacquemont, Sebastien

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Psychology, Mental Health, Clinical Research, Pediatric, Genetics, Basic Behavioral and Social Science, Human Genome, Prevention, Brain Disorders, Behavioral and Social Science, Neurosciences, Aetiology, 2.1 Biological and endogenous factors, Mental health, Neurological, Brain, DNA Copy Number Variations, Humans, Magnetic Resonance Imaging, Mental Disorders, Multicenter Studies as Topic, Neurodevelopmental Disorders, Neuroimaging, brain structural imaging, copy number variant, diffusion tensor imaging, evolution, genetics-first approach, neurodevelopmental disorders, psychiatric disorders, ENIGMA-CNV Working Group, ENIGMA 22q11.2 Deletion Syndrome Working Group, Cognitive Sciences, Experimental Psychology, Biological psychology, Cognitive and computational psychology
Abstract

The Enhancing NeuroImaging Genetics through Meta-Analysis copy number variant (ENIGMA-CNV) and 22q11.2 Deletion Syndrome Working Groups (22q-ENIGMA WGs) were created to gain insight into the involvement of genetic factors in human brain development and related cognitive, psychiatric and behavioral manifestations. To that end, the ENIGMA-CNV WG has collated CNV and magnetic resonance imaging (MRI) data from ~49,000 individuals across 38 global research sites, yielding one of the largest studies to date on the effects of CNVs on brain structures in the general population. The 22q-ENIGMA WG includes 12 international research centers that assessed over 533 individuals with a confirmed 22q11.2 deletion syndrome, 40 with 22q11.2 duplications, and 333 typically developing controls, creating the largest-ever 22q11.2 CNV neuroimaging data set. In this review, we outline the ENIGMA infrastructure and procedures for multi-site analysis of CNVs and MRI data. So far, ENIGMA has identified effects of the 22q11.2, 16p11.2 distal, 15q11.2, and 1q21.1 distal CNVs on subcortical and cortical brain structures. Each CNV is associated with differences in cognitive, neurodevelopmental and neuropsychiatric traits, with characteristic patterns of brain structural abnormalities. Evidence of gene-dosage effects on distinct brain regions also emerged, providing further insight into genotype-phenotype relationships. Taken together, these results offer a more comprehensive picture of molecular mechanisms involved in typical and atypical brain development. This "genotype-first" approach also contributes to our understanding of the etiopathogenesis of brain disorders. Finally, we outline future directions to better understand effects of CNVs on brain structure and behavior.

Published
2022

9. Effects of eight neuropsychiatric copy number variants on human brain structure.

Author

Modenato, Claudia, Kumar, Kuldeep, Moreau, Clara, Martin-Brevet, Sandra, Huguet, Guillaume, Schramm, Catherine, Jean-Louis, Martineau, Martin, Charles-Olivier, Younis, Nadine, Tamer, Petra, Douard, Elise, Thébault-Dagher, Fanny, Côté, Valérie, Charlebois, Audrey-Rose, Deguire, Florence, Maillard, Anne M, Rodriguez-Herreros, Borja, Pain, Aurèlie, Richetin, Sonia, 16p11.2 European Consortium, Simons Searchlight Consortium, Melie-Garcia, Lester, Kushan, Leila, Silva, Ana I, van den Bree, Marianne BM, Linden, David EJ, Owen, Michael J, Hall, Jeremy, Lippé, Sarah, Chakravarty, Mallar, Bzdok, Danilo, Bearden, Carrie E, Draganski, Bogdan, and Jacquemont, Sébastien

Subjects
16p11.2 European Consortium, Simons Searchlight Consortium, Brain, Humans, Magnetic Resonance Imaging, Schizophrenia, DNA Copy Number Variations, Neuroimaging, Clinical Sciences, Public Health and Health Services, Psychology
Abstract

Many copy number variants (CNVs) confer risk for the same range of neurodevelopmental symptoms and psychiatric conditions including autism and schizophrenia. Yet, to date neuroimaging studies have typically been carried out one mutation at a time, showing that CNVs have large effects on brain anatomy. Here, we aimed to characterize and quantify the distinct brain morphometry effects and latent dimensions across 8 neuropsychiatric CNVs. We analyzed T1-weighted MRI data from clinically and non-clinically ascertained CNV carriers (deletion/duplication) at the 1q21.1 (n = 39/28), 16p11.2 (n = 87/78), 22q11.2 (n = 75/30), and 15q11.2 (n = 72/76) loci as well as 1296 non-carriers (controls). Case-control contrasts of all examined genomic loci demonstrated effects on brain anatomy, with deletions and duplications showing mirror effects at the global and regional levels. Although CNVs mainly showed distinct brain patterns, principal component analysis (PCA) loaded subsets of CNVs on two latent brain dimensions, which explained 32 and 29% of the variance of the 8 Cohen's d maps. The cingulate gyrus, insula, supplementary motor cortex, and cerebellum were identified by PCA and multi-view pattern learning as top regions contributing to latent dimension shared across subsets of CNVs. The large proportion of distinct CNV effects on brain morphology may explain the small neuroimaging effect sizes reported in polygenic psychiatric conditions. Nevertheless, latent gene brain morphology dimensions will help subgroup the rapidly expanding landscape of neuropsychiatric variants and dissect the heterogeneity of idiopathic conditions.

Published
2021

10. The transcriptional landscape of Shh medulloblastoma.

Author

Skowron, Patryk, Farooq, Hamza, Cavalli, Florence MG, Morrissy, A Sorana, Ly, Michelle, Hendrikse, Liam D, Wang, Evan Y, Djambazian, Haig, Zhu, Helen, Mungall, Karen L, Trinh, Quang M, Zheng, Tina, Dai, Shizhong, Stucklin, Ana S Guerreiro, Vladoiu, Maria C, Fong, Vernon, Holgado, Borja L, Nor, Carolina, Wu, Xiaochong, Abd-Rabbo, Diala, Bérubé, Pierre, Wang, Yu Chang, Luu, Betty, Suarez, Raul A, Rastan, Avesta, Gillmor, Aaron H, Lee, John JY, Zhang, Xiao Yun, Daniels, Craig, Dirks, Peter, Malkin, David, Bouffet, Eric, Tabori, Uri, Loukides, James, Doz, François P, Bourdeaut, Franck, Delattre, Olivier O, Masliah-Planchon, Julien, Ayrault, Olivier, Kim, Seung-Ki, Meyronet, David, Grajkowska, Wieslawa A, Carlotti, Carlos G, de Torres, Carmen, Mora, Jaume, Eberhart, Charles G, Van Meir, Erwin G, Kumabe, Toshihiro, French, Pim J, Kros, Johan M, Jabado, Nada, Lach, Boleslaw, Pollack, Ian F, Hamilton, Ronald L, Rao, Amulya A Nageswara, Giannini, Caterina, Olson, James M, Bognár, László, Klekner, Almos, Zitterbart, Karel, Phillips, Joanna J, Thompson, Reid C, Cooper, Michael K, Rubin, Joshua B, Liau, Linda M, Garami, Miklós, Hauser, Peter, Li, Kay Ka Wai, Ng, Ho-Keung, Poon, Wai Sang, Yancey Gillespie, G, Chan, Jennifer A, Jung, Shin, McLendon, Roger E, Thompson, Eric M, Zagzag, David, Vibhakar, Rajeev, Ra, Young Shin, Garre, Maria Luisa, Schüller, Ulrich, Shofuda, Tomoko, Faria, Claudia C, López-Aguilar, Enrique, Zadeh, Gelareh, Hui, Chi-Chung, Ramaswamy, Vijay, Bailey, Swneke D, Jones, Steven J, Mungall, Andrew J, Moore, Richard A, Calarco, John A, Stein, Lincoln D, Bader, Gary D, Reimand, Jüri, Ragoussis, Jiannis, Weiss, William A, Marra, Marco A, Suzuki, Hiromichi, and Taylor, Michael D

Subjects
Humans, Medulloblastoma, Cerebellar Neoplasms, Signal Transduction, Gene Expression Regulation, Neoplastic, Adolescent, Adult, Middle Aged, Child, Child, Preschool, Infant, Female, Male, Hedgehog Proteins, Gene Regulatory Networks, Genetic Variation, Young Adult, Transcriptome, Pediatric Research Initiative, Brain Cancer, Pediatric, Rare Diseases, Genetics, Pediatric Cancer, Clinical Research, Brain Disorders, Neurosciences, Biotechnology, Human Genome, Cancer, 2.1 Biological and endogenous factors
Abstract

Sonic hedgehog medulloblastoma encompasses a clinically and molecularly diverse group of cancers of the developing central nervous system. Here, we use unbiased sequencing of the transcriptome across a large cohort of 250 tumors to reveal differences among molecular subtypes of the disease, and demonstrate the previously unappreciated importance of non-coding RNA transcripts. We identify alterations within the cAMP dependent pathway (GNAS, PRKAR1A) which converge on GLI2 activity and show that 18% of tumors have a genetic event that directly targets the abundance and/or stability of MYCN. Furthermore, we discover an extensive network of fusions in focally amplified regions encompassing GLI2, and several loss-of-function fusions in tumor suppressor genes PTCH1, SUFU and NCOR1. Molecular convergence on a subset of genes by nucleotide variants, copy number aberrations, and gene fusions highlight the key roles of specific pathways in the pathogenesis of Sonic hedgehog medulloblastoma and open up opportunities for therapeutic intervention.

Published
2021

11. Genetic Studies of Leptin Concentrations Implicate Leptin in the Regulation of Early Adiposity

Author

Yaghootkar, Hanieh, Zhang, Yiying, Spracklen, Cassandra N, Karaderi, Tugce, Huang, Lam Opal, Bradfield, Jonathan, Schurmann, Claudia, Fine, Rebecca S, Preuss, Michael H, Kutalik, Zoltan, Wittemans, Laura BL, Lu, Yingchang, Metz, Sophia, Willems, Sara M, Li-Gao, Ruifang, Grarup, Niels, Wang, Shuai, Molnos, Sophie, Sandoval-Zárate, América A, Nalls, Mike A, Lange, Leslie A, Haesser, Jeffrey, Guo, Xiuqing, Lyytikäinen, Leo-Pekka, Feitosa, Mary F, Sitlani, Colleen M, Venturini, Cristina, Mahajan, Anubha, Kacprowski, Tim, Wang, Carol A, Chasman, Daniel I, Amin, Najaf, Broer, Linda, Robertson, Neil, Young, Kristin L, Allison, Matthew, Auer, Paul L, Blüher, Matthias, Borja, Judith B, Bork-Jensen, Jette, Carrasquilla, Germán D, Christofidou, Paraskevi, Demirkan, Ayse, Doege, Claudia A, Garcia, Melissa E, Graff, Mariaelisa, Guo, Kaiying, Hakonarson, Hakon, Hong, Jaeyoung, Ida Chen, Yii-Der, Jackson, Rebecca, Jakupović, Hermina, Jousilahti, Pekka, Justice, Anne E, Kähönen, Mika, Kizer, Jorge R, Kriebel, Jennifer, LeDuc, Charles A, Li, Jin, Lind, Lars, Luan, Jian'an, Mackey, David A, Mangino, Massimo, Männistö, Satu, Martin Carli, Jayne F, Medina-Gomez, Carolina, Mook-Kanamori, Dennis O, Morris, Andrew P, de Mutsert, Renée, Nauck, Matthias, Prokic, Ivana, Pennell, Craig E, Pradhan, Arund D, Psaty, Bruce M, Raitakari, Olli T, Scott, Robert A, Skaaby, Tea, Strauch, Konstantin, Taylor, Kent D, Teumer, Alexander, Uitterlinden, Andre G, Wu, Ying, Yao, Jie, Walker, Mark, North, Kari E, Kovacs, Peter, Ikram, M Arfan, van Duijn, Cornelia M, Ridker, Paul M, Lye, Stephen, Homuth, Georg, Ingelsson, Erik, Spector, Tim D, McKnight, Barbara, Province, Michael A, Lehtimäki, Terho, Adair, Linda S, Rotter, Jerome I, Reiner, Alexander P, and Wilson, James G

Subjects
Genetics, Nutrition, Prevention, Obesity, Aetiology, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Metabolic and endocrine, Cardiovascular, Stroke, Cancer, Adiposity, Gene Expression Regulation, Developmental, Genetic Variation, Genotype, Humans, Leptin, Models, Molecular, Protein Conformation, Racial Groups, Medical and Health Sciences, Endocrinology & Metabolism
Abstract

Leptin influences food intake by informing the brain about the status of body fat stores. Rare LEP mutations associated with congenital leptin deficiency cause severe early-onset obesity that can be mitigated by administering leptin. However, the role of genetic regulation of leptin in polygenic obesity remains poorly understood. We performed an exome-based analysis in up to 57,232 individuals of diverse ancestries to identify genetic variants that influence adiposity-adjusted leptin concentrations. We identify five novel variants, including four missense variants, in LEP, ZNF800, KLHL31, and ACTL9, and one intergenic variant near KLF14. The missense variant Val94Met (rs17151919) in LEP was common in individuals of African ancestry only, and its association with lower leptin concentrations was specific to this ancestry (P = 2 × 10-16, n = 3,901). Using in vitro analyses, we show that the Met94 allele decreases leptin secretion. We also show that the Met94 allele is associated with higher BMI in young African-ancestry children but not in adults, suggesting that leptin regulates early adiposity.

Published
2020

12. Rapid deployment of SARS-CoV-2 testing: The CLIAHUB.

Author

Crawford, Emily D, Acosta, Irene, Ahyong, Vida, Anderson, Erika C, Arevalo, Shaun, Asarnow, Daniel, Axelrod, Shannon, Ayscue, Patrick, Azimi, Camillia S, Azumaya, Caleigh M, Bachl, Stefanie, Bachmutsky, Iris, Bhaduri, Aparna, Brown, Jeremy Bancroft, Batson, Joshua, Behnert, Astrid, Boileau, Ryan M, Bollam, Saumya R, Bonny, Alain R, Booth, David, Borja, Michael Jerico B, Brown, David, Buie, Bryan, Burnett, Cassandra E, Byrnes, Lauren E, Cabral, Katelyn A, Cabrera, Joana P, Caldera, Saharai, Canales, Gabriela, Castañeda, Gloria R, Chan, Agnes Protacio, Chang, Christopher R, Charles-Orszag, Arthur, Cheung, Carly, Chio, Unseng, Chow, Eric D, Citron, Y Rose, Cohen, Allison, Cohn, Lillian B, Chiu, Charles, Cole, Mitchel A, Conrad, Daniel N, Constantino, Angela, Cote, Andrew, Crayton-Hall, Tre'Jon, Darmanis, Spyros, Detweiler, Angela M, Dial, Rebekah L, Dong, Shen, Duarte, Elias M, Dynerman, David, Egger, Rebecca, Fanton, Alison, Frumm, Stacey M, Fu, Becky Xu Hua, Garcia, Valentina E, Garcia, Julie, Gladkova, Christina, Goldman, Miriam, Gomez-Sjoberg, Rafael, Gordon, M Grace, Grove, James CR, Gupta, Shweta, Haddjeri-Hopkins, Alexis, Hadley, Pierce, Haliburton, John, Hao, Samantha L, Hartoularos, George, Herrera, Nadia, Hilberg, Melissa, Ho, Kit Ying E, Hoppe, Nicholas, Hosseinzadeh, Shayan, Howard, Conor J, Hussmann, Jeffrey A, Hwang, Elizabeth, Ingebrigtsen, Danielle, Jackson, Julia R, Jowhar, Ziad M, Kain, Danielle, Kim, James YS, Kistler, Amy, Kreutzfeld, Oriana, Kulsuptrakul, Jessie, Kung, Andrew F, Langelier, Charles, Laurie, Matthew T, Lee, Lena, Leng, Kun, Leon, Kristoffer E, Leonetti, Manuel D, Levan, Sophia R, Li, Sam, Li, Aileen W, Liu, Jamin, Lubin, Heidi S, Lyden, Amy, Mann, Jennifer, Mann, Sabrina, and Margulis, Gorica

Subjects
Humans, Pneumonia, Viral, Coronavirus Infections, Clinical Laboratory Techniques, California, Workflow, Pandemics, Clinical Laboratory Services, Betacoronavirus, COVID-19, SARS-CoV-2, COVID-19 Testing, Pneumonia, Viral, Microbiology, Immunology, Medical Microbiology, Virology
Published
2020

13. Clinical Observership Opportunities in North America for International Orthopaedic Surgeons.

Author

Carrillo, Laura A, Segarra, Borja, and Sabharwal, Sanjeev

Subjects
Canada, Humans, International Educational Exchange, Orthopedics, United States, Biomedical Engineering, Clinical Sciences
Abstract

BackgroundAlthough efforts have been made to address the inequities of surgical care globally, to our knowledge, there has been no comprehensive analysis of orthopaedic clinical observerships in North America that are available for international surgeons.MethodsTwo investigators performed a systematic online search to identify orthopaedic clinical observerships that are available in the United States and Canada for international surgeons. Variables such as host type, geographic location of host site, program type, eligibility criteria, subspecialty focus, application and participation fees, availability of funding, duration of observership, and the quality of online information that is available based on an online content (OC) score were collected.ResultsOf the 113 available observership sponsors in North America, 36 (32%) were professional-society-based, 69 (61%) were academic/institution-based, and 8 (7%) were private-practice-based. Most observerships were located in the U.S. (n = 85) and, of these, the Northeast was the most common U.S. region (n = 29, p = 0.008). Of the observerships with a focus, pediatrics was the most frequent orthopaedic subspecialty (p < 0.0001), followed by spine and trauma. Professional-society-sponsored observerships offered funding to international surgeons more often than academic/institution-based and privately sponsored programs (p < 0.0001). The average OC score for the entire cohort was 2.35 and was similar among the 3 host types (p = 0.954). The program structure and requirements such as applicant eligibility, application and participation fees, and duration of observership varied widely.ConclusionsThere are opportunities for international orthopaedic surgeons to participate in clinical observerships in North America. Given the greater funding support and lack of fees for professional-society-sponsored observerships, these observerships may pose fewer financial barriers for surgeons from low and middle-income countries (LMICs). The quality of online information was similar among the 3 different host types and can be improved.Clinical relevanceThe relevance and impact of a clinical observership experience in North America for a practicing orthopaedic surgeon from an LMIC need to be explored further.

Published
2020

14. Impact of first-line antiretroviral therapy regimens on the restoration of the CD4/CD8 ratio in the CNICS cohort

Author

Herrera, Sabina, Fernandez-Felix, Borja M, Hunt, Peter W, Deeks, Steven G, Sainz, Talía, Heath, Sonya L, Achenbach, Chad J, Rodríguez, Benigno, Mathews, Christopher, Christopoulos, Katerina, Mayer, Kenneth, Napravnik, Sonia, Moreno, Santiago, and Serrano-Villar, Sergio

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Clinical Sciences, Immunology, HIV/AIDS, Infectious Diseases, Clinical Research, Sexually Transmitted Infections, Clinical Trials and Supportive Activities, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Infection, Good Health and Well Being, Adult, Anti-HIV Agents, CD4-CD8 Ratio, CD8-Positive T-Lymphocytes, Cohort Studies, HIV Infections, Humans, Viral Load, Microbiology, Pharmacology and Pharmaceutical Sciences, Clinical sciences, Pharmacology and pharmaceutical sciences
Abstract

BackgroundThe CD4/CD8 ratio is an indicator of immunosenescence and a predictor of all-cause mortality in HIV-infected patients. The effects of different ART regimens on CD4/CD8 ratio recovery remain unclear.MethodsClinical cohort study of ART-treated patients from the CFAR Network of Integrated Clinical Systems (CNICS). We included ART-naive adults with HIV infection who achieved undetectable HIV RNA during the first 48 weeks of treatment and had additional follow-up 48 weeks after virological suppression (VS). Primary endpoints included increase in CD4/CD8 ratio at both timepoints and secondary endpoints were CD4/CD8 ratio recovery at cut-offs of ≥0.5 or ≥1.0.ResultsOf 3971 subjects who met the study criteria, 1876 started ART with an NNRTI, 1804 with a PI and 291 with an integrase strand transfer inhibitor (INSTI). After adjusting for age, sex, race, year of entry, risk group, HCV serostatus, baseline viral load and baseline CD4/CD8 ratio, subjects on an NNRTI showed a significantly greater CD4/CD8 ratio gain compared with those on a PI, either 48 weeks after ART initiation or after 48 weeks of HIV RNA VS. The greater CD4/CD8 ratio improvement in the NNRTI arm was driven by a higher decline in CD8 counts. The INSTI group showed increased rates of CD4/CD8 ratio normalization at the ≥1.0 cut-off compared with the PI group.ConclusionsNNRTI therapy was associated with a greater increase in the CD4/CD8 ratio compared with PIs. NNRTI- and INSTI-based first-line ART were associated with higher rates of CD4/CD8 ratio normalization at a cut-off of 1.0 than a PI-based regimen, which might have clinical implications.

Published
2020

15. Transition of Macrophages to Fibroblast-Like Cells in Healing Myocardial Infarction.

Author

Haider, Nezam, Boscá, Lisardo, Zandbergen, H, Kovacic, Jason, Narula, Navneet, González-Ramos, Silvia, Fernandez-Velasco, María, Agrawal, Sudhanshu, Paz-García, Marta, Gupta, Sudhir, DeLeon-Pennell, Kristine, Fuster, Valentin, Ibañez, Borja, and Narula, Jagat

Subjects
cardiac fibroblast, fibroblast markers, infiltration, macrophage/fibroblast-like transition, myeloid tracers, myocardial infarction, Animals, Biomarkers, Cell Transdifferentiation, Fibroblasts, Humans, Macrophages, Mice, Transgenic, Myocardial Infarction
Abstract

BACKGROUND: Macrophages and fibroblasts are 2 major cell types involved in healing after myocardial infarction (MI), contributing to myocardial remodeling and fibrosis. Post-MI fibrosis progression is characterized by a decrease in cardiac macrophage content. OBJECTIVES: This study explores the potential of macrophages to express fibroblast genes and the direct role of these cells in post-MI cardiac fibrosis. METHODS: Prolonged in vitro culture of human macrophages was used to evaluate the capacity to express fibroblast markers. Infiltrating cardiac macrophages was tracked in vivo after experimental MI of LysM(Cre/+);ROSA26(EYFP/+) transgenic mice. The expression of Yellow Fluorescent Protein (YFP) in these animals is restricted to myeloid lineage allowing the identification of macrophage-derived fibroblasts. The expression in YFP-positive cells of fibroblast markers was determined in myocardial tissue sections of hearts from these mice after MI. RESULTS: Expression of the fibroblast markers type I collagen, prolyl-4-hydroxylase, fibroblast specific protein-1, and fibroblast activation protein was evidenced in YFP-positive cells in the heart after MI. The presence of fibroblasts after MI was evaluated in the hearts of animals after depletion of macrophages with clodronate liposomes. This macrophage depletion significantly reduced the number of Mac3+Col1A1+ cells in the heart after MI. CONCLUSIONS: The data provide both in vitro and in vivo evidence for the ability of macrophages to transition and adopt a fibroblast-like phenotype. Therapeutic manipulation of this macrophage-fibroblast transition may hold promise for favorably modulating the fibrotic response after MI and after other cardiovascular pathological processes.

Published
2019

16. BPG: Seamless, automated and interactive visualization of scientific data

Author

P’ng, Christine, Green, Jeffrey, Chong, Lauren C, Waggott, Daryl, Prokopec, Stephenie D, Shamsi, Mehrdad, Nguyen, Francis, Mak, Denise YF, Lam, Felix, Albuquerque, Marco A, Wu, Ying, Jung, Esther H, Starmans, Maud HW, Chan-Seng-Yue, Michelle A, Yao, Cindy Q, Liang, Bianca, Lalonde, Emilie, Haider, Syed, Simone, Nicole A, Sendorek, Dorota, Chu, Kenneth C, Moon, Nathalie C, Fox, Natalie S, Grzadkowski, Michal R, Harding, Nicholas J, Fung, Clement, Murdoch, Amanda R, Houlahan, Kathleen E, Wang, Jianxin, Garcia, David R, de Borja, Richard, Sun, Ren X, Lin, Xihui, Chen, Gregory M, Lu, Aileen, Shiah, Yu-Jia, Zia, Amin, Kearns, Ryan, and Boutros, Paul C

Subjects
Information and Computing Sciences, Applied Computing, Networking and Information Technology R&D (NITRD), Data Analysis, Humans, Simulation Training, Software, Data-visualization, Interactive plotting, Web-resources, Mathematical Sciences, Biological Sciences, Bioinformatics, Biological sciences, Information and computing sciences, Mathematical sciences
Abstract

BackgroundWe introduce BPG, a framework for generating publication-quality, highly-customizable plots in the R statistical environment.ResultsThis open-source package includes multiple methods of displaying high-dimensional datasets and facilitates generation of complex multi-panel figures, making it suitable for complex datasets. A web-based interactive tool allows online figure customization, from which R code can be downloaded for integration with computational pipelines.ConclusionBPG provides a new approach for linking interactive and scripted data visualization and is available at http://labs.oicr.on.ca/boutros-lab/software/bpg or via CRAN at https://cran.r-project.org/web/packages/BoutrosLab.plotting.general.

Published
2019

17. Application of machine learning methodology to assess the performance of DIABETIMSS program for patients with type 2 diabetes in family medicine clinics in Mexico.

Author

You, Yue, Doubova, Svetlana, Pinto-Masis, Diana, Pérez-Cuevas, Ricardo, Borja-Aburto, Víctor, and Hubbard, Alan

Subjects
Diabetes program, Family medicine clinics, Machine learning methodology, Mexico, Adult, Ambulatory Care, Cross-Sectional Studies, Diabetes Mellitus, Type 2, Electronic Health Records, Family Practice, Female, Humans, Logistic Models, Machine Learning, Male, Mexico, Middle Aged
Abstract

BACKGROUND: The study aimed to assess the performance of a multidisciplinary-team diabetes care program called DIABETIMSS on glycemic control of type 2 diabetes (T2D) patients, by using available observational patient data and machine-learning-based targeted learning methods. METHODS: We analyzed electronic health records and laboratory databases from the year 2012 to 2016 of T2D patients from six family medicine clinics (FMCs) delivering the DIABETIMSS program, and five FMCs providing routine care. All FMCs belong to the Mexican Institute of Social Security and are in Mexico City and the State of Mexico. The primary outcome was glycemic control. The study covariates included: patient sex, age, anthropometric data, history of glycemic control, diabetic complications and comorbidity. We measured the effects of DIABETIMSS program through 1) simple unadjusted mean differences; 2) adjusted via standard logistic regression and 3) adjusted via targeted machine learning. We treated the data as a serial cross-sectional study, conducted a standard principal components analysis to explore the distribution of covariates among clinics, and performed regression tree on data transformed to use the prediction model to identify patient sub-groups in whom the program was most successful. To explore the robustness of the machine learning approaches, we conducted a set of simulations and the sensitivity analysis with process-of-care indicators as possible confounders. RESULTS: The study included 78,894 T2D patients, from which 37,767patients received care through DIABETIMSS. The impact of DIABETIMSS ranged, among clinics, from 2 to 8% improvement in glycemic control, with an overall (pooled) estimate of 5% improvement. T2D patients with fewer complications have more significant benefit from DIABETIMSS than those with more complications. At the FMCs delivering the conventional model the predicted impacts were like what was observed empirically in the DIABETIMSS clinics. The sensitivity analysis did not change the overall estimate average across clinics. CONCLUSIONS: DIABETIMSS program had a small, but significant increase in glycemic control. The use of machine learning methods yields both population-level effects and pinpoints the sub-groups of patients the program benefits the most. These methods exploit the potential of routine observational patient data within complex healthcare systems to inform decision-makers.

Published
2019

18. Associations of autozygosity with a broad range of human phenotypes.

Author

Clark, David W, Okada, Yukinori, Moore, Kristjan HS, Mason, Dan, Pirastu, Nicola, Gandin, Ilaria, Mattsson, Hannele, Barnes, Catriona LK, Lin, Kuang, Zhao, Jing Hua, Deelen, Patrick, Rohde, Rebecca, Schurmann, Claudia, Guo, Xiuqing, Giulianini, Franco, Zhang, Weihua, Medina-Gomez, Carolina, Karlsson, Robert, Bao, Yanchun, Bartz, Traci M, Baumbach, Clemens, Biino, Ginevra, Bixley, Matthew J, Brumat, Marco, Chai, Jin-Fang, Corre, Tanguy, Cousminer, Diana L, Dekker, Annelot M, Eccles, David A, van Eijk, Kristel R, Fuchsberger, Christian, Gao, He, Germain, Marine, Gordon, Scott D, de Haan, Hugoline G, Harris, Sarah E, Hofer, Edith, Huerta-Chagoya, Alicia, Igartua, Catherine, Jansen, Iris E, Jia, Yucheng, Kacprowski, Tim, Karlsson, Torgny, Kleber, Marcus E, Li, Shengchao Alfred, Li-Gao, Ruifang, Mahajan, Anubha, Matsuda, Koichi, Meidtner, Karina, Meng, Weihua, Montasser, May E, van der Most, Peter J, Munz, Matthias, Nutile, Teresa, Palviainen, Teemu, Prasad, Gauri, Prasad, Rashmi B, Priyanka, Tallapragada Divya Sri, Rizzi, Federica, Salvi, Erika, Sapkota, Bishwa R, Shriner, Daniel, Skotte, Line, Smart, Melissa C, Smith, Albert Vernon, van der Spek, Ashley, Spracklen, Cassandra N, Strawbridge, Rona J, Tajuddin, Salman M, Trompet, Stella, Turman, Constance, Verweij, Niek, Viberti, Clara, Wang, Lihua, Warren, Helen R, Wootton, Robyn E, Yanek, Lisa R, Yao, Jie, Yousri, Noha A, Zhao, Wei, Adeyemo, Adebowale A, Afaq, Saima, Aguilar-Salinas, Carlos Alberto, Akiyama, Masato, Albert, Matthew L, Allison, Matthew A, Alver, Maris, Aung, Tin, Azizi, Fereidoun, Bentley, Amy R, Boeing, Heiner, Boerwinkle, Eric, Borja, Judith B, de Borst, Gert J, Bottinger, Erwin P, Broer, Linda, Campbell, Harry, Chanock, Stephen, Chee, Miao-Li, and Chen, Guanjie

Subjects
Humans, Body Size, Risk-Taking, Cognition, Health Status, Consanguinity, Fertility, Haplotypes, Homozygote, Alleles, Inbreeding Depression
Abstract

In many species, the offspring of related parents suffer reduced reproductive success, a phenomenon known as inbreeding depression. In humans, the importance of this effect has remained unclear, partly because reproduction between close relatives is both rare and frequently associated with confounding social factors. Here, using genomic inbreeding coefficients (FROH) for >1.4 million individuals, we show that FROH is significantly associated (p

Published
2019

19. Study of Optimal Perimetric Testing in Children (OPTIC): evaluation of kinetic approaches in childhood neuro-ophthalmic disease

Author

Patel, Dipesh E, Cumberland, Phillippa M, Walters, Bronwen C, Cortina-Borja, Mario, Rahi, Jugnoo S, Khaw, Peng Tee, Walters, Bronwen, Russell-Eggitt, Isabelle, Timms, Chris, Brookes, John, Moore, Anthony, Papadopoulos, Maria, Garway-Heath, David, Viswanathan, Ananth, Liasis, Alki, and Crabb, David

Subjects
Biomedical and Clinical Sciences, Ophthalmology and Optometry, Pediatric, Neurosciences, Clinical Research, Adolescent, Child, Child, Preschool, Cross-Sectional Studies, Feasibility Studies, Female, Follow-Up Studies, Humans, Infant, Male, Prospective Studies, Reproducibility of Results, Vision Disorders, Visual Acuity, Visual Field Tests, Visual Fields, OPTIC study group, child health, diagnostic tests/investigation, field of vision, visual pathway, Clinical Sciences, Opthalmology and Optometry, Public Health and Health Services, Ophthalmology & Optometry, Clinical sciences, Ophthalmology and optometry
Abstract

AimsWe compared feasibility, quality and outcomes of visual field (VF) testing in children with neuro-ophthalmic disease between the discontinued 'gold-standard' Goldmann and Octopus perimeters.MethodsChildren with neuro-ophthalmic disease, attending Great Ormond Street Hospital, London, were assessed using standardised protocols by one examiner in a single sitting, using Goldmann and Octopus kinetic perimetry. Outputs were classified to compare severity of loss and defect type. Test quality was assessed using both qualitative and quantitative methods.ResultsThirty children (40% female) aged 5-15 years participated. Goldmann perimetry was completed in full by 90.0% vs 72.4% for Octopus. Inability to plot the blind spot was the most common reason for not completing testing. Over 75% completed a test in ≤20 min. Duration was similar between perimeters (paired t-test, mean difference: 0.48min (-1.2, 2.2), p=0.559). The lowest quality tests were for Octopus perimetry in children

Published
2019

20. Exome-Derived Adiponectin-Associated Variants Implicate Obesity and Lipid Biology

Author

Spracklen, Cassandra N, Karaderi, Tugce, Yaghootkar, Hanieh, Schurmann, Claudia, Fine, Rebecca S, Kutalik, Zoltan, Preuss, Michael H, Lu, Yingchang, Wittemans, Laura BL, Adair, Linda S, Allison, Matthew, Amin, Najaf, Auer, Paul L, Bartz, Traci M, Blüher, Matthias, Boehnke, Michael, Borja, Judith B, Bork-Jensen, Jette, Broer, Linda, Chasman, Daniel I, Chen, Yii-Der Ida, Chirstofidou, Paraskevi, Demirkan, Ayse, van Duijn, Cornelia M, Feitosa, Mary F, Garcia, Melissa E, Graff, Mariaelisa, Grallert, Harald, Grarup, Niels, Guo, Xiuqing, Haesser, Jeffrey, Hansen, Torben, Harris, Tamara B, Highland, Heather M, Hong, Jaeyoung, Ikram, M Arfan, Ingelsson, Erik, Jackson, Rebecca, Jousilahti, Pekka, Kähönen, Mika, Kizer, Jorge R, Kovacs, Peter, Kriebel, Jennifer, Laakso, Markku, Lange, Leslie A, Lehtimäki, Terho, Li, Jin, Li-Gao, Ruifang, Lind, Lars, Luan, Jian'an, Lyytikäinen, Leo-Pekka, MacGregor, Stuart, Mackey, David A, Mahajan, Anubha, Mangino, Massimo, Männistö, Satu, McCarthy, Mark I, McKnight, Barbara, Medina-Gomez, Carolina, Meigs, James B, Molnos, Sophie, Mook-Kanamori, Dennis, Morris, Andrew P, de Mutsert, Renee, Nalls, Mike A, Nedeljkovic, Ivana, North, Kari E, Pennell, Craig E, Pradhan, Aruna D, Province, Michael A, Raitakari, Olli T, Raulerson, Chelsea K, Reiner, Alex P, Ridker, Paul M, Ripatti, Samuli, Roberston, Neil, Rotter, Jerome I, Salomaa, Veikko, Sandoval-Zárate, America A, Sitlani, Colleen M, Spector, Tim D, Strauch, Konstantin, Stumvoll, Michael, Taylor, Kent D, Thuesen, Betina, Tönjes, Anke, Uitterlinden, Andre G, Venturini, Cristina, Walker, Mark, Wang, Carol A, Wang, Shuai, Wareham, Nicholas J, Willems, Sara M, Willems van Dijk, Ko, Wilson, James G, Wu, Ying, Yao, Jie, Young, Kristin L, Langenberg, Claudia, and Frayling, Timothy M

Subjects
Epidemiology, Biological Sciences, Health Sciences, Genetics, Human Genome, Nutrition, Obesity, 2.1 Biological and endogenous factors, Aetiology, Metabolic and endocrine, Cardiovascular, Adiponectin, Adipose Tissue, Adolescent, Adult, Black or African American, Aged, Aged, 80 and over, Exome, Female, Genetic Predisposition to Disease, Hispanic or Latino, Humans, Lipids, Male, Middle Aged, Phenotype, Polymorphism, Single Nucleotide, Quantitative Trait Loci, White People, Young Adult, adiponectin, cardio metabolic traits, exome, genetics, genome-wide association study, lipids, obesity, Medical and Health Sciences, Genetics & Heredity, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Circulating levels of adiponectin, an adipocyte-secreted protein associated with cardiovascular and metabolic risk, are highly heritable. To gain insights into the biology that regulates adiponectin levels, we performed an exome array meta-analysis of 265,780 genetic variants in 67,739 individuals of European, Hispanic, African American, and East Asian ancestry. We identified 20 loci associated with adiponectin, including 11 that had been reported previously (p < 2 × 10-7). Comparison of exome array variants to regional linkage disequilibrium (LD) patterns and prior genome-wide association study (GWAS) results detected candidate variants (r2 > .60) spanning as much as 900 kb. To identify potential genes and mechanisms through which the previously unreported association signals act to affect adiponectin levels, we assessed cross-trait associations, expression quantitative trait loci in subcutaneous adipose, and biological pathways of nearby genes. Eight of the nine loci were also associated (p < 1 × 10-4) with at least one obesity or lipid trait. Candidate genes include PRKAR2A, PTH1R, and HDAC9, which have been suggested to play roles in adipocyte differentiation or bone marrow adipose tissue. Taken together, these findings provide further insights into the processes that influence circulating adiponectin levels.

Published
2019

21. Human iPSC-Derived Retinal Pigment Epithelium: A Model System for Prioritizing and Functionally Characterizing Causal Variants at AMD Risk Loci

Author

Smith, Erin N, D'Antonio-Chronowska, Agnieszka, Greenwald, William W, Borja, Victor, Aguiar, Lana R, Pogue, Robert, Matsui, Hiroko, Benaglio, Paola, Borooah, Shyamanga, D'Antonio, Matteo, Ayyagari, Radha, and Frazer, Kelly A

Subjects
Biological Sciences, Genetics, Neurodegenerative, Aging, Human Genome, Stem Cell Research - Embryonic - Human, Eye Disease and Disorders of Vision, Macular Degeneration, Stem Cell Research, Stem Cell Research - Induced Pluripotent Stem Cell - Human, Neurosciences, Stem Cell Research - Induced Pluripotent Stem Cell, Human Fetal Tissue, Aetiology, 2.1 Biological and endogenous factors, Eye, Female, Genetic Loci, Humans, Induced Pluripotent Stem Cells, Retinal Pigment Epithelium, Sequence Analysis, RNA, Vascular Endothelial Growth Factor A, VEGFA, age-related macular degeneration, chromatin accessibility, fine mapping, genome-wide association, iPSC-RPE, induced pluripotent stem cells, regulatory variants, retinal pigment epithelium, Biochemistry and Cell Biology, Clinical Sciences, Biochemistry and cell biology
Abstract

We evaluate whether human induced pluripotent stem cell-derived retinal pigment epithelium (iPSC-RPE) cells can be used to prioritize and functionally characterize causal variants at age-related macular degeneration (AMD) risk loci. We generated iPSC-RPE from six subjects and show that they have morphological and molecular characteristics similar to those of native RPE. We generated RNA-seq, ATAC-seq, and H3K27ac ChIP-seq data and observed high similarity in gene expression and enriched transcription factor motif profiles between iPSC-RPE and human fetal RPE. We performed fine mapping of AMD risk loci by integrating molecular data from the iPSC-RPE, adult retina, and adult RPE, which identified rs943080 as the probable causal variant at VEGFA. We show that rs943080 is associated with altered chromatin accessibility of a distal ATAC-seq peak, decreased overall gene expression of VEGFA, and allele-specific expression of a non-coding transcript. Our study thus provides a potential mechanism underlying the association of the VEGFA locus with AMD.

Published
2019

22. BPG: Seamless, automated and interactive visualization of scientific data.

Author

P'ng, Christine, Green, Jeffrey, Chong, Lauren C, Waggott, Daryl, Prokopec, Stephenie D, Shamsi, Mehrdad, Nguyen, Francis, Mak, Denise YF, Lam, Felix, Albuquerque, Marco A, Wu, Ying, Jung, Esther H, Starmans, Maud HW, Chan-Seng-Yue, Michelle A, Yao, Cindy Q, Liang, Bianca, Lalonde, Emilie, Haider, Syed, Simone, Nicole A, Sendorek, Dorota, Chu, Kenneth C, Moon, Nathalie C, Fox, Natalie S, Grzadkowski, Michal R, Harding, Nicholas J, Fung, Clement, Murdoch, Amanda R, Houlahan, Kathleen E, Wang, Jianxin, Garcia, David R, de Borja, Richard, Sun, Ren X, Lin, Xihui, Chen, Gregory M, Lu, Aileen, Shiah, Yu-Jia, Zia, Amin, Kearns, Ryan, and Boutros, Paul C

Subjects
Humans, Software, Simulation Training, Data Analysis, Data-visualization, Interactive plotting, Web-resources, Networking and Information Technology R&D, Biological Sciences, Information and Computing Sciences, Mathematical Sciences, Bioinformatics
Abstract

BackgroundWe introduce BPG, a framework for generating publication-quality, highly-customizable plots in the R statistical environment.ResultsThis open-source package includes multiple methods of displaying high-dimensional datasets and facilitates generation of complex multi-panel figures, making it suitable for complex datasets. A web-based interactive tool allows online figure customization, from which R code can be downloaded for integration with computational pipelines.ConclusionBPG provides a new approach for linking interactive and scripted data visualization and is available at http://labs.oicr.on.ca/boutros-lab/software/bpg or via CRAN at https://cran.r-project.org/web/packages/BoutrosLab.plotting.general.

Published
2019

23. Grammatical licensing and relative clause parsing in a flexible word-order language.

Author

Wagers, Matthew W, Borja, Manuel F, and Chung, Sandra

Subjects
Humans, Comprehension, Reading, Linguistics, Adult, Aged, Middle Aged, Female, Male, Young Adult, Austronesian, Chamorro, Parsing, Relative clauses, Subject preference, Word order, Behavioral and Social Science, Experimental Psychology, Information and Computing Sciences, Psychology and Cognitive Sciences, Language, Communication and Culture
Abstract

Evidence from two experiments reveals that in Chamorro, a verb-first language, the comprehension of relative clauses (RCs) is sensitive to the order of the RC with respect to the head. Unlike most other languages, Chamorro allows both postnominal and prenominal RCs, so it is possible to compare how the two types are processed within the same language. Moreover, Chamorro is a small language whose speakers do not fit the typical profile of participants in cognitive science experiments. We found that RC comprehension is affected by the relative order of RC and head, and by other language-specific factors. However, we also found new support for a subject gap advantage in all RC types. This advantage emerged in early response measures and was reinforced in postnominal RCs, but often outcompeted in prenominal RCs by other pressures. We frame this competition in terms of a model in which grammatical licensing requirements play a key role in comprehension.

Published
2018

24. Racial differences in completion of the living kidney donor evaluation process.

Author

Kumar, Komal, Tonascia, James, Muzaale, Abimereki, Purnell, Tanjala, Ottmann, Shane, Al Ammary, Fawaz, Bowring, Mary, Poon, Anna, King, Elizabeth, Massie, Allan, Chow, Eric, Thomas, Alvin, Ying, Hao, Borja, Marvin, Konel, Jonathan, Henderson, Macey, Cameron, Andrew, Garonzik-Wang, Jacqueline, and Segev, Dorry

Subjects
donor candidates, listed candidates, living donation, Adult, Black or African American, Donor Selection, Female, Follow-Up Studies, Healthcare Disparities, Humans, Kidney Failure, Chronic, Kidney Transplantation, Living Donors, Male, Middle Aged, Needs Assessment, Treatment Outcome, United States, White People
Abstract

Racial disparities in living donor kidney transplantation (LDKT) persist but the most effective target to eliminate these disparities remains unknown. One potential target could be delays during completion of the live donor evaluation process. We studied racial differences in progression through the evaluation process for 247 African American (AA) and 664 non-AA living donor candidates at our center between January 2011 and March 2015. AA candidates were more likely to be obese (38% vs 22%: P

Published
2018

25. A Hematogenous Route for Medulloblastoma Leptomeningeal Metastases

Author

Garzia, Livia, Kijima, Noriyuki, Morrissy, A Sorana, De Antonellis, Pasqualino, Guerreiro-Stucklin, Ana, Holgado, Borja L, Wu, Xiaochong, Wang, Xin, Parsons, Michael, Zayne, Kory, Manno, Alex, Kuzan-Fischer, Claudia, Nor, Carolina, Donovan, Laura K, Liu, Jessica, Qin, Lei, Garancher, Alexandra, Liu, Kun-Wei, Mansouri, Sheila, Luu, Betty, Thompson, Yuan Yao, Ramaswamy, Vijay, Peacock, John, Farooq, Hamza, Skowron, Patryk, Shih, David JH, Li, Angela, Ensan, Sherine, Robbins, Clinton S, Cybulsky, Myron, Mitra, Siddhartha, Ma, Yussanne, Moore, Richard, Mungall, Andy, Cho, Yoon-Jae, Weiss, William A, Chan, Jennifer A, Hawkins, Cynthia E, Massimino, Maura, Jabado, Nada, Zapotocky, Michal, Sumerauer, David, Bouffet, Eric, Dirks, Peter, Tabori, Uri, Sorensen, Poul HB, Brastianos, Priscilla K, Aldape, Kenneth, Jones, Steven JM, Marra, Marco A, Woodgett, James R, Wechsler-Reya, Robert J, Fults, Daniel W, and Taylor, Michael D

Subjects
Brain Cancer, Cancer, Neurosciences, Pediatric Cancer, Pediatric, Rare Diseases, Brain Disorders, Allografts, Animals, Cell Line, Tumor, Chemokine CCL2, Chromosomes, Human, Pair 10, Female, Humans, Male, Medulloblastoma, Meningeal Neoplasms, Mice, SCID, Neoplastic Cells, Circulating, Parabiosis, brain tumors, circulating tumor cells, medulloblastoma, metastases, pediatric cancer, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

While the preponderance of morbidity and mortality in medulloblastoma patients are due to metastatic disease, most research focuses on the primary tumor due to a dearth of metastatic tissue samples and model systems. Medulloblastoma metastases are found almost exclusively on the leptomeningeal surface of the brain and spinal cord; dissemination is therefore thought to occur through shedding of primary tumor cells into the cerebrospinal fluid followed by distal re-implantation on the leptomeninges. We present evidence for medulloblastoma circulating tumor cells (CTCs) in therapy-naive patients and demonstrate in vivo, through flank xenografting and parabiosis, that medulloblastoma CTCs can spread through the blood to the leptomeningeal space to form leptomeningeal metastases. Medulloblastoma leptomeningeal metastases express high levels of the chemokine CCL2, and expression of CCL2 in medulloblastoma in vivo is sufficient to drive leptomeningeal dissemination. Hematogenous dissemination of medulloblastoma offers a new opportunity to diagnose and treat lethal disseminated medulloblastoma.

Published
2018

26. Dysfunctional high-density lipoprotein from HIV+ individuals promotes monocyte-derived foam cell formation in vitro

Author

Angelovich, Thomas A, Hearps, Anna C, Oda, Michael N, Borja, Mark S, Huynh, Diana, Homann, Stefanie, Jaworowski, Anthony, and Kelesidis, Theodoros

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Atherosclerosis, HIV/AIDS, Heart Disease, Cardiovascular, Prevention, Clinical Research, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Adult, Antioxidants, Cross-Sectional Studies, Foam Cells, HIV Infections, Humans, Lipoproteins, HDL, Male, Middle Aged, Young Adult, atherosclerosis, cardiovascular disease, high-density lipoprotein function, human immunodeficiency virus, monocyte-derived foam cells, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Virology, Biomedical and clinical sciences, Health sciences
Abstract

ObjectiveThe role of high-density lipoprotein (HDL) function in HIV-related atherosclerotic cardiovascular disease (CVD) is unclear. HDLs isolated from HIV [HIV(+)HDL] and HIV-uninfected individuals [HIV(-)HDL] were assessed for HDL function and ability to promote monocyte-derived foam cell formation (MDFCF; a key event in HIV-related CVD) ex vivo.Design/methodsUsing an established in-vitro model of atherogenesis and plasma samples from an established cross-sectional study of virologically suppressed HIV men on stable effective antiretroviral therapy and with low CVD risk (median age: 42 years; n = 10), we explored the impact of native HDL [HIV(+)HDL] on MDFCF. In this exploratory study, we selected HIV(+)HDL known to be dysfunctional based on two independent measures of impaired HDL function: antioxidant (high HDLox) ability of HDL to release apolipoprotein A-I (ApoA-I) (low HDL-ApoA-I exchange). Five healthy men matched by age and race to the HIV group were included. Given that oxidation of HDL leads to abnormal HDL function, we also compared proatherogenic effects of HIV(+)HDL vs. chemically derived HDLox. The ex-vivo atherogenesis assay was performed using lipoproteins (purchased or isolated from plasma using ultracentrifugation) and monocytes purified via negative selection from healthy donors.ResultsHIV(+)HDL known to have reduced antioxidant function and rate of HDL/ApoAI exchange promoted MDFCF to a greater extent than HDL (33.0 vs. 26.2% foam cells; P = 0.015). HDL oxidized in vitro also enhanced foam cell formation as compared with nonoxidized HDL (P

Published
2017

27. Comprehensive Analysis of Hypermutation in Human Cancer

Author

Campbell, Brittany B, Light, Nicholas, Fabrizio, David, Zatzman, Matthew, Fuligni, Fabio, de Borja, Richard, Davidson, Scott, Edwards, Melissa, Elvin, Julia A, Hodel, Karl P, Zahurancik, Walter J, Suo, Zucai, Lipman, Tatiana, Wimmer, Katharina, Kratz, Christian P, Bowers, Daniel C, Laetsch, Theodore W, Dunn, Gavin P, Johanns, Tanner M, Grimmer, Matthew R, Smirnov, Ivan V, Larouche, Valérie, Samuel, David, Bronsema, Annika, Osborn, Michael, Stearns, Duncan, Raman, Pichai, Cole, Kristina A, Storm, Phillip B, Yalon, Michal, Opocher, Enrico, Mason, Gary, Thomas, Gregory A, Sabel, Magnus, George, Ben, Ziegler, David S, Lindhorst, Scott, Issai, Vanan Magimairajan, Constantini, Shlomi, Toledano, Helen, Elhasid, Ronit, Farah, Roula, Dvir, Rina, Dirks, Peter, Huang, Annie, Galati, Melissa A, Chung, Jiil, Ramaswamy, Vijay, Irwin, Meredith S, Aronson, Melyssa, Durno, Carol, Taylor, Michael D, Rechavi, Gideon, Maris, John M, Bouffet, Eric, Hawkins, Cynthia, Costello, Joseph F, Meyn, M Stephen, Pursell, Zachary F, Malkin, David, Tabori, Uri, and Shlien, Adam

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Oncology and Carcinogenesis, Human Genome, Cancer, Rare Diseases, Cancer Genomics, 2.1 Biological and endogenous factors, Good Health and Well Being, Adult, Child, Cluster Analysis, DNA Polymerase II, DNA Polymerase III, DNA Replication, Humans, Mutation, Neoplasms, Poly-ADP-Ribose Binding Proteins, DNA repair, DNA replication, cancer genomics, cancer predisposition, hypermutation, immune checkpoint inhibitors, mismatch repair, mutator, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

We present an extensive assessment of mutation burden through sequencing analysis of >81,000 tumors from pediatric and adult patients, including tumors with hypermutation caused by chemotherapy, carcinogens, or germline alterations. Hypermutation was detected in tumor types not previously associated with high mutation burden. Replication repair deficiency was a major contributing factor. We uncovered new driver mutations in the replication-repair-associated DNA polymerases and a distinct impact of microsatellite instability and replication repair deficiency on the scale of mutation load. Unbiased clustering, based on mutational context, revealed clinically relevant subgroups regardless of the tumors' tissue of origin, highlighting similarities in evolutionary dynamics leading to hypermutation. Mutagens, such as UV light, were implicated in unexpected cancers, including sarcomas and lung tumors. The order of mutational signatures identified previous treatment and germline replication repair deficiency, which improved management of patients and families. These data will inform tumor classification, genetic testing, and clinical trial design.

Published
2017

28. Genome-wide physical activity interactions in adiposity - A meta-analysis of 200,452 adults.

Author

Graff, Mariaelisa, Scott, Robert A, Justice, Anne E, Young, Kristin L, Feitosa, Mary F, Barata, Llilda, Winkler, Thomas W, Chu, Audrey Y, Mahajan, Anubha, Hadley, David, Xue, Luting, Workalemahu, Tsegaselassie, Heard-Costa, Nancy L, den Hoed, Marcel, Ahluwalia, Tarunveer S, Qi, Qibin, Ngwa, Julius S, Renström, Frida, Quaye, Lydia, Eicher, John D, Hayes, James E, Cornelis, Marilyn, Kutalik, Zoltan, Lim, Elise, Luan, Jian'an, Huffman, Jennifer E, Zhang, Weihua, Zhao, Wei, Griffin, Paula J, Haller, Toomas, Ahmad, Shafqat, Marques-Vidal, Pedro M, Bien, Stephanie, Yengo, Loic, Teumer, Alexander, Smith, Albert Vernon, Kumari, Meena, Harder, Marie Neergaard, Justesen, Johanne Marie, Kleber, Marcus E, Hollensted, Mette, Lohman, Kurt, Rivera, Natalia V, Whitfield, John B, Zhao, Jing Hua, Stringham, Heather M, Lyytikäinen, Leo-Pekka, Huppertz, Charlotte, Willemsen, Gonneke, Peyrot, Wouter J, Wu, Ying, Kristiansson, Kati, Demirkan, Ayse, Fornage, Myriam, Hassinen, Maija, Bielak, Lawrence F, Cadby, Gemma, Tanaka, Toshiko, Mägi, Reedik, van der Most, Peter J, Jackson, Anne U, Bragg-Gresham, Jennifer L, Vitart, Veronique, Marten, Jonathan, Navarro, Pau, Bellis, Claire, Pasko, Dorota, Johansson, Åsa, Snitker, Søren, Cheng, Yu-Ching, Eriksson, Joel, Lim, Unhee, Aadahl, Mette, Adair, Linda S, Amin, Najaf, Balkau, Beverley, Auvinen, Juha, Beilby, John, Bergman, Richard N, Bergmann, Sven, Bertoni, Alain G, Blangero, John, Bonnefond, Amélie, Bonnycastle, Lori L, Borja, Judith B, Brage, Søren, Busonero, Fabio, Buyske, Steve, Campbell, Harry, Chines, Peter S, Collins, Francis S, Corre, Tanguy, Smith, George Davey, Delgado, Graciela E, Dueker, Nicole, Dörr, Marcus, Ebeling, Tapani, Eiriksdottir, Gudny, Esko, Tõnu, and Faul, Jessica D

Subjects
CHARGE Consortium, EPIC-InterAct Consortium, PAGE Consortium, Humans, Obesity, Genetic Predisposition to Disease, Body Mass Index, Waist-Hip Ratio, Exercise, Genotype, Female, Male, Adiposity, Waist Circumference, Genome-Wide Association Study, Epigenomics, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Genetics, Developmental Biology
Abstract

Physical activity (PA) may modify the genetic effects that give rise to increased risk of obesity. To identify adiposity loci whose effects are modified by PA, we performed genome-wide interaction meta-analyses of BMI and BMI-adjusted waist circumference and waist-hip ratio from up to 200,452 adults of European (n = 180,423) or other ancestry (n = 20,029). We standardized PA by categorizing it into a dichotomous variable where, on average, 23% of participants were categorized as inactive and 77% as physically active. While we replicate the interaction with PA for the strongest known obesity-risk locus in the FTO gene, of which the effect is attenuated by ~30% in physically active individuals compared to inactive individuals, we do not identify additional loci that are sensitive to PA. In additional genome-wide meta-analyses adjusting for PA and interaction with PA, we identify 11 novel adiposity loci, suggesting that accounting for PA or other environmental factors that contribute to variation in adiposity may facilitate gene discovery.

Published
2017

29. iPSCORE: A Resource of 222 iPSC Lines Enabling Functional Characterization of Genetic Variation across a Variety of Cell Types

Author

Panopoulos, Athanasia D, D'Antonio, Matteo, Benaglio, Paola, Williams, Roy, Hashem, Sherin I, Schuldt, Bernhard M, DeBoever, Christopher, Arias, Angelo D, Garcia, Melvin, Nelson, Bradley C, Harismendy, Olivier, Jakubosky, David A, Donovan, Margaret KR, Greenwald, William W, Farnam, KathyJean, Cook, Megan, Borja, Victor, Miller, Carl A, Grinstein, Jonathan D, Drees, Frauke, Okubo, Jonathan, Diffenderfer, Kenneth E, Hishida, Yuriko, Modesto, Veronica, Dargitz, Carl T, Feiring, Rachel, Zhao, Chang, Aguirre, Aitor, McGarry, Thomas J, Matsui, Hiroko, Li, He, Reyna, Joaquin, Rao, Fangwen, O'Connor, Daniel T, Yeo, Gene W, Evans, Sylvia M, C., Neil, Jepsen, Kristen, Nariai, Naoki, Müller, Franz-Josef, Goldstein, Lawrence SB, Belmonte, Juan Carlos Izpisua, Adler, Eric, Loring, Jeanne F, Berggren, W Travis, D'Antonio-Chronowska, Agnieszka, Smith, Erin N, and Frazer, Kelly A

Subjects
Biological Sciences, Genetics, Stem Cell Research - Induced Pluripotent Stem Cell - Non-Human, Clinical Research, Stem Cell Research - Induced Pluripotent Stem Cell - Human, Human Genome, Stem Cell Research, Stem Cell Research - Induced Pluripotent Stem Cell, Aetiology, 2.1 Biological and endogenous factors, Arrhythmias, Cardiac, Cell Differentiation, Cell Line, Cellular Reprogramming, Databases, Factual, Genetic Association Studies, Genetic Variation, Genotype, High-Throughput Nucleotide Sequencing, Humans, Induced Pluripotent Stem Cells, Multigene Family, Myocytes, Cardiac, Oligonucleotide Array Sequence Analysis, Phenotype, Polymorphism, Single Nucleotide, Racial Groups, GWAS, KCNH2, LQT2, NHLBI Next Gen, cardiac disease, iPSC, iPSC-derived cardiomyocytes, iPSCORE, molecular traits, physiological traits, Biochemistry and Cell Biology, Clinical Sciences, Biochemistry and cell biology
Abstract

Large-scale collections of induced pluripotent stem cells (iPSCs) could serve as powerful model systems for examining how genetic variation affects biology and disease. Here we describe the iPSCORE resource: a collection of systematically derived and characterized iPSC lines from 222 ethnically diverse individuals that allows for both familial and association-based genetic studies. iPSCORE lines are pluripotent with high genomic integrity (no or low numbers of somatic copy-number variants) as determined using high-throughput RNA-sequencing and genotyping arrays, respectively. Using iPSCs from a family of individuals, we show that iPSC-derived cardiomyocytes demonstrate gene expression patterns that cluster by genetic background, and can be used to examine variants associated with physiological and disease phenotypes. The iPSCORE collection contains representative individuals for risk and non-risk alleles for 95% of SNPs associated with human phenotypes through genome-wide association studies. Our study demonstrates the utility of iPSCORE for examining how genetic variants influence molecular and physiological traits in iPSCs and derived cell lines.

Published
2017

30. Genome-wide Association Studies of Posttraumatic Stress Disorder in 2 Cohorts of US Army Soldiers

Author

Stein, Murray B, Chen, Chia-Yen, Ursano, Robert J, Cai, Tianxi, Gelernter, Joel, Heeringa, Steven G, Jain, Sonia, Jensen, Kevin P, Maihofer, Adam X, Mitchell, Colter, Nievergelt, Caroline M, Nock, Matthew K, Neale, Benjamin M, Polimanti, Renato, Ripke, Stephan, Sun, Xiaoying, Thomas, Michael L, Wang, Qian, Ware, Erin B, Borja, Susan, Kessler, Ronald C, and Smoller, Jordan W

Subjects
Mental Health, Clinical Research, Anxiety Disorders, Human Genome, Genetics, Post-Traumatic Stress Disorder (PTSD), Brain Disorders, 2.3 Psychological, social and economic factors, Aetiology, Inflammatory and immune system, Mental health, Good Health and Well Being, Adult, Carrier Proteins, Case-Control Studies, Chromosomes, Human, Pair 19, Chromosomes, Human, Pair 5, Cohort Studies, Female, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Military Personnel, Polymorphism, Single Nucleotide, Stress Disorders, Post-Traumatic, Young Adult, Army Study to Assess Risk and Resilience in Servicemembers (STARRS) Collaborators, Other Medical and Health Sciences, Psychology, Cognitive Sciences
Abstract

ImportancePosttraumatic stress disorder (PTSD) is a prevalent, serious public health concern, particularly in the military. The identification of genetic risk factors for PTSD may provide important insights into the biological foundation of vulnerability and comorbidity.ObjectiveTo discover genetic loci associated with the lifetime risk for PTSD in 2 cohorts from the Army Study to Assess Risk and Resilience in Servicemembers (Army STARRS).Design, setting, and participantsTwo coordinated genome-wide association studies of mental health in the US military contributed participants. The New Soldier Study (NSS) included 3167 unique participants with PTSD and 4607 trauma-exposed control individuals; the Pre/Post Deployment Study (PPDS) included 947 unique participants with PTSD and 4969 trauma-exposed controls. The NSS data were collected from February 1, 2011, to November 30, 2012; the PDDS data, from January 9 to April 30, 2012. The primary analysis compared lifetime DSM-IV PTSD cases with trauma-exposed controls without lifetime PTSD. Data were analyzed from March 18 to December 27, 2015.Main outcomes and measuresAssociation analyses for PTSD used logistic regression models within each of 3 ancestral groups (European, African, and Latino American) by study, followed by meta-analysis. Heritability and genetic correlation and pleiotropy with other psychiatric and immune-related disorders were estimated.ResultsThe NSS population was 80.7% male (6277 of 7774 participants; mean [SD] age, 20.9 [3.3] years); the PPDS population, 94.4% male (5583 of 5916 participants; mean [SD] age, 26.5 [6.0] years). A genome-wide significant locus was found in ANKRD55 on chromosome 5 (rs159572; odds ratio [OR], 1.62; 95% CI, 1.37-1.92; P = 2.34 × 10-8) and persisted after adjustment for cumulative trauma exposure (adjusted OR, 1.64; 95% CI, 1.39-1.95; P = 1.18 × 10-8) in the African American samples from the NSS. A genome-wide significant locus was also found in or near ZNF626 on chromosome 19 (rs11085374; OR, 0.77; 95% CI, 0.70-0.85; P = 4.59 × 10-8) in the European American samples from the NSS. Similar results were not found for either single-nucleotide polymorphism in the corresponding ancestry group from the PPDS sample, in other ancestral groups, or in transancestral meta-analyses. Single-nucleotide polymorphism-based heritability was nonsignificant, and no significant genetic correlations were observed between PTSD and 6 mental disorders or 9 immune-related disorders. Significant evidence of pleiotropy was observed between PTSD and rheumatoid arthritis and, to a lesser extent, psoriasis.Conclusions and relevanceIn the largest genome-wide association study of PTSD to date, involving a US military sample, limited evidence of association for specific loci was found. Further efforts are needed to replicate the genome-wide significant association with ANKRD55-associated in prior research with several autoimmune and inflammatory disorders-and to clarify the nature of the genetic overlap observed between PTSD and rheumatoid arthritis and psoriasis.

Published
2016

31. Divergent clonal selection dominates medulloblastoma at recurrence

Author

Morrissy, A Sorana, Garzia, Livia, Shih, David JH, Zuyderduyn, Scott, Huang, Xi, Skowron, Patryk, Remke, Marc, Cavalli, Florence MG, Ramaswamy, Vijay, Lindsay, Patricia E, Jelveh, Salomeh, Donovan, Laura K, Wang, Xin, Luu, Betty, Zayne, Kory, Li, Yisu, Mayoh, Chelsea, Thiessen, Nina, Mercier, Eloi, Mungall, Karen L, Ma, Yusanne, Tse, Kane, Zeng, Thomas, Shumansky, Karey, Roth, Andrew JL, Shah, Sohrab, Farooq, Hamza, Kijima, Noriyuki, Holgado, Borja L, Lee, John JY, Matan-Lithwick, Stuart, Liu, Jessica, Mack, Stephen C, Manno, Alex, Michealraj, KA, Nor, Carolina, Peacock, John, Qin, Lei, Reimand, Juri, Rolider, Adi, Thompson, Yuan Y, Wu, Xiaochong, Pugh, Trevor, Ally, Adrian, Bilenky, Mikhail, Butterfield, Yaron SN, Carlsen, Rebecca, Cheng, Young, Chuah, Eric, Corbett, Richard D, Dhalla, Noreen, He, An, Lee, Darlene, Li, Haiyan I, Long, William, Mayo, Michael, Plettner, Patrick, Qian, Jenny Q, Schein, Jacqueline E, Tam, Angela, Wong, Tina, Birol, Inanc, Zhao, Yongjun, Faria, Claudia C, Pimentel, José, Nunes, Sofia, Shalaby, Tarek, Grotzer, Michael, Pollack, Ian F, Hamilton, Ronald L, Li, Xiao-Nan, Bendel, Anne E, Fults, Daniel W, Walter, Andrew W, Kumabe, Toshihiro, Tominaga, Teiji, Collins, V Peter, Cho, Yoon-Jae, Hoffman, Caitlin, Lyden, David, Wisoff, Jeffrey H, Garvin, James H, Stearns, Duncan S, Massimi, Luca, Schüller, Ulrich, Sterba, Jaroslav, Zitterbart, Karel, Puget, Stephanie, Ayrault, Olivier, Dunn, Sandra E, Tirapelli, Daniela PC, Carlotti, Carlos G, Wheeler, Helen, Hallahan, Andrew R, Ingram, Wendy, MacDonald, Tobey J, Olson, Jeffrey J, Van Meir, Erwin G, Lee, Ji-Yeoun, and Wang, Kyu-Chang

Subjects
Pediatric, Biotechnology, Genetics, Brain Disorders, Human Genome, Brain Cancer, Rare Diseases, Cancer, Animals, Cerebellar Neoplasms, Clone Cells, Craniospinal Irradiation, DNA Mutational Analysis, Disease Models, Animal, Drosophila melanogaster, Female, Genome, Human, Humans, Male, Medulloblastoma, Mice, Molecular Targeted Therapy, Neoplasm Recurrence, Local, Radiotherapy, Image-Guided, Selection, Genetic, Signal Transduction, Xenograft Model Antitumor Assays, General Science & Technology
Abstract

The development of targeted anti-cancer therapies through the study of cancer genomes is intended to increase survival rates and decrease treatment-related toxicity. We treated a transposon-driven, functional genomic mouse model of medulloblastoma with 'humanized' in vivo therapy (microneurosurgical tumour resection followed by multi-fractionated, image-guided radiotherapy). Genetic events in recurrent murine medulloblastoma exhibit a very poor overlap with those in matched murine diagnostic samples (

Published
2016

32. Higher dose corticosteroids in patients admitted to hospital with COVID-19 who are hypoxic but not requiring ventilatory support (RECOVERY)

Author

Obbina Abani, Ali Abbas, Fatima Abbas, Joshua Abbas, Kasim Abbas, Mustafa Abbas, Sadia Abbasi, Hakam Abbass, Alfie Abbott, Alison Abbott, Nabeel Abdallah, Ammar Abdelaziz, Ashraf Abdelaziz, Mohamed Abdelfattah, Bushra Abdelqader, Audrey Abdul, Basir Abdul, Siddiqui Abdul, Althaf Abdul Rasheed, Ajibode Abdulakeem, Rezan Abdul-Kadir, Abdullah Abdullah, Abdulfatahi Abdulmumeen, Rasheed Abdul-Raheem, Niyaz Abdulshukkoor, Kula Abdusamad, Yazeed Abed El Khaleq, Mai Abedalla, Abeer Abeer Ul Amna, Lynn Abel, Katrina Abernethy, Movin Abeywickrema, Chandra Abhinaya, Affyarsyah Abidin, Adebanke Aboaba, Abigail Aboagye-Odei, Christopher Aboah, Heba Aboelela, Hani Abo-Leyah, Karim Abouelela, Ahmed Abou-Haggar, Mahmoud Abouibrahim, Ahmed Abousamra, Mona Abouzaid, Miriam Abraham, Tizzy Abraham, Abraheem Abraheem, Judith Abrams, Rebecca Abrams, Hyacinth-John Abu, Ahmed Abu-Arafeh, Syed M Abubacker, Akata Abung, Yousuf Abusamra, Yaa Aceampong, Amaka Achara, Devikumar Acharya, Faustina Acheampong, Prince Acheampong, Sarah Acheampong, Janet Acheson, Shiella Achieng, Andres Acosta, Rebecca Acquah, Catherine Acton, Jacqueline Adabie-Ankrah, Paul Adair, Fiona Adam, Matthew Adam, Huzaifa Adamali, Marta Adamczyk, Carol Adams, Charlotte Adams, Daniel Adams, Kate Adams, Laura Adams, Nikkita Adams, Richard Adams, Tim Adams, Laura Adamu-Ikeme, Krishma Adatia, Kirsty Adcock, Lawrence Addai-Boampong, Afua Addo, Oluwatobi Adeagbo, Ade Adebiyi, Ogunlana Adedeji, Yewande Adegeye, Ken Adegoke, Vicki Adell, Sherna Adenwalla, Femi W Adeoye, Oluwasegun A Adesemoye, Emmanuel O Adewunmi, Adedamola Adeyanju, Joyce Adeyemi, Tenifayo Adeyemo, Binay Adhikari, Shanti A Adhikari, Rina Adhikary, Adhikarla Aditya, Patience Adjepong, Gabrielle Adkins, Adnan Adnan, Marguerite Adriaanse, John Aeron-Thomas, Debbie Affleck, Carmel Afnan, Muhammad Afridi, Patricia Afrim, Felicia Akua Afriyie, Zainab A Aftab, Meenakshi Agarwal, Rachel Agbeko, Chris Agbo, Sunil Aggarwal, Arameh Aghababaie, Laura Aguilar Jimenez, Jacqueline Afrakomah Agyekum, Kwame Agyen, Shafana Ahamed Sadiq, Mohamed H Ahammed Nazeer, Mohammad Ahmad, Syed Ahmad, Afshan Ahmed, Ashar Ahmed, Asim Ahmed, Basheer A R Ahmed, Bilal Ahmed, Forizuddin Ahmed, Hamze Ahmed, Hanad Ahmed, Irshad Ahmed, Khaled Ahmed, Khalil Ahmed, Liban Ahmed, Mahin Ahmed, Maria C Ahmed, Muhammad S Ahmed, Naseer Ahmed, Nausheen Ahmed, Osama Ahmed, Rajia A Ahmed, Rawya Ahmed, Rizwan Ahmed, Saif Ahmed, Sammiya Ahmed, Sana G Ahmed, Syed Ahmed, Syed H Ahmed, Roa Ahmed Ali, Bilal Ahmed Mohamud, Sana Ahmed, Sana Ahmer, Augustine Ahonia, Christine Aiken, Dhiraj Ail, Mark Ainsworth, Myriam Aissa, Lindianne Aitken, Bini Ajay, Abdulakeem Ajibode, Ayesha Ajmi, Nasim Akhtar, Nauman Akhtar, Suha Akili, Bolutito Akinbiyi, Oludoyinsola Akindolie, Yinka Akinfenwa, Olugbenga Akinkugbe, Ibrahim Akinpelu, Mohammad Akram, Olugbenro Aktinade, Uzayr Akudi, Ahmad S A R Al Aaraj, Asma Al Balushi, Majd Al Dakhola, Aladdin Al Swaifi, Eslam Al-Abadi, Adegoke Alabi, Narendra Aladangady, Mohamed Alafifi, Ayaz Alam, Sajid Alam, Abbas Al-Asadi, Kyriaki Alatzoglou, Paul Albert, Albertus Albertus, Lorraine Albon, Angela Alcala, Gemma Alcorn, Stephen Alcorn, Aggie Aldana, David Alderdice, Abdullah Aldesouki, Rayan Aldouri, Jonathan Aldridge, Nicolas Aldridge, Ram Maya Ale, Ana Alegria, Alison Alexander, Courtney Alexander, John Alexander, Peter D G Alexander, Julyan Al-fori, Laith Alghazawi, Osama Alhabsha, Bahij Al-Hakim, Rafil Alhameed, Mohammed Al-Hayali, Shams Al-Hity, Ali Ali, Amanda Ali, Asad Ali, Fawzia R Ali, Jawad Ali, Mariam Ali, Mohamed Ali, Mohammad Ali, Muhammad S Ali, Nayab Ali, Oudai Ali, Ramla Ali, Sakina Ali, Syed Ali, Emilio Aliberti, Jade Alin, Abid Alina, Analyn Alipustain, Bachti Alisjahbana, Fine Aliyuda, Katrin Alizadeh, Maithem Al-Jibury, Saba Al-Juboori, Majid Al-Khalil, Abdullah Alkhudhayri, Moutaz Alkhusheh, Fiona Allan, Nataliya Allan, Alison Allanson, Robert Allcock, Eireann Allen, Jade Allen, Kerry Allen, Louise Allen, Poppy Allen, 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Thomas Cope, Sinead Corbet, Carolyn Corbett, Ailsa Corbishley, John Corcoran, Chris Cordell, Jessica Cordle, Alasdair Corfield, John Corless, Alison Corlett, Joe Cornwell, Michael Cornwell, Diana Corogeanu, Aisling Corr, Mirella Corredera, Ruth Corrigan, P Corry, Rita Corser, Jon Cort, Denise Cosgrove, Tracey Cosier, Patricia Costa, Telma Costa, Charlie Coston, Susannah Cotgrove, Zoe Coton, Lisa-Jayne Cottam, Rhiannon Cotter, Donna Cotterill, Caroline Cotton, George Couch, Martina Coulding, Andrew Coull, David Counsell, David Counter, Cherry Coupland, Ellie Courtney, Julia Courtney, Rebecca Cousins, Amanda J Coutts, Alexander Cowan, Elena Cowan, Richard Cowan, Richard Cowell, Louise Cowen, Steve Cowman, Amanda Cowton, Ellie Cox, Emma Cox, Giles Cox, Helen Cox, Karina Cox, Miriam Cox, Karen Coy, Andrea Cradduck-Bamford, Hannah Craig, Jayne Craig, John Craig, Victoria Craig, Felicity Craighead, Matthew Cramp, Hayley Cranston, Sheetal S Crasta, Jacolene Crause, Angie Crawford, Emma 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Czekaj, Patrycja Czylok, Shane D'Souza, Joana da Rocha, Mohammed Dafalla, Andrew Dagens, Helen Daggett, Jacqui Daglish, Sandeep Dahiya, Anne Dale, Katie Dale, Michaela Dale, Sam Dale, Susan Dale, Jolyon Dales, Umberto D'Alessandro, Helen Dalgleish, Helen Dallow, Carlo D'aloia, Dermot Dalton, Morag Dalton, Zoe Daly, Mansi Damani, Eleanor Damm, Akila Danga, Joanne Dangerfield, Amelia Daniel, Priya Daniel, Allison Daniels, Adela Dann, Kwaku Gyasi Danso, Sandra Danso-Bamfo, Quang Tung Dao, Suzanne Darby, Alex Darbyshire, Janet Darbyshire, Paul Dargan, Paul Dark, Kate Darlington, Sarah Darnell, Thomas Darton, Guledew Darylile, Avisnata Das, Manjusha Das, Sukamal Das, Martin Daschel, Joanne Dasgin, Dibyendu Datta, Anna Daunt, Vaishali Dave, Emily Davenport, Mark Davey, Miriam Davey, Molly Davey, Mini David, Alexander Davidson, Laura Davidson, Neil Davidson, Richard Davidson, Albert Davies, Alison Davies, Amanda Davies, Amy Davies, Angela Davies, Bethan Davies, Caroline Davies, Carolyn 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Souza, Anthony De Soyza, Natasha de Vere, Johannes de Vos, Bethan Deacon, Sharon Dealing, Anna Dean, Julie Dean, Katrina Dean, Stephen Dean, Tessa Dean, Jill Deane, James Dear, Effie Dearden, Catherine Deas, Samuel Debbie, Gabor Debreceni, Vashist Deelchand, Matthew Deeley, Joanne Deery, Emmanuel Defever, Manuela Del Forno, Arnold Dela Rosa, Gonzalo De-La-Cedra, Amanda Dell, Carrie Demetriou, David DeMets, Jane Democratis, Jacqueline Denham, Emmanuelle Denis, Laura Denley, Craig Denmade, Alexandra Dent, Kathy Dent, Martin Dent, Elise Denton, Tom Denwood, Nishigandh Deole, Darshita Depala, Maria Depante, Susan Dermody, Amisha Desai, Asmita Desai, Purav Desai, Sanjeev Deshpande, Vai Deshpande, Sirjana Devkota, Usha Devkota, Debbie Devonport, Matthew Devonport, Prakash Dey, Vishal Dey, Rogin Deylami, Kevin Dhaliwal, Sundip Dhani, Amandeep Dhanoa, Mili Dhar, Ankush Dhariwal, Dawpadee Dharmasena, Devesh Dhasmana, Ekanjali Dhillon, Reiss Dhillon, Syra Dhillon, Meghnath Dhimal, Dipali Dhiru, Trupti Dhorajiwala, Priya Dias, Stephanie Diaz, Kayleigh Diaz-Pratt, Mohammed Dibas, Debbie Dickerson, Pamela Dicks, Matt Dickson, Stuart Dickson, J Digby, Ronneil Digpal, Sean Dillane, Sarah Diment, Paul Dimitri, Georgios Dimitriadis, Sajeel Din, Thai H Dinh, Thi T T Dinh, Alex Dipper, Sabiq Dipro, Laura Dirmantaite, Lorelle Dismore, Lisa Ditchfield, Sarah Diver, Lavanya Diwakar, Preeti Diwan, Caroline Dixon, Giles Dixon, Kate Dixon, Brice Djeugam, Sipho Dlamini, Petr Dlouhy, Andrea D'Mello, Paul Dmitri, Thi Tien Do, Laurence Dobbie, Marinela Dobranszky Oroian, Charlotte Dobson, Lee Dobson, Marie Docherty, David Dockrell, Jacqueline Dodd, James Dodd, Jackie Dodds, Rebecca Dodds, Steve Dodds, Richi Dogra, Conor Doherty, Erin Doherty, Warren Doherty, Yumiko Doi, Iain Doig, Eleanor Doke, Daniel Dolan, Mark Dolman, Rozzie Dolman, Lisa Donald, Katie Donald, Callum Donaldson, Christopher Donaldson, Denise Donaldson, Gillian Donaldson, Kate Donaldson, Phu Khiem Dong, Martha Donkor, Sinead Donlon, Joanne Donnachie, Eilish Donnelly, Ronan Donnelly, Phil Donnison, Aravindhan Donohoe, Gemma Donohoe, Bryan Donohue, Emma Dooks, Reece J Doonan, Rogier Van Doorn, Grainne Doran, Rachael Dore, Kane Dorey, Sharon Dorgan, Kataryna Dos Santos, Moonira Dosani, Davinder Dosanjh, Paula Dospinescu, Isabelle Doss, Theonymfi Doudouliaki, Andrew Dougherty, Jill Doughty, Katie Douglas, Jonathan Douse, Allyn Dow, Lucy Dowden, Michelle Dower, Sud Dowling, Nicola Downer, Charlotte Downes, Rob Downes, Thomas Downes, Damian Downey, Robert Downey, Caroline Downing, Louise Downs, Simon Dowson, Cornel Dragan, Cristina Dragos, Maire Drain, Chelsea Drake, Victoria Drew, Olivia Drewett, Anthony Drexel, Celine Driscoll, Helena Drogan, Odysseas Drosos, Graham Drummond, Katie Drury, Kay Druryk, Ronald Druyeh, Jack Dryburgh-Jones, Simon Drysdale, An Du Thinh, Hazel Dube, Judith Dube, Stephen Duberley, Paige K Duckenfield, Hayley Duckles-Leech, Nicola Duff, Emma Duffield, Heather Duffy, Helen Duffy, Katharine Duffy, Lionel Dufour, Annette Duggan, Parveen Dugh, Rauand Duhoky, Janice Duignan, Jennifer Dulay, Simon Dummer, Alexis Duncan, Andrew Duncan, Christopher Duncan, Fullerton Duncan, Gregory Duncan, Holly Duncan, Robert Duncan, Stephanie Dundas, Do Van Dung, Aileen Dunleavy, Julia Dunleavy, Alessia Dunn, Charlotte Dunn, Damian Dunn, Laura Dunn, Paul Dunn, Charlene Dunne, Karen Dunne, Fiona Dunning, Aidan Dunphy, Tran Thi Hai Duong, Venkat Duraiswamy, Beatriz Duran, Ingrid DuRand, Leanne Durdle, Natalie Duric, Alison Durie, Emily Durie, Samuel Durogbola, Chris Durojaiye, Laura Durrans, Katie Durrant, Hannah Durrington, Iheukwumere Duru, Haris Duvnjak, Akshay Dwarakanath, Laasya Dwarakanath, Dennis Dwomoh Nkrumah, Ellen Dwyer, Zara Dyar, Claudia Dyball, Kristyn Dyer, Harvey Dymond, Tom Dymond, Chris Eades, Lauren Eadie, Rebekah Eadie, Laura Eagles, Beena Eapen, Naomi Earl, Joanne Early, Melissa Earwaker, Nicholas Easom, Clare East, Amy Easthope, Fraser Easton, Jack Easton, Patrick Easton, Ruth Eatough, Oluwadamilola Ebigbola, Martin Ebon, Alison Eccles, Sinan Eccles, Chloe Eddings, Michael Eddleston, Maureen Edgar, Katharine Edgerley, Nicholas Edmond, Mary Edmondson, Tracy Edmunds, Abby Edwards, Alexandra Edwards, Catherine Edwards, Joy Edwards, Kennedy Edwards, Mandy Edwards, Martin Edwards, Sophie Edwards, Jenny Eedle, Aline Eggink, Dawn Egginton, Sam Eggleston, Loveth Ehiorobo, Sarah Eisen, Ugochukwu Ekeowa, Mohamed Ekoi, Ayomide Ekunola, Soha El Behery, Nagla Elashhar, Lisa Elawamy, Mohamed Elbeshy, Kate El-Bouzidi, Jennifer Elder, Mohammed El-Din, Emma Eldridge, Diana Eleanor, Uchenna Elenwa, Ibrahim Eletu, Eman Elfar, Mayy Magdy Elgamal, Amr Elgohary, Mohamed A A Elhadi, Stellios Elia, Jennifer Elias, Tania Elias, Nadia Elkaram, Andrew V Elkins, Julie Ellam, Nikki Ellard, Laura N Ellerton, Lucy Elliot, Amy Elliott, Fiona Elliott, Kerry Elliott, Scott Elliott, Sian Elliott, Annie Ellis, Christine Ellis, Kaytie Ellis, Leila Ellis, Rupert Ellis, Tak-Yan Ellis, Yvette Ellis, Alison C Ellwood, Rahma Elmahdi, Einas Elmahi, Hannah-May Elmasry, Mohammed El-Naggar, Najla Elndari, Omer Elneima, Mohamed Elokl, Ahmed Elradi, Mohamed Elsaadany, Mohammed A S A Elsayed, Sally El-Sayeh, Hana El-Sbahi, Mohammad Elsebaei, Tarek Elsefi, Karim El-Shakankery, Alguili Elsheikh, Hosni El-Taweel, Sarah Elyoussfi, Jonathan Emberey, Jonathan R Emberson, John Emberton, Anna Emery, Julian Emmanuel, Ingrid Emmerson, Michael Emms, Florence Emond, Marieke Emonts, Nicu Enachi, Dickson Enenche, Angila Engden, Katy English, Emma Entwistle, Hene Enyi, Marios Erotocritou, Peter Eskander, Hanif Esmail, Fatheha Essa, Brynach Evans, Chris Evans, Debra Evans, E Evans, Emrys Evans, Gail Evans, Gareth Evans, Isabel Evans, Jack Evans, Jacqueline Evans, Jennifer Evans, John Evans, Jolanta Evans, Lisa Evans, Lynn Evans, Mim Evans, Morgan Evans, Ranoromanana Evans, Sharon Evans, Sian Evans, Teriann Evans, Tomos Evans, Caroline Everden, Serenydd Everden, Lynette Every, Hayley Evison, Lynsey Evison, Chiamaka Ezenduka, Jacqueline Faccenda, Leila Fahel, Youstina Fahmay, Ian Fairbairn, Sara Fairbairn, Terry Fairbairn, Andy Fairclough, Louise Fairlie, Mark Fairweather, Anne Fajardo, Naomi Falcone, Euan Falconer, John Fallon, Andrea Fallow, David Faluyi, Victoria Fancois, Ayaan Farah, Muna Farah, Qayyum Farah, Nowin Z Fard, Leila Fares, Amr Farg, Adam Farmer, Katie Farmer, Toni Farmery, Samantha Farnworth, Faiyaz Farook, Hadia Farooq, Sidrah Farooq, Fiona Farquhar, Holly Farr, Aaron Farrell, Barbara Farrell, Fayed Farrukh, James Farthing, Syeda Farzana, Rahmatu Fasina, Azam Fatemi, Mina Fatemi, Suman Fathima, Nibah Fatimah, Maria Faulkner, Saul N Faust, Clair Favager, Joe Fawke, Sinmidele Fawohunre, Abul Fazal, Aisthath Fazleen, Simon Fearby, Connie Fearnley, Alex Feben, Federico Fedel, Daria Fedorova, Christopher Fegan, Mae Felongo, Lynsey Felton, Tim Felton, Kate Fenlon, Andrea Fenn, Ruth Fennelly, Isabelle Fenner, Ciara Fenton, Melisa Fenton, Gloria Ferenando, Cameron Ferguson, Jenny Ferguson, Kathryn Ferguson, Katie Ferguson, Susan Ferguson, Susie Ferguson, Victoria Ferguson, Denzil Fernandes, Candida Fernandez, Eduardo Fernandez, Maria Fernandez, Sonia Fernandez Lopez, Jaime Fernandez Roman, Callum J Fernando, Jessica Fernando, Ahmed Feroz, Pietro Ferranti, Thais Ferrari, Eleanor Ferrelly, Alexandra Ferrera, Emma Ferriman, Sheldon Ferron, Nicholas Fethers, Ben Field, Janet Field, Rebecca Field, Karen Fielder, Lindsey Fieldhouse, Andra Fielding, Julie Fielding, Sarah Fielding, Asma Fikree, Santos Filipa, Sarah A Filson, Shona Finan, Sarah Finbow, Deborah J Finch, Joanne Finch, Laurie Finch, Simon Finch, Spencer Finch, Natalie Fineman, Jim Finlayson, Lauren Finlayson, Adam Finn, Joanne Finn, Dylan Finnerty, Clare Finney, Deborah Finucane, Sofia Fiouni, Jo Fiquet, Promise Firi, James Fisher, Neil Fisher, Daniel Fishman, Krystofer Fishwick, Carolyn Fitton, Felicity Fitzgerald, Fiona Fitzgerald, Karen Fitzjohn, Jan Flaherty, Michael Flanagan, Charles Flanders, Nikolaos Flaris, Gail Fleming, Julie Fleming, Lucy Fleming, Paul Fleming, William Flesher, Alison Fletcher, Anna Fletcher, Jonathan Fletcher, Lucy Fletcher, Simon Fletcher, Sophie Fletcher, Fiona Flett, Karen Flewitt, Sarah Flockhart, Christopher Flood, Ian Floodgate, Jonathan Flor, Vincent Florence, Mary Flowerdew, Sharon Floyd, Margaret J Flynn, Rachel Flynn, Claire Foden, Adama Fofana, Georgina Fogarty, Paul Foley, Linda Folkes, Tracey Fong, Daniela M Font, Aiwyne Foo, Jane Foo, Andrew Foot, Helen R Foot, Jayne Foot, Jane Forbes, Amber Ford, Jamie Ford, Imogen Fordham, Jennifer Foreman, Matthew Forester, Mohammad Forkan, Caroline Fornolles, Adam Forrest, Ellie Forsey, Miranda Forsey, Thomas Forshall, Elliot Forster, Abigail Forsyth, Julian Forton, Conrad Foster, Emily Foster, Joseph Foster, Rachel A Foster, Tracy Foster, Angela Foulds, Ian Foulds, Folakemi Fowe, Natasha Fowkes, Emily Fowler, Robert Fowler, Stephen Fowler, Amy Fox, Claire Fox, Heather Fox, Jonathan Fox, Laura Fox, Lauren Fox, Natalie Fox, Olivia Fox, Simon Fox, Sarah-Jane Foxton, Eva Fraile, Rebecca Frake, Alex Francioni, Olesya Francis, Rebecca Francis, Sarah Francis, Theodora Francis-Bacon, Helen Frankland, Jessica Franklin, Siobhan Franklin, Catherine Fraser, Andi Fratila, Sharon Frayling, Martyn Fredlund, Anna Freeman, Carol Freeman, Elaine Freeman, Hannah Freeman, Nicola Freeman, Clare Freer, Eleanor French, Thomas French, Karen Freshwater, Matthew Frise, Renate Fromson, Adam Frosh, John Frost, Victoria Frost, Oliver Froud, Rachel Frowd, Arun Fryatt, Andrzej Frygier, Bridget Fuller, Liz Fuller, Lucy Fuller, Tracy Fuller, Duncan Fullerton, Carrie Fung, Gayle Fung, Sarah Funnell, John Furness, Andrew Fyfe, Nytianandan G, Elizabeth Gabbitas, Claire Gabriel, Zoë Gabriel, Hadiza Gachi, Sophie Gaffarena, Sarah Gage, Joshua Gahir, Sarveen Gajebasia, Katarzyna Gajewska-Knapik, Babita Gajmer, Zacharoula Galani, Christopher Gale, Hugo Gale, Linda Gale, Rebecca Gale, Swetha Gali, Bernadette Gallagher, Jude Gallagher, Rosie Gallagher, William Gallagher, Feroze Gallam, Joanne Galliford, Catherine Galloway, Chris Galloway, Emma Galloway, Jacqui Galloway, James Galloway, Anna Galvin, Victoria Galvis, Gareth Gamble, Laura Gamble, Liz Gamble, Brian Gammon, Chien N Gan, Muhammad B Ganaie, Jaikumar Ganapathi, Ramesh Ganapathy, Kaminiben Gandhi, Sarah Gandhi, Usha Ganesh, Thenugan Ganeshanathan, Saibal Ganguly, Abrar Gani, Pauline Ganley, Ukraina Garcia, Emma-James Garden, Antoni D Gardener, Emma Gardiner, Michael Gardiner, Phil Gardiner, Siobhan Gardiner, Caroline Gardiner-Hill, Jonathan Gardner, Louis Gardner, Mark Garfield, Atul Garg, Isha Garg, Nathan Garlick, Daniel Garner, Justin Garner, Lucie Garner, Zoe Garner, Rosaline Garr, Kathryn A Garrero, Manisha Gartaula, Florence Garty, Rachel Gascoyne, Hyeriju Gashau, Aoife Gatenby, Erin Gaughan, Alok Gaurav, Mariana Gavrila, Jane Gaylard, Sophie Gayle, Catherine Geddie, Ian Gedge, Sarah Gee, Fartuun Geele, Kalaichelvi Geerthan, Minnie Gellamucho, Karzan Gelly, Leila Gelmon, Sandra Gelves-Zapata, Gemma Genato, Neal Gent, Susan Gent, Natalie Geoghegan, Aparna George, Bini George, Sam George, Susan George, Tina George, Valerie P George, Simon Georges, Domonique Georgiou, Peter Gerard, Leigh Gerdes, Louise Germain, Helen Gerrish, Abel Getachew, Louise Gethin, Siobhan Gettings, Hisham Ghanayem, Bijan Ghavami Kia, Shaista Ghazal, Anca Gherman, Alison Ghosh, Dipansu Ghosh, Justin Ghosh, Subhamay Ghosh, Sarra Giannopoulou, Malick Gibani, Chris Gibb, Ben Gibbison, Kerry Gibbons, Alex Gibson, Bethan Gibson, Jamie Gibson, Kimberley Gibson, Kirsty Gibson, Sian Gibson, Mary Gigi, Cat Gilbert, Jeanette Gilbert, Kayleigh Gilbert, Benjamin Giles, James Gilham, Mandy Gill, Lynne Gill, Paul Gillen, Annelies Gillesen, Katherine Gillespie, Elizabeth Gillham, Andrew Gillian, Deborah Gilliland, Robert Gillott, Danielle Gilmour, Kate Gilmour, Lesley Gilmour, Louis Ginn, Franciscus Ginting, Theodora Giokanini-Royal, Anna Gipson, Barbie Giri, Joanna Girling, Rhian Gisby, Angelena Gkioni, Aikaterini Gkoritsa, Effrossyni Gkrania-Klotsas, Amy Gladwell, James Glanville, Jessica Glasgow, Susannah Glasgow, Jon Glass, Lynn Glass, Sharon Glaysher, Lisa Gledhill, Eleanor Glenday, Ana Glennon, Jodie Glossop, John Glover, Kyle Glover, Michelle Glover, Jan Glover Bengtsson, Deborah Glowski, Sharon Glynn, Chevanthy Gnanalingam, Julie Goddard, Wendy Goddard, Emily Godden, Jo Godden, Sarah Godlee, Emma Godson, Gillian Godwin, Sukanya Gogoi, Aiky Goh, Manjinder Gohel, Rebeca Goiriz, Sriya Gokaraju, Raphael Goldacre, Arthur Goldsmith, Portia Goldsmith, Darren Gomersall, Lucia Gomez, Raquel Gomez-Marcos, Ali Gondal, Celia Gonzalez, Jack Goodall, Vicky Goodall, Bob Goodenough, Anna Goodfellow, Laura Goodfellow, James Goodlife, Camelia Goodwin, Elizabeth Goodwin, Jayne Goodwin, Paula Goodyear, Rajiv Gooentilleke, Michelle Goonasekara, Sheila Gooseman, Shameer Gopal, Chris Gordon, Sally Gordon, Robin Gore, Hugh Gorick, Caitlin Gorman, Claire Gorman, Stuart Gormely, Maria Gorniok, Diana Gorog, Michelle Gorst, Thomas Gorsuch, Jayshreebahen Gosai, Rebecca Gosling, Sally Gosling, Georgina Gosney, Vanessa Goss, Dzintars Gotham, Naomi Gott, Elizabeth Goudie, Nicole Gould, Susan Gould, Charlotte Goumalatsou, Lysander Gourbault, Abha Govind, Rajesh Govindan, Sharon Gowans, Girish Gowda, Rohit Gowda, Hannah Gower, Pankaj Goyal, Sunil Goyal, Sushant Goyal, Cheryl Graham, Clive Graham, Jonathan Graham, Justin Graham, Libby Graham, Rachel Graham, Sharon Graham, Matthew Graham-Brown, Julia Grahamslaw, Gianluca Grana, Tracyanne Grandison, Louis Grandjean, Alison Grant, Ann Grant, David Grant, Kirstie Grant, Matthew Grant, Pauleen Grant, Rhys Gravell, Jenny Graves, Alasdair Gray, Catherine Gray, Georgina Gray, Glaxy Gray, Jackie Gray, Karen Gray, Nicola Gray, Roxanne Gray, Sebastian Gray, Alan Grayson, Fiona Greaves, Paul Greaves, Alastair Green, Amy Green, Amy S Green, Charlotte Green, Christopher A Green, David Green, Frederick Green, Joel Green, Marie Green, Nicola Green, Stacey Green, Diarra Greene, Philippa Greenfield, Alan Greenhalgh, Daniel Greenwood, Sandra Greer, James Gregory, Jane Gregory, Katie Gregory, Tamsin Gregory, Jill Greig, Julia Greig, Rebecca Grenfell, Teena Grenier, Jack Grenville, Jo Gresty, Susan Grevatt, Glaxy Grey, Samuel Gribben, Andrew Gribbin, Amy Gribble, Natasha Grieg, Douglas Grieve, Ben Griffin, Denise Griffin, Mel Griffin, Sian Griffith, Andrew Griffiths, Daniel Griffiths, David Griffiths, Donna Griffiths, Isabel Griffiths, Mark Griffiths, Nicola Griffiths, Oliver Griffiths, Sandra Griffiths, Sarah Griffiths, Scott Griffiths, Yvonne Griffiths, Sofia Grigoriadou, Steph Grigsby, Paul Grist, Evelina Grobovaite, Dorothy Grogono, Clarissa Grondin, Rachel Groome, Pauline Grose, Liliana Grosu, Jenny Grounds, Margaret Grout, Helen Grover, Jayne Groves, Neil Grubb, Julie Grundy, Francesca Guarino, Sharada Gudur, Jacinta Guerin, Sharazeq 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Hale, Jennie Hale, Carmel Halevy, Paul Halford, William Halford, Alaina Halim, Alistair Hall, Anthony Hall, Claire Hall, Elizabeth Hall, Fiona Hall, Helen Hall, Jennifer Hall, Kathryn Hall, Laura Hall, Jan Hallas, Kyle Hallas, Charles Hallett, Jackie Halliday, Akmal Hallman, Heather Halls, Maryam Hamdollah-Zadeh, Ifedadepo A Hamed-Adekale, Bilal Hameed, Mohammed Hameed, Raph L Hamers, Imran Hamid, Mohamad Hamie, Raymond Hamill, Bethany Hamilton, Fergus Hamilton, Gus Hamilton, Leigh Hamilton, Melanie Hamilton, Nicola Hamilton, Sara Hamilton, Ruth Hamlin, Eleanor Hamlyn, Beatrice Hammans, Shirley Hammersley, Kate Hammerton, Bev Hammond, Emily Hammond, Leah Hammond, Sally Hammond, Fiona Hammonds, Ibrahim Hamoodi, Karen Hampshire, James A Hampson, Jude Hampson, Lucy Hampson, Lisa Hamzah, Jenny Han, Ozan Hanci, Sadiyah Hand, Lala Handayani, Jasmine Handford, Soran Handrean, Nina K Handzewniak, Sarah Haney, Vu Thi Kim Hang, Sheharyar Hanif, E Hanison, Esther Hanison, Jennifer Hannah, Amy Hannington, Merhej Hannun, Aidan Hanrath, Helena Hanratty, Daniel Hansen, Anita Hanson, Ashley Hanson, Helen Hanson, Jane Hanson, Kathryn Hanson, Steve Hanson, Ala Haqiqi, Monjurul Haque, Henry Harcourt, Lesley Harden, Zoe Harding, Simon Hardman, Marc Hardwick, Gareth Hardy, Joanna Hardy, Yasmine Hardy, Kumar Haresh, Rachel Harford, Beverley Hargadon, James Hargraves, Carolyn Hargreaves, Alice Harin, Mohammed Haris, Edward Harlock, Paula Harman, Tracy Harman, Mark Harmer, Muhammad A Haroon, Charlie Harper, Heather Harper, James Harper, Peter Harper, Rosemary Harper, Sarah Harrhy, Kate Harrington, Sian Harrington, Yasmin Harrington-Davies, Jade Harris, Jess Harris, John Harris, Laura Harris, Marie-Clare Harris, Nichola Harris, Sophie Harris, David Harrison, Laura Harrison, Melanie Harrison, Olakunbi A Harrison, Rachael Harrison, Rowan Harrison, Susie Harrison, Thomas Harrison, Wendy Harrison, Elizabeth Harrod, Ciaran Hart, Dominic Hart, Jessica Hartley, Lisa Hartley, Rosemary Hartley, Ruth Hartley, Tom Hartley, William Hartrey, Phillipa Hartridge, Stuart Hartshorn, Alice Harvey, Angela Harvey, Anna Harvey, Max Harvey, Catherine Harwood, Helen Harwood, Zoe Harzeli, Brigitte Haselden, Kazi Hashem, Mohammed Hashimm, Tadaaki Hashimoto, Imranullah Hashmi, Jack Haslam, Zena Haslam, Grace Hasnip, Adil Hassan, Ali Hassan, Amro Hassan, Awab Hassan, Zeinab Hassan, Sapna Hassasing, Jane Hassell, Philip Hassell, Alex Hastings, Bethany Hastings, Janice Hastings, Sarah Hathaway-Lees, Jonathan Hatton, Jennifer Hau, May Havinden-Williams, Stefan Havlik, Daniel B Hawcutt, Kadean Hawes, Liz Hawes, Nicola Hawes, Lydia Hawker, Annie Hawkins, Joe Hawkins, Nancy Hawkins, W John Hawkins, Dan Hawley, Ed Hawley-Jones, Edward Haworth, Alasdair W Hay, Cathy Hay, Amna Hayat, Jamal Hayat, Mohamed-Riyal Hayathu, Anne Hayes, Jonas Hayes, Kate Hayes, Melony Hayes, Fiona Hayes, Patrick Hayle, Chloe Haylett, Antara Hayman, Melanie Hayman, Matthew Haynes, Richard Haynes, Rachel Hayre, Carole Hays, Sarah Haysom, James Hayward, Patrick Haywood, Hazel Haywood Hasford, Tracy Hazelton, Phoebe Hazenberg, Zhengmai He, Elizabeth Headon, Carrie Heal, Brendan Healy, Jessica L Healy, Amy Hearn, David Heasman, Angela Heath, Debbie Heath, Rowan Heath, Diane Heaton, Adam Heavens, Kerry Hebbron, Catherine Heckman, Gemma Hector, Sadie Heddon, Andy Hedges, Katrine Hedges, Cheryl Heeley, Elaine Heeney, Richard Heinink, Rajdeep Heire, Ingvild Helgesen, Joanne Hemingway, Ulla Hemmila, Beth Hemmings, Scott Hemphill, Deborah Hemsley, Abigail Henderson, Eilidh Henderson, Jennifer Henderson, Steven Henderson, Joanne Henry, Karol Henry, Lavinia Henry, Margo Henry, Natalie Henry, David Henshall, Gillian Herdman, Rosaleen Herdman-Grant, Morag Herkes, Lucas E Hermans, Fe Marie Hernandez, Emma Heron, Lisa Heron, William Herrington, Emilia Heselden, Peta Heslop, Tracey Heslop, Simon Hester, Emily Hetherington, Joseph Hetherington, Chamila Hettiarachchi, Pramodh Hettiarachchi, Hayley Hewer, John Hewertson, 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Chloe Vansomeren, William Van't Hoff, Sejal Vara, Stehen J Vardy, Anu Varghese, Maria Varghese, William Varney, Giulia Varnier, Anna-Nektaria Varouxaki, Resti Varquez, Valeria Vasadi, Olivia Vass, Katherine Vassell, Vimal Vasu, Vasanthi Vasudevan, Manu Vatish, Sue Vaughan, Heloyes Vayalaman, Darini Vayapooree, Christopher Vaz, Niki Veale, Sachuda Veerasamy, Swati Velankar, Luxmi Velauthar, Neyme Veli, Nicola Vella, Aravind Velugupati, Anitha Velusamy, Ian Venables, Mavi Venditti, Ramya Venkataramakrishnan, Richard Venn, Robert Venn, Michelle Venter, Lyn Ventilacion, Joanne Vere, Mark Veres, Stefania Vergnano, Will Verling, Amit Verma, Rachel Vernall, Britney Vernon, Mark Vertue, Liberty Verueco, Jerik Verula, Anna Veterini, Natalie Vethanayagam, Shambavi Vettikumaran, Lucy Veys, Carinna Vickers, Saji Victor, SImpson Victoria, Celine P Vidaillac, Jennifer Vidler, Bavithra Vijayakumar, Vinod W Vijayaraghavan Nalini, Brigita Vilcinskaite, Alicija Vileito, Neringa Vilimiene, Lynn Vinall, Sylvia Vinay, Latha Vinayakarao, Olivia Vincent, Rachel Vincent, Rosie Vincent, Pritpal Virdee, Emma Virgilio, Abdullah M Virk, Elisa Visentin, Martina Vitaglione, Karunakaran Vithian, Sorice Vittoria, Sankkita Vivekananthan, Elena Vlad, Ben Vlies, Linda von Oven, Claire Vooght, Kim Thi Vu Thai, Kritchai Vutipongsatorn, Alain Vuylsteke, Eleftheria Vyras, Richard Wach, Beverley Wadams, Susan Wadd, Natalia Waddington, Phillip Wade, Jonathan Wadsley, Kirsten Wadsworth, Syed E I Wafa, Daniel Wagstaff, Lynda Wagstaff, Dalia Wahab, Zaroug Wahbi, Abiodun Waheed Adigun, Sawan Waidyanatha, Alicia Waite, Rachel Wake, Alice Wakefield, William Wakeford, Fiona Wakinshaw, Emma Waldeck, Andrew Walden, Lorna Walding, Alexandria Waldron, Joanne Waldron, Emma Wales, Batool Wali, Danielle Walker, Gemma Walker, Harriet Walker, Ian Walker, Kevin Walker, Kim Walker, Lauren Walker, Linda Walker, Lynne Walker, Olivia Walker, Rachel Walker, Rebecca Walker, Sara Walker, Susan Walker, Gillian Wallace, Rebecca Wallbutton, Jessica Wallen, Karl Wallendszus, Arabella Waller, Rosemary Waller, Gabiel Wallis, Gabriel Wallis, Louise Wallis, Matthew Wallis, Emma Walmsley, Donna Walsh, Elizabeth Walsh, Livia Walsh, Deborah Walstow, Daniel Walter, Alex Walters, Holt Walters, James Walters, Jocelyn Walters, Eileen Walton, Lucy Walton, Maisie Walton, Michael Walton, Olivia Walton, Sharon Walton, Susan Walton, Mandy Wan, Junita Wanda, Mary Wands, Rachel Wane, Frank Wang, Nick Wang, Ran Wang, Shentong Wang, Deborah Warbrick, Samantha Warburton, Christopher Ward, Deborah Ward, Emma Ward, Hannah Ward, Janice Ward, Joanna Ward, Luke Ward, Nicola Ward, Rachael Ward, Thomas Ward, Tom Ward, Scott A Warden, Gibril Wardere, Steve Wardle, Hassan Wardy, Gareth Waring, Scott Waring, Jenny Warmington, Ben Warner, Christian Warner, Lewis Warnock, Sarah Warran, Jade Warren, Lisa Warren, Rebecca Warren, Yolanda Warren, Davina Warrender, Hannah Warren-Miell, Adilia Warris, Gill Warwick, Helen Wassall, Sean Wasserman, Elizabeth Wasson, Hazel J Watchorn, Holly Waterfall, Abby Waters, Donald Waters, Mark Waterstone, Abigail Watkin, Catherine Watkins, Catrin Watkins, Eleanor Watkins, Karen Watkins, Lynn Watkins, Abigail Watson, Adam J R Watson, Ekaterina Watson, Eleanor Watson, Felicity Watson, J G R Watson, Louisa Watson, Paul Watson, Rebecca Watson, Robert Watson, Kathleen Watson, Malcolm Watters, Donna Watterson, Khairiah Wattimena, Daniel Watts, John Watts, Merlin Watts, Victoria Waugh, Emma Wayman, Matthew Wayman, Akhlaq Wazir, Mark Weatherhead, Nick Weatherly, Chloe Webb, Claire Webb, Hayley Webb, Kathryn Webb, Kylie Webb, Stephen Webb, Cheryl Websdale, Deborah Webster, Ian Webster, Jemma Webster, Tim Webster, Jordan Wedlin, Ling Wee, Rebecca Weerakoon, Thanuja Weerasinghe, Janaka Weeratunga, Maria Weetman, Shuying Wei, Immo Weichert, Emma Welch, Hugh Welch, James Welch, Leanne Welch, Steven Welch, Benjamin Welham, Samantha Weller, Lucy Wellings, Brian Wells, Susan Wellstead, Berni Welsh, Richard Welsh, Ingeborg Welters, Rachael Welton, Victoria Wenn, Lauren Wentworth, Joan Wesonga, Kate Wesseldine, Joe West, Magdelena West, Raha West, Ruth West, Sophie West, Luke Western, Ruth Westhead, Heather Weston, Alice Westwood, Kelly Westwood, Sharon Westwood, Bill Wetherill, Sharon Wheaver, Helen Wheeler, Ben Whelan, Matthew Whelband, Amanda Whileman, Alison Whitcher, Andrew White, Ayesha White, Benjamin White, Catherine White, Christopher White, Duncan White, James White, Jonathan White, Katie White, Marie White, Nick White, Nikki White, Sarah White, Sonia White, Tracey White, Catherine Whitehead, Kelly Whitehorn, Anne Whitehouse, Claire Whitehouse, Tony Whitehouse, Julia Whiteley, Louiza Whiteley, Sophie Whiteley, Rachael Whitham, Gabriel Whitlingum, David Whitmore, Elizabeth Whittaker, Lindsay Whittam, Ashley Whittington, Helen Whittle, Robert Whittle, Eunice Wiafe, Lou Wiblin, Olivia Wickens, John Widdrington, Jason Wieboldt, Hannah Wieringa, Cornelia Wiesender, Laura Wiffen, Andrew Wight, Ashleigh Wignall, Christopher Wignall, Annamaria Wilce, Danielle Wilcock, Emma Wilcock, Louise Wilcox, Ben Wild, Laura Wild, Stephen Wild, Michael Wilde, Laura Wilding, Peter Wilding, Tracey Wildsmith, Joe Wileman, Joy Wiles, Kate Wiles, Elva Wilhelmsen, Thomas Wiliams, Janet Wilkie, David Wilkin, Hannah Wilkins, Joy Wilkins, Suzanne Wilkins, Iain Wilkinson, Lesley Wilkinson, Nicola Wilkinson, Sophia Wilkinson, Susan Wilkinson, Tim Wilkinson, Sylvia Willetts, Aimee Williams, Alexandra Williams, Alison Williams, Angharad Williams, Anna Williams, Ava Williams, Carl Williams, Caroline V Williams, Claire Williams, Dewi Williams, Eleri Williams, Gail Williams, Gemma Williams, Gina Williams, Hannah Williams, Heledd Williams, James Williams, Jennie Williams, Jill Williams, John Williams, Joseph Williams, Karen Williams, Kathryn Williams, Mandy Williams, Marie Williams, Mark Williams, Matthew Williams, Patricia Williams, Penny Williams, Rachel Williams, Robin Williams, Rupert Williams, Samson Williams, Sarah Williams, Sophie Williams, Steffan Williams, Tamanna Williams, Tania Williams, Annie Williamson, Cath Williamson, Catherine Williamson, Dawn Williamson, James D Williamson, Jodie Williamson, Rachel Williamson, Helen Williamson, Elaine Willis, Elizabeth Willis, Emily Willis, Heather Willis, Herika Willis, Joanna Willis, Louise Wills, Lucy Willsher, Catherine Willshire, Francesca Willson, Jayne Willson, Alison Wilson, Andrea Wilson, Anna Wilson, Antoinette Wilson, Billy Wilson, David Wilson, Imogen Wilson, James Wilson, Karen Wilson, Kate Wilson, Kristy-Ann Wilson, Lucinda Wilson, Mark Wilson, Stephen Wilson, Toni Wilson, John Wilson, Khin Lei Yee Win, Marlar Win, Than Win, Tin Tin Win, Wut Yee Win Win, Lucinda Winckworth, Laura Winder, Piers Winder, Stuart Winearl, Helen Winmill, Simon Winn, Carmen Winpenny, Helen Winslow, Helen Winter, Jonathan Winter, Barbara Winter-Goodwin, Joseph Winterton, Hannah Winwood, Jack Wischhusen, Stephen Wisdom, Matthew Wise, Martin Wiselka, Rebecca Wiseman, Sophie Wiseman, Steven Wishart, Tabitha WIshlade, Eric Witele, Nicholas Withers, Janet Wittes, Donna Wixted, Therese Wodehouse, Will Wolf, Nicola Wolff, Kirsten Wolffsohn, Rebecca Wolf-Roberts, Elena Wolodimeroff, Adam Wolstencroft, Alan Wong, Charlotte Wong, Chi-Hung Wong, Chi-Man Wong, Edwin Wong, Jessica S Y Wong, Kit Y Wong, Mei Yin Wong, Nick Wong, Sam Wong, Ting Wong, Aaron B Wongkyezeng, Amanda Wood, Caroline Wood, Dianne Wood, Fiona Wood, Gordon Wood, Hannah Wood, Jennifer Wood, Joe Wood, Lisa Wood, Louise Wood, Madeleine Wood, Stephen Wood, Tracy Wood, Katharine Woodall, Rebecca Woodfield, Christopher Woodford, Elizabeth Woodford, Jill Woodford, Louise Woodhead, Timothy Woodhead, Philip Woodland, Marc Woodman, Myles Woodman, Stephen Woodmansey, Charlotte Woods, Jane Woods, Katherine Woods, Sarah Woods, Zoe Woodward, Megan Woolcock, Gemma Wooldridge, Rebecca Woolf, Chris Woollard, Christopher Woollard, Louisa Woollen, Emma Woolley, Jade Woolley, Daniel Woosey, Dan Wootton, Joanne Wootton, Daniel Worley, Stephy Worton, Jonathan Wraight, Maria Wray, Kim Wren, Lynn Wren, Caroline Wrey Brown, Catherine Wright, Demi Wright, Francesca Wright, Holly Wright, Imogen Wright, Lianne Wright, Rachel Wright, Sarah Wright, Stephanie Wright, Tim Wright, Caroline Wroe, Hannah Wroe, Henry Wu, Peishan Wu, Pensee Wu, Jonathan Wubetu, Fitria Wulandari, Retno Wulandari, Subie Wurie, Craig Wyatt, Frederick Wyn-Griffiths, Inez Wynter, Bindhu Xavier, Arnold Xhikola, Bingru E Xia, Zhongyang Xia, Effua Yacoba, Santosh Yadav, Masseh Yakubi, May Yan, Yuuki Yanagisawa, Freda Yang, Yingjia Yang, Michael Yanney, Woei Lin Yap, Nabil Yaqoob, Salima Yasmin, Bryan Yates, David Yates, Edward Yates, Helen Yates, Thomas Yates, Mark Yates, Jessica Ye, Charlotte Yearwood Martin, Khin Yein, Fiona Yelnoorkar, Lam Minh Yen, Alastair Yeoh, Chun Yu Yeung, Peter Yew, Durgesh Yewatkar, Laura Ylquimiche Melly, Inez Ynter, H Yong, Jemma Yorke, Jasmine Youens, Abdel Younes Ibrahim, Eoin Young, Gail Young, Louise Young, Asfand Yousafzar, Sajeda Youssouf, Ahmed Yousuf, Hartantri Yovita, Chrissie Yu, Jack S J Yuan, Nindya Yufaniaputri, Bernard Yung, Daniel Yusef, Said Yusef, Intekhab Yusuf, Anna-Sophia Zafar, Silvia Zagalo, Su Zaher, Aqsa Zahoor, Mahrukh Zainab, Thornton Zak, Kareem Zaki, Nabhan Zakir, Kasia Zalewska, Ane Zamalloa, Mohsin Zaman, Shakir Zaman, Julie Zamikula, Louise Zammit, Marie Zammit-Mangion, Marcelina Zawadzka, Mohammed Zayed, Esther Zebracki, Daniel Zehnder, Lisa Zeidan, Darius Zeinali, Jing Zhang, Xiaobei Zhao, Dongling Zheng, Doreen Zhu, Madiha Zia, Omar Zibdeh, Rabia Zill-E-Huma, Ei Thankt Zin, Eva Zincone, Garikai Zindoga, Eleanor Zinkin, Vivian Zinyemba, Christos Zipitis, Letizia Zitter, Arkadiusz Zmierczak, Garazi Zubikarai, Azam Zubir, Naz Zuhra, Rasha Zulaikha, Sabrina Zulfikar, Carol Zullo, Ana Zuriaga-Alvaro, University of St Andrews. Infection and Global Health Division, University of St Andrews. School of Medicine, and Group, RECOVERY Collaborative

Subjects
Adult, Male, Hypoxia/etiology, SARS-CoV-2, COVID-19, 3rd-DAS, General Medicine, Adrenal Cortex Hormones/therapeutic use, AC, Dexamethasone/therapeutic use, Hospitals, Oxygen, Treatment Outcome, SDG 3 - Good Health and Well-being, MCP, Humans, Female
Abstract

Background Low-dose corticosteroids have been shown to reduce mortality for patients with COVID-19 requiring oxygen or ventilatory support (non-invasive mechanical ventilation, invasive mechanical ventilation, or extracorporeal membrane oxygenation). We evaluated the use of a higher dose of corticosteroids in this patient group. Methods This randomised, controlled, open-label platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]) is assessing multiple possible treatments in patients hospitalised for COVID-19. Eligible and consenting adult patients with clinical evidence of hypoxia (ie, receiving oxygen or with oxygen saturation Findings Between May 25, 2021, and May 13, 2022, 1272 patients with COVID-19 and hypoxia receiving no oxygen (eight [1%]) or simple oxygen only (1264 [99%]) were randomly allocated to receive usual care plus higher dose corticosteroids (659 patients) versus usual care alone (613 patients, of whom 87% received low-dose corticosteroids during the follow-up period). Of those randomly assigned, 745 (59%) were in Asia, 512 (40%) in the UK, and 15 (1%) in Africa. 248 (19%) had diabetes and 769 (60%) were male. Overall, 123 (19%) of 659 patients allocated to higher dose corticosteroids versus 75 (12%) of 613 patients allocated to usual care died within 28 days (rate ratio 1·59 [95% CI 1·20–2·10]; p=0·0012). There was also an excess of pneumonia reported to be due to non-COVID infection (64 cases [10%] vs 37 cases [6%]; absolute difference 3·7% [95% CI 0·7–6·6]) and an increase in hyperglycaemia requiring increased insulin dose (142 [22%] vs 87 [14%]; absolute difference 7·4% [95% CI 3·2–11·5]). Interpretation In patients hospitalised for COVID-19 with clinical hypoxia who required either no oxygen or simple oxygen only, higher dose corticosteroids significantly increased the risk of death compared with usual care, which included low-dose corticosteroids. The RECOVERY trial continues to assess the effects of higher dose corticosteroids in patients hospitalised with COVID-19 who require non-invasive ventilation, invasive mechanical ventilation, or extracorporeal membrane oxygenation. Funding UK Research and Innovation (Medical Research Council), National Institute of Health and Care Research, and Wellcome Trust.

Published
2023

33. Stigma related to labels and symptoms in individuals at clinical high-risk for psychosis

Author

Yang, Lawrence H, Link, Bruce G, Ben-David, Shelly, Gill, Kelly E, Girgis, Ragy R, Brucato, Gary, Wonpat-Borja, Ahtoy J, and Corcoran, Cheryl M

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Clinical Research, Depression, Prevention, Behavioral and Social Science, Brain Disorders, Mental Health, Serious Mental Illness, Mental health, Good Health and Well Being, Adolescent, Awareness, Child, Female, Humans, Male, Prodromal Symptoms, Psychiatric Status Rating Scales, Psychotic Disorders, Risk Assessment, Self Concept, Social Stigma, Stereotyping, Young Adult, Clinical high risk state for psychosis, At risk, Early psychosis, Stigma, Prodrome, Discrimination, Adolescents, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry, Clinical sciences
Abstract

BackgroundDespite advances that the psychosis "clinical high-risk" (CHR) identification offers, risk of stigma exists. Awareness of and agreement with stereotypes has not yet been evaluated in CHR individuals. Furthermore, the relative stigma associated with symptoms, as opposed to the label of risk, is not known, which is critical because CHR identification may reduce symptom-related stigma.MethodsThirty-eight CHR subjects were ascertained using standard measures from the Center of Prevention and Evaluation/New York State Psychiatric Institute/ Columbia University. Labeling-related measures adapted to the CHR group included "stereotype awareness and self-stigma" ("Stereotype awareness", "Stereotype Agreement", "Negative emotions [shame]"), and a parallel measure of "Negative emotions (shame)" for symptoms. These measures were examined in relation to symptoms of anxiety and depression, adjusting for core CHR symptoms (e.g. attenuated psychotic symptoms).ResultsCHR participants endorsed awareness of mental illness stereotypes, but largely did not themselves agree with these stereotypes. Furthermore, CHR participants described more stigma associated with symptoms than they did with the risk-label itself. Shame related to symptoms was associated with depression, while shame related to the risk-label was associated with anxiety.ConclusionBoth stigma of the risk-label and of symptoms contribute to the experience of CHR individuals. Stereotype awareness was relatively high and labeling-related shame was associated with increased anxiety. Yet limited agreement with stereotypes indicated that labeling-related stigma had not fully permeated self-conceptions. Furthermore, symptom-related stigma appeared more salient overall and was linked with increased depression, suggesting that alleviating symptom-related shame via treating symptoms might provide major benefit.

Published
2015

34. Early clinical outcomes of ultrasound-guided CT-planned high-dose-rate interstitial brachytherapy for primary locally advanced cervical cancer

Author

Mesko, Shane, Swamy, Uma, Park, Sang-June, Borja, Lalaine, Wang, Jason, Demanes, D Jeffrey, and Kamrava, Mitchell

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Cancer, Prevention, Cervical Cancer, 6.5 Radiotherapy and other non-invasive therapies, Evaluation of treatments and therapeutic interventions, Adult, Aged, Aged, 80 and over, Brachytherapy, Disease-Free Survival, Female, Gastrointestinal Tract, Humans, Middle Aged, Neoplasm Metastasis, Radiation Injuries, Radiotherapy Dosage, Radiotherapy Planning, Computer-Assisted, Retrospective Studies, Survival Rate, Tomography, X-Ray Computed, Treatment Outcome, Ultrasonography, Interventional, Urogenital System, Uterine Cervical Neoplasms, Young Adult, Cervical cancer, High-dose-rate, Interstitial, Image-guided brachytherapy, Oncology & Carcinogenesis, Clinical sciences
Abstract

PurposeTo report early clinical outcomes of high-dose-rate interstitial image-guided brachytherapy (BT) in the definitive management of locally advanced cervical cancer.MethodsWe retrospectively analyzed 31 locally advanced cervical cancer patients treated at our institution between January 2010 and April 2013. About 88% had advanced disease based on the International Federation of Gynecology and Obstetrics guidelines, and 87% received concurrent chemotherapy. All patients were treated with external beam radiation therapy to a median dose of 45 Gy (range, 39.6-58 Gy) before receiving BT. High-dose-rate BT was delivered in a single implant to a median dose of 6 Gy × five fractions to a CT-defined volume. Median total equivalent 2-Gy dose, dose covered by 90% of the high-risk clinical target volume (HR-CTV D90), and HR-CTV were 84, 87.4, and 49.9 cc, respectively. Kaplan-Meier method was used for actuarial survival analysis, and toxicity was graded using Common Terminology Criteria for Adverse Events, version 4.0.ResultsMedian followup was 19.3 months. Two-year actuarial local control, regional control, and distant metastasis (DM) were 90%, 93%, and 23.6%, respectively. Two-year disease-free survival was 55%. Genitourinary, gastrointestinal, or gynecologic Grade 3 toxicity was seen in 5 patients (3 T4a and 2 T3b) for crude rates of 13%, 7%, and 3%, respectively. Stratifying HR-CTV by 30 cc and then by HR-CTV D90 of 90 Gy showed that 100% of the local failures, regional failures, DM, and G3 toxicity occurred in >30 cc group. The rate of DM was also significantly higher in the >30 cc group (p = 0.036).ConclusionsAn interstitial approach can achieve excellent outcomes in cases where intracavitary and/or hybrid approaches are either not suitable or not available.

Published
2015

35. Palaeogenomics of Upper Palaeolithic to Neolithic European hunter-gatherers

Author

Cosimo Posth, He Yu, Ayshin Ghalichi, Hélène Rougier, Isabelle Crevecoeur, Yilei Huang, Harald Ringbauer, Adam B. Rohrlach, Kathrin Nägele, Vanessa Villalba-Mouco, Rita Radzeviciute, Tiago Ferraz, Alexander Stoessel, Rezeda Tukhbatova, Dorothée G. Drucker, Martina Lari, Alessandra Modi, Stefania Vai, Tina Saupe, Christiana L. Scheib, Giulio Catalano, Luca Pagani, Sahra Talamo, Helen Fewlass, Laurent Klaric, André Morala, Mathieu Rué, Stéphane Madelaine, Laurent Crépin, Jean-Baptiste Caverne, Emmy Bocaege, Stefano Ricci, Francesco Boschin, Priscilla Bayle, Bruno Maureille, Foni Le Brun-Ricalens, Jean-Guillaume Bordes, Gregorio Oxilia, Eugenio Bortolini, Olivier Bignon-Lau, Grégory Debout, Michel Orliac, Antoine Zazzo, Vitale Sparacello, Elisabetta Starnini, Luca Sineo, Johannes van der Plicht, Laure Pecqueur, Gildas Merceron, Géraldine Garcia, Jean-Michel Leuvrey, Coralie Bay Garcia, Asier Gómez-Olivencia, Marta Połtowicz-Bobak, Dariusz Bobak, Mona Le Luyer, Paul Storm, Claudia Hoffmann, Jacek Kabaciński, Tatiana Filimonova, Svetlana Shnaider, Natalia Berezina, Borja González-Rabanal, Manuel R. González Morales, Ana B. Marín-Arroyo, Belén López, Carmen Alonso-Llamazares, Annamaria Ronchitelli, Caroline Polet, Ivan Jadin, Nicolas Cauwe, Joaquim Soler, Neus Coromina, Isaac Rufí, Richard Cottiaux, Geoffrey Clark, Lawrence G. Straus, Marie-Anne Julien, Silvia Renhart, Dorothea Talaa, Stefano Benazzi, Matteo Romandini, Luc Amkreutz, Hervé Bocherens, Christoph Wißing, Sébastien Villotte, Javier Fernández-López de Pablo, Magdalena Gómez-Puche, Marco Aurelio Esquembre-Bebia, Pierre Bodu, Liesbeth Smits, Bénédicte Souffi, Rimantas Jankauskas, Justina Kozakaitė, Christophe Cupillard, Hartmut Benthien, Kurt Wehrberger, Ralf W. Schmitz, Susanne C. Feine, Tim Schüler, Corinne Thevenet, Dan Grigorescu, Friedrich Lüth, Andreas Kotula, Henny Piezonka, Franz Schopper, Jiří Svoboda, Sandra Sázelová, Andrey Chizhevsky, Aleksandr Khokhlov, Nicholas J. Conard, Frédérique Valentin, Katerina Harvati, Patrick Semal, Bettina Jungklaus, Alexander Suvorov, Rick Schulting, Vyacheslav Moiseyev, Kristiina Mannermaa, Alexandra Buzhilova, Thomas Terberger, David Caramelli, Eveline Altena, Wolfgang Haak, Johannes Krause, Helsinki Institute of Sustainability Science (HELSUS), Department of Cultures, Faculty Common Matters (Faculty of Arts), Universidad de Cantabria, Posth, Cosimo [0000-0002-8206-3907], Yu, He [0000-0003-1323-4730], Rougier, Hélène [0000-0003-0358-0285], Ringbauer, Harald [0000-0002-4884-9682], Rohrlach, Adam B [0000-0002-4204-5018], Nägele, Kathrin [0000-0003-3861-8677], Villalba-Mouco, Vanessa [0000-0002-9357-5238], Radzeviciute, Rita [0000-0002-5800-3787], Stoessel, Alexander [0000-0003-2434-2542], Drucker, Dorothée G [0000-0003-0854-4371], Lari, Martina [0000-0002-7832-8212], Modi, Alessandra [0000-0001-9514-9868], Vai, Stefania [0000-0003-3844-5147], Scheib, Christiana L [0000-0003-4158-8296], Rué, Mathieu [0000-0001-7948-9459], Boschin, Francesco [0000-0001-5795-9050], Maureille, Bruno [0000-0002-7616-0073], Bortolini, Eugenio [0000-0001-6751-5680], Starnini, Elisabetta [0000-0002-3933-0854], Sineo, Luca [0000-0001-8634-2295], Garcia, Géraldine [0000-0001-5777-7126], Połtowicz-Bobak, Marta [0000-0003-1973-4971], Bobak, Dariusz [0000-0002-5216-6630], Le Luyer, Mona [0000-0001-7999-0294], Kabaciński, Jacek [0000-0002-2118-2005], Berezina, Natalia [0000-0001-5704-9153], González-Rabanal, Borja [0000-0002-1802-994X], Amkreutz, Luc [0000-0003-4664-5552], Bocherens, Hervé [0000-0002-0494-0126], Jankauskas, Rimantas [0000-0001-7611-2576], Conard, Nicholas J [0000-0002-4633-0385], Valentin, Frédérique [0000-0002-0575-7681], Harvati, Katerina [0000-0001-5998-4794], Schulting, Rick [0000-0002-4444-766X], Mannermaa, Kristiina [0000-0002-8510-1120], Buzhilova, Alexandra [0000-0001-6398-2177], Caramelli, David [0000-0001-6468-1675], Altena, Eveline [0000-0001-8911-7771], Haak, Wolfgang [0000-0003-2475-2007], Krause, Johannes [0000-0001-9144-3920], Apollo - University of Cambridge Repository, Rohrlach, Adam B. [0000-0002-4204-5018], Drucker, Dorothée G. [0000-0003-0854-4371], Scheib, Christiana L. [0000-0003-4158-8296], Conard, Nicholas J. [0000-0002-4633-0385], Posth, Cosimo, Yu, He, Ghalichi, Ayshin, Rougier, Hélène, Crevecoeur, Isabelle, Huang, Yilei, Ringbauer, Harald, Rohrlach, Adam B, Nägele, Kathrin, Villalba-Mouco, Vanessa, Radzeviciute, Rita, Ferraz, Tiago, Stoessel, Alexander, Tukhbatova, Rezeda, Drucker, Dorothée G, Lari, Martina, Modi, Alessandra, Vai, Stefania, Saupe, Tina, Scheib, Christiana L, Catalano, Giulio, Pagani, Luca, Talamo, Sahra, Fewlass, Helen, Klaric, Laurent, Morala, André, Rué, Mathieu, Madelaine, Stéphane, Crépin, Laurent, Caverne, Jean-Baptiste, Bocaege, Emmy, Ricci, Stefano, Boschin, Francesco, Bayle, Priscilla, Maureille, Bruno, Le Brun-Ricalens, Foni, Bordes, Jean-Guillaume, Oxilia, Gregorio, Bortolini, Eugenio, Bignon-Lau, Olivier, Debout, Grégory, Orliac, Michel, Zazzo, Antoine, Sparacello, Vitale, Starnini, Elisabetta, Sineo, Luca, van der Plicht, Johanne, Pecqueur, Laure, Merceron, Gilda, Garcia, Géraldine, Leuvrey, Jean-Michel, Garcia, Coralie Bay, Gómez-Olivencia, Asier, Połtowicz-Bobak, Marta, Bobak, Dariusz, Le Luyer, Mona, Storm, Paul, Hoffmann, Claudia, Kabaciński, Jacek, Filimonova, Tatiana, Shnaider, Svetlana, Berezina, Natalia, González-Rabanal, Borja, González Morales, Manuel R, Marín-Arroyo, Ana B, López, Belén, Alonso-Llamazares, Carmen, Ronchitelli, Annamaria, Polet, Caroline, Jadin, Ivan, Cauwe, Nicola, Soler, Joaquim, Coromina, Neu, Rufí, Isaac, Cottiaux, Richard, Clark, Geoffrey, Straus, Lawrence G, Julien, Marie-Anne, Renhart, Silvia, Talaa, Dorothea, Benazzi, Stefano, Romandini, Matteo, Amkreutz, Luc, Bocherens, Hervé, Wißing, Christoph, Villotte, Sébastien, de Pablo, Javier Fernández-López, Gómez-Puche, Magdalena, Esquembre-Bebia, Marco Aurelio, Bodu, Pierre, Smits, Liesbeth, Souffi, Bénédicte, Jankauskas, Rimanta, Kozakaitė, Justina, Cupillard, Christophe, Benthien, Hartmut, Wehrberger, Kurt, Schmitz, Ralf W, Feine, Susanne C, Schüler, Tim, Thevenet, Corinne, Grigorescu, Dan, Lüth, Friedrich, Kotula, Andrea, Piezonka, Henny, Schopper, Franz, Svoboda, Jiří, Sázelová, Sandra, Chizhevsky, Andrey, Khokhlov, Aleksandr, Conard, Nicholas J, Valentin, Frédérique, Harvati, Katerina, Semal, Patrick, Jungklaus, Bettina, Suvorov, Alexander, Schulting, Rick, Moiseyev, Vyacheslav, Mannermaa, Kristiina, Buzhilova, Alexandra, Terberger, Thoma, Caramelli, David, Altena, Eveline, Haak, Wolfgang, Krause, Johannes, Universidad de Alicante. Instituto Universitario de Investigación en Arqueología y Patrimonio Histórico, Prehistoria y Protohistoria, Pagani, Luca [0000-0002-6639-524X], and Alonso-Llamazares, Carmen [0000-0002-1053-1388]

Subjects
History, Ancient dna, Interactions, Cave, 45/23, Admixture, Settore BIO/08 - Antropologia, 631/208/457, 631/181/27, 6160 Other humanities, Contamination, Humans, Hunting, Palaeogenomics, Population-structure, Archaeology, Biological anthropology, Evolutionary genetics, Population genetics, History, Ancient, Human evolution, Diversity, Occupation, Multidisciplinary, 45, Genome, Human, article, Paleontology, Last glacial maximum, Human Genetics, Gene Pool, Genomics, 631/181/19/2471, Pleistocene, Europe, Genomic transformations, 631/181/2474, Anthropology, Hunter-gatherers, Genome sequence
Abstract

Acknowledgements: The authors thank G. Marciani and O. Jöris for comments on archaeology; C. Jeong, M. Spyrou and K. Prüfer for comments on genetics; M. O’Reilly for graphical support for Fig. 5 and Extended Data Fig. 9; the entire IT and laboratory teams at the Department of Archaeogenetics of MPI-SHH for technical assistance; M. Meyer and S. Nagel for support with single-stranded library preparation; K. Post, P. van Es, J. Glimmerveen, M. Medendorp, M. Sier, S. Dikstra, M. Dikstra, R. van Eerden, D. Duineveld and A. Hoekman for providing access to human specimens from the North Sea (The Netherlands); M. D. Garralda and A. Estalrrich for providing access to human specimens from La Riera (Spain); J. Górski and M. Zając for providing access to human specimens from Maszycka cave; C. Di Patti for providing access to human specimens from San Teodoro 2 (Italy); P. Blaževičius for providing access to the Donkalnis human remains and the new radiocarbon dates; the Italian Ministry of Culture and Soprintendenza Archeologia Belle Arti e Paesaggio for the Provinces of Verona, Rovigo, and Vicenza for granting access to the human remains of Tagliente 2; F. Fontana, who carries out investigations of the Riparo Tagliente site (Italy); the Friuli Venezia Giulia Superintendency for providing access to the human tooth Pradis 1; and the Soprintendenza Archeologia Belle Arti e Paesaggio for the Provinces of Barletta-Andria-Trani and Foggia for providing access to the Paglicci human remains. This project has received funding by the European Research Council under the European Union’s Horizon 2020 research and innovation programme under grant agreements no. 803147-RESOLUTION (to S.T.), no. 771234-PALEoRIDER (to W.H.), no. 864358 (to K.M.), no. 724703 and no. 101019659 (to K.H.). K.H. is also supported by the Deutsche Forschungsgemeinschaft (DFG FOR 2237). E.A. has received funding from the Van de Kamp fonds. PACEA co-authors of this research benefited from the scientific framework of the University of Bordeaux’s IdEx Investments for the Future programme/GPR Human Past. A.G.-O. is supported by a Ramón y Cajal fellowship (RYC-2017-22558). L. Sineo, M.L. and D.C. have received funding from the Italian Ministry of University and Research (MUR) PRIN 2017 grants 20177PJ9XF and 20174BTC4R_002. H. Rougier received support from the College of Social and Behavioral Sciences of CSUN and the CSUN Competition for RSCA Awards. C.L.S. and T. Saupe received support from the European Union through the European Regional Development Fund (project no. 2014-2020.4.01.16-0030) and C.L.S. received support from the Estonian Research Council grant PUT (PRG243). S. Shnaider received support from the Russian Science Foundation (no. 19-78-10053)., Modern humans have populated Europe for more than 45,000 years1,2. Our knowledge of the genetic relatedness and structure of ancient hunter-gatherers is however limited, owing to the scarceness and poor molecular preservation of human remains from that period3. Here we analyse 356 ancient hunter-gatherer genomes, including new genomic data for 116 individuals from 14 countries in western and central Eurasia, spanning between 35,000 and 5,000 years ago. We identify a genetic ancestry profile in individuals associated with Upper Palaeolithic Gravettian assemblages from western Europe that is distinct from contemporaneous groups related to this archaeological culture in central and southern Europe4, but resembles that of preceding individuals associated with the Aurignacian culture. This ancestry profile survived during the Last Glacial Maximum (25,000 to 19,000 years ago) in human populations from southwestern Europe associated with the Solutrean culture, and with the following Magdalenian culture that re-expanded northeastward after the Last Glacial Maximum. Conversely, we reveal a genetic turnover in southern Europe suggesting a local replacement of human groups around the time of the Last Glacial Maximum, accompanied by a north-to-south dispersal of populations associated with the Epigravettian culture. From at least 14,000 years ago, an ancestry related to this culture spread from the south across the rest of Europe, largely replacing the Magdalenian-associated gene pool. After a period of limited admixture that spanned the beginning of the Mesolithic, we find genetic interactions between western and eastern European hunter-gatherers, who were also characterized by marked differences in phenotypically relevant variants.

Published
2023
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36. Hotspot activating PRKD1 somatic mutations in polymorphous low-grade adenocarcinomas of the salivary glands

Author

Weinreb, Ilan, Piscuoglio, Salvatore, Martelotto, Luciano G, Waggott, Daryl, Ng, Charlotte KY, Perez-Ordonez, Bayardo, Harding, Nicholas J, Alfaro, Javier, Chu, Kenneth C, Viale, Agnes, Fusco, Nicola, da Cruz Paula, Arnaud, Marchio, Caterina, Sakr, Rita A, Lim, Raymond, Thompson, Lester DR, Chiosea, Simion I, Seethala, Raja R, Skalova, Alena, Stelow, Edward B, Fonseca, Isabel, Assaad, Adel, How, Christine, Wang, Jianxin, de Borja, Richard, Chan-Seng-Yue, Michelle, Howlett, Christopher J, Nichols, Anthony C, Wen, Y Hannah, Katabi, Nora, Buchner, Nicholas, Mullen, Laura, Kislinger, Thomas, Wouters, Bradly G, Liu, Fei-Fei, Norton, Larry, McPherson, John D, Rubin, Brian P, Clarke, Blaise A, Weigelt, Britta, Boutros, Paul C, and Reis-Filho, Jorge S

Subjects
Agricultural, Veterinary and Food Sciences, Biological Sciences, Bioinformatics and Computational Biology, Genetics, Agricultural Biotechnology, Cancer, Digestive Diseases, Adenocarcinoma, Amino Acid Sequence, Animals, Humans, Immunohistochemistry, Immunoprecipitation, Mice, Microscopy, Confocal, Models, Molecular, Molecular Sequence Data, Mutagenesis, Mutation, Missense, NIH 3T3 Cells, Protein Kinase C, Salivary Gland Neoplasms, Sequence Alignment, Sequence Analysis, DNA, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

Polymorphous low-grade adenocarcinoma (PLGA) is the second most frequent type of malignant tumor of the minor salivary glands. We identified PRKD1 hotspot mutations encoding p.Glu710Asp in 72.9% of PLGAs but not in other salivary gland tumors. Functional studies demonstrated that this kinase-activating alteration likely constitutes a driver of PLGA.

Published
2014

37. Global, regional, and national levels and causes of maternal mortality during 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013

Author

Kassebaum, Nicholas J, Bertozzi-Villa, Amelia, Coggeshall, Megan S, Shackelford, Katya A, Steiner, Caitlyn, Heuton, Kyle R, Gonzalez-Medina, Diego, Barber, Ryan, Huynh, Chantal, Dicker, Daniel, Templin, Tara, Wolock, Timothy M, Ozgoren, Ayse Abbasoglu, Abd-Allah, Foad, Abera, Semaw Ferede, Abubakar, Ibrahim, Achoki, Tom, Adelekan, Ademola, Ademi, Zanfina, Adou, Arsène Kouablan, Adsuar, José C, Agardh, Emilie E, Akena, Dickens, Alasfoor, Deena, Alemu, Zewdie Aderaw, Alfonso-Cristancho, Rafael, Alhabib, Samia, Ali, Raghib, Al Kahbouri, Mazin J, Alla, François, Allen, Peter J, AlMazroa, Mohammad A, Alsharif, Ubai, Alvarez, Elena, Alvis-Guzmán, Nelson, Amankwaa, Adansi A, Amare, Azmeraw T, Amini, Hassan, Ammar, Walid, Antonio, Carl AT, Anwari, Palwasha, Arnlöv, Johan, Arsenijevic, Valentina S Arsic, Artaman, Ali, Asad, Majed Masoud, Asghar, Rana J, Assadi, Reza, Atkins, Lydia S, Badawi, Alaa, Balakrishnan, Kalpana, Basu, Arindam, Basu, Sanjay, Beardsley, Justin, Bedi, Neeraj, Bekele, Tolesa, Bell, Michelle L, Bernabe, Eduardo, Beyene, Tariku J, Bhutta, Zulfiqar, Bin Abdulhak, Aref, Blore, Jed D, Basara, Berrak Bora, Bose, Dipan, Breitborde, Nicholas, Cárdenas, Rosario, Castañeda-Orjuela, Carlos A, Castro, Ruben Estanislao, Catalá-López, Ferrán, Cavlin, Alanur, Chang, Jung-Chen, Che, Xuan, Christophi, Costas A, Chugh, Sumeet S, Cirillo, Massimo, Colquhoun, Samantha M, Cooper, Leslie Trumbull, Cooper, Cyrus, da Costa Leite, Iuri, Dandona, Lalit, Dandona, Rakhi, Davis, Adrian, Dayama, Anand, Degenhardt, Louisa, De Leo, Diego, del Pozo-Cruz, Borja, Deribe, Kebede, Dessalegn, Muluken, deVeber, Gabrielle A, Dharmaratne, Samath D, Dilmen, Uğur, Ding, Eric L, Dorrington, Rob E, Driscoll, Tim R, Ermakov, Sergei Petrovich, Esteghamati, Alireza, Faraon, Emerito Jose A, Farzadfar, Farshad, Felicio, Manuela Mendonca, Fereshtehnejad, Seyed-Mohammad, and de Lima, Graça Maria Ferreira

Subjects
2.4 Surveillance and distribution, Aetiology, Infection, Reproductive health and childbirth, Good Health and Well Being, Age Distribution, Cause of Death, Female, Global Health, HIV Infections, Humans, Maternal Mortality, Models, Statistical, Organizational Objectives, Pregnancy, Pregnancy Complications, Infectious, Risk Factors, Socioeconomic Factors, Time Factors, Medical and Health Sciences, General & Internal Medicine
Abstract

BackgroundThe fifth Millennium Development Goal (MDG 5) established the goal of a 75% reduction in the maternal mortality ratio (MMR; number of maternal deaths per 100,000 livebirths) between 1990 and 2015. We aimed to measure levels and track trends in maternal mortality, the key causes contributing to maternal death, and timing of maternal death with respect to delivery.MethodsWe used robust statistical methods including the Cause of Death Ensemble model (CODEm) to analyse a database of data for 7065 site-years and estimate the number of maternal deaths from all causes in 188 countries between 1990 and 2013. We estimated the number of pregnancy-related deaths caused by HIV on the basis of a systematic review of the relative risk of dying during pregnancy for HIV-positive women compared with HIV-negative women. We also estimated the fraction of these deaths aggravated by pregnancy on the basis of a systematic review. To estimate the numbers of maternal deaths due to nine different causes, we identified 61 sources from a systematic review and 943 site-years of vital registration data. We also did a systematic review of reports about the timing of maternal death, identifying 142 sources to use in our analysis. We developed estimates for each country for 1990-2013 using Bayesian meta-regression. We estimated 95% uncertainty intervals (UIs) for all values.Findings292,982 (95% UI 261,017-327,792) maternal deaths occurred in 2013, compared with 376,034 (343,483-407,574) in 1990. The global annual rate of change in the MMR was -0·3% (-1·1 to 0·6) from 1990 to 2003, and -2·7% (-3·9 to -1·5) from 2003 to 2013, with evidence of continued acceleration. MMRs reduced consistently in south, east, and southeast Asia between 1990 and 2013, but maternal deaths increased in much of sub-Saharan Africa during the 1990s. 2070 (1290-2866) maternal deaths were related to HIV in 2013, 0·4% (0·2-0·6) of the global total. MMR was highest in the oldest age groups in both 1990 and 2013. In 2013, most deaths occurred intrapartum or postpartum. Causes varied by region and between 1990 and 2013. We recorded substantial variation in the MMR by country in 2013, from 956·8 (685·1-1262·8) in South Sudan to 2·4 (1·6-3·6) in Iceland.InterpretationGlobal rates of change suggest that only 16 countries will achieve the MDG 5 target by 2015. Accelerated reductions since the Millennium Declaration in 2000 coincide with increased development assistance for maternal, newborn, and child health. Setting of targets and associated interventions for after 2015 will need careful consideration of regions that are making slow progress, such as west and central Africa.FundingBill & Melinda Gates Foundation.

Published
2014

38. Global, regional, and national incidence and mortality for HIV, tuberculosis, and malaria during 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013

Author

Murray, Christopher JL, Ortblad, Katrina F, Guinovart, Caterina, Lim, Stephen S, Wolock, Timothy M, Roberts, D Allen, Dansereau, Emily A, Graetz, Nicholas, Barber, Ryan M, Brown, Jonathan C, Wang, Haidong, Duber, Herbert C, Naghavi, Mohsen, Dicker, Daniel, Dandona, Lalit, Salomon, Joshua A, Heuton, Kyle R, Foreman, Kyle, Phillips, David E, Fleming, Thomas D, Flaxman, Abraham D, Phillips, Bryan K, Johnson, Elizabeth K, Coggeshall, Megan S, Abd-Allah, Foad, Abera, Semaw Ferede, Abraham, Jerry P, Abubakar, Ibrahim, Abu-Raddad, Laith J, Abu-Rmeileh, Niveen Me, Achoki, Tom, Adeyemo, Austine Olufemi, Adou, Arsène Kouablan, Adsuar, José C, Agardh, Emilie Elisabet, Akena, Dickens, Al Kahbouri, Mazin J, Alasfoor, Deena, Albittar, Mohammed I, Alcalá-Cerra, Gabriel, Alegretti, Miguel Angel, Alemu, Zewdie Aderaw, Alfonso-Cristancho, Rafael, Alhabib, Samia, Ali, Raghib, Alla, Francois, Allen, Peter J, Alsharif, Ubai, Alvarez, Elena, Alvis-Guzman, Nelson, Amankwaa, Adansi A, Amare, Azmeraw T, Amini, Hassan, Ammar, Walid, Anderson, Benjamin O, Antonio, Carl Abelardo T, Anwari, Palwasha, Arnlöv, Johan, Arsenijevic, Valentina S Arsic, Artaman, Ali, Asghar, Rana J, Assadi, Reza, Atkins, Lydia S, Badawi, Alaa, Balakrishnan, Kalpana, Banerjee, Amitava, Basu, Sanjay, Beardsley, Justin, Bekele, Tolesa, Bell, Michelle L, Bernabe, Eduardo, Beyene, Tariku Jibat, Bhala, Neeraj, Bhalla, Ashish, Bhutta, Zulfiqar A, Abdulhak, Aref Bin, Binagwaho, Agnes, Blore, Jed D, Basara, Berrak Bora, Bose, Dipan, Brainin, Michael, Breitborde, Nicholas, Castañeda-Orjuela, Carlos A, Catalá-López, Ferrán, Chadha, Vineet K, Chang, Jung-Chen, Chiang, Peggy Pei-Chia, Chuang, Ting-Wu, Colomar, Mercedes, Cooper, Leslie Trumbull, Cooper, Cyrus, Courville, Karen J, Cowie, Benjamin C, Criqui, Michael H, Dandona, Rakhi, Dayama, Anand, De Leo, Diego, Degenhardt, Louisa, Del Pozo-Cruz, Borja, and Deribe, Kebede

Subjects
HIV/AIDS, Prevention, Rare Diseases, Vector-Borne Diseases, Infectious Diseases, 2.2 Factors relating to the physical environment, 2.4 Surveillance and distribution, Aetiology, Infection, Good Health and Well Being, Age Distribution, Epidemics, Female, Global Health, HIV Infections, Humans, Incidence, Malaria, Male, Mortality, Organizational Objectives, Sex Distribution, Tuberculosis, Medical and Health Sciences, General & Internal Medicine
Abstract

BackgroundThe Millennium Declaration in 2000 brought special global attention to HIV, tuberculosis, and malaria through the formulation of Millennium Development Goal (MDG) 6. The Global Burden of Disease 2013 study provides a consistent and comprehensive approach to disease estimation for between 1990 and 2013, and an opportunity to assess whether accelerated progress has occured since the Millennium Declaration.MethodsTo estimate incidence and mortality for HIV, we used the UNAIDS Spectrum model appropriately modified based on a systematic review of available studies of mortality with and without antiretroviral therapy (ART). For concentrated epidemics, we calibrated Spectrum models to fit vital registration data corrected for misclassification of HIV deaths. In generalised epidemics, we minimised a loss function to select epidemic curves most consistent with prevalence data and demographic data for all-cause mortality. We analysed counterfactual scenarios for HIV to assess years of life saved through prevention of mother-to-child transmission (PMTCT) and ART. For tuberculosis, we analysed vital registration and verbal autopsy data to estimate mortality using cause of death ensemble modelling. We analysed data for corrected case-notifications, expert opinions on the case-detection rate, prevalence surveys, and estimated cause-specific mortality using Bayesian meta-regression to generate consistent trends in all parameters. We analysed malaria mortality and incidence using an updated cause of death database, a systematic analysis of verbal autopsy validation studies for malaria, and recent studies (2010-13) of incidence, drug resistance, and coverage of insecticide-treated bednets.FindingsGlobally in 2013, there were 1·8 million new HIV infections (95% uncertainty interval 1·7 million to 2·1 million), 29·2 million prevalent HIV cases (28·1 to 31·7), and 1·3 million HIV deaths (1·3 to 1·5). At the peak of the epidemic in 2005, HIV caused 1·7 million deaths (1·6 million to 1·9 million). Concentrated epidemics in Latin America and eastern Europe are substantially smaller than previously estimated. Through interventions including PMTCT and ART, 19·1 million life-years (16·6 million to 21·5 million) have been saved, 70·3% (65·4 to 76·1) in developing countries. From 2000 to 2011, the ratio of development assistance for health for HIV to years of life saved through intervention was US$4498 in developing countries. Including in HIV-positive individuals, all-form tuberculosis incidence was 7·5 million (7·4 million to 7·7 million), prevalence was 11·9 million (11·6 million to 12·2 million), and number of deaths was 1·4 million (1·3 million to 1·5 million) in 2013. In the same year and in only individuals who were HIV-negative, all-form tuberculosis incidence was 7·1 million (6·9 million to 7·3 million), prevalence was 11·2 million (10·8 million to 11·6 million), and number of deaths was 1·3 million (1·2 million to 1·4 million). Annualised rates of change (ARC) for incidence, prevalence, and death became negative after 2000. Tuberculosis in HIV-negative individuals disproportionately occurs in men and boys (versus women and girls); 64·0% of cases (63·6 to 64·3) and 64·7% of deaths (60·8 to 70·3). Globally, malaria cases and deaths grew rapidly from 1990 reaching a peak of 232 million cases (143 million to 387 million) in 2003 and 1·2 million deaths (1·1 million to 1·4 million) in 2004. Since 2004, child deaths from malaria in sub-Saharan Africa have decreased by 31·5% (15·7 to 44·1). Outside of Africa, malaria mortality has been steadily decreasing since 1990.InterpretationOur estimates of the number of people living with HIV are 18·7% smaller than UNAIDS's estimates in 2012. The number of people living with malaria is larger than estimated by WHO. The number of people living with HIV, tuberculosis, or malaria have all decreased since 2000. At the global level, upward trends for malaria and HIV deaths have been reversed and declines in tuberculosis deaths have accelerated. 101 countries (74 of which are developing) still have increasing HIV incidence. Substantial progress since the Millennium Declaration is an encouraging sign of the effect of global action.FundingBill & Melinda Gates Foundation.

Published
2014

39. Identification of genes expressed by immune cells of the colon that are regulated by colorectal cancer‐associated variants

Author

Peltekova, Vanya D, Lemire, Mathieu, Qazi, Aamer M, Zaidi, Syed HE, Trinh, Quang M, Bielecki, Ryszard, Rogers, Marianne, Hodgson, Lyndsey, Wang, Mike, D’Souza, David JA, Zandi, Sasan, Chong, Taryne, Kwan, Jennifer YY, Kozak, Krystian, De Borja, Richard, Timms, Lee, Rangrej, Jagadish, Volar, Milica, Chan-Seng-Yue, Michelle, Beck, Timothy, Ash, Colleen, Lee, Shawna, Wang, Jianxin, Boutros, Paul C, Stein, Lincoln D, Dick, John E, Gryfe, Robert, McPherson, John D, Zanke, Brent W, Pollett, Aaron, Gallinger, Steven, and Hudson, Thomas J

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Genetics, Colo-Rectal Cancer, Biotechnology, Cancer, Digestive Diseases, Human Genome, Aetiology, 2.1 Biological and endogenous factors, Inflammatory and immune system, Amino Acid Sequence, Blotting, Western, Caco-2 Cells, Cell Line, Tumor, Colon, Colorectal Neoplasms, Gene Expression Regulation, Neoplastic, Genetic Predisposition to Disease, HCT116 Cells, HEK293 Cells, HL-60 Cells, HT29 Cells, HeLa Cells, Humans, Immune System, Immunohistochemistry, Jurkat Cells, K562 Cells, MCF-7 Cells, Molecular Sequence Data, Neoplasm Proteins, Phylogeny, Polymorphism, Single Nucleotide, RNA, Reverse Transcriptase Polymerase Chain Reaction, Sequence Homology, Amino Acid, U937 Cells, genome-wide association study, genetic risk factors, colon cancer, tumor microenvironment, Hela Cells, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

A locus on human chromosome 11q23 tagged by marker rs3802842 was associated with colorectal cancer (CRC) in a genome-wide association study; this finding has been replicated in case-control studies worldwide. In order to identify biologic factors at this locus that are related to the etiopathology of CRC, we used microarray-based target selection methods, coupled to next-generation sequencing, to study 103 kb at the 11q23 locus. We genotyped 369 putative variants from 1,030 patients with CRC (cases) and 1,061 individuals without CRC (controls) from the Ontario Familial Colorectal Cancer Registry. Two previously uncharacterized genes, COLCA1 and COLCA2, were found to be co-regulated genes that are transcribed from opposite strands. Expression levels of COLCA1 and COLCA2 transcripts correlate with rs3802842 genotypes. In colon tissues, COLCA1 co-localizes with crystalloid granules of eosinophils and granular organelles of mast cells, neutrophils, macrophages, dendritic cells and differentiated myeloid-derived cell lines. COLCA2 is present in the cytoplasm of normal epithelial, immune and other cell lineages, as well as tumor cells. Tissue microarray analysis demonstrates the association of rs3802842 with lymphocyte density in the lamina propria (p = 0.014) and levels of COLCA1 in the lamina propria (p = 0.00016) and COLCA2 (tumor cells, p = 0.0041 and lamina propria, p = 6 × 10(-5)). In conclusion, genetic, expression and immunohistochemical data implicate COLCA1 and COLCA2 in the pathogenesis of colon cancer. Histologic analyses indicate the involvement of immune pathways.

Published
2014

40. The secondary structure of apolipoprotein A-I on 9.6-nm reconstituted high-density lipoprotein determined by EPR spectroscopy.

Author

Oda, Michael N, Budamagunta, Madhu S, Borja, Mark S, Petrlova, Jitka, Voss, John C, and Lagerstedt, Jens O

Subjects
Humans, Lipoproteins, HDL, Apolipoprotein A-I, Electron Spin Resonance Spectroscopy, Protein Structure, Secondary, Protein Structure, Tertiary, Models, Molecular, EPR spectroscopy, apolipoprotein A-I, cardiovascular, cholesterol, high-density lipoprotein, Cardiovascular, Clinical Research, Atherosclerosis, apolipoproteinA-I, Medicinal and Biomolecular Chemistry, Biochemistry and Cell Biology, Medical Biochemistry and Metabolomics, Biochemistry & Molecular Biology
Abstract

Apolipoprotein A-I (ApoA-I) is the major protein component of high-density lipoprotein (HDL), and is critical for maintenance of cholesterol homeostasis. During reverse cholesterol transport, HDL transitions between an array of subclasses, differing in size and composition. This process requires ApoA-I to adapt to changes in the shape of the HDL particle, transiting from an apolipoprotein to a myriad of HDL subclass-specific conformations. Changes in ApoA-I structure cause alterations in HDL-specific enzyme and receptor-binding properties, and thereby direct the HDL particle through the reverse cholesterol transport pathway. In this study, we used site-directed spin label spectroscopy to examine the conformational details of the ApoA-I central domain on HDL. The motional dynamics and accessibility to hydrophobic/hydrophilic relaxation agents of ApoA-I residues 99-163 on 9.6-nm reconstituted HDL was analyzed by EPR. In previous analyses, we examined residues 6-98 and 164-238 (of ApoA-I's 243 residues), and combining these findings with the current results, we have generated a full-length map of the backbone structure of reconstituted HDL-associated ApoA-I. Remarkably, given that the majority of ApoA-I's length is composed of amphipathic helices, we have identified nonhelical residues, specifically the presence of a β-strand (residues 149-157). The significance of these nonhelical residues is discussed, along with the other features, in the context of ApoA-I function in contrast to recent models derived by other methods.

Published
2013

41. Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes.

Author

Biankin, Andrew, Waddell, Nicola, Kassahn, Karin, Gingras, Marie-Claude, Muthuswamy, Lakshmi, Johns, Amber, Miller, David, Wilson, Peter, Patch, Ann-Marie, Wu, Jianmin, Chang, David, Cowley, Mark, Gardiner, Brooke, Song, Sarah, Harliwong, Ivon, Idrisoglu, Senel, Nourse, Craig, Nourbakhsh, Ehsan, Manning, Suzanne, Wani, Shivangi, Gongora, Milena, Pajic, Marina, Scarlett, Christopher, Gill, Anthony, Pinho, Andreia, Rooman, Ilse, Anderson, Matthew, Holmes, Oliver, Leonard, Conrad, Taylor, Darrin, Wood, Scott, Xu, Qinying, Nones, Katia, Fink, J, Christ, Angelika, Bruxner, Tim, Cloonan, Nicole, Kolle, Gabriel, Newell, Felicity, Pinese, Mark, Mead, R, Humphris, Jeremy, Kaplan, Warren, Jones, Marc, Colvin, Emily, Nagrial, Adnan, Humphrey, Emily, Chou, Angela, Chin, Venessa, Chantrill, Lorraine, Mawson, Amanda, Samra, Jaswinder, Kench, James, Lovell, Jessica, Daly, Roger, Merrett, Neil, Toon, Christopher, Epari, Krishna, Nguyen, Nam, Barbour, Andrew, Zeps, Nikolajs, Kakkar, Nipun, Zhao, Fengmei, Wu, Yuan, Wang, Min, Muzny, Donna, Fisher, William, Brunicardi, F, Hodges, Sally, Reid, Jeffrey, Drummond, Jennifer, Chang, Kyle, Han, Yi, Lewis, Lora, Dinh, Huyen, Buhay, Christian, Beck, Timothy, Timms, Lee, Sam, Michelle, Begley, Kimberly, Brown, Andrew, Pai, Deepa, Panchal, Ami, Buchner, Nicholas, De Borja, Richard, Denroche, Robert, Yung, Christina, Serra, Stefano, Onetto, Nicole, Mukhopadhyay, Debabrata, Tsao, Ming-Sound, Shaw, Patricia, Petersen, Gloria, Gallinger, Steven, Hruban, Ralph, Maitra, Anirban, Iacobuzio-Donahue, Christine, Schulick, Richard, Wolfgang, Christopher, and Morgan, Richard

Subjects
Animals, Axons, Carcinoma, Pancreatic Ductal, Gene Dosage, Gene Expression Regulation, Neoplastic, Genome, Humans, Kaplan-Meier Estimate, Mice, Mutation, Pancreatic Neoplasms, Proteins, Signal Transduction
Abstract

Pancreatic cancer is a highly lethal malignancy with few effective therapies. We performed exome sequencing and copy number analysis to define genomic aberrations in a prospectively accrued clinical cohort (n = 142) of early (stage I and II) sporadic pancreatic ductal adenocarcinoma. Detailed analysis of 99 informative tumours identified substantial heterogeneity with 2,016 non-silent mutations and 1,628 copy-number variations. We define 16 significantly mutated genes, reaffirming known mutations (KRAS, TP53, CDKN2A, SMAD4, MLL3, TGFBR2, ARID1A and SF3B1), and uncover novel mutated genes including additional genes involved in chromatin modification (EPC1 and ARID2), DNA damage repair (ATM) and other mechanisms (ZIM2, MAP2K4, NALCN, SLC16A4 and MAGEA6). Integrative analysis with in vitro functional data and animal models provided supportive evidence for potential roles for these genetic aberrations in carcinogenesis. Pathway-based analysis of recurrently mutated genes recapitulated clustering in core signalling pathways in pancreatic ductal adenocarcinoma, and identified new mutated genes in each pathway. We also identified frequent and diverse somatic aberrations in genes described traditionally as embryonic regulators of axon guidance, particularly SLIT/ROBO signalling, which was also evident in murine Sleeping Beauty transposon-mediated somatic mutagenesis models of pancreatic cancer, providing further supportive evidence for the potential involvement of axon guidance genes in pancreatic carcinogenesis.

Published
2012

42. Novel loci for adiponectin levels and their influence on type 2 diabetes and metabolic traits: a multi-ethnic meta-analysis of 45,891 individuals.

Author

Dastani, Zari, Hivert, Marie-France, Timpson, Nicholas, Perry, John RB, Yuan, Xin, Scott, Robert A, Henneman, Peter, Heid, Iris M, Kizer, Jorge R, Lyytikäinen, Leo-Pekka, Fuchsberger, Christian, Tanaka, Toshiko, Morris, Andrew P, Small, Kerrin, Isaacs, Aaron, Beekman, Marian, Coassin, Stefan, Lohman, Kurt, Qi, Lu, Kanoni, Stavroula, Pankow, James S, Uh, Hae-Won, Wu, Ying, Bidulescu, Aurelian, Rasmussen-Torvik, Laura J, Greenwood, Celia MT, Ladouceur, Martin, Grimsby, Jonna, Manning, Alisa K, Liu, Ching-Ti, Kooner, Jaspal, Mooser, Vincent E, Vollenweider, Peter, Kapur, Karen A, Chambers, John, Wareham, Nicholas J, Langenberg, Claudia, Frants, Rune, Willems-Vandijk, Ko, Oostra, Ben A, Willems, Sara M, Lamina, Claudia, Winkler, Thomas W, Psaty, Bruce M, Tracy, Russell P, Brody, Jennifer, Chen, Ida, Viikari, Jorma, Kähönen, Mika, Pramstaller, Peter P, Evans, David M, St Pourcain, Beate, Sattar, Naveed, Wood, Andrew R, Bandinelli, Stefania, Carlson, Olga D, Egan, Josephine M, Böhringer, Stefan, van Heemst, Diana, Kedenko, Lyudmyla, Kristiansson, Kati, Nuotio, Marja-Liisa, Loo, Britt-Marie, Harris, Tamara, Garcia, Melissa, Kanaya, Alka, Haun, Margot, Klopp, Norman, Wichmann, H-Erich, Deloukas, Panos, Katsareli, Efi, Couper, David J, Duncan, Bruce B, Kloppenburg, Margreet, Adair, Linda S, Borja, Judith B, DIAGRAM+ Consortium, MAGIC Consortium, GLGC Investigators, MuTHER Consortium, Wilson, James G, Musani, Solomon, Guo, Xiuqing, Johnson, Toby, Semple, Robert, Teslovich, Tanya M, Allison, Matthew A, Redline, Susan, Buxbaum, Sarah G, Mohlke, Karen L, Meulenbelt, Ingrid, Ballantyne, Christie M, Dedoussis, George V, Hu, Frank B, Liu, Yongmei, Paulweber, Bernhard, Spector, Timothy D, Slagboom, P Eline, Ferrucci, Luigi, and Jula, Antti

Subjects
DIAGRAM+ Consortium, MAGIC Consortium, GLGC Investigators, MuTHER Consortium, DIAGRAM Consortium, GIANT Consortium, Global B Pgen Consortium, Procardis Consortium, MAGIC investigators, GLGC Consortium, Humans, Diabetes Mellitus, Type 2, Insulin Resistance, Genetic Predisposition to Disease, Glucose Tolerance Test, Waist-Hip Ratio, Gene Expression, Polymorphism, Single Nucleotide, African Americans, Asian Continental Ancestry Group, European Continental Ancestry Group, Female, Male, Adiponectin, Cholesterol, HDL, Metabolic Networks and Pathways, Genome-Wide Association Study, Diabetes Mellitus, Type 2, Polymorphism, Single Nucleotide, Cholesterol, HDL, Genetics, Developmental Biology
Abstract

Circulating levels of adiponectin, a hormone produced predominantly by adipocytes, are highly heritable and are inversely associated with type 2 diabetes mellitus (T2D) and other metabolic traits. We conducted a meta-analysis of genome-wide association studies in 39,883 individuals of European ancestry to identify genes associated with metabolic disease. We identified 8 novel loci associated with adiponectin levels and confirmed 2 previously reported loci (P = 4.5×10(-8)-1.2×10(-43)). Using a novel method to combine data across ethnicities (N = 4,232 African Americans, N = 1,776 Asians, and N = 29,347 Europeans), we identified two additional novel loci. Expression analyses of 436 human adipocyte samples revealed that mRNA levels of 18 genes at candidate regions were associated with adiponectin concentrations after accounting for multiple testing (p

Published
2012

43. The ABC membrane transporter ABCG2 prevents access of FAAH inhibitor URB937 to the central nervous system

Author

Moreno-Sanz, Guillermo, Barrera, Borja, Guijarro, Ana, d’Elia, Ilaria, Otero, Jon Andoni, Alvarez, Ana I, Bandiera, Tiziano, Merino, Gracia, and Piomelli, Daniele

Subjects
Neurosciences, Substance Misuse, Drug Abuse (NIDA only), Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Neurological, ATP Binding Cassette Transporter, Subfamily G, Member 2, ATP-Binding Cassette Transporters, Amidohydrolases, Animals, Cannabinoids, Cell Line, Central Nervous System, Dogs, Gene Deletion, Humans, Male, Mice, Models, Molecular, Neoplasm Proteins, Up-Regulation, Fatty-acid amide hydrolase, URB937, Breast cancer resistance protein, Blood-brain barrier, Central nervous system, Abcg2-deficient mice, Pharmacology and Pharmaceutical Sciences, Pharmacology & Pharmacy
Abstract

The O-arylcarbamate URB937 is a potent inhibitor of fatty-acid amide hydrolase (FAAH), an intracellular serine hydrolase responsible for the deactivation of the endocannabinoid anandamide. URB937 is unique among FAAH inhibitors in that is actively extruded from the central nervous system (CNS), and therefore increases anandamide levels exclusively in peripheral tissues. Despite its limited distribution, URB937 exhibits marked analgesic properties in rodent models of pain. Pharmacological evidence suggests that the extrusion of URB937 from the CNS may be mediated by the ABC membrane transporter ABCG2 (also called Breast cancer resistance protein, BCRP). In the present study, we show that URB937 is a substrate for both mouse and human orthologues of ABCG2. The relative transport ratios for URB937 in Madin-Darby canine kidney (MDCKII) cells monolayers over-expressing either mouse Abcg2 or human ABCG2 were significantly higher compared to parental monolayers (13.6 and 13.1 vs. 1.5, respectively). Accumulation of the compound in the luminal/apical side was prevented by co-administration of the selective ABCG2 inhibitor, Ko-143. In vivo studies in mice showed that URB937 (25 mg kg(-1)) readily entered the brain and spinal cord of Abcg2-deficient mice following intraperitoneal administration, whereas the same dose of drug remained restricted to peripheral tissues in wild-type mice. By identifying ABCG2 as a transport mechanism responsible for the extrusion of URB937 from the CNS, the present results should facilitate the rational design of novel peripherally restricted FAAH inhibitors.

Published
2011

44. Incidence, risk factors, and evolution of venous thromboembolic events in patients diagnosed with pancreatic carcinoma and treated with chemotherapy on an outpatient basis

Author

Silvia García Adrián, Adán Rodríguez González, Eva Martínez de Castro, Vanessa Pachón Olmos, Laura Ortega Morán, Purificación Martínez del Prado, Mercedes Salgado Fernández, José David Cumplido Burón, Ignacio García Escobar, Joaquina Martínez Galán, Ana Isabel Ferrer Pérez, Fernando Neria, Diego Cacho Lavin, Borja López de San Vicente Hernández, Paula Jiménez-Fonseca, and Andrés J. Muñoz Martín

Subjects
Risk Factors, Incidence, Venous thrombosis, Outpatients, Internal Medicine, Humans, Khorana score, Venous Thromboembolism, Pancreatic carcinoma, Retrospective Studies
Abstract

Background Pancreatic carcinoma is one of the tumors associated with a higher risk for thromboembolic events, with incidence rates ranging from 5% to 41% in previous retrospective series. Patients and methods We conducted a retrospective study in eleven Spanish hospitals that included 666 patients diagnosed with pancreatic carcinoma (any stage) between 2008 and 2011 and treated with chemotherapy. The main objective was to evaluate the incidence of venous thromboembolic events (VTE) in this population, as well as potential risk factors for thrombosis. The impact of VTE on mortality was also assessed. Results With a median follow-up of 9.3 months, the incidence of VTE was 22.1%; 52% were diagnosed incidentally. Our study was unable to confirm the ability of the Khorana score to discriminate between patients in the intermediate or high risk category for thrombosis. The presence of VTE proved to be an independent prognostic factor associated with increased risk of death (HR 2.39, 95% CI 1.96–2.92). Symptomatic events correlated with higher mortality than asymptomatic events (HR 1.72; 95% CI, 1.21–2.45; p = 0.002), but incidental VTE, including visceral vein thrombosis (VVT), negatively affected survival compared to patients without VTE. Subjects who developed VTE within the first 3 months of diagnosis of pancreatic carcinoma had lower survival rates than those with VTE after 3 months (HR 1.92, 95% CI 1.30–2.84; p

Published
2022

45. Safety of tongue base procedures for sleep apnoea in adults: A systematic review and metanalysis from the YO-IFOS study group

Author

Christian Calvo-Henriquez, Borja Boronat-Catala, Irene Rivero-Fernández, Giovanni Cammarotto, Badr Ibrahim, Jerome R. Lechien, Gabriel Martínez-Capoccioni, Marina Carrasco-Llatas, Robson Capasso, and Carlos Martin-Martin

Subjects
Adult, Sleep Apnea, Obstructive, Sleep Apnea Syndromes, Otorhinolaryngology, Tongue, Polysomnography, Humans, General Medicine, Larynx
Abstract

Tongue base and hypopharynx are the major sites of obstruction in OSA patients with failed palatal surgery. In recent years, several minimally invasive procedures have been developed to address tongue base obstruction. However, the research focus has consistently been on the effectiveness of surgery in reducing obstructive sleep apnoea rather than on postoperative complications. In this systematic review and metanalysis we aim to review the complication rate of minimally invasive base of tongue procedures for OSAS in adults.PubMed (Medline), the Cochrane Library, EMBASE, Scopus, SciELO and Trip Database.Data sources were checked by three authors of the YO-IFOS sleep apnoea study group. Three authors extracted the data. Main outcome was expressed as the complication rate and 95% confidence interval for each surgical technique.20 studies (542 patients) met the inclusion criteria. The mean complication rate is 12.79%; 4.65% for minor complications, 6.42% if they are moderate, and 1.77% if severe. The most reported complication overall is infection, in 1.95% of cases, followed by transient swallowing disorder, occurring in 1.30% of the total sample.The heterogeneity amongst the included studies prevents us from obtaining solid conclusions. The available evidence suggests that minimally invasive base of tongue procedures may present a wide spectrum of complication rates, ranging from 4.4% in tongue base radiofrequency to up to 42.42% in tongue base ablation.

Published
2022

46. Incidence of hypertension in young transgender people after a 5-year follow-up: association with gender-affirming hormonal therapy

Author

Francisco Javier, Martinez-Martin, Agnieszka, Kuzior, Alba, Hernandez-Lazaro, Ricardo Jose, de Leon-Durango, Carlos, Rios-Gomez, Borja, Santana-Ojeda, Jennifer Maria, Perez-Rivero, Paula Maria, Fernandez-Trujillo-Comenge, Paula, Gonzalez-Diaz, Claudia, Arnas-Leon, Carmen, Acosta-Calero, Esperanza, Perdomo-Herrera, Alba Lucia, Tocino-Hernandez, Maria, Del Sol Sanchez-Bacaicoa, and Maria, Del Pino Perez-Garcia

Subjects
Male, Physiology, Incidence, Gender Identity, Androgen Antagonists, Transgender Persons, Hypertension, Androgens, Internal Medicine, Humans, Female, Cyproterone Acetate, Cardiology and Cardiovascular Medicine, Retrospective Studies
Abstract

In order to assess the risk of hypertension development, we performed a retrospective analysis of the clinical records of consecutive transgender patients who began gender-affirming hormonal therapy in our Outpatient Gender Identity Clinic with30 years of age and had a follow-up5 years. 149 transgender women treated with estradiol and 153 transgender men treated with testosterone were included; 129 of the transgender women received also androgen blockers (54 spironolactone, 49 cyproterone acetate and 26 LHRH agonists). The annual incidence of hypertension in young transgender men (1.18%) seemed comparable to that of the general population. In young transgender women, it seemed higher (2.14%); we found that the choice of androgen blocker had a remarkable effect, with a highly significant increase in patients treated with cyproterone acetate (4.90%) vs. the rest (0.80%); the adjusted hazard-ratio was 0.227 (p = 0.001). Correlation, logistic regression and mediation analyses were performed for the associations of the available clinical variables with the increase in systolic blood pressure and the onset of hypertension, but besides the use of cyproterone acetate, only the ponderal gain was found significant (Spearman's r: 0.361, p 0.001); with a 36.7% mediation effect (31.2-42.3%). Cyproterone acetate has additional known risks, such as meningioma; although we cannot conclusively prove that it has a role in the development of hypertension, we conclude that the use of cyproterone acetate for this indication should be reconsidered.

Published
2022

47. Effects of a comprehensive lifestyle intervention on cardiovascular health

Author

Ines Garcia-Lunar, Hidde P van der Ploeg, Juan Miguel Fernández Alvira, Femke van Nassau, Jose Maria Castellano Vázquez, Allard J van der Beek, Xavier Rossello, Antonio Fernández-Ortiz, Jennifer Coffeng, Johanna M van Dongen, Jose Maria Mendiguren, Borja Ibáñez, Willem van Mechelen, Valentin Fuster, Public and occupational health, APH - Health Behaviors & Chronic Diseases, Epidemiology and Data Science, AMS - Sports, APH - Societal Participation & Health, VU University medical center, Fundación Centro Nacional de Investigaciones Cardiovasculares, AstraZeneca, Banco Santander, Instituto de Salud Carlos III, Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF), Ministerio de Ciencia e Innovación (España), Ministerio de Ciencia e Innovación. Centro de Excelencia Severo Ochoa (España), Fundación ProCNIC, Health Sciences, Health Economics and Health Technology Assessment, AMS - Musculoskeletal Health, and APH - Mental Health

Subjects
Lifestyle intervention, Adult, Blood Pressure, Middle Aged, Cardiovascular, Atherosclerosis, SDG 3 - Good Health and Well-being, Randomized controlled trial, Humans, Subclinical atherosclerosis, Cardiology and Cardiovascular Medicine, Workplace, Life Style, Exercise
Abstract

To investigate the effectiveness of a 3-year worksite lifestyle intervention on cardiovascular metrics and to study whether outcomes are influenced by baseline subclinical atherosclerosis (SA) by non-invasive imaging. A randomized controlled trial was performed to compare a lifestyle intervention with standard of care in asymptomatic middle-aged subjects, stratified by SA. The intervention consisted of nine motivational interviews during the first year, followed by three further sessions between Years 1 and 3. The primary outcome was the change in a pre-specified adaptation of the Fuster-BEWAT score (Blood pressure, Exercise, Weight, Alimentation, and Tobacco) between baseline and follow-up Years 1-3. A total of 1020 participants (mean age 50 ± 4 years) were enrolled, of whom 510 were randomly assigned to the intervention and 510 to the control group. The baseline adapted Fuster-BEWAT score was 16.2 ± 3.7 points in the intervention group and 16.5 ± 3.5 points in the control group. At Year 1, the score improved significantly in intervention participants compared with controls [estimate 0.83 (95% CI 0.52-1.15) points]. However, intervention effectiveness decreased to non-significant levels at Year 3 [0.24 (95% CI -0.10 to 0.59) points]. Over the 3-year period, the intervention was effective in participants having low baseline SA [0.61 (95% CI 0.30-0.93) points] but not in those with high baseline SA [0.19 (95% CI -0.26 to 0.64) points]. In middle-aged asymptomatic adults, a lifestyle intervention was associated with a significant improvement in cardiovascular health and behavioural metrics. The effect attenuated after 1 year as the intensity of the intervention was reduced. ClinicalTrials.gov (NCT02561065). TANSNIP-PESA is funded by Fundación Centro Nacional de Investigaciones Cardiovasculares (CNIC) Carlos III through an Investigator-initiated Study grant to Icahn School of Medicine from AstraZeneca. The PESA study is cofunded by the CNIC and Banco Santander. The study also received funding from the Instituto de Salud Carlos III (PI15/02019) and the European Regional Development Fund (ERDF) ‘A way to make Europe’. The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the Ministerio de Ciencia e Innovación (MCIN), and the Pro CNIC Foundation and is a Severo Ochoa Center of Excellence (grant CEX2020-001041-S funded by MICIN/AEI/10.13039/501100011033. The study funders were not involved in the study design; the collection, analysis, or interpretation of data; the writing of the report; or the decision to submit the paper for publication. Sí

Published
2022

48. Physical activity phenotypes and mortality in older adults: a novel distributional data analysis of accelerometry in the NHANES

Author

Marcos Matabuena, Paulo Félix, Ziad Akram Ali Hammouri, Jorge Mota, Borja del Pozo Cruz, and Universidade de Santiago de Compostela. Centro de Investigación en Tecnoloxías da Información

Subjects
Aged, 80 and over, Data Analysis, Aging, Physical activity, Precision medicine, Longevity, Distributional representation, Nutrition Surveys, Phenotype, Accelerometry, Humans, Geriatrics and Gerontology, Exercise, Aged
Abstract

Physical activity is deemed critical to successful ageing. Despite evidence and progress, there is still a need to determine more precisely the direction, magnitude, intensity, and volume of physical activity that should be performed on a daily basis to effectively promote the health of individuals. This study aimed to assess the clinical validity of new physical activity phenotypes derived from a novel distributional functional analysis of accelerometer data in older adults. A random sample of participants aged between 65 and 80 years with valid accelerometer data from the National Health and Nutrition Examination Survey (NHANES) 2011–2014 was used. Five major clinical phenotypes were identified, which provided a greater sensitivity for predicting 5-year mortality and survival outcomes than age alone, and our results confirm the importance of moderate-to-vigorous physical activity. The new clinical physical activity phenotypes are a promising tool for improving patient prognosis and for directing to more targeted intervention planning, according to the principles of precision medicine. The use of distributional representations shows clear advantages over more traditional metrics to explore the effects of the full spectrum of the physical activity continuum on human health Open Access funding provided thanks to the CRUE-CSIC agreement with Springer Nature. This research was funded by the Ministry of Science and Innovation of Spain, under Grant No. PID2021-123152OB-C21 SI

Published
2022

49. Predicting major complications in patients undergoing laparoscopic and open hysterectomy for benign indications

Author

Krupa, Madhvani, Silvia Fernandez, Garcia, Borja M, Fernandez-Felix, Javier, Zamora, Tyrone, Carpenter, and Khalid S, Khan

Subjects
Postoperative Complications, Humans, Female, Laparoscopy, General Medicine, Hysterectomy, State Medicine, Retrospective Studies
Abstract

Background: Hysterectomy, the most common gynecological operation, requires surgeons to counsel women about their operative risks. We aimed to develop and validate multivariable logistic regression models to predict major complications of laparoscopic or abdominal hysterectomy for benign conditions. Methods: We obtained routinely collected health administrative data from the English National Health Service (NHS) from 2011 to 2018. We defined major complications based on core outcomes for postoperative complications including ureteric, gastrointestinal and vascular injury, and wound complications. We specified 11 predictors a priori. We used internal–external cross-validation to evaluate discrimination and calibration across 7 NHS regions in the development cohort. We validated the final models using data from an additional NHS region. Results: We found that major complications occurred in 4.4% (3037/68 599) of laparoscopic and 4.9% (6201/125 971) of abdominal hysterectomies. Our models showed consistent discrimination in the development cohort (laparoscopic, C-statistic 0.61, 95% confidence interval [CI] 0.60 to 0.62; abdominal, C-statistic 0.67, 95% CI 0.64 to 0.70) and similar or better discrimination in the validation cohort (laparoscopic, C-statistic 0.67, 95% CI 0.65 to 0.69; abdominal, C-statistic 0.67, 95% CI 0.65 to 0.69). Adhesions were most predictive of complications in both models (laparoscopic, odds ratio [OR] 1.92, 95% CI 1.73 to 2.13; abdominal, OR 2.46, 95% CI 2.27 to 2.66). Other factors predictive of complications included adenomyosis in the laparoscopic model, and Asian ethnicity and diabetes in the abdominal model. Protective factors included age and diagnoses of menstrual disorders or benign adnexal mass in both models and diagnosis of fibroids in the abdominal model. Interpretation: Personalized risk estimates from these models, which showed moderate discrimination, can inform clinical decision-making for people with benign conditions who may require hysterectomy., British Society for Gynaecological Endoscopy

Published
2022

50. STIM/Orai Inhibition as a Strategy for Alleviating Diabetic Erectile Dysfunction Through Modulation of Rat and Human Penile Tissue Contractility and in vivo Potentiation of Erectile Responses

Author

Alejandro Sevilleja-Ortiz, Mariam El Assar, Borja García-Gómez, José M. La Fuente, Manuel Alonso-Isa, Javier Romero-Otero, Juan I. Martínez-Salamanca, Argentina Fernández, Leocadio Rodríguez-Mañas, and Javier Angulo

Subjects
Male, Penile Erection, Urology, Endocrinology, Diabetes and Metabolism, Thromboxanes, Phosphodiesterase 5 Inhibitors, Rats, Diabetes Mellitus, Experimental, Psychiatry and Mental health, Adrenergic Agents, Endocrinology, Diabetes Mellitus, Type 2, Erectile Dysfunction, Reproductive Medicine, Stromal Interaction Molecules, Animals, Humans, Penis
Abstract

Background Stromal interaction molecule (STIM)/Orai calcium entry system appears to have a role in erectile dysfunction (ED) pathophysiology but its specific contribution to diabetic ED was not elucidated. Aim To evaluate STIM/Orai inhibition on functional alterations associated with diabetic ED in rat and human penile tissues and on in vivo erectile responses in diabetic rats. Methods Rat corpus cavernosum (RCC) strips from nondiabetic (No DM) and streptozotocin-induced diabetic (DM) rats and human penile resistance arteries (HPRA) and corpus cavernosum (HCC) from ED patients undergoing penile prosthesis insertion were functionally evaluated in organ chambers and wire myographs. Erectile function in vivo in rats was assessed by intracavernosal pressure (ICP) responses to cavernous nerve electrical stimulation (CNES). Expression of STIM/Orai elements in HCC was determined by immunofluorescence and immunoblot. Main Outcome Measures Functional responses in RCC, HCC and HPRA and STIM/Orai protein expression in HCC. In vivo erectile responses to CNES. Results Inhibition of Orai channels with YM-58483 (20 µM) significantly reduced adrenergic contractions in RCC but more effectively in DM. Thromboxane-induced and neurogenic contractions were reduced by STIM/Orai inhibition while defective endothelial, neurogenic and PDE5 inhibitor-induced relaxations were enhanced by YM-58483 (10 µM) in RCC from DM rats. In vivo, YM-58483 caused erections and attenuated diabetes-related impairment of erectile responses. YM-58483 potentiated the effects of PDE5 inhibition. In human tissues, STIM/Orai inhibition depressed adrenergic and thromboxane-induced contractions in ED patients more effectively in those with type 2 diabetes. Diabetes was associated with increased expression of Orai1 and Orai3 in ED patients. Clinical Translation Targeting STIM/Orai to alleviate diabetes-related functional alterations of penile vascular tissue could improve erectile function and potentiate therapeutic effects of PDE5 inhibitors in diabetic ED. Strengths and Limitations Improving effects of STIM/Orai inhibition on diabetes-related functional impairment was evidenced in vitro and in vivo in an animal model and validated in human tissues from ED patients. Functional findings were complemented with expression results. Main limitation was low numbers of human experiments due to limited human tissue availability. Conclusions STIM/Orai inhibition alleviated alterations of functional responses in vitro and improved erectile responses in vivo in diabetic rats, potentiating the effects of PDE5 inhibition. STIM/Orai inhibition was validated as a target to modulate functional alterations of human penile vascular tissue in diabetic ED where Orai1 and Orai3 channels were upregulated. STIM/Orai inhibition could be a potential therapeutic strategy to overcome poor response to conventional ED therapy in diabetic patients.

Published
2022

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