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1. Implications of TP53 allelic state for genome stability, clinical presentation and outcomes in myelodysplastic syndromes

Author

Bernard, Elsa, Nannya, Yasuhito, Hasserjian, Robert P, Devlin, Sean M, Tuechler, Heinz, Medina-Martinez, Juan S, Yoshizato, Tetsuichi, Shiozawa, Yusuke, Saiki, Ryunosuke, Malcovati, Luca, Levine, Max F, Arango, Juan E, Zhou, Yangyu, Solé, Francesc, Cargo, Catherine A, Haase, Detlef, Creignou, Maria, Germing, Ulrich, Zhang, Yanming, Gundem, Gunes, Sarian, Araxe, van de Loosdrecht, Arjan A, Jädersten, Martin, Tobiasson, Magnus, Kosmider, Olivier, Follo, Matilde Y, Thol, Felicitas, Pinheiro, Ronald F, Santini, Valeria, Kotsianidis, Ioannis, Boultwood, Jacqueline, Santos, Fabio PS, Schanz, Julie, Kasahara, Senji, Ishikawa, Takayuki, Tsurumi, Hisashi, Takaori-Kondo, Akifumi, Kiguchi, Toru, Polprasert, Chantana, Bennett, John M, Klimek, Virginia M, Savona, Michael R, Belickova, Monika, Ganster, Christina, Palomo, Laura, Sanz, Guillermo, Ades, Lionel, Della Porta, Matteo Giovanni, Elias, Harold K, Smith, Alexandra G, Werner, Yesenia, Patel, Minal, Viale, Agnès, Vanness, Katelynd, Neuberg, Donna S, Stevenson, Kristen E, Menghrajani, Kamal, Bolton, Kelly L, Fenaux, Pierre, Pellagatti, Andrea, Platzbecker, Uwe, Heuser, Michael, Valent, Peter, Chiba, Shigeru, Miyazaki, Yasushi, Finelli, Carlo, Voso, Maria Teresa, Shih, Lee-Yung, Fontenay, Michaela, Jansen, Joop H, Cervera, José, Atsuta, Yoshiko, Gattermann, Norbert, Ebert, Benjamin L, Bejar, Rafael, Greenberg, Peter L, Cazzola, Mario, Hellström-Lindberg, Eva, Ogawa, Seishi, and Papaemmanuil, Elli

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Hematology, Stem Cell Research, Cancer, Clinical Research, Rare Diseases, Genetics, 2.1 Biological and endogenous factors, Aetiology, Alleles, Cohort Studies, DNA Copy Number Variations, DNA Mutational Analysis, Female, Gene Frequency, Genomic Instability, Humans, Loss of Heterozygosity, Male, Mutation, Myelodysplastic Syndromes, Phenotype, Prognosis, Survival Analysis, Treatment Outcome, Tumor Suppressor Protein p53, Medical and Health Sciences, Immunology, Biomedical and clinical sciences, Health sciences
Abstract

Tumor protein p53 (TP53) is the most frequently mutated gene in cancer1,2. In patients with myelodysplastic syndromes (MDS), TP53 mutations are associated with high-risk disease3,4, rapid transformation to acute myeloid leukemia (AML)5, resistance to conventional therapies6-8 and dismal outcomes9. Consistent with the tumor-suppressive role of TP53, patients harbor both mono- and biallelic mutations10. However, the biological and clinical implications of TP53 allelic state have not been fully investigated in MDS or any other cancer type. We analyzed 3,324 patients with MDS for TP53 mutations and allelic imbalances and delineated two subsets of patients with distinct phenotypes and outcomes. One-third of TP53-mutated patients had monoallelic mutations whereas two-thirds had multiple hits (multi-hit) consistent with biallelic targeting. Established associations with complex karyotype, few co-occurring mutations, high-risk presentation and poor outcomes were specific to multi-hit patients only. TP53 multi-hit state predicted risk of death and leukemic transformation independently of the Revised International Prognostic Scoring System (IPSS-R)11. Surprisingly, monoallelic patients did not differ from TP53 wild-type patients in outcomes and response to therapy. This study shows that consideration of TP53 allelic state is critical for diagnostic and prognostic precision in MDS as well as in future correlative studies of treatment response.

Published
2020

2. Neuroprotective activation of astrocytes by methylmercury exposure in the inferior colliculus.

Author

Ishihara, Yasuhiro, Itoh, Kouichi, Oguro, Ami, Chiba, Yoichi, Ueno, Masaki, Tsuji, Mayumi, Vogel, Christoph, and Yamazaki, Takeshi

Subjects
Animals, Astrocytes, Brain-Derived Neurotrophic Factor, Glial Fibrillary Acidic Protein, Inferior Colliculi, Male, Methylmercury Compounds, Mice, Mice, Inbred ICR, Neurons, Neuroprotection
Abstract

Methylmercury (MeHg) is well known to induce auditory disorders such as dysarthria. When we performed a global analysis on the brains of mice exposed to MeHg by magnetic resonance imaging, an increase in the T1 signal in the inferior colliculus (IC), which is localized in the auditory pathway, was observed. Therefore, the purpose of this study is to examine the pathophysiology and auditory dysfunction induced by MeHg, focusing on the IC. Measurement of the auditory brainstem response revealed increases in latency and decreases in threshold in the IC of mice exposed to MeHg for 4 weeks compared with vehicle mice. Incoordination in MeHg-exposed mice was noted after 6 weeks of exposure, indicating that IC dysfunction occurs earlier than incoordination. There was no change in the number of neurons or microglial activity, while the expression of glial fibrillary acidic protein, a marker for astrocytic activity, was elevated in the IC of MeHg-exposed mice after 4 weeks of exposure, indicating that astrogliosis occurs in the IC. Suppression of astrogliosis by treatment with fluorocitrate exacerbated the latency and threshold in the IC evaluated by the auditory brainstem response. Therefore, astrocytes in the IC are considered to play a protective role in the auditory pathway. Astrocytes exposed to MeHg increased the expression of brain-derived neurotrophic factor in the IC, suggesting that astrocytic brain-derived neurotrophic factor is a potent protectant in the IC. This study showed that astrogliosis in the IC could be an adaptive response to MeHg toxicity. The overall toxicity of MeHg might be determined on the basis of the balance between MeHg-mediated injury to neurons and protective responses from astrocytes.

Published
2019

3. The BRG1/SOX9 axis is critical for acinar cell–derived pancreatic tumorigenesis

Author

Tsuda, Motoyuki, Fukuda, Akihisa, Roy, Nilotpal, Hiramatsu, Yukiko, Leonhardt, Laura, Kakiuchi, Nobuyuki, Hoyer, Kaja, Ogawa, Satoshi, Goto, Norihiro, Ikuta, Kozo, Kimura, Yoshito, Matsumoto, Yoshihide, Takada, Yutaka, Yoshioka, Takuto, Maruno, Takahisa, Yamaga, Yuichi, Kim, Grace E, Akiyama, Haruhiko, Ogawa, Seishi, Wright, Christopher V, Saur, Dieter, Takaori, Kyoichi, Uemoto, Shinji, Hebrok, Matthias, Chiba, Tsutomu, and Seno, Hiroshi

Subjects
Digestive Diseases, Genetics, Rare Diseases, Cancer, Pancreatic Cancer, 2.1 Biological and endogenous factors, Aetiology, Animals, Carcinoma, Pancreatic Ductal, Cell Transformation, Neoplastic, DNA Helicases, Female, Gene Expression Regulation, Humans, Male, Mice, Mice, Transgenic, Nuclear Proteins, Pancreatic Neoplasms, Response Elements, SOX9 Transcription Factor, Signal Transduction, Transcription Factors, Tumor Suppressor Protein p53, Epigenetics, Gastroenterology, Mouse models, Oncology, Medical and Health Sciences, Immunology
Abstract

Chromatin remodeler Brahma related gene 1 (BRG1) is silenced in approximately 10% of human pancreatic ductal adenocarcinomas (PDAs). We previously showed that BRG1 inhibits the formation of intraductal pancreatic mucinous neoplasm (IPMN) and that IPMN-derived PDA originated from ductal cells. However, the role of BRG1 in pancreatic intraepithelial neoplasia-derived (PanIN-derived) PDA that originated from acinar cells remains elusive. Here, we found that exclusive elimination of Brg1 in acinar cells of Ptf1a-CreER; KrasG12D; Brg1fl/fl mice impaired the formation of acinar-to-ductal metaplasia (ADM) and PanIN independently of p53 mutation, while PDA formation was inhibited in the presence of p53 mutation. BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. SOX9 expression was downregulated in BRG1-depleted ADMs/PanINs. Notably, Sox9 overexpression canceled this PanIN-attenuated phenotype in KBC mice. Furthermore, Brg1 deletion in established PanIN by using a dual recombinase system resulted in regression of the lesions in mice. Finally, BRG1 expression correlated with SOX9 expression in human PDAs. In summary, BRG1 is critical for PanIN initiation and progression through positive regulation of SOX9. Thus, the BRG1/SOX9 axis is a potential target for PanIN-derived PDA.

Published
2018

4. Genome-wide association meta-analysis in 269,867 individuals identifies new genetic and functional links to intelligence

Author

Savage, Jeanne E, Jansen, Philip R, Stringer, Sven, Watanabe, Kyoko, Bryois, Julien, de Leeuw, Christiaan A, Nagel, Mats, Awasthi, Swapnil, Barr, Peter B, Coleman, Jonathan RI, Grasby, Katrina L, Hammerschlag, Anke R, Kaminski, Jakob A, Karlsson, Robert, Krapohl, Eva, Lam, Max, Nygaard, Marianne, Reynolds, Chandra A, Trampush, Joey W, Young, Hannah, Zabaneh, Delilah, Hägg, Sara, Hansell, Narelle K, Karlsson, Ida K, Linnarsson, Sten, Montgomery, Grant W, Muñoz-Manchado, Ana B, Quinlan, Erin B, Schumann, Gunter, Skene, Nathan G, Webb, Bradley T, White, Tonya, Arking, Dan E, Avramopoulos, Dimitrios, Bilder, Robert M, Bitsios, Panos, Burdick, Katherine E, Cannon, Tyrone D, Chiba-Falek, Ornit, Christoforou, Andrea, Cirulli, Elizabeth T, Congdon, Eliza, Corvin, Aiden, Davies, Gail, Deary, Ian J, DeRosse, Pamela, Dickinson, Dwight, Djurovic, Srdjan, Donohoe, Gary, Conley, Emily Drabant, Eriksson, Johan G, Espeseth, Thomas, Freimer, Nelson A, Giakoumaki, Stella, Giegling, Ina, Gill, Michael, Glahn, David C, Hariri, Ahmad R, Hatzimanolis, Alex, Keller, Matthew C, Knowles, Emma, Koltai, Deborah, Konte, Bettina, Lahti, Jari, Le Hellard, Stephanie, Lencz, Todd, Liewald, David C, London, Edythe, Lundervold, Astri J, Malhotra, Anil K, Melle, Ingrid, Morris, Derek, Need, Anna C, Ollier, William, Palotie, Aarno, Payton, Antony, Pendleton, Neil, Poldrack, Russell A, Räikkönen, Katri, Reinvang, Ivar, Roussos, Panos, Rujescu, Dan, Sabb, Fred W, Scult, Matthew A, Smeland, Olav B, Smyrnis, Nikolaos, Starr, John M, Steen, Vidar M, Stefanis, Nikos C, Straub, Richard E, Sundet, Kjetil, Tiemeier, Henning, Voineskos, Aristotle N, Weinberger, Daniel R, Widen, Elisabeth, Yu, Jin, Abecasis, Goncalo, Andreassen, Ole A, Breen, Gerome, and Christiansen, Lene

Subjects
Biological Sciences, Genetics, Brain Disorders, Mental Health, Human Genome, Biotechnology, Neurosciences, Underpinning research, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Aetiology, Mental health, Neurological, Adolescent, Brain, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Intelligence, Male, Middle Aged, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

Intelligence is highly heritable1 and a major determinant of human health and well-being2. Recent genome-wide meta-analyses have identified 24 genomic loci linked to variation in intelligence3-7, but much about its genetic underpinnings remains to be discovered. Here, we present a large-scale genetic association study of intelligence (n = 269,867), identifying 205 associated genomic loci (190 new) and 1,016 genes (939 new) via positional mapping, expression quantitative trait locus (eQTL) mapping, chromatin interaction mapping, and gene-based association analysis. We find enrichment of genetic effects in conserved and coding regions and associations with 146 nonsynonymous exonic variants. Associated genes are strongly expressed in the brain, specifically in striatal medium spiny neurons and hippocampal pyramidal neurons. Gene set analyses implicate pathways related to nervous system development and synaptic structure. We confirm previous strong genetic correlations with multiple health-related outcomes, and Mendelian randomization analysis results suggest protective effects of intelligence for Alzheimer's disease and ADHD and bidirectional causation with pleiotropic effects for schizophrenia. These results are a major step forward in understanding the neurobiology of cognitive function as well as genetically related neurological and psychiatric disorders.

Published
2018

5. Sagittal plane walking patterns are related to MRI changes over 18‐months in people with and without mild‐moderate hip osteoarthritis

Author

Kumar, Deepak, Wyatt, Cory, Lee, Sonia, Okazaki, Narihiro, Chiba, Ko, Link, Thomas M, Souza, Richard B, and Majumdar, Sharmila

Subjects
Allied Health and Rehabilitation Science, Health Sciences, Aging, Clinical Research, Arthritis, Pain Research, 2.1 Biological and endogenous factors, Aetiology, Musculoskeletal, Adult, Aged, Biomechanical Phenomena, Disease Progression, Female, Gait, Humans, Logistic Models, Longitudinal Studies, Magnetic Resonance Imaging, Male, Middle Aged, Osteoarthritis, Hip, Prospective Studies, Walking, hip, osteoarthritis, gait, disease progression, MRI, Biomedical Engineering, Clinical Sciences, Human Movement and Sports Sciences, Orthopedics, Biomedical engineering, Sports science and exercise
Abstract

The purpose was to evaluate the association of sagittal plane gait mechanics with MRI changes in the hip joint over 18-months. Subjects with and without radiographic hip OA (n = 57) underwent MRI at baseline and 18 months for grading of cartilage lesions, bone marrow lesions (BML), cysts, and labral tears. 3D gait analyses at baseline were used for sagittal plane hip kinematics and kinetics during the stance phase. Subjects were classified as progressors or non-progressors based on increase in any MRI OA parameter. Multivariate ANOVA were used for differences in sagittal gait parameters between progressors and non-progressors at baseline while adjusting for age. Logistic regression was used to estimate the probability of being classified as a progressor or non-progressor with increasing hip flexion while adjusting for age, BMI, sex, and presence of radiographic hip OA. Of the 57, 35 were classified as non-progressors and 22 were classified as progressors. At baseline, the progressors walked with 4.5° greater hip flexion during early stance (p = 0.021) and 3.5° lesser hip extension in late stance that was nearly significant (p = 0.059). Walking with greater hip flexion at baseline was associated with a greater risk of increase in MRI defined structural changes in the hip joint (Odds Ratio = 1.1, p = 0.038). Greater hip flexion during walking was associated with a risk of structural progression of hip OA. The results may guide future interventions to alter the walking patterns and slow structural hip OA progression.© 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:1472-1477, 2018.

Published
2018

6. Large-Scale Cognitive GWAS Meta-Analysis Reveals Tissue-Specific Neural Expression and Potential Nootropic Drug Targets

Author

Lam, Max, Trampush, Joey W, Yu, Jin, Knowles, Emma, Davies, Gail, Liewald, David C, Starr, John M, Djurovic, Srdjan, Melle, Ingrid, Sundet, Kjetil, Christoforou, Andrea, Reinvang, Ivar, DeRosse, Pamela, Lundervold, Astri J, Steen, Vidar M, Espeseth, Thomas, Räikkönen, Katri, Widen, Elisabeth, Palotie, Aarno, Eriksson, Johan G, Giegling, Ina, Konte, Bettina, Roussos, Panos, Giakoumaki, Stella, Burdick, Katherine E, Payton, Antony, Ollier, William, Chiba-Falek, Ornit, Attix, Deborah K, Need, Anna C, Cirulli, Elizabeth T, Voineskos, Aristotle N, Stefanis, Nikos C, Avramopoulos, Dimitrios, Hatzimanolis, Alex, Arking, Dan E, Smyrnis, Nikolaos, Bilder, Robert M, Freimer, Nelson A, Cannon, Tyrone D, London, Edythe, Poldrack, Russell A, Sabb, Fred W, Congdon, Eliza, Conley, Emily Drabant, Scult, Matthew A, Dickinson, Dwight, Straub, Richard E, Donohoe, Gary, Morris, Derek, Corvin, Aiden, Gill, Michael, Hariri, Ahmad R, Weinberger, Daniel R, Pendleton, Neil, Bitsios, Panos, Rujescu, Dan, Lahti, Jari, Le Hellard, Stephanie, Keller, Matthew C, Andreassen, Ole A, Deary, Ian J, Glahn, David C, Malhotra, Anil K, and Lencz, Todd

Subjects
Biological Sciences, Genetics, Mental Health, Aging, Brain Disorders, Biotechnology, Autoimmune Disease, Neurosciences, Human Genome, 2.1 Biological and endogenous factors, Aetiology, Underpinning research, 1.1 Normal biological development and functioning, Mental health, Neurological, Cefotaxime, Cognition, Female, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Nootropic Agents, Polymorphism, Single Nucleotide, Synapses, GWAS, calcium channel, cerebellum, gene expression, general cognitive ability, neurodevelopment, nootropics, potassium channel, synapse, Biochemistry and Cell Biology, Medical Physiology, Biological sciences
Abstract

Here, we present a large (n = 107,207) genome-wide association study (GWAS) of general cognitive ability ("g"), further enhanced by combining results with a large-scale GWAS of educational attainment. We identified 70 independent genomic loci associated with general cognitive ability. Results showed significant enrichment for genes causing Mendelian disorders with an intellectual disability phenotype. Competitive pathway analysis implicated the biological processes of neurogenesis and synaptic regulation, as well as the gene targets of two pharmacologic agents: cinnarizine, a T-type calcium channel blocker, and LY97241, a potassium channel inhibitor. Transcriptome-wide and epigenome-wide analysis revealed that the implicated loci were enriched for genes expressed across all brain regions (most strongly in the cerebellum). Enrichment was exclusive to genes expressed in neurons but not oligodendrocytes or astrocytes. Finally, we report genetic correlations between cognitive ability and disparate phenotypes including psychiatric disorders, several autoimmune disorders, longevity, and maternal age at first birth.

Published
2017

7. Cholinergic shaping of neural correlations

Author

Minces, Victor, Pinto, Lucas, Dan, Yang, and Chiba, Andrea A

Subjects
Dementia, Neurosciences, Behavioral and Social Science, Mental Health, Acquired Cognitive Impairment, Basic Behavioral and Social Science, Brain Disorders, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), 1.1 Normal biological development and functioning, Underpinning research, Neurological, Acetylcholine, Action Potentials, Animals, Cholinergic Agonists, Cholinergic Neurons, Female, Male, Mice, Photic Stimulation, Visual Cortex, acetylcholine, neural coding, neural correlations, neuromodulation, sensory processing
Abstract

A primary function of the brain is to form representations of the sensory world. Its capacity to do so depends on the relationship between signal correlations, associated with neuronal receptive fields, and noise correlations, associated with neuronal response variability. It was recently shown that the behavioral relevance of sensory stimuli can modify the relationship between signal and noise correlations, presumably increasing the encoding capacity of the brain. In this work, we use data from the visual cortex of the awake mouse watching naturalistic stimuli and show that a similar modification is observed under heightened cholinergic modulation. Increasing cholinergic levels in the cortex through optogenetic stimulation of basal forebrain cholinergic neurons decreases the dependency that is commonly observed between signal and noise correlations. Simulations of correlated neural networks with realistic firing statistics indicate that this change in the correlation structure increases the encoding capacity of the network.

Published
2017

8. GWAS meta-analysis reveals novel loci and genetic correlates for general cognitive function: a report from the COGENT consortium

Author

Trampush, JW, Yang, MLZ, Yu, J, Knowles, E, Davies, G, Liewald, DC, Starr, JM, Djurovic, S, Melle, I, Sundet, K, Christoforou, A, Reinvang, I, DeRosse, P, Lundervold, AJ, Steen, VM, Espeseth, T, Räikkönen, K, Widen, E, Palotie, A, Eriksson, JG, Giegling, I, Konte, B, Roussos, P, Giakoumaki, S, Burdick, KE, Payton, A, Ollier, W, Horan, M, Chiba-Falek, O, Attix, DK, Need, AC, Cirulli, ET, Voineskos, AN, Stefanis, NC, Avramopoulos, D, Hatzimanolis, A, Arking, DE, Smyrnis, N, Bilder, RM, Freimer, NA, Cannon, TD, London, E, Poldrack, RA, Sabb, FW, Congdon, E, Conley, ED, Scult, MA, Dickinson, D, Straub, RE, Donohoe, G, Morris, D, Corvin, A, Gill, M, Hariri, AR, Weinberger, DR, Pendleton, N, Bitsios, P, Rujescu, D, Lahti, J, Le Hellard, S, Keller, MC, Andreassen, OA, Deary, IJ, Glahn, DC, Malhotra, AK, and Lencz, T

Subjects
Biomedical and Clinical Sciences, Biological Psychology, Clinical and Health Psychology, Clinical Sciences, Psychology, Basic Behavioral and Social Science, Genetics, Behavioral and Social Science, Mental Health, Biotechnology, Prevention, Human Genome, Clinical Research, Aetiology, 2.1 Biological and endogenous factors, Mental health, Adult, Alleles, Cognition, Female, Gene Frequency, Genetic Association Studies, Genetic Loci, Genetic Predisposition to Disease, Genetic Variation, Genome-Wide Association Study, Humans, Male, Middle Aged, Multifactorial Inheritance, Neurocognitive Disorders, Polymorphism, Single Nucleotide, White People, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry, Clinical sciences, Biological psychology, Clinical and health psychology
Abstract

The complex nature of human cognition has resulted in cognitive genomics lagging behind many other fields in terms of gene discovery using genome-wide association study (GWAS) methods. In an attempt to overcome these barriers, the current study utilized GWAS meta-analysis to examine the association of common genetic variation (~8M single-nucleotide polymorphisms (SNP) with minor allele frequency ⩾1%) to general cognitive function in a sample of 35 298 healthy individuals of European ancestry across 24 cohorts in the Cognitive Genomics Consortium (COGENT). In addition, we utilized individual SNP lookups and polygenic score analyses to identify genetic overlap with other relevant neurobehavioral phenotypes. Our primary GWAS meta-analysis identified two novel SNP loci (top SNPs: rs76114856 in the CENPO gene on chromosome 2 and rs6669072 near LOC105378853 on chromosome 1) associated with cognitive performance at the genome-wide significance level (P

Published
2017

9. CD8+ T Cells Contribute to the Development of Coronary Arteritis in the Lactobacillus casei Cell Wall Extract–Induced Murine Model of Kawasaki Disease

Author

Rivas, Magali Noval, Lee, Youngho, Wakita, Daiko, Chiba, Norika, Dagvadorj, Jargalsaikhan, Shimada, Kenichi, Chen, Shuang, Fishbein, Michael C, Lehman, Thomas JA, Crother, Timothy R, and Arditi, Moshe

Subjects
Biomedical and Clinical Sciences, Immunology, Autoimmune Disease, Heart Disease - Coronary Heart Disease, Heart Disease, Cardiovascular, HIV/AIDS, 2.1 Biological and endogenous factors, Aetiology, Animals, Arteritis, CD8-Positive T-Lymphocytes, Cell Extracts, Cell Wall, Coronary Artery Disease, Disease Models, Animal, Lacticaseibacillus casei, Male, Mice, Inbred C57BL, Mucocutaneous Lymph Node Syndrome, Clinical Sciences, Public Health and Health Services, Arthritis & Rheumatology, Clinical sciences
Abstract

ObjectiveKawasaki disease (KD) is the leading cause of acquired heart disease among children in developed countries. Coronary lesions in KD in humans are characterized by an increased presence of infiltrating CD3+ T cells; however, the specific contributions of the different T cell subpopulations in coronary arteritis development remain unknown. Therefore, we sought to investigate the function of CD4+ and CD8+ T cells, Treg cells, and natural killer (NK) T cells in the pathogenesis of KD.MethodsWe addressed the function of T cell subsets in KD development by using a well-established murine model of Lactobacillus casei cell wall extract (LCWE)-induced KD vasculitis. We determined which T cell subsets were required for development of KD vasculitis by using several knockout murine strains and depleting monoclonal antibodies.ResultsLCWE-injected mice developed coronary lesions characterized by the presence of inflammatory cell infiltrates. Frequently, this chronic inflammation resulted in complete occlusion of the coronary arteries due to luminal myofibroblast proliferation (LMP) as well as the development of coronary arteritis and aortitis. We found that CD8+ T cells, but not CD4+ T cells, NK T cells, or Treg cells, were required for development of KD vasculitis.ConclusionThe LCWE-induced murine model of KD vasculitis mimics many histologic features of the disease in humans, such as the presence of CD8+ T cells and LMP in coronary artery lesions as well as epicardial coronary arteritis. Moreover, CD8+ T cells functionally contribute to the development of KD vasculitis in this murine model. Therapeutic strategies targeting infiltrating CD8+ T cells might be useful in the management of KD in humans.

Published
2017

10. BRCC3 mutations in myeloid neoplasms

Author

Huang, Dayong, Nagata, Yasunobu, Grossmann, Vera, Radivoyevitch, Tomas, Okuno, Yusuke, Nagae, Genta, Hosono, Naoko, Schnittger, Susanne, Sanada, Masashi, Przychodzen, Bartlomiej, Kon, Ayana, Polprasert, Chantana, Shen, Wenyi, Clemente, Michael J, Phillips, James G, Alpermann, Tamara, Yoshida, Kenichi, Nadarajah, Niroshan, Sekeres, Mikkael A, Oakley, Kevin, Nguyen, Nhu, Shiraishi, Yuichi, Shiozawa, Yusuke, Chiba, Kenichi, Tanaka, Hiroko, Koeffler, H Phillip, Klein, Hans-Ulrich, Dugas, Martin, Aburatani, Hiroyuki, Miyano, Satoru, Haferlach, Claudia, Kern, Wolfgang, Haferlach, Torsten, Du, Yang, Ogawa, Seishi, and Makishima, Hideki

Subjects
Human Genome, Rare Diseases, Cancer, Genetics, Hematology, Stem Cell Research, Stem Cell Research - Nonembryonic - Non-Human, Aged, Aged, 80 and over, Alleles, Animals, BRCA1 Protein, Chromosome Aberrations, DNA Mutational Analysis, Deubiquitinating Enzymes, Female, Gene Frequency, Gene Knockdown Techniques, Genetic Association Studies, Genotype, Humans, Male, Membrane Proteins, Mice, Middle Aged, Mutation, Myeloproliferative Disorders, Phenotype, RNA, Small Interfering, Immunology
Abstract

Next generation sequencing technologies have provided insights into the molecular heterogeneity of various myeloid neoplasms, revealing previously unknown somatic genetic events. In our cohort of 1444 cases analyzed by next generation sequencing, somatic mutations in the gene BRCA1-BRCA2-containing complex 3 (BRCC3) were identified in 28 cases (1.9%). BRCC3 is a member of the JAMM/MPN+ family of zinc metalloproteases capable of cleaving Lys-63 linked polyubiquitin chains, and is implicated in DNA repair. The mutations were located throughout its coding region. The average variant allelic frequency of BRCC3 mutations was 30.1%, and by a serial sample analysis at two different time points a BRCC3 mutation was already identified in the initial stage of a myelodysplastic syndrome. BRCC3 mutations commonly occurred in nonsense (n=12), frameshift (n=4), and splice site (n=5) configurations. Due to the marginal male dominance (odds ratio; 2.00, 0.84-4.73) of BRCC3 mutations, the majority of mutations (n=23; 82%) were hemizygous. Phenotypically, BRCC3 mutations were frequently observed in myelodysplastic syndromes and myelodysplastic/myeloproliferative neoplasms and associated with -Y abnormality (odds ratio; 3.70, 1.25-11.0). Clinically, BRCC3 mutations were also related to higher age (P=0.01), although prognosis was not affected. Knockdown of Brcc3 gene expression in murine bone marrow lineage negative, Sca1 positive, c-kit positive cells resulted in 2-fold more colony formation and modest differentiation defect. Thus, BRCC3 likely plays a role as tumor-associated gene in myelodysplastic syndromes and myelodysplastic/myeloproliferative neoplasms.

Published
2015

11. Anatomic correlates of reduced hip extension during walking in mild-moderate radiographic hip osteoarthritis

Author

Kumar, D, Wyatt, CR, Chiba, K, Lee, S, Link, TM, Majumdar, S, and Souza, RB

Subjects
Biomedical and Clinical Sciences, Health Sciences, Clinical Sciences, Sports Science and Exercise, Allied Health and Rehabilitation Science, Engineering, Biomedical Engineering, Biomedical Imaging, Pain Research, Chronic Pain, Aging, Arthritis, Osteoarthritis, Clinical Research, Aetiology, 2.1 Biological and endogenous factors, Musculoskeletal, Adult, Analysis of Variance, Biomechanical Phenomena, Cohort Studies, Female, Gait, Hip Joint, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Male, Middle Aged, Osteoarthritis, Hip, Radiography, Range of Motion, Articular, Walking, minute walk test, HOOS, Labrum, cartilage, gait, Human Movement and Sports Sciences, Orthopedics, Biomedical engineering, Sports science and exercise
Abstract

To identify radiographic and MR features of hip osteoarthritis (OA) related to reduced hip extension during walking. Sixty six subjects, were stratified into those with (n = 36, KL = 2, 3) and without (n = 30, KL = 0, 1) radiographic hip OA. Cartilage and labrum lesions were graded semi-quantitatively on hip MRI. Alpha angle and lateral center edge (LCE) angle were measured. Sagittal kinematics and kinetics were calculated during walking at speed of 1.35 m/s using 3-D motion capture. All subjects completed Hip disability and Osteoarthritis Outcome Score (HOOS), timed up and go, and 6 min walk tests. Variables were compared between the two groups using one-way ANOVA (adjusting for age). Correlations of radiographic and MR parameters with peak hip extension were calculated. The OA group was older, had greater pain, and limitation of function. They also had lower peak hip extension and higher peak hip flexion; and worse acetabular and femoral cartilage lesions. Peak hip extension and flexion correlated with KL grade, cartilage lesions in the inferior and posterior femur. Reduced hip extension and greater hip flexion during walking are present in high functioning (HOOS > 85%) individuals with mild-moderate hip OA, and are associated with cartilage lesions.

Published
2014

12. Landscape of genetic lesions in 944 patients with myelodysplastic syndromes

Author

Haferlach, T, Nagata, Y, Grossmann, V, Okuno, Y, Bacher, U, Nagae, G, Schnittger, S, Sanada, M, Kon, A, Alpermann, T, Yoshida, K, Roller, A, Nadarajah, N, Shiraishi, Y, Shiozawa, Y, Chiba, K, Tanaka, H, Koeffler, HP, Klein, H-U, Dugas, M, Aburatani, H, Kohlmann, A, Miyano, S, Haferlach, C, Kern, W, and Ogawa, S

Subjects
Genetic Testing, Clinical Research, Rare Diseases, Human Genome, Genetics, Biotechnology, Cancer, Hematology, Adult, Aged, Aged, 80 and over, Female, Gene Frequency, Genetic Association Studies, Genetic Markers, High-Throughput Nucleotide Sequencing, Humans, Male, Middle Aged, Mutation, Mutation Rate, Myelodysplastic Syndromes, Polymorphism, Single Nucleotide, Prognosis, Proportional Hazards Models, Young Adult, next-generation sequencing, molecular markers, myelodysplastic syndromes, prognostic score, Clinical Sciences, Oncology and Carcinogenesis, Immunology
Abstract

High-throughput DNA sequencing significantly contributed to diagnosis and prognostication in patients with myelodysplastic syndromes (MDS). We determined the biological and prognostic significance of genetic aberrations in MDS. In total, 944 patients with various MDS subtypes were screened for known/putative mutations/deletions in 104 genes using targeted deep sequencing and array-based genomic hybridization. In total, 845/944 patients (89.5%) harbored at least one mutation (median, 3 per patient; range, 0-12). Forty-seven genes were significantly mutated with TET2, SF3B1, ASXL1, SRSF2, DNMT3A, and RUNX1 mutated in >10% of cases. Many mutations were associated with higher risk groups and/or blast elevation. Survival was investigated in 875 patients. By univariate analysis, 25/48 genes (resulting from 47 genes tested significantly plus PRPF8) affected survival (P

Published
2014

13. Acetylation-Mediated Proteasomal Degradation of Core Histones during DNA Repair and Spermatogenesis

Author

Qian, Min-Xian, Pang, Ye, Liu, Cui Hua, Haratake, Kousuke, Du, Bo-Yu, Ji, Dan-Yang, Wang, Guang-Fei, Zhu, Qian-Qian, Song, Wei, Yu, Yadong, Zhang, Xiao-Xu, Huang, Hai-Tao, Miao, Shiying, Chen, Lian-Bin, Zhang, Zi-Hui, Liang, Ya-Nan, Liu, Shan, Cha, Hwangho, Yang, Dong, Zhai, Yonggong, Komatsu, Takuo, Tsuruta, Fuminori, Li, Haitao, Cao, Cheng, Li, Wei, Li, Guo-Hong, Cheng, Yifan, Chiba, Tomoki, Wang, Linfang, Goldberg, Alfred L, Shen, Yan, and Qiu, Xiao-Bo

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Contraception/Reproduction, Neurodegenerative, Genetics, 1.1 Normal biological development and functioning, Underpinning research, Generic health relevance, Acetylation, Amino Acid Sequence, Animals, DNA Breaks, Double-Stranded, DNA Repair, Histones, Humans, Male, Mice, Molecular Sequence Data, Nuclear Proteins, Proteasome Endopeptidase Complex, Protein Structure, Tertiary, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Sequence Alignment, Spermatogenesis, Testis, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Histone acetylation plays critical roles in chromatin remodeling, DNA repair, and epigenetic regulation of gene expression, but the underlying mechanisms are unclear. Proteasomes usually catalyze ATP- and polyubiquitin-dependent proteolysis. Here, we show that the proteasomes containing the activator PA200 catalyze the polyubiquitin-independent degradation of histones. Most proteasomes in mammalian testes ("spermatoproteasomes") contain a spermatid/sperm-specific α subunit α4 s/PSMA8 and/or the catalytic β subunits of immunoproteasomes in addition to PA200. Deletion of PA200 in mice abolishes acetylation-dependent degradation of somatic core histones during DNA double-strand breaks and delays core histone disappearance in elongated spermatids. Purified PA200 greatly promotes ATP-independent proteasomal degradation of the acetylated core histones, but not polyubiquitinated proteins. Furthermore, acetylation on histones is required for their binding to the bromodomain-like regions in PA200 and its yeast ortholog, Blm10. Thus, PA200/Blm10 specifically targets the core histones for acetylation-mediated degradation by proteasomes, providing mechanisms by which acetylation regulates histone degradation, DNA repair, and spermatogenesis.

Published
2013

14. Bing-Neel Syndrome Successfully Treated with Tirabrutinib

Author

Takashi, Oyama, Kazuki, Taoka, Akira, Chiba, Kensuke, Matsuda, Hiroaki, Maki, Yosuke, Masamoto, and Mineo, Kurokawa

Subjects
Male, Brain Diseases, Pyrimidines, Internal Medicine, Humans, Neurodegenerative Diseases, Syndrome, General Medicine, Middle Aged, Waldenstrom Macroglobulinemia
Abstract

Bing-Neel syndrome (BNS) is a rare central nervous system manifestation of lymphoplasmacytic lymphoma/Waldenström macroglobulinemia (LPL/WM). We herein report a 62-year-old man with LPL/WM after multiple chemotherapies. He had weakness of lower extremities and elevated serum IgM levels. A bone marrow examination showed lymphoplasmacytic cells infiltration. Contrast-enhanced magnetic resonance imaging suggested enhancing lesions in the cauda equina roots. He was diagnosed with BNS and started on treatment with tirabrutinib 480 mg daily. Within three months, he showed clinical and radiologic improvement. Tirabrutinib may have utility as an effective treatment for BNS.

Published
2022

15. Improved diagnostic accuracy for pediatric obstructive sleep apnea using an out-of-center sleep test

Author

Nao Isaka, Shintaro Chiba, Masaaki Suzuki, Konomi Ikeda, Masahiro Miura, Tomoko Yagi, and Hiromi Kojima

Subjects
Male, Sleep Apnea, Obstructive, Otorhinolaryngology, Child, Preschool, Polysomnography, Humans, Reproducibility of Results, Female, Surgery, General Medicine, Child, Sleep, Retrospective Studies
Abstract

Polysomnography (PSG) is considered the gold standard for diagnosing obstructive sleep apnea syndrome (OSA) in children. However, many hospitals do not carry out PSG evaluations, and use out-of-center sleep test (OCST) devices for diagnosis instead. The aim of this study was to confirm the reliability of OCSTs for the diagnosis of pediatric OSA. We also investigated the factors influencing diagnostic reliability of OCST for the severe OSA patients who should be treated earlier.This was a retrospective study using the Ota Memorial Sleep Center database. We analyzed the data of children who underwent Type 4 OCST at home and Type 1 PSG in the sleep lab between April 2006 to April 2015. Cephalometric parameters and anthropometric findings such as enlarged tonsils were also evaluated. We compared the 3% oxygen desaturation index (ODI3%) measured by OCST with the apnea-hypopnea index (AHI) measured by PSG. We used Receiver Operator Curve (ROC) to calculate the optimal OCST- ODI3% value to diagnose PSG-AHI ≥10 per hour. In order to determine which factors increase the accuracy of OCST, we calculated the accuracy, sensitivity and specificity in regard to the predicted values using multiple logistic regression analysis. The Ethics Committee of Ota General Hospital approved the study (approval no. 21018).A total of 191 children were enrolled in this study. The study included 127 boys and 64 girls, with a mean age of 5.4 years (range: 3-8 years), BMI of 15.7 kg/m² (range: 11.5-35.7 kg/m²), PSG-AHI of 17.4 per hour (range: 0.3-89.8 per hour). The sensitivity, specificity and accuracy with an OCST-ODI cutoff of 6.3 per hour were 64.4%, 70.3% and 67.5%, respectively, to detect PSG-AHI ≥ 10 per hour for children with suspected OSA. Multivariable stepwise regression revealed that increases of sensitivity, specificity and accuracy with an OCST-ODI cutoff of 6.3 per hour were independently predicted by facial axis, which is cephalometric angle of 81° or less, and tonsil hypertrophy, which is Brodsky +3 or +4, showing increases to 73.3%, 71.3%, and 72.3%, respectively, whereas age, gender, body mass index, adenoid size and other cephalometric parameters were not significant predictors.The results of the statistical analyses suggest that it would be useful to add the assessment of tonsil size and facial axis as well as OCST to determine whether the threshold of PSG-AHI ≥ 10 per hour has been crossed.

Published
2022

16. Expansion of the Parkinson disease-associated SNCA- Rep1 allele upregulates human α-synuclein in transgenic mouse brain

Author

Cronin, Kenneth D, Ge, Dongliang, Manninger, Paul, Linnertz, Colton, Rossoshek, Anna, Orrison, Bonnie M, Bernard, David J, El-Agnaf, Omar MA, Schlossmacher, Michael G, Nussbaum, Robert L, and Chiba-Falek, Ornit

Subjects
Biological Sciences, Genetics, Acquired Cognitive Impairment, Neurodegenerative, Parkinson's Disease, Neurosciences, Aging, Dementia, Prevention, Brain Disorders, 2.1 Biological and endogenous factors, Aetiology, Neurological, Alleles, Animals, Brain, Female, Humans, Male, Mice, Mice, Transgenic, Microsatellite Repeats, Parkinson Disease, Polymorphism, Genetic, Up-Regulation, alpha-Synuclein, Medical and Health Sciences, Genetics & Heredity
Abstract

Alpha-synuclein (SNCA) gene has been implicated in the development of rare forms of familial Parkinson disease (PD). Recently, it was shown that an increase in SNCA copy numbers leads to elevated levels of wild-type SNCA-mRNA and protein and is sufficient to cause early-onset, familial PD. A critical question concerning the molecular pathogenesis of PD is what contributory role, if any, is played by the SNCA gene in sporadic PD. The expansion of SNCA-Rep1, an upstream, polymorphic microsatellite of the SNCA gene, is associated with elevated risk for sporadic PD. However, whether SNCA-Rep1 is the causal variant and the underlying mechanism with which its effect is mediated by remained elusive. We report here the effects of three distinct SNCA-Rep1 variants in the brains of 72 mice transgenic for the entire human SNCA locus. Human SNCA-mRNA and protein levels were increased 1.7- and 1.25-fold, respectively, in homozygotes for the expanded, PD risk-conferring allele compared with homozygotes for the shorter, protective allele. When adjusting for the total SNCA-protein concentration (endogenous mouse and transgenic human) expressed in each brain, the expanded risk allele contributed 2.6-fold more to the SNCA steady-state than the shorter allele. Furthermore, targeted deletion of Rep1 resulted in the lowest human SNCA-mRNA and protein concentrations in murine brain. In contrast, the Rep1 effect was not observed in blood lysates from the same mice. These results demonstrate that Rep1 regulates human SNCA expression by enhancing its transcription in the adult nervous system and suggest that homozygosity for the expanded Rep1 allele may mimic locus multiplication, thereby elevating PD risk.

Published
2009

17. Expansion of the Parkinson disease-associated SNCA-Rep1 allele upregulates human alpha-synuclein in transgenic mouse brain.

Author

Cronin, Kenneth D, Ge, Dongliang, Manninger, Paul, Linnertz, Colton, Rossoshek, Anna, Orrison, Bonnie M, Bernard, David J, El-Agnaf, Omar MA, Schlossmacher, Michael G, Nussbaum, Robert L, and Chiba-Falek, Ornit

Subjects
Brain, Animals, Mice, Transgenic, Humans, Mice, Parkinson Disease, Up-Regulation, Microsatellite Repeats, Polymorphism, Genetic, Alleles, Female, Male, alpha-Synuclein, Transgenic, Polymorphism, Genetic, Biological Sciences, Medical and Health Sciences, Genetics & Heredity
Abstract

Alpha-synuclein (SNCA) gene has been implicated in the development of rare forms of familial Parkinson disease (PD). Recently, it was shown that an increase in SNCA copy numbers leads to elevated levels of wild-type SNCA-mRNA and protein and is sufficient to cause early-onset, familial PD. A critical question concerning the molecular pathogenesis of PD is what contributory role, if any, is played by the SNCA gene in sporadic PD. The expansion of SNCA-Rep1, an upstream, polymorphic microsatellite of the SNCA gene, is associated with elevated risk for sporadic PD. However, whether SNCA-Rep1 is the causal variant and the underlying mechanism with which its effect is mediated by remained elusive. We report here the effects of three distinct SNCA-Rep1 variants in the brains of 72 mice transgenic for the entire human SNCA locus. Human SNCA-mRNA and protein levels were increased 1.7- and 1.25-fold, respectively, in homozygotes for the expanded, PD risk-conferring allele compared with homozygotes for the shorter, protective allele. When adjusting for the total SNCA-protein concentration (endogenous mouse and transgenic human) expressed in each brain, the expanded risk allele contributed 2.6-fold more to the SNCA steady-state than the shorter allele. Furthermore, targeted deletion of Rep1 resulted in the lowest human SNCA-mRNA and protein concentrations in murine brain. In contrast, the Rep1 effect was not observed in blood lysates from the same mice. These results demonstrate that Rep1 regulates human SNCA expression by enhancing its transcription in the adult nervous system and suggest that homozygosity for the expanded Rep1 allele may mimic locus multiplication, thereby elevating PD risk.

Published
2009

18. Association of dual sensory impairment with changes in life space: A longitudinal study with two-year follow-up

Author

Kouki Tomida, Sangyoon Lee, Seongryu Bae, Keitaro Makino, Ippei Chiba, Kenji Harada, Osamu Katayama, Masanori Morikawa, and Hiroyuki Shimada

Subjects
Male, Activities of Daily Living, Vision Disorders, Humans, Obstetrics and Gynecology, Female, Longitudinal Studies, Hearing Loss, General Biochemistry, Genetics and Molecular Biology, Aged, Follow-Up Studies
Abstract

Dual sensory impairment (DSI) of hearing and vision in older adults may limit lifestyle activities of daily living and contribute to a reduced life space. This study aimed to investigate how DSI is associated with specific lifestyle activities and predicts changes in mobility in life space.Participants comprised 4214 older adults (52.3 % female, mean age 75.8 years) who met the study's inclusion criteria. The participants were divided into three groups according to the number of sensory impairments: (1) no sensory impairment (NSI), (2) single sensory impairment (SSI), and (3) DSI.We investigated the association between DSI and specific lifestyle activities at baseline. The Active Mobility Index (AMI) was used to assess life-space. Two years later, the association between DSI and life-space mobility was verified using multinomial logistic regression analysis.DSI was more likely to have limited people's instrumental activities of daily living and cognitive, social, and productive activities at baseline (P 0.05). In the adjusted model with potential covariates, people with DSI had a lower life-space score at 2 years than people with NSI (odds ratio [OR] = 1.40, 95 % confidence interval [CI]: 1.01-1.95), but the difference was not significant for SSI (OR = 0.98, 95 % CI: 0.78-1.24).This study suggested that DSI was a factor that limited various activities and narrowed the life-space mobility of older adults. Prevention of DSI may be important for community-dwelling older adults to maintain a more active lifestyle.

Published
2022

19. Partially hydrolyzed guar gum alleviates hepatic steatosis and alters specific gut microbiota in a murine liver injury model

Author

Takayuki Fujii, Haruyuki Nakayama-Imaohji, Aya Tanaka, Hiroto Katami, Kazuya Tanaka, Yoichi Chiba, Machi Kawauchi, Masaki Ueno, Tomomi Kuwahara, and Ryuichi Shimono

Subjects
Male, Mice, Inbred C57BL, Mice, Intestinal Diseases, Liver, Tumor Necrosis Factor-alpha, RNA, Ribosomal, 16S, Pediatrics, Perinatology and Child Health, Animals, Surgery, General Medicine, Gastrointestinal Microbiome
Abstract

The gut microbiota, via the gut-liver axis, plays an important role in the development of intestinal failure-associated liver disease. Here, we investigated whether partially hydrolyzed guar gum (PHGG), a dietary fiber could alleviate liver damage and modulate the gut microbiota in a murine liver injury (LI) model.Liver injury was induced in 6-week-old male C57BL/6 mice using an enteral liquid diet composed of parenteral nutrition (LI group) and treated with 5% PHGG (LI/PHGG group). Liver histopathology was examined using oil red O and a tumor necrosis factor-α (TNF-α) labeling. The gut microbiota was examined using 16S rRNA gene sequencing.Lipid accumulation was significantly decreased in the LI /PHGG group when compared with that of the LI group. The area of TNF-α-positive cells was significantly higher in the LI group when compared with that of the control. The principal coordinate analysis (PCoA) revealed pronounced changes in the gut microbiota after PHGG treatment. Linear discriminant analysis of effect size showed that PHGG treatment significantly increased cecal abundance of Parabacteroides.PHGG alleviated hepatic steatosis following liver injury in mice. The protective effect of PHGG treatment could be associated with increased abundance of Parabacteroides in the cecum.

Published
2022

20. Etrolizumab versus infliximab for the treatment of moderately to severely active ulcerative colitis (GARDENIA): a randomised, double-blind, double-dummy, phase 3 study

Author

Silvio Danese, Jean-Frederic Colombel, Milan Lukas, Javier P Gisbert, Geert D'Haens, Bu'hussain Hayee, Remo Panaccione, Hyun-Soo Kim, Walter Reinisch, Helen Tyrrell, Young S Oh, Swati Tole, Akiko Chai, Kirsten Chamberlain-James, Meina Tao Tang, Stefan Schreiber, Nazimuddin Aboo, Tariq Ahmad, Xavier Aldeguer Mante, Matthieu Allez, Sven Almer, Romain Altwegg, Montserrat Andreu Garcia, Ramesh Arasaradnam, Sandro Ardizzone, Alessandro Armuzzi, Ian Arnott, Guy Aumais, Irit Avni-Biron, Peter Barrow, Ian Beales, Fernando Bermejo San Jose, Abraham Bezuidenhout, Livia Biancone, Michael Blaeker, Stuart Bloom, Bernd Bokemeyer, Fabrizio Bossa, Peter Bossuyt, Guillaume Bouguen, Yoram Bouhnik, Gerd Bouma, Raymond Bourdages, Arnaud Bourreille, Christian Boustiere, Tomas Brabec, Stephan Brand, Carsten Buening, Anthony Buisson, Guillaume Cadiot, Xavier Calvet Calvo, Franck Carbonnel, Daniel Carpio, Jae Hee Cheon, Naoki Chiba, Camelia Chioncel, Nicoleta-Claudia Cimpoeru, Martin Clodi, Gino Roberto Corazza, Rocco Cosintino, Jose Cotter, Thomas Creed, Fraser Cummings, Gian Luigi de' Angelis, Marc De Maeyer, Milind Desai, Etienne Desilets, Pierre Desreumaux, Olivier Dewit, Johanna Dinter, Ecaterina Daniela Dobru, Tomas Douda, Dan Lucian Dumitrascu, Matthias Ebert, Ana Echarri Piudo, Magdy Elkhashab, Chang Soo Eun, Brian Feagan, Roland Fejes, Catarina Fidalgo, Sigal Fishman, Bernard Flourié, Sharyle Fowler, Walter Fries, Csaba Fulop, Mathurin Fumery, Gyula G Kiss, Sonja Gassner, Daniel Gaya, Bastianello Germanà, Liliana Simona Gheorghe, Cyrielle Gilletta de Saint Joseph, Paolo Gionchetti, Adrian-Eugen Goldis, Raquel Gonçalves, Jean-Charles Grimaud, Tibor Gyökeres, Herve Hagege, Andrei Haidar, Heinz Hartmann, Peter Hasselblatt, Buhussain Hayee, Xavier Hebuterne, Per Hellström, Pieter Hindryckx, Helena Hlavova, Frank Hoentjen, Stefanie Howaldt, Ludek Hrdlicka, Kyu Chan Huh, Maria Isabel Iborra Colomino, Florentina Ionita-Radu, Peter Irving, Jørgen Jahnsen, ByungIk Jang, Jeroen Jansen, Seong Woo Jeon, Rodrigo Jover Martinez, Pascal Juillerat, Per Karlén, Arthur Kaser, Radan Keil, Deepak Kejariwal, Dan Keret, Reena Khanna, Dongwoo Kim, Duk Hwan Kim, Hyo-Jong Kim, Joo Sung Kim, Kueongok Kim, Kyung-Jo Kim, Sung Kook Kim, Young-Ho Kim, Jochen Klaus, Anna Kohn, Vladimir Kojecky, Ja Seol Koo, Robert Kozak, Milan Kremer, Tunde Kristof, Frederik Kruger, David Laharie, Adi Lahat-zok, Evgeny Landa, Jonghun Lee, Kang-Moon Lee, Kook Lae Lee, YooJin Lee, Frank Lenze, Wee Chian Lim, Jimmy Limdi, James Lindsay, Pilar Lopez Serrano, Edouard Louis, Stefan Lueth, Giovanni Maconi, Fazia Mana, Steven Mann, John Mansfield, Santino Marchi, Marco Marino, John Marshall, Maria Dolores Martin Arranz, Radu-Bogdan Mateescu, John McLaughlin, Simon McLaughlin, Ehud Melzer, Jessica Mertens, Paul Mitrut, Tamas Molnar, Vinciane Muls, Pushpakaran Munuswamy, Charles Murray, Timna Naftali, Visvakuren Naidoo, Yusuf Nanabhay, Lucian Negreanu, Augustin Nguyen, Thomas Ochsenkuehn, Ambrogio Orlando, Julian Panes Diaz, Maya Paritsky, Dong Il Park, Jihye Park, Luca Pastorelli, Markus Peck-Radosavljevic, Farhad Peerani, Javier Perez Gisbert, Laurent Peyrin-Biroulet, Laurence Picon, Marieke Pierik, Terry Ponich, Francisco Portela, Maartens Jeroen Prins, Istvan Racz, Khan Fareed Rahman, Jean-Marie Reimund, Max Reinshagen, Xavier Roblin, Rodolfo Rocca, Francesca Rogai, Gerhard Rogler, Agnes Salamon, Ennaliza Salazar, Zoltan Sallo, Sunil Samuel, Miquel de los Santos Sans Cuffi, Edoardo Vincenzo Savarino, Vincenzo Savarino, Guillaume Savoye, Andrada Seicean, Christian Selinger, David Martins Serra, Hang Hock Shim, SungJae Shin, Britta Siegmund, Jesse Siffledeen, Wayne Simmonds, Jan Smid, Jose Sollano, Geun Am Song, Alexander Speight, Ioan Sporea, Dirk Staessen, George Stancu, Alan Steel, David Stepek, Victor Stoica, Andreas Sturm, Gyorgy Szekely, Teck Kiang Tan, Carlos Taxonera Samso, John Thomson, Michal Tichy, Gabor Tamas Toth, Zsolt Tulassay, Marcello Vangeli, Marta Varga, Ana Vieira, Stephanie Viennot, Erica Villa, Petr Vitek, Harald Vogelsang, Petr Vyhnalek, Peter Wahab, Jens Walldorf, Byong Duk Ye, Christopher Ziady, Danese S., Colombel J.-F., Lukas M., Gisbert J.P., D'Haens G., Hayee B., Panaccione R., Kim H.-S., Reinisch W., Tyrrell H., Oh Y.S., Tole S., Chai A., Chamberlain-James K., Tang M.T., Schreiber S., Aboo N., Ahmad T., Aldeguer Mante X., Allez M., Almer S., Altwegg R., Andreu Garcia M., Arasaradnam R., Ardizzone S., Armuzzi A., Arnott I., Aumais G., Avni-Biron I., Barrow P., Beales I., Bermejo San Jose F., Bezuidenhout A., Biancone L., Blaeker M., Bloom S., Bokemeyer B., Bossa F., Bossuyt P., Bouguen G., Bouhnik Y., Bouma G., Bourdages R., Bourreille A., Boustiere C., Brabec T., Brand S., Buening C., Buisson A., Cadiot G., Calvet Calvo X., Carbonnel F., Carpio D., Cheon J.H., Chiba N., Chioncel C., Cimpoeru N.-C., Clodi M., Corazza G.R., Cosintino R., Cotter J., Creed T., Cummings F., de' Angelis G.L., De Maeyer M., Desai M., Desilets E., Desreumaux P., Dewit O., Dinter J., Dobru E.D., Douda T., Dumitrascu D.L., Ebert M., Echarri Piudo A., Elkhashab M., Eun C.S., Feagan B., Fejes R., Fidalgo C., Fishman S., Flourie B., Fowler S., Fries W., Fulop C., Fumery M., G Kiss G., Gassner S., Gaya D., Germana B., Gheorghe L.S., Gilletta de Saint Joseph C., Gionchetti P., Goldis A.-E., Goncalves R., Grimaud J.-C., Gyokeres T., Hagege H., Haidar A., Hartmann H., Hasselblatt P., Hebuterne X., Hellstrom P., Hindryckx P., Hlavova H., Hoentjen F., Howaldt S., Hrdlicka L., Huh K.C., Iborra Colomino M.I., Ionita-Radu F., Irving P., Jahnsen J., Jang B., Jansen J., Jeon S.W., Jover Martinez R., Juillerat P., Karlen P., Kaser A., Keil R., Kejariwal D., Keret D., Khanna R., Kim D., Kim D.H., Kim H.-J., Kim J.S., Kim K., Kim K.-J., Kim S.K., Kim Y.-H., Klaus J., Kohn A., Kojecky V., Koo J.S., Kozak R., Kremer M., Kristof T., Kruger F., Laharie D., Lahat-zok A., Landa E., Lee J., Lee K.-M., Lee K.L., Lee Y., Lenze F., Lim W.C., Limdi J., Lindsay J., Lopez Serrano P., Louis E., Lueth S., Maconi G., Mana F., Mann S., Mansfield J., Marchi S., Marino M., Marshall J., Martin Arranz M.D., Mateescu R.-B., McLaughlin J., McLaughlin S., Melzer E., Mertens J., Mitrut P., Molnar T., Muls V., Munuswamy P., Murray C., Naftali T., Naidoo V., Nanabhay Y., Negreanu L., Nguyen A., Ochsenkuehn T., Orlando A., Panes Diaz J., Paritsky M., Park D.I., Park J., Pastorelli L., Peck-Radosavljevic M., Peerani F., Perez Gisbert J., Peyrin-Biroulet L., Picon L., Pierik M., Ponich T., Portela F., Prins M.J., Racz I., Rahman K.F., Reimund J.-M., Reinshagen M., Roblin X., Rocca R., Rogai F., Rogler G., Salamon A., Salazar E., Sallo Z., Samuel S., Sans Cuffi M.D.L.S., Savarino E.V., Savarino V., Savoye G., Seicean A., Selinger C., Serra D.M., Shim H.H., Shin S., Siegmund B., Siffledeen J., Simmonds W., Smid J., Sollano J., Song G.A., Speight A., Sporea I., Staessen D., Stancu G., Steel A., Stepek D., Stoica V., Sturm A., Szekely G., Tan T.K., Taxonera Samso C., Thomson J., Tichy M., Toth G.T., Tulassay Z., Vangeli M., Varga M., Vieira A., Viennot S., Villa E., Vitek P., Vogelsang H., Vyhnalek P., Wahab P., Walldorf J., Ye B.D., and Ziady C.

Subjects
Adult, Male, medicine.medical_specialty, Adolescent, Population, Antibodies, Monoclonal, Humanized, Injections, Subcutaneou, Placebo, Severity of Illness Index, Gastroenterology, Young Adult, Double-Blind Method, Internal medicine, Gastrointestinal Agent, Clinical endpoint, medicine, education, Adverse effect, Aged, Aged, 80 and over, education.field_of_study, Hepatology, business.industry, Middle Aged, medicine.disease, Ulcerative colitis, Infliximab, Treatment Outcome, Etrolizumab, Concomitant, Colitis, Ulcerative, Female, business, Inflammatory diseases Radboud Institute for Molecular Life Sciences [Radboudumc 5], Human, medicine.drug
Abstract

Item does not contain fulltext BACKGROUND: Etrolizumab is a gut-targeted anti-β7 integrin monoclonal antibody. In a previous phase 2 induction study, etrolizumab significantly improved clinical remission versus placebo in patients with moderately to severely active ulcerative colitis. We aimed to compare the safety and efficacy of etrolizumab with infliximab in patients with moderately to severely active ulcerative colitis. METHODS: We conducted a randomised, double-blind, double-dummy, parallel-group, phase 3 study (GARDENIA) across 114 treatment centres worldwide. We included adults (age 18-80 years) with moderately to severely active ulcerative colitis (Mayo Clinic total score [MCS] of 6-12 with an endoscopic subscore of ≥2, a rectal bleeding subscore of ≥1, and a stool frequency subscore of ≥1) who were naive to tumour necrosis factor inhibitors. Patients were required to have had an established diagnosis of ulcerative colitis for at least 3 months, corroborated by both clinical and endoscopic evidence, and evidence of disease extending at least 20 cm from the anal verge. Participants were randomly assigned (1:1) to receive subcutaneous etrolizumab 105 mg once every 4 weeks or intravenous infliximab 5 mg/kg at 0, 2, and 6 weeks and every 8 weeks thereafter for 52 weeks. Randomisation was stratified by baseline concomitant treatment with corticosteroids, concomitant treatment with immunosuppressants, and baseline disease activity. All participants and study site personnel were masked to treatment assignment. The primary endpoint was the proportion of patients who had both clinical response at week 10 (MCS ≥3-point decrease and ≥30% reduction from baseline, plus ≥1-point decrease in rectal bleeding subscore or absolute rectal bleeding score of 0 or 1) and clinical remission at week 54 (MCS ≤2, with individual subscores ≤1); efficacy was analysed using a modified intention-to-treat population (all randomised patients who received at least one dose of study drug). GARDENIA was designed to show superiority of etrolizumab over infliximab for the primary endpoint. This trial is registered with ClinicalTrials.gov, NCT02136069, and is now closed to recruitment. FINDINGS: Between Dec 24, 2014, and June 23, 2020, 730 patients were screened for eligibility and 397 were enrolled and randomly assigned to etrolizumab (n=199) or infliximab (n=198). 95 (48%) patients in the etrolizumab group and 103 (52%) in the infliximab group completed the study through week 54. At week 54, 37 (18·6%) of 199 patients in the etrolizumab group and 39 (19·7%) of 198 in the infliximab group met the primary endpoint (adjusted treatment difference -0·9% [95% CI -8·7 to 6·8]; p=0·81). The number of patients reporting one or more adverse events was similar between treatment groups (154 [77%] of 199 in the etrolizumab group and 151 [76%] of 198 in the infliximab group); the most common adverse event in both groups was ulcerative colitis (55 [28%] patients in the etrolizumab group and 43 [22%] in the infliximab group). More patients in the etrolizumab group reported serious adverse events (including serious infections) than did those in the infliximab group (32 [16%] vs 20 [10%]); the most common serious adverse event was ulcerative colitis (12 [6%] and 11 [6%]). There was one death during follow-up, in the infliximab group due to a pulmonary embolism, which was not considered to be related to study treatment. INTERPRETATION: To our knowledge, this trial is the first phase 3 maintenance study in moderately to severely active ulcerative colitis to use infliximab as an active comparator. Although the study did not show statistical superiority for the primary endpoint, etrolizumab performed similarly to infliximab from a clinical viewpoint. FUNDING: F Hoffmann-La Roche.

Published
2022

21. Are we choosing wisely? Drivers of preoperative MRI use in breast cancer patients

Author

Eric Brown, Amanda Mendiola, Melissa Lazar, Naveenraj L. Solomon, David W. Ollila, Marissa Howard-McNatt, Edward A. Levine, Anees B. Chagpar, Sonali V Pandya, Elisabeth Dupont, Carlos Garcia-Cantu, Mary Murray, Kristalyn K. Gallagher, Andrew Fenton, Jennifer Gass, Sharon S. Lum, Akiko Chiba, Laura Walters, and Jukes P. Namm

Subjects
Male, medicine.medical_specialty, Multivariate analysis, medicine.medical_treatment, Breast Neoplasms, Mastectomy, Segmental, law.invention, Breast cancer, Randomized controlled trial, Patient age, law, Preoperative Care, medicine, Breast-conserving surgery, Humans, Breast, Stage (cooking), Neoadjuvant therapy, Tumor histology, business.industry, General Medicine, medicine.disease, Magnetic Resonance Imaging, Neoadjuvant Therapy, Female, Surgery, Radiology, business
Abstract

Factors contributing to the use of preoperative MRI remain poorly understood.Data from a randomized controlled trial of stage 0-3 breast cancer patients undergoing breast conserving surgery between 2016 and 2018 were analyzed.Of the 396 patients in this trial, 32.6% had a preoperative MRI. Patient age, race, ethnicity, tumor histology, and use of neoadjuvant therapy were significant predictors of MRI use. On multivariate analysis, younger patients with invasive lobular tumors were more likely to have a preoperative MRI. Rates also varied significantly by individual surgeon (p 0.001); in particular, female surgeons (39.9% vs. 24.0% for male surgeons, p = 0.001) and those in community practice (58.9% vs. 14.2% for academic, p 0.001) were more likely to order preoperative MRI. Rates declined over the two years of the study, particularly among female surgeons.Preoperative MRI varies with patient age and tumor histology; however, there remains variability by individual surgeon.

Published
2022

22. Real-world outcomes and risk stratification in patients with metastatic castration-sensitive prostate cancer treated with upfront abiraterone acetate and docetaxel

Author

Shintaro Narita, Takahiro Kimura, Shingo Hatakeyama, Kenichi Hata, Takafumi Yanagisawa, Shinya Maita, Shuji Chiba, Hiromi Sato, Soki Kashima, Atsushi Koizumi, Ryohei Yamamoto, Koichiro Takayama, Katsumi Okane, Toshiya Ishida, Yohei Horikawa, Teruaki Kumazawa, Jiro Shimoda, Takehiro Suzuki, Chikara Ohyama, Shin Egawa, and Tomonori Habuchi

Subjects
Male, Abiraterone Acetate, Androgen Antagonists, Docetaxel, Hematology, General Medicine, Risk Assessment, Prostatic Neoplasms, Castration-Resistant, Treatment Outcome, Oncology, Antineoplastic Combined Chemotherapy Protocols, Humans, Surgery, Castration, Retrospective Studies
Abstract

We assessed clinical outcomes in patients with metastatic castration-sensitive prostate cancer (mCSPC) treated with two upfront therapies.The medical records of 301 patients with mCSPC treated with androgen deprivation therapy plus upfront abiraterone acetate (ABI) or docetaxel (DOC) between 2014 and 2021 were retrospectively reviewed. Propensity score matching (PSM) was performed to compare survival outcomes. Subgroup analyses of risk factors for second progression were conducted.A total of 95 patients received upfront DOC, whereas 206 received upfront ABI. After PSM, the ABI group had a significantly better castration-resistant prostate cancer (CRPC)-free survival than the DOC group [hazard ratio (HR), 0.53; 95% confidence interval (CI), 0.34-0.82]. Second progression-free survival (PFS2) tended to be longer in the ABI group than in the DOC group, but the difference was not statistically significant (HR, 0.64; 95% CI, 0.33-1.22). No significant difference in overall survival (OS) was found between the two groups (HR, 0.92; 95% CI, 0.42-2.03). In the subgroup analysis, upfront ABI had significantly favorable PFS2 in patients aged ≥ 75 years compared with upfront DOC (p = 0.038). Four risk factors for second progression (primary Gleason 5, liver metastasis, high serum alkaline phosphatase level, and high serum lactate dehydrogenase level) successfully stratified patients into three risk groups.Upfront ABI provided better CRPC-free survival than upfront DOC; however, no significant differences in PFS2 or OS were observed between the two groups. Personalized management based on prognostic risk factors may benefit patients with mCSPC treated with upfront intensified therapies.

Published
2022

23. Inducing Cortical Plasticity to Manipulate and Consolidate Subjective Time Interval Production

Author

Atsuro Chiba, Takeshi Atsumi, Yasuo Terao, Shoko Saito, Shin-ichi Tokushige, Motoyasu Honma, and Satomi Inomata-Terada

Subjects
Male, medicine.medical_treatment, Temporoparietal junction, Prefrontal Cortex, 03 medical and health sciences, 0302 clinical medicine, Neuroplasticity, medicine, Humans, Neuronal Plasticity, business.industry, Motor Cortex, General Medicine, Time perception, Evoked Potentials, Motor, Transcranial Magnetic Stimulation, Dorsolateral prefrontal cortex, Transcranial magnetic stimulation, Anesthesiology and Pain Medicine, medicine.anatomical_structure, Neurology, Duration (music), Female, Memory consolidation, Neurology (clinical), Primary motor cortex, business, Neuroscience, 030217 neurology & neurosurgery
Abstract

OBJECTIVES: Time awareness may change depending on the mental state or disease conditions, although each individual perceives his/her own sense of time as stable and accurate. Nevertheless, the processes that consolidate altered duration production remain unclear. The present study aimed to manipulate the subjective duration production via memory consolidation through the modulation of neural plasticity. MATERIALS AND METHODS: We first performed false feedback training of duration or length production and examined the period required for natural recovery from the altered production. Next, persistent neural plasticity was promoted by quadripulse transcranial magnetic stimulation (QPS) over the right dorsolateral prefrontal cortex (DLPFC), temporoparietal junction (TPJ), and primary motor cortex (M1). We conducted the same feedback training in the individual and studied how the time course of false learning changed. RESULTS: We observed that altered duration production after false feedback returned to baseline within two hours. Next, immediate exposure to false feedback during neural plasticity enhancement revealed that in individuals who received QPS over the right DLPFC, but not over TPJ or M1, false duration production was maintained for four hours; furthermore, the efficacy persisted for at least one week. CONCLUSION: These findings suggest that, while learned altered duration production decays over several hours, QPS over the right DLPFC enables the consolidation of newly learned duration production.

Published
2022

24. Protective effects of tadalafil against cisplatin-induced spermatogenic dysfunction

Author

Yasuhiro Kaku, Koji Chiba, Katsuya Sato, Atsushi Onishi, Takaki Ishida, Keisuke Okada, and Masato Fujisawa

Subjects
Male, Biophysics, Cell Biology, Biochemistry, Antioxidants, Rats, Tadalafil, Oxidative Stress, Testicular Neoplasms, Animals, Humans, Dimethyl Sulfoxide, Atrophy, Cisplatin, Molecular Biology
Abstract

Cisplatin (CDDP) is an effective anticancer drug for the treatment of malignant tumors, such as lung cancer, bladder cancer, and testicular cancer. However, oligozoospermia and azoospermia after administration of CDDP are clinical problems. One of the testicular toxicities of CDDP is known to cause oxidative stress. Tadalafil has been reported to exhibit antioxidant effects and is widely used in clinical practice to treat benign prostatic hyperplasia and erectile dysfunction. Rho-kinase α (ROCK2) regulates cell migration and apoptosis and has been reported to be involved in CDDP-induced nephrotoxicity. The excessive expression of ROCK2 is known to cause oxidative stress.The objective of the current study was to test the effect of tadalafil on the testicular toxicity of CDDP.Thirty-two rats were used and divided into the following four groups. (1) The control group (CONT), treated with saline on day 1 and saline and dimethyl sulfoxide (DMSO) on days 1-10 intraperitoneally (i.p.) (2) The Tadalafil Group (TAD), treated with saline on day 1, and 0.4 mg/kg tadalafil on days 1-10 i.p. (3) The CDDP group (CD), treated with 7 mg/kg CDDP, saline, and DMSO on days 1-10 i.p. and (4) The CDDP + TAD group (CDT) was treated with 7 mg/kg CDDP on day 1, and 0.4 mg/kg tadalafil on days 1-10 i.p. Testes and epididymides samples were collected on day 11. Biochemical and pathological analyses and quantitative polymerase chain reaction were performed on the excised specimens.CDDP treatment resulted in testicular atrophy, decreased sperm concentration, and atrophy of seminiferous tubules as observed from the testicular histology. Increased apoptosis of seminiferous tubules, oxidative stress, and ROCK2 mRNA expression were observed after CDDP treatment. Treatment with tadalafil improved these adverse effects.Tadalafil is a potential drug for reducing CDDP-induced spermatogenic dysfunction. The antioxidant effect of tadalafil may be partly responsible for this phenomenon. ROCK2 and oxidative stress markers may be involved in the possible antioxidant effects of tadalafil. Tadalafil may be considered as one of a treatment option for reducing spermatogenic dysfunction after administration of CDDP.

Published
2022

25. Minocycline-induced black thyroid with black pigmentation of the thyroid cartilage, cricoid cartilage, and trachea found during reconstructive surgery for hypopharyngeal cancer

Author

Munehide Nakatsugawa, Kiyoaki Tsukahara, Akira Okimura, Takahito Kondo, Yuji Hirai, Atsuo Takeda, Yuujin Chiba, Naiue Kikawada, Hiroshi Hirano, Yusuke Aihara, and Yasuo Ogawa

Subjects
Male, Reconstructive surgery, medicine.medical_specialty, medicine.medical_treatment, Thyroid Gland, Minocycline, Cricoid Cartilage, 03 medical and health sciences, 0302 clinical medicine, Prurigo, Cricoid cartilage, Humans, Medicine, Thyroid Neoplasms, 030223 otorhinolaryngology, Aged, Hypopharyngeal Neoplasms, Pigmentation, business.industry, Thyroid, Head and neck cancer, Neck dissection, Hypopharyngeal cancer, General Medicine, Plastic Surgery Procedures, respiratory system, Thyroid cartilage, medicine.disease, Surgery, Trachea, medicine.anatomical_structure, Otorhinolaryngology, Thyroid Cartilage, 030220 oncology & carcinogenesis, business
Abstract

Black thyroid is characterized by a rare pigment change observed almost exclusively in patients taking minocycline. We present the case of a 72-year-old man diagnosed with T3N3bM0 stage IVB hypopharyngeal squamous cell carcinoma who had been taking minocycline for approximately 18 months as a treatment for prurigo chronica multiformis. Initial treatment consisted of total pharyngolaryngoesophagectomy, bilateral neck dissection, total thyroidectomy, pharyngeal reconstruction using a free jejunal autograft, and creation of a permanent tracheostoma. During surgery, black discoloration of the thyroid and trachea was observed. Postoperative histological findings confirmed the black discoloration, with deposits of dark-brown, melanin-like granules observed in the thyroid, trachea, thyroid cartilage, and cricoid cartilage. Therefore, the black discoloration of the thyroid associated with the use of minocycline can extend to the thyroid cartilage, cricoid cartilage, and trachea. This information is important for surgeons to recognize in order to prevent unnecessary resection due to misdiagnosis.

Published
2022

26. Real-world survival outcomes of adding docetaxel or abiraterone in patients with high-volume metastatic castration-sensitive prostate cancer: historically controlled, propensity score matched comparison with androgen deprivation therapy

Author

Shintaro Narita, Takahiro Kimura, Shingo Hatakeyama, Kenichi Hata, Takafumi Yanagisawa, Shinya Maita, Shuji Chiba, Hiromi Sato, Soki Kashima, Atsushi Koizumi, Ryohei Yamamoto, Koichiro Takayama, Katsumi Okane, Toshiya Ishida, Yohei Horikawa, Teruaki Kumazawa, Jiro Shimoda, Takehiro Suzuki, Chikara Ohyama, Shin Egawa, Kyoko Nomura, and Tomonori Habuchi

Subjects
Male, Prostatic Neoplasms, Castration-Resistant, Urology, Antineoplastic Combined Chemotherapy Protocols, Androgens, Humans, Prostatic Neoplasms, Androgen Antagonists, Androstenes, Castration, Docetaxel, Propensity Score, Retrospective Studies
Abstract

This study investigated the impact of treatment intensification with upfront docetaxel (DOC) or abiraterone (ABI) plus prednisolone on survival outcomes in patients with metastatic castration-sensitive prostate cancer (mCSPC) by comparing it with androgen deprivation therapy (ADT) monotherapy or combined androgen blockade (CAB) using propensity score matching (PSM).Outcomes from 278 CHAARTED high-volume patients receiving upfront DOC (92 patients) or upfront ABI (186 patients) were compared to those from 354 patients receiving ADT or CAB. PSM was conducted to assess castration-resistant prostate cancer-free survival (CRPCFS) and overall survival (OS).After PSM, patient distributions between the three groups were well balanced. After 1:1 PSM, patients receiving upfront ABI had significantly better CRPCFS than those receiving ADT/CAB or upfront DOC [hazard ratio (HR) 0.39; 95% CI 0.27-0.56 vs. HR 0.50; 95% CI 0.30-0.82, respectively]. No significant difference in CRPCFS was observed between the upfront DOC and ADT/CAB groups (HR 0.75; 95% CI 0.50-1.12). Patients receiving upfront DOC and upfront ABI had significantly better OS than those receiving ADT/CAB (HR 0.54; 95% CI 0.0.30-0.98 vs. HR 0.49; 95% CI 0.29-0.84, respectively). However, no significant difference in OS was observed between upfront ABI and upfront DOC (hazard ratio 0.84; 95% CI 0.34-2.06).The comparison of real-world retrospective cohorts showed that treatment intensification with upfront DOC or upfront ABI promoted better OS compared to ADT alone or CAB in patients with high-volume mCSPC after PSM. However, no difference in OS was observed between upfront DOC and upfront ABI.

Published
2022

27. Enhanced fusogenicity and pathogenicity of SARS-CoV-2 Delta P681R mutation

Author

Saito, Akatsuki, Irie, Takashi, Suzuki, Rigel, Maemura, Tadashi, Nasser, Hesham, Uriu, Keiya, Kosugi, Yusuke, Shirakawa, Kotaro, Sadamasu, Kenji, Kimura, Izumi, Ito, Jumpei, Wu, Jiaqi, Iwatsuki-Horimoto, Kiyoko, Ito, Mutsumi, Yamayoshi, Seiya, Loeber, Samantha, Tsuda, Masumi, Wang, Lei, Ozono, Seiya, Butlertanaka, Erika P., Tanaka, Yuri L., Shimizu, Ryo, Shimizu, Kenta, Yoshimatsu, Kumiko, Kawabata, Ryoko, Sakaguchi, Takemasa, Tokunaga, Kenzo, Yoshida, Isao, Asakura, Hiroyuki, Nagashima, Mami, Kazuma, Yasuhiro, Nomura, Ryosuke, Horisawa, Yoshihito, Yoshimura, Kazuhisa, Takaori-Kondo, Akifumi, Imai, Masaki, Chiba, Mika, Furihata, Hirotake, Hasebe, Haruyo, Kitazato, Kazuko, Kubo, Haruko, Misawa, Naoko, Morizako, Nanami, Noda, Kohei, Oide, Akiko, Suganami, Mai, Takahashi, Miyoko, Tsushima, Kana, Yokoyama, Miyabishara, Yuan, Yue, Tanaka, Shinya, Nakagawa, So, Ikeda, Terumasa, Fukuhara, Takasuke, Kawaoka, Yoshihiro, and Sato, Kei

Subjects
Delta, Male, Lineage (genetic), Viral pathogenesis, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Biology, medicine.disease_cause, Antibodies, Viral, Virus Replication, Genome, Giant Cells, Membrane Fusion, Virus, Cricetinae, medicine, Animals, Phylogeny, Mutation, Multidisciplinary, Mesocricetus, Virulence, SARS-CoV-2, COVID-19, Phenotype, Virology, Antibodies, Neutralizing, Amino Acid Substitution, Spike Glycoprotein, Coronavirus
Abstract

During the current SARS-CoV-2 pandemic, a variety of mutations have accumulated in the viral genome, and currently, four variants of concern (VOCs) are considered potentially hazardous to human society1. The recently emerged B.1.617.2/Delta VOC is closely associated with the COVID-19 surge that occurred in India in the spring of 20212. However, its virological properties remain unclear. Here, we show that the B.1.617.2/Delta variant is highly fusogenic and notably more pathogenic than prototypic SARS-CoV-2 in infected hamsters. The P681R mutation in the spike protein, which is highly conserved in this lineage, facilitates spike protein cleavage and enhances viral fusogenicity. Moreover, we demonstrate that the P681R-bearing virus exhibits higher pathogenicity than its parental virus. Our data suggest that the P681R mutation is a hallmark of the virological phenotype of the B.1.617.2/Delta variant and is associated with enhanced pathogenicity., SARS-CoV-2デルタ株に特徴的なP681R変異は ウイルスの病原性を増大させる. 京都大学プレスリリース. 2021-11-26.

Published
2022

28. Altered TMPRSS2 usage by SARS-CoV-2 Omicron impacts infectivity and fusogenicity

Author

Meng, B., Abdullahi, A., Ferreira, I. A. T. M., Goonawardane, N., Saito, A., Kimura, I., Yamasoba, D., Gerber, P. P., Fatihi, S., Rathore, S., Zepeda, S. K., Papa, G., Kemp, S. A., Ikeda, T., Toyoda, M., Tan, T. S., Kuramochi, J., Mitsunaga, S., Ueno, T., Shirakawa, K., Takaori-Kondo, A., Brevini, T., Mallery, D. L., Charles, O. J., Baker, S., Dougan, G., Hess, C., Kingston, N., Lehner, P. J., Lyons, P. A., Matheson, N. J., Ouwehand, W. H., Saunders, C., Summers, C., Thaventhiran, J. E. D., Toshner, M., Weekes, M. P., Maxwell, P., Shaw, A., Bucke, A., Calder, J., Canna, L., Domingo, J., Elmer, A., Fuller, S., Harris, J., Hewitt, S., Kennet, J., Jose, S., Kourampa, J., Meadows, A., O'Brien, C., Price, J., Publico, C., Rastall, R., Ribeiro, C., Rowlands, J., Ruffolo, V., Tordesillas, H., Bullman, B., Dunmore, B. J., Graf, S., Hodgson, J., Huang, C., Hunter, K., Jones, E., Legchenko, E., Matara, C., Martin, J., Mescia, F., O'Donnell, C., Pointon, L., Shih, J., Sutcliffe, R., Tilly, T., Treacy, C., Tong, Z., Wood, J., Wylot, M., Betancourt, A., Bower, G., Cossetti, C., De Sa, A., Epping, M., Fawke, S., Gleadall, N., Grenfell, R., Hinch, A., Jackson, S., Jarvis, I., Krishna, B., Nice, F., Omarjee, O., Perera, M., Potts, M., Richoz, N., Romashova, V., Stefanucci, L., Strezlecki, M., Turner, L., De Bie, E. M. D. D., Bunclark, K., Josipovic, M., Mackay, M., Butcher, H., Caputo, D., Chandler, M., Chinnery, P., Clapham-Riley, D., Dewhurst, E., Fernandez, C., Furlong, A., Graves, B., Gray, J., Hein, S., Ivers, T., Le Gresley, E., Linger, R., Kasanicki, M., King, R., Meloy, S., Moulton, A., Muldoon, F., Ovington, N., Papadia, S., Penkett, C. J., Phelan, I., Ranganath, V., Paraschiv, R., Sage, A., Sambrook, J., Scholtes, I., Schon, K., Stark, H., Stirrups, K. E., Townsend, P., Walker, N., Webster, J., Butlertanaka, E. P., Tanaka, Y. L., Ito, J., Uriu, K., Kosugi, Y., Suganami, M., Oide, A., Yokoyama, M., Chiba, M., Motozono, C., Nasser, H., Shimizu, R., Kitazato, K., Hasebe, H., Irie, T., Nakagawa, S., Wu, J., Takahashi, M., Fukuhara, T., Shimizu, K., Tsushima, K., Kubo, H., Kazuma, Y., Nomura, R., Horisawa, Y., Nagata, K., Kawai, Y., Yanagida, Y., Tashiro, Y., Tokunaga, K., Ozono, S., Kawabata, R., Morizako, N., Sadamasu, K., Asakura, H., Nagashima, M., Yoshimura, K., Cardenas, P., Munoz, E., Barragan, V., Marquez, S., Prado-Vivar, B., Becerra-Wong, M., Caravajal, M., Trueba, G., Rojas-Silva, P., Grunauer, M., Gutierrez, B., Guadalupe, J. J., Fernandez-Cadena, J. C., Andrade-Molina, D., Baldeon, M., Pinos, A., Bowen, J. E., Joshi, A., Walls, A. C., Jackson, L., Martin, D., Smith, K. G. C., Bradley, J., Briggs, J. A. G., Choi, J., Madissoon, E., Meyer, K. B., Mlcochova, P., Ceron-Gutierrez, L., Doffinger, R., Teichmann, S. A., Fisher, A. J., Pizzuto, M. S., de Marco, A., Corti, D., Hosmillo, M., Lee, J. H., James, L. C., Thukral, L., Veesler, D., Sigal, A., Sampaziotis, F., Goodfellow, I. G., Sato, K., and Gupta, R. K.

Subjects
Adult, Male, COVID-19 Vaccines, Virus Replication, Membrane Fusion, Antibodies, Cell Line, Tissue Culture Techniques, Chlorocebus aethiops, 80 and over, Animals, Humans, Viral, Neutralizing, Lung, Aged, Multidisciplinary, Virulence, SARS-CoV-2, Immune Sera, Cell Membrane, Serine Endopeptidases, COVID-19, Convalescence, Middle Aged, Virus Internalization, Spike Glycoprotein, Intestines, Coronavirus, Nasal Mucosa, Mutation, Female, Angiotensin-Converting Enzyme 2, Aged, 80 and over, Antibodies, Neutralizing, Antibodies, Viral, Spike Glycoprotein, Coronavirus
Abstract

The SARS-CoV-2 Omicron BA.1 variant emerged in 20211 and has multiple mutations in its spike protein2. Here we show that the spike protein of Omicron has a higher affinity for ACE2 compared with Delta, and a marked change in its antigenicity increases Omicron’s evasion of therapeutic monoclonal and vaccine-elicited polyclonal neutralizing antibodies after two doses. mRNA vaccination as a third vaccine dose rescues and broadens neutralization. Importantly, the antiviral drugs remdesivir and molnupiravir retain efficacy against Omicron BA.1. Replication was similar for Omicron and Delta virus isolates in human nasal epithelial cultures. However, in lung cells and gut cells, Omicron demonstrated lower replication. Omicron spike protein was less efficiently cleaved compared with Delta. The differences in replication were mapped to the entry efficiency of the virus on the basis of spike-pseudotyped virus assays. The defect in entry of Omicron pseudotyped virus to specific cell types effectively correlated with higher cellular RNA expression of TMPRSS2, and deletion of TMPRSS2 affected Delta entry to a greater extent than Omicron. Furthermore, drug inhibitors targeting specific entry pathways3 demonstrated that the Omicron spike inefficiently uses the cellular protease TMPRSS2, which promotes cell entry through plasma membrane fusion, with greater dependency on cell entry through the endocytic pathway. Consistent with suboptimal S1/S2 cleavage and inability to use TMPRSS2, syncytium formation by the Omicron spike was substantially impaired compared with the Delta spike. The less efficient spike cleavage of Omicron at S1/S2 is associated with a shift in cellular tropism away from TMPRSS2-expressing cells, with implications for altered pathogenesis.

Published
2022

29. Trastuzumab-Induced Negative Chronotropic and Lusitropic Effects in Cynomolgus Monkeys

Author

Yu Maeda, Kazuhiko Mori, Yu Yoshimatsu, Katsuyoshi Chiba, and Tomomichi Ishizaka

Subjects
Male, Chronotropic, Cardiac function curve, medicine.medical_specialty, Time Factors, Lusitropy, Risk Assessment, Drug Administration Schedule, Ventricular Function, Left, Ventricular Dysfunction, Left, Antineoplastic Agents, Immunological, Heart Rate, Risk Factors, Trastuzumab, Internal medicine, Heart rate, Ventricular Pressure, medicine, Animals, skin and connective tissue diseases, Pharmacology, Dose-Response Relationship, Drug, business.industry, medicine.disease, Cardiotoxicity, Macaca fascicularis, Preload, Heart failure, Ventricular pressure, Cardiology, Cardiology and Cardiovascular Medicine, business, medicine.drug
Abstract

Treatment with trastuzumab, an antihuman epidermal growth factor receptor type 2 humanized monoclonal antibody, has been associated with heart failure in certain patients with cancer; however, the mechanism underlying trastuzumab-induced cardiac dysfunction remains unclear. This study was conducted to clarify the cardiac effects of trastuzumab in cynomolgus monkeys, which are commonly used as cross-reactive species in preclinical safety evaluation. Monkeys were treated with trastuzumab weekly for 1 month (5 doses in total). At first and fifth doses for pressure-volume loop analysis, trastuzumab at 20 mg·kg-1·10 min-1, equivalent to the human therapeutic dose, was administered intravenously to isoflurane-anesthetized animals, followed by 60 mg·kg-1·10 min-1 at a 30-minute interval. The other doses were fixed at 80 mg·kg-1·10 min-1 under unanesthetized conditions. After the first dose, reduced heart rate, decreases in maximal rate of fall of left ventricular pressure, and prolonged time constant for isovolumic relaxation, which are predictors of drug-induced changes in lusitropy, were observed at 20 and 60 mg·kg-1. The changes after the fifth dose were comparable with those after the first dose, indicating trastuzumab did not show exacerbation of cardiac function during the 1-month trial. No significant changes in slope of preload recruitable stroke work, which is a load-independent inotropic parameter, were observed at either dose. In conclusion, trastuzumab-induced little inotropic effect but induced negative chronotropic or lusitropic effects in monkeys, which might be associated with impaired left ventricular diastolic function.

Published
2022

30. Monte Carlo simulation of tilted contact plaque brachytherapy placement for juxtapapillary retinoblastoma

Author

Satoshi Nakamura, Naoya Murakami, Shigenobu Suzuki, Kimiteru Ito, Mihiro Takemori, Hiroki Nakayama, Keita Kaga, Takahito Chiba, Kotaro Iijima, Kana Takahashi, Tomonori Goka, Jun Itami, Hiroyuki Okamoto, and Hiroshi Igaki

Subjects
Male, Retinal Neoplasms, 106Ru plaque applicator, Brachytherapy, Retinoblastoma, R895-920, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, Case Report, Medical physics. Medical radiology. Nuclear medicine, Oncology, Child, Preschool, Juxtapapillary tumor, Humans, Radiology, Nuclear Medicine and imaging, Monte Carlo Method, Monte Carlo simulation, RC254-282
Abstract

Background The 106-Ruthenium contact plaque applicator is utilized for the treatment of intraocular tumor within a thickness of less than 6 mm. If anything obstructs the placement of the plaque applicator, the treatment is generally difficult because the applicator has to be temporarily located just on the opposite side of the retinal tumor. Furthermore, the plaque applicator edge of approximately 1 mm does not contain 106Ru, estimating the delivered radiation dose for eccentric tumor is challenging because the lateral dose profile is inadequately provided by the manufacture’s certification. This study aims to simulate tumor coverage of the tilted applicator placement for treating an infant with juxtapapillary retinoblastoma and to achieve the effective treatment. Case presentation We present an infant with retinoblastoma whose tumor involved macular and was invading just temporal side of the optic disc. Additionally, posterior staphyloma was induced by a series of previous treatments, making it more difficult to treat the standard plaque placement. Thus, the applicator type of CCA was intentionally tilted to the eyeball and the distance between the posterior edge of the applicator and the eyeball had to be then equal to or more than 2 mm based on the dose distribution of the applicator calculated using Monte Carlo simulation to minimize damage to surrounding tissues while covering the tumor. It was then comparable to the certification and previous reports. Based on the acquired dose distribution, the optimal placement of the applicator was derived from varying the distance between the applicator’s edge and the eyeball, and the distance was then determined to be 2 mm. In this case, the minimum dose rate in the tumor was 25.5 mGy/min, and the time required to deliver the prescribed dose was 26.2 h. Therefore, the tilted 106Ru plaque applicator placement could deliver the required dose for the treatment. The physical examination revealed no active tumor as a result of the treatment. Conclusions Optimizing the placement of the 106Ru plaque applicator, it was possible to guarantee that the prescribed dose will be delivered to the tumor even if the standard placement is not possible for the juxtapapillary tumor.

Published
2022

31. A triple-blind randomized clinical trial of different associations between dexamethasone and non-steroids anti-inflammatories for preemptive action in third molar extractions

Author

Gustavo Antonio Correa Momesso, Gustavo Augusto Grossi-Oliveira, William Phillip Pereira Silva, Renan Akira, Fernando Chiba, Tárik Ocon Braga Polo, Tiburtino José de Lima Neto, Bárbara Ribeiro Rios, Ana Paula Farnezi Bassi, Doris Hissako Sumida, Michael Han, Michael Miloro, Leonardo Perez Faverani, Universidade Estadual Paulista (UNESP), and University of Illinois at Chicago (UIC)

Subjects
Adult, Male, endocrine system, Adolescent, Science, Ibuprofen, Oral analgesics, Dexamethasone, Article, Young Adult, polycyclic compounds, Humans, Prospective Studies, Glucocorticoids, Analgesics, Multidisciplinary, Phenylpropionates, Anti-Inflammatory Agents, Non-Steroidal, Clinical trial design, Tooth Extraction, Etodolac, Medicine, Drug Therapy, Combination, Female, Molar, Third, Ketorolac, hormones, hormone substitutes, and hormone antagonists
Abstract

Made available in DSpace on 2022-05-01T11:54:04Z (GMT). No. of bitstreams: 0 Previous issue date: 2021-12-01 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) The aim of this study is to evaluate the preemptive analgesic effects of dexamethasone (DEX) alone or combined with non-steroidal anti-inflammatory drugs (NSAIDs) in third molar surgeries. The subjects were divided into five groups (n = 20 teeth/group); subjects received only 8 mg of dexamethasone 1 h before the surgical procedure (DEX group), or in combination with etodolac (DEX + ETO), ketorolac (DEX + KET), ibuprofen (DEX + IBU), loxoprofen (DEX + LOX). Paracetamol 750 mg was provided as the number of rescue analgesics (NRA). Salivary PGE2 expression was measured preoperatively and at 48 h. Edema and Maximum mouth opening (MMO) were measured postoperatively at 48 h and 7 days. A visual analog scale (VAS) was performed postoperatively at 6, 12, 24, 48, 72 h, and 7 days. Salivary expression of PGE2 showed a decrease only for the DEX group. Edema and MMO and NRA consumption showed no significant differences among the groups (P > 0.05). The VAS showed a significantly lower pain perception at 6 h after the surgery for the DEX + ETO and DEX + KET groups (P < 0.05). The combination of DEX and NSAIDS should be considered for preemptive acute postsurgical pain management in third molar surgery. In some drug associations such as dexamethasone 8 mg + NSAIDS (ETO and KET) in the pre-operative time, only a few rescue analgesics are necessary. Department of Diagnosis and Surgery School of Dentistry São Paulo State University (UNESP), Rua Jose Bonifacio, 1193 Department of Basic Sciences School of Dentistry São Paulo State University (UNESP) Department of Oral and Maxillofacial Surgery UIH Medical Center; College of Dentistry University of Illinois at Chicago (UIC) Department of Diagnosis and Surgery School of Dentistry São Paulo State University (UNESP), Rua Jose Bonifacio, 1193 Department of Basic Sciences School of Dentistry São Paulo State University (UNESP) CAPES: 001

Published
2021

32. Exogenous insulin‐like growth factor 1 attenuates cisplatin‐induced muscle atrophy in mice

Author

Junzo Kamei, Satoshi Yoshida, Nobutomo Ikarashi, Yu Miyauchi, Yuta Suzuki, Maho Asami, Satoko Kitora, Hiroaki Naito, Rei Tachinooka, Yoshihiko Chiba, Risako Kon, and Hiroyasu Sakai

Subjects
Male, medicine.medical_specialty, Ubiquitin-Protein Ligases, Insulin‐like growth factor 1, Muscle Proteins, Diseases of the musculoskeletal system, Mice, Phosphatidylinositol 3-Kinases, Atrophy, Downregulation and upregulation, Physiology (medical), Internal medicine, medicine, Animals, Humans, Orthopedics and Sports Medicine, Insulin-Like Growth Factor I, PI3K/AKT/mTOR pathway, Mecasermin, Cisplatin, Myogenesis, business.industry, QM1-695, Skeletal muscle, Original Articles, medicine.disease, Muscle atrophy, Mice, Inbred C57BL, Muscular Atrophy, Endocrinology, medicine.anatomical_structure, RC925-935, Human anatomy, Original Article, medicine.symptom, business, medicine.drug
Abstract

Background A reduction in the skeletal muscle mass worsens the prognosis of patients with various cancers. Our previous studies indicated that cisplatin administration to mice caused muscle atrophy. This is a concern for human patients receiving cisplatin. The insulin‐like growth factor 1 (IGF‐1)/phosphoinositide 3‐kinase (PI3K)/Akt pathway stimulates the rate of protein synthesis in skeletal muscle. Thus, IGF‐I can be a central therapeutic target for preventing the loss of skeletal muscle mass in muscle atrophy, although it remains unclear whether pharmacological activation of the IGF‐1/PI3K/Akt pathway attenuates muscle atrophy induced by cisplatin. In this study, we examined whether exogenous recombinant human IGF‐1 attenuated cisplatin‐induced muscle atrophy. Methods Male C57BL/6J mice (8–9 weeks old) were injected with cisplatin or saline for four consecutive days. On Day 5, quadriceps muscles were isolated. Mecasermin (recombinant human IGF‐1) or the vehicle control was subcutaneously administered 30 min prior to cisplatin administration. A dietary restriction group achieving weight loss equivalent to that caused by cisplatin administration was used as a second control. C2C12 myotubes were treated with cisplatin with/without recombinant mouse IGF‐1. The skeletal muscle protein synthesis/degradation pathway was analysed by histological and biochemical methods. Results Cisplatin reduced protein level of IGF‐1 by about 85% compared with the vehicle group and also reduced IGF‐1/PI3K/Akt signalling in skeletal muscle. Under this condition, the protein levels of muscle ring finger protein 1 (MuRF1) and atrophy gene 1 (atrogin‐1) were increased in quadriceps muscles (MuRF1; 3.0 ± 0.1 folds, atrogin‐1; 3.0 ± 0.3 folds, P

Published
2021

33. Alteration of the immune environment in bone marrow from children with recurrent B cell precursor acute lymphoblastic leukemia

Author

Seishi Ogawa, Katsuyoshi Koh, Kenichi Chiba, Yuki Arakawa, Tomoya Isobe, Satoru Miyano, Shimon Sakaguchi, Satoshi Saida, Hiroko Tanaka, Hirohito Kubota, Ai Okada, Junko Takita, Koichi Oshima, Yuichi Shiraishi, James B. Wing, Katsutsugu Umeda, Keiko Iwaisako, Hidefumi Hiramatsu, Keiji Tasaka, Hiroo Ueno, Mitsuteru Hiwatari, Souichi Adachi, Itaru Kato, Kuniaki Tanaka, and Takashi Mikami

Subjects
Male, regulatory T cell, Cancer Research, Adolescent, Regulatory T cell, medicine.medical_treatment, immune response, Th1, Young Adult, Basic and Clinical Immunology, Immune system, Immunophenotyping, Cancer immunotherapy, Bone Marrow, Precursor B-Cell Lymphoblastic Leukemia-Lymphoma, hemic and lymphatic diseases, B cell leukemia, Biomarkers, Tumor, Tumor Microenvironment, medicine, Humans, Child, B cell, relapse, Sequence Analysis, RNA, business.industry, Gene Expression Profiling, Infant, Original Articles, General Medicine, biochemical phenomena, metabolism, and nutrition, Flow Cytometry, medicine.disease, Up-Regulation, Gene Expression Regulation, Neoplastic, Leukemia, medicine.anatomical_structure, Oncology, Child, Preschool, B-cell leukemia, Cancer research, bacteria, Original Article, Female, Bone marrow, Neoplasm Recurrence, Local, Single-Cell Analysis, business
Abstract

Due to the considerable success of cancer immunotherapy for leukemia, the tumor immune environment has become a focus of intense research; however, there are few reports on the dynamics of the tumor immune environment in leukemia. Here, we analyzed the tumor immune environment in pediatric B cell precursor acute lymphoblastic leukemia by analyzing serial bone marrow samples from nine patients with primary and recurrent disease by mass cytometry using 39 immunophenotype markers, and transcriptome analysis. High‐dimensional single‐cell mass cytometry analysis elucidated a dynamic shift of T cells from naïve to effector subsets, and clarified that, during relapse, the tumor immune environment comprised a T helper 1‐polarized immune profile, together with an increased number of effector regulatory T cells. These results were confirmed in a validation cohort using conventional flow cytometry. Furthermore, RNA transcriptome analysis identified the upregulation of immune‐related pathways in B cell precursor acute lymphoblastic leukemia cells during relapse, suggesting interaction with the surrounding environment. In conclusion, a tumor immune environment characterized by a T helper 1‐polarized immune profile, with an increased number of effector regulatory T cells, could contribute to the pathophysiology of recurrent B cell precursor acute lymphoblastic leukemia. This information could contribute to the development of effective immunotherapeutic approaches against B cell precursor acute lymphoblastic leukemia relapse., Tumor immune environment characterized by a T helper 1‐polarized immune profile was observed in recurrent B cell precursor acute lymphoblastic leukemia. Regulatory T cells were activated in recurrent B cell precursor acute lymphoblastic leukemia.

Published
2021

34. Claudin-9 constitutes tight junctions of folliculo-stellate cells in the anterior pituitary gland

Author

Kyoko Furuse, Tomohito Higashi, Kana Ozeki, Mikio Furuse, Atsuko Y. Higashi, and Hideki Chiba

Subjects
Male, Pituitary gland, Immunoelectron microscopy, Science, Enteroendocrine cell, Occludin, Article, Cell Physiological Phenomena, Tight Junctions, Mice, Anterior pituitary, Pituitary Gland, Anterior, medicine, Animals, Claudin, Multidisciplinary, Tight junction, Chemistry, Cell biology, Mice, Inbred C57BL, medicine.anatomical_structure, Astrocytes, Claudins, Hepatic stellate cell, Medicine, Female
Abstract

The anterior pituitary gland regulates growth, metabolism, and reproduction by secreting hormones. Folliculo-stellate (FS) cells are non-endocrine cells located among hormone-producing cells in the anterior pituitary glands. They form follicular lumens, which are sealed by tight junctions (TJs). Although FS cells are hypothesized to contribute to fine-tuning of endocrine cells, little is known about the exact roles of FS cells. Here, we investigated the molecular composition of TJs in FS cells. We demonstrated that occludin is a good marker for TJs in the pituitary gland and examined the structure of the lumens surrounded by FS cells. We also found that claudin-9 is a major component of TJs in the FS cells. In immunoelectron microscopy, claudin-9 was specifically localized at TJs of the FS cells. The expression of claudin-9 was gradually increased in the pituitary gland after birth, suggesting that claudin-9 is developmentally regulated and performs some specific functions on the paracellular barrier of follicles in the pituitary gland. Furthermore, we found that angulin-1, angulin-2, and tricellulin are localized at the tricellular contacts of the FS cells. Our findings provide a first comprehensive molecular profile of TJs in the FS cells, and may lead us towards unveiling the FS cell functions.

Published
2021

35. Involvement of the Peripheral μ-Opioid Receptor in Tramadol-Induced Constipation in Rodents

Author

Tsutomu Suzuki, Hirokazu Mishima, Mika Kobayashi, Masahide Fujita, Yasuhide Morioka, Motoji Kitaura, Katsumi Koike, Kana Yasufuku, Shino Takenouchi, Hiroki Chiba, and Minoru Hasegawa

Subjects
Male, Nociception, Constipation, Side effect, medicine.drug_class, Receptors, Opioid, mu, Pharmaceutical Science, Pharmacology, Rats, Sprague-Dawley, Naldemedine, Opioid receptor, Intestine, Small, Animals, Medicine, Rats, Wistar, Receptor, Tramadol, business.industry, Antagonist, General Medicine, Naltrexone, Rats, Analgesics, Opioid, Opioid, medicine.symptom, business, Opioid-Induced Constipation, medicine.drug
Abstract

Tramadol is a weak opioid that produces analgesic effect via both the μ-opioid receptor (MOR) and non-opioid targets. Constipation is the most common opioid-related side effect in patients with cancer and non-cancer pain. However, the contribution of MOR to tramadol-induced constipation is unclear. Therefore, we used naldemedine, a peripherally acting MOR antagonist, and MOR-knockout mice to investigate the involvement of peripheral MOR in tramadol-induced constipation using a small intestinal transit model. A single dose of tramadol (3-100 mg/kg, per os (p.o.)) inhibited small intestinal transit dose-dependently in rats. Naldemedine (0.01-10 mg/kg, p.o.) blocked the inhibition of small intestinal transit induced by tramadol (30 mg/kg, p.o.) in rats. The transition rate increased dose-dependently over the range of naldemedine 0.01-0.3 mg/kg, and complete recovery was observed at 0.3-10 m/kg. Additionally, tramadol (30 and 100 mg/kg, subcutaneously (s.c.)) inhibited small intestinal transit in wild-type mice but not in MOR-knockout mice. These results suggest that peripheral MOR participates in tramadol-induced constipation.

Published
2021

36. Pathophysiological background and prognosis of common atrial flutter in non-elderly patients: Comparison to Atrial Fibrillation

Author

Yoshio Kobayashi, Miyo Nakano, Yusuke Kondo, Ryo Ito, Haruhiro Takahira, Masahiro Nakano, Toshinori Chiba, Takatsugu Kajiyama, Mari Kitagawa, and Masafumi Sugawara

Subjects
Male, medicine.medical_specialty, medicine.medical_treatment, Catheter ablation, 030204 cardiovascular system & hematology, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Atrial Fibrillation, Humans, Medicine, Sinus rhythm, Heart Atria, 030212 general & internal medicine, business.industry, Atrial fibrillation, Myocardial Disorder, Middle Aged, Prognosis, medicine.disease, Ablation, Pathophysiology, Treatment Outcome, Atrial Flutter, Cohort, Catheter Ablation, Cardiology, Cardiology and Cardiovascular Medicine, business, Atrial flutter
Abstract

It is unclear whether there is any difference in the background and prognosis between non-elderly patients who undergo catheter ablation of atrial fibrillation (AF) and common atrial flutter (CAFL).To investigate the difference between the patient background of both CAFL and AF in the non-elderly.In 526 consecutive patients who underwent catheter ablation of clinical paroxysmal/persistent CAFL or AF in our hospital, we enrolled only patients under 60 years old. Cases harboring both AFL and AF were excluded. We analyzed the patient characteristics, echocardiographic findings, electrocardiographic (ECG) abnormalities during sinus rhythm, and clinical course after ablation.In total, 196 patients (Cohort 1: 142 males, 156 AF cases) were analyzed. AFL patients were younger than AF patients (47.4 ± 10.6 vs. 50.2 ± 6.4years, p = 0.031) and organic heart disease (OHD) was significantly more common in AFL patients than AF patients (42.5% vs. 11.5%, p0.001). In 161 patients excluding OHD (Cohort 2), ECG abnormalities were more frequent in AFL than in AF patients (78.3% vs. 39.1%, p = 0.001). There were no significant differences in all-cause death, onset of heart failure, and cerebral strokes. On the other hand, the number of cases that required a pacemaker was significantly higher in the CAFL group than AF group (0.0% vs. 26.1%, p-value0.001). These results suggested that CAFL may reflect occurrence of any atrial myocardial damage, even if it does not lead to heart failure.Our present study suggested that CAFL may be associated with a broader atrial myocardial disorder in non-elderly patients.

Published
2021

37. Effects of Enhanced Intracranial Pressure on Blood Pressure and the Cardio-Ankle Vascular Index in Rabbits

Author

Tatsuo Chiba, Kazuhiro Shimizu, Tomoyuki Yamamoto, Chikao Miyazaki, Kiyoshi Sakuma, Akira Takahara, Nobuo Sugo, Mao Takahashi, Yoshinobu Nagasawa, Megumi Aimoto, and Kohji Shirai

Subjects
Male, medicine.medical_specialty, Intracranial Pressure, medicine.medical_treatment, Blood Pressure, 030204 cardiovascular system & hematology, Cisterna magna, Central venous pressure, 03 medical and health sciences, chemistry.chemical_compound, Vascular Stiffness, 0302 clinical medicine, Internal medicine, Carotid blood flow, Internal Medicine, medicine, Animals, Saline, Intracranial pressure, business.industry, musculoskeletal, neural, and ocular physiology, Biochemistry (medical), Cardio-ankle vascular index, medicine.disease, Autonomic nervous system, Blood pressure, Cardio Ankle Vascular Index, chemistry, Cardiology, Arterial stiffness, Original Article, Hexamethonium, Rabbits, Ankle, Cardiology and Cardiovascular Medicine, business, 030217 neurology & neurosurgery
Abstract

Aim: Stroke is well known to lead to hypertension; nevertheless, the role of vascular function in hypertension remains unclear. In this study, we aimed to clarify the mechanism underlying increased arterial stiffness following stroke. Methods: The cardio-ankle vascular index (CAVI) was measured in five New Zealand White rabbits. Under general anesthesia, intracranial pressure (ICP) was increased by injecting saline (15 mL) into the cisterna magna. ICP was monitored using a catheter inserted into the subarachnoid space via right frontal bone craniotomy. Blood pressure (BP), CAVI, and common carotid flow (CCF) were evaluated, and the responses of these parameters to increased ICP were analyzed. Results: Saline injection into the cisterna magna increased the ICP by over 20 mmHg. Both BP and CAVI increased from 63.2±4.84 to 128.8±14.68 mmHg and from 4.02±0.28 to 4.9±0.53, respectively. Similarly, BP and CCF increased. When hexamethonium was administered before the increase in ICP, the increase in BP (132.2±9.41 mmHg with 10 mg/kg hexamethonium vs. 105.6±11.01 mmHg with 100 mg/kg hexamethonium) and CAVI (5.02±0.64 with 10 mg/kg hexamethonium vs. 4.82±0.42 with 100 mg/kg hexamethonium) were suppressed in a dose-dependent manner. Conclusion: Increased ICP causes an increase in BP and CAVI, suggesting that enhanced stiffness of the muscular arteries contributes to high BP. Blocking the autonomic nervous system with hexamethonium suppresses the increase in BP and CAVI, indicating that these increases are mediated by activation of the autonomic nervous system.

Published
2021

38. Trauma Computed Tomography in the Modern Era: Not Always Quick and Safe

Author

Cameron Ghafil, Renqing Wu, Kazuhide Matsushima, Kenji Inaba, Heeseop Shin, Michael Menchine, and Hiroto Chiba

Subjects
Adult, Male, medicine.medical_specialty, Resuscitation, Time Factors, Computed tomography, Trauma Centers, Risk Factors, Transfusion requirement, medicine, Humans, Trauma team, Whole Body Imaging, Clinical significance, Prospective Studies, Adverse effect, Retrospective Studies, medicine.diagnostic_test, business.industry, Incidence (epidemiology), Trauma center, General Medicine, Middle Aged, Los Angeles, Wounds and Injuries, Female, Radiology, Tomography, X-Ray Computed, business
Abstract

Background Computed tomography (CT) has emerged as the diagnostic modality of choice in trauma patients. Recent studies suggest its use in hemodynamically unstable patients is safe and potentially lifesaving; however, the incidence of adverse events (AE) during the trauma CT scanning process remains unknown. Study Design Over a 6-month period at a Level 1 trauma center, data on patients undergoing trauma CT (whole-body CT (WBCT) +/− additional CT studies) were prospectively collected. All patients requiring a trauma team activation (TTA) were included. Adverse events and specific time intervals were recorded from the time of TTA notification to the time of return to the resuscitation bay from the CT suite. Results Of the 94 consecutive patients included in the study, 47.9% experienced 1 or more AE. Median duration away from the resuscitation bay for all patients was 24 minutes. Patients with AE spent a significantly longer time away from the resuscitation bay and had longer scan times. Vasopressor support and ongoing transfusion requirement at the time of CT scanning were associated with AE. Conclusion Adverse events of varying clinical significance occur frequently in patients undergoing emergent trauma CT. A standard trauma CT protocol could improve the efficiency and safety of the scanning process.

Published
2021

39. Sphingosine-1-phosphate interactions in the spleen and heart reflect extent of cardiac repair in mice and failing human hearts

Author

SiddabasaveGowda B. Gowda, Ganesh V. Halade, Vibhu Parcha, Shu-Ping Hui, Divyavani Gowda, Pankaj Arora, Hitoshi Chiba, Charles E. Chalfant, and Vasundhara Kain

Subjects
Male, medicine.medical_specialty, Physiology, Myocardial Infarction, Spleen, Disease, Mice, chemistry.chemical_compound, Sphingosine, Lectins, Physiology (medical), Internal medicine, medicine, Animals, Humans, Regeneration, Myocytes, Cardiac, Myocardial infarction, Sphingosine-1-phosphate, Sphingosine-1-Phosphate Receptors, Cells, Cultured, Chemokine CCL2, Heart Failure, Arginase, Tumor Necrosis Factor-alpha, business.industry, Macrophages, LC/MS, medicine.disease, ischemic heart disease, beta-N-Acetylhexosaminidases, Mice, Inbred C57BL, medicine.anatomical_structure, chemistry, Heart failure, Cardiac repair, sphingosine-1-phosphate, Cardiology, lipids (amino acids, peptides, and proteins), Lysophospholipids, Cardiology and Cardiovascular Medicine, business, Research Article
Abstract

Sphingosine-1-phosphate (S1P) is a bioactive mediator in inflammation. Dysregulated S1P is demonstrated as a cause of heart failure (HF). However, the time-dependent and integrative role of S1P interaction with receptors in HF is unclear after myocardial infarction (MI). In this study, the sphingolipid mediators were quantified in ischemic human hearts. We also measured the time kinetics of these mediators post-MI in murine spleen and heart as an integrative approach to understand the interaction of S1P and respective S1P receptors in the transition of acute (AHF) to chronic HF (CHF). Risk-free 8-12 wk male C57BL/6 mice were subjected to MI surgery, and MI was confirmed by echocardiography and histology. Mass spectrometry was used to quantify sphingolipids in plasma, infarcted heart, spleen of mice, and ischemic and healthy human heart. The physiological cardiac repair was observed in mice with a notable increase of S1P quantity (pmol/g) in the heart and spleen significantly reduced in patients with ischemic HF. The circulating murine S1P levels were increased during AHF and CHF despite lowered substrate in CHF. The S1PR1 receptor expression was observed to coincide with the respective S1P quantity in mice and human hearts. Furthermore, selective S1P1 agonist limited inflammatory markers CCL2 and TNF-alpha and accelerated reparative markers ARG-1 and YM-1 in macrophages in the presence of Kdo2-Lipid A (KLA; potent inflammatory stimulant). This report demonstrated the importance of S1P/S1PR1 signaling in physiological inflammation during cardiac repair in mice. Alteration in these axes may serve as the signs of pathological remodeling in patients with ischemia. NEW & NOTEWORTHY Previous studies indicate that sphingosine-1-phosphate (S1P) has some role in cardiovascular disease. This study adds quantitative and integrative systems-based approaches that are necessary for discovery and bedside translation. Here, we quantitated sphinganine, sphingosine, sphingosine-1-phosphate (S1P) in mice and human cardiac pathobiology. Interorgan S1P quantity and respective systems-based receptor activation suggest cardiac repair after myocardial infarction. Thus, S1P serves as a therapeutic target for cardiac protection in clinical translation.

Published
2021

40. Evaluation of auto-segmentation accuracy of cloud-based artificial intelligence and atlas-based models

Author

Mihiro Takemori, Satoshi Nakamura, Hiroshi Igaki, Kotaro Iijima, Junichi Kuwahara, Takahito Chiba, Weishan Chang, Tomoya Kaneda, Tairo Kashihara, Naoya Murakami, Hiroki Nakayama, Shouichi Katsuta, Yuka Urago, Hidetoshi Saitoh, and Hiroyuki Okamoto

Subjects
Male, Organs at Risk, Artificial intelligence, medicine.medical_treatment, R895-920, Prostate cancer, Medical physics. Medical radiology. Nuclear medicine, Atlases as Topic, Atlas (anatomy), Prostate, medicine, Humans, Radiology, Nuclear Medicine and imaging, Segmentation, Deep learning neural network, Head and neck cancer, RC254-282, Observer Variation, business.industry, Auto segmentation, Research, Prostatic Neoplasms, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, Cloud Computing, medicine.disease, Radiation therapy, medicine.anatomical_structure, Oncology, Head and Neck Neoplasms, Automatic segmentation, business
Abstract

Background Contour delineation, a crucial process in radiation oncology, is time-consuming and inaccurate due to inter-observer variation has been a critical issue in this process. An atlas-based automatic segmentation was developed to improve the delineation efficiency and reduce inter-observer variation. Additionally, automated segmentation using artificial intelligence (AI) has recently become available. In this study, auto-segmentations by atlas- and AI-based models for Organs at Risk (OAR) in patients with prostate and head and neck cancer were performed and delineation accuracies were evaluated. Methods Twenty-one patients with prostate cancer and 30 patients with head and neck cancer were evaluated. MIM Maestro was used to apply the atlas-based segmentation. MIM Contour ProtégéAI was used to apply the AI-based segmentation. Three similarity indices, the Dice similarity coefficient (DSC), Hausdorff distance (HD), and mean distance to agreement (MDA), were evaluated and compared with manual delineations. In addition, radiation oncologists visually evaluated the delineation accuracies. Results Among patients with prostate cancer, the AI-based model demonstrated higher accuracy than the atlas-based on DSC, HD, and MDA for the bladder and rectum. Upon visual evaluation, some errors were observed in the atlas-based delineations when the boundary between the small bowel or the seminal vesicle and the bladder was unclear. For patients with head and neck cancer, no significant differences were observed between the two models for almost all OARs, except small delineations such as the optic chiasm and optic nerve. The DSC tended to be lower when the HD and the MDA were smaller in small volume delineations. Conclusions In terms of efficiency, the processing time for head and neck cancers was much shorter than manual delineation. While quantitative evaluation with AI-based segmentation was significantly more accurate than atlas-based for prostate cancer, there was no significant difference for head and neck cancer. According to the results of visual evaluation, less necessity of manual correction in AI-based segmentation indicates that the segmentation efficiency of AI-based model is higher than that of atlas-based model. The effectiveness of the AI-based model can be expected to improve the segmentation efficiency and to significantly shorten the delineation time.

Published
2021

41. Genetic profiles of Barrett’s esophagus and esophageal adenocarcinoma in Japanese patients

Author

Hirotaka Oura, Mamoru Tokunaga, Ariki Nagashima, Motoi Nishimura, Wataru Shiratori, Tatsuya Kaneko, Masao Omata, Yuki Ohta, Yosuke Hirotsu, Takashi Taida, Kengo Kanayama, Naoki Akizue, Kentaro Ishikawa, Jun Kato, Jun-ichiro Ikeda, Keiko Saito, Hitoshi Mochizuki, Naoya Kato, Tsubasa Ishikawa, Kenichiro Okimoto, Masayuki Ota, Tomoaki Matsumura, Tetsuhiro Chiba, Kenji Amemiya, Kazuyuki Matsushita, Makoto Arai, and Keisuke Matsusaka

Subjects
Adult, Male, medicine.medical_specialty, Esophageal Neoplasms, Science, Esophageal adenocarcinoma, Adenocarcinoma, Gastroenterology, Article, Lesion, Barrett Esophagus, Young Adult, Esophagus, Japan, Internal medicine, medicine, Genetics, Humans, Aged, Cancer, Aged, 80 and over, Multidisciplinary, business.industry, Endoscopic biopsy, Gene Expression Profiling, Significant difference, High-Throughput Nucleotide Sequencing, Japanese population, Middle Aged, medicine.disease, Gene Expression Regulation, Neoplastic, medicine.anatomical_structure, Dysplasia, Barrett's esophagus, Medicine, Female, medicine.symptom, business
Abstract

The genetic characteristics of Barrett’s esophagus (BE) and esophageal adenocarcinoma (EAC) in the Japanese population is unclear. This study aims to investigate the genetic characteristics from nondysplastic BE (NDBE) to early EAC in Japan. Clinical information was collected. Moreover, the genetic profile of NDBE without concurrent dysplasia, early EAC, and surrounding BE were also investigated using endoscopic biopsy samples and formalin-fixed, paraffin-embedded specimens from Japanese patients by targeted next-generation sequencing. Immunohistochemical staining for p53 was also performed for EAC lesions. Targeted NGS was performed for 33 cases with 77 specimens. No significant difference exists in the NDBE group between the number of putative drivers per lesion in the short-segment Barrett’s esophagus (SSBE) and long-segment Barrett’s esophagus (LSBE) [0 (range, 0–1) vs. 0 (range, 0–1). p = 1.00]. TP53 putative drivers were found in two patients (16.7%) with nondysplastic SSBE. TP53 was the majority of putative drivers in both BE adjacent to EAC and EAC, accounting for 66.7% and 66.7%, respectively. More putative drivers per lesion were found in the EAC than in the NDBE group [1 (range, 0–3) vs. 0 (range, 0–1). p TP53 in the Japanese early EAC were similar to those in western countries. However, TP53 putative drivers were detected even in Japanese patients with nondysplastic SSBE. This is significant because such nondysplastic SSBE might have higher risk of progressing to high-grade dysplasia or EAC. The risks of progression may not be underestimated and appropriate follow-ups may be necessary even in patients with SSBE.Trial registration: This study was registered at the University Hospital Medical Information Network (UMIN000034247).

Published
2021

42. Mapping the human genetic architecture of COVID-19

Author

Niemi, MEK, Karjalainen, J, Liao, RG, Neale, BM, Daly, M, Ganna, A, Pathak, GA, Andrews, SJ, Kanai, M, Veerapen, K, Fernandez-Cadenas, I, Schulte, EC, Striano, P, Marttila, M, Minica, C, Marouli, E, Karim, MA, Wendt, FR, Savage, J, Sloofman, L, Butler-Laporte, G, Kim, H-N, Kanoni, S, Okada, Y, Byun, J, Han, Y, Uddin, MJ, Smith, GD, Willer, CJ, Buxbaum, JD, Mehtonen, J, Finucane, H, Cordioli, M, Martin, AR, Zhou, W, Pasaniuc, B, Julienne, H, Aschard, H, Shi, H, Yengo, L, Polimanti, R, Ghoussaini, M, Schwartzentruber, J, Dunham, I, Chwialkowska, K, Francescatto, M, Trankiem, A, Balaconis, MK, Davis, L, Lee, S, Priest, J, Renieri, A, Sankaran, VG, van Heel, D, Deelen, P, Richards, JB, Nakanishi, T, Biesecker, L, Kerchberger, VE, Kenneth, J, Mari, F, Bernasconi, A, Ceri, S, Canakoglu, A, Wolford, B, Faucon, A, Dutta, AK, Schurmann, C, Harry, E, Birney, E, Nguyen, H, Nasir, J, Kaunisto, M, Solomonson, M, Dueker, N, Vadgama, N, Limou, S, Rahmouni, S, Mbarek, H, Darwish, D, Uddin, MM, Albertos, R, Perez-Tur, J, Li, R, Folkersen, L, Moltke, I, Koelling, N, Teumer, A, Kousathanas, A, Utrilla, A, Verdugo, RA, Zarate, R, Medina-Gomez, C, Gomez-Cabrero, D, Carnero-Montoro, E, Cadilla, CL, Moreno-Estrada, A, Garmendia, A, Moya, L, Sedaghati-Khayat, B, Boua, PR, Fave, M-J, Francioli, L, Lemacon, A, Migeotte, I, Patel, S, Varnai, R, Szentpeteri, JL, Sipeky, C, Colombo, F, von Hohenstaufen, K, Lio, P, Vallerga, C, Wang, Q, Tanigawa, Y, Im, H, Han, C, Song, H, Lim, J, Lee, Y, Kim, S, Im, S, Atanasovska, B, Ahmad, HF, Boer, C, Jansen, P, Franke, L, Kaja, E, Pasko, D, Kennis-Szilagyi, I, Kornilov, SA, Prijatelj, V, Prokic, I, Sivanadhan, I, Perumal, S, Esmaeeli, S, Pearson, NM, Auton, A, Shelton, JF, Shastri, AJ, Filshtein-Sonmez, T, Coker, D, Symons, A, Esparza-Gordillo, J, Aslibekyan, S, O'Connell, J, Ye, C, Weldon, CH, Perera, M, O'Leary, K, Tuck, M, O'Brien, T, Meltzer, D, O'Donnell, P, Nutescu, E, Yang, G, Alarcon, C, Herrmann, S, Mazurek, S, Banagan, J, Hamidi, Z, Barbour, A, Raffat, N, Moreno, D, Friedman, P, Ferwerda, B, van de Beek, D, Brouwer, MC, Vlaar, APJ, Wiersinga, WJ, Posthuma, D, Tissink, E, Zwinderman, AHK, Uffelmann, E, van Agtmael, M, Algera, AG, van Baarle, F, Bax, D, Beudel, M, Bogaard, HJ, Bomers, M, Bonta, PI, Bos, L, Botta, M, de Brabander, J, de Bree, G, de Bruin, S, Bugiani, M, Bulle, E, Chouchane, O, Cloherty, A, Dongelmans, D, Elbers, P, Fleuren, L, Geerlings, S, Geerts, B, Geijtenbeek, T, Girbes, A, Goorhuis, B, Grobusch, MP, Hafkamp, F, Hagens, L, Hamann, J, Harris, V, Hemke, R, Hermans, SM, Heunks, L, Hollmann, M, Horn, J, Hovius, JW, de Jong, MD, Koning, R, van Mourik, N, Nellen, J, Nossent, EJ, Paulus, F, Peters, E, van der Poll, T, Preckel, B, Prins, JM, Raasveld, J, Reijnders, T, Schinkel, M, Schultz, MJ, Schuurman, A, Sigaloff, K, Smit, M, Stijnis, CS, Stilma, W, Teunissen, C, Thoral, P, Tsonas, A, van der Valk, M, Veelo, D, de Vries, H, van Vugt, M, Wouters, D, Minnaar, RP, Kromhout, A, van Uffelen, KWJ, 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Hirofumi, Ikemura, Shinnosuke, Chubachi, Shotaro, Okamori, Satoshi, Terai, Hideki, Tanaka, Hiromu, Morita, Atsuho, Lee, Ho, Asakura, Takanori, Sasaki, Junichi, Morisaki, Hiroshi, Uwamino, Yoshifumi, Nanki, Kosaku, Mikami, Yohei, Tomono, Kazunori, Kato, Kazuto, Matsuda, Fumihiko, Takahashi, Meiko, Hizawa, Nobuyuki, Takeda, Yoshito, Hirata, Haruhiko, Shiroyama, Takayuki, Miyawaki, Satoru, Suzuki, Ken, Maeda, Yuichi, Nii, Takuro, Noda, Yoshimi, Niitsu, Takayuki, Adachi, Yuichi, Enomoto, Takatoshi, Amiya, Saori, Hara, Reina, Takahashi, Kunihiko, Anzai, Tatsuhiko, Hasegawa, Takanori, Ito, Satoshi, Koike, Ryuji, Endo, Akifumi, Uchimura, Yuji, Miyazaki, Yasunari, Honda, Takayuki, Tateishi, Tomoya, Tohda, Shuji, Ichimura, Naoya, Sonobe, Kazunari, Sassa, Chihiro, Nakajima, Jun, Nannya, Yasuhito, Omae, Yosuke, Takahashi, Kazuhisa, Harada, Norihiro, Hiki, Makoto, Takagi, Haruhi, Nakamura, Ai, Tagaya, Etsuko, Kawana, Masatoshi, Arimura, Ken, Ishiguro, Takashi, Takayanagi, Noboru, Isono, Taisuke, Takaku, Yotaro, Takano, Kenji, Anan, Ryusuke, Nakajima, Yukiko, Nakano, Yasushi, Nishio, Kazumi, Ueda, Soichiro, Hayashi, Reina, Tateno, Hiroki, Hase, Isano, Yoshida, Shuichi, Suzuki, Shoji, Mitamura, Keiko, Saito, Fumitake, Ueda, Tetsuya, Azuma, Masanori, Nagasaki, Tadao, Yasui, Yoshinori, Hasegawa, Yoshinori, Mutoh, Yoshikazu, Yoshiyama, Takashi, Shoko, Tomohisa, Kojima, Mitsuaki, Adachi, Tomohiro, Ishikawa, Motonao, Takahashi, Kenichiro, Watanabe, Kazuyoshi, Manabe, Tadashi, Ito, Fumimaro, Fukui, Takahiro, Funatsu, Yohei, Koh, Hidefumi, Hirai, Yoshihiro, Kawashima, Hidetoshi, Narita, Atsuya, Niwa, Kazuki, Sekikawa, Yoshiyuki, Saito, Fukuki, Yoshiya, Kazuhisa, Yoshihara, Tomoyuki, Suzuki, Yusuke, Nakayama, Sohei, Masuzawa, Keita, Nishi, Koichi, Nishitsuji, Masaru, Tani, Maiko, Inoue, Takashi, Hirano, Toshiyuki, Kobayashi, Keigo, Miyazawa, Naoki, Kimura, Yasuhiro, Sado, Reiko, Ogura, Takashi, Kitamura, Hideya, Murohashi, Kota, Nakachi, Ichiro, Baba, Rie, Arai, Daisuke, Fuke, Satoshi, Saito, Hiroshi, Kuwahara, Naota, Fujiwara, Akiko, Okada, Takenori, Baba, Tomoya, Noda, Junya, Mashimo, Shuko, Yagi, Kazuma, Shiomi, Tetsuya, Hashiguchi, Mizuha, Odani, Toshio, Mochimaru, Takao, Oyamada, Yoshitaka, Mori, Nobuaki, Izumi, Namiki, Nagata, Kaoru, Taki, Reiko, Murakami, Koji, Yamada, Mitsuhiro, Sugiura, Hisatoshi, Hayashi, Kentaro, Shimizu, Tetsuo, Gon, Yasuhiro, Fujitani, Shigeki, Tsuchida, Tomoya, Yoshida, Toru, Kagaya, Takashi, Kita, Toshiyuki, Sakagami, Satoru, Kimizuka, Yoshifumi, Kawana, Akihiko, Nakamura, Yoshihiko, Ishikura, Hiroyasu, Takata, Tohru, Kikuchi, Takahide, Taniyama, Daisuke, Nakamura, Morio, Kodama, Nobuhiro, Kaneyama, Yasunari, Maeda, Shunsuke, Nagasaki, Yoji, Okamoto, Masaki, Ishihara, Sayoko, Ito, Akihiro, Chihara, Yusuke, Takeuchi, Mayumi, Onoi, Keisuke, Hashimoto, Naozumi, Wakahara, Keiko, Ando, Akira, Masuda, Makoto, Wakabayashi, Aya, Watanabe, Hiroki, Sageshima, Hisako, Nakada, Taka-Aki, Abe, Ryuzo, Shimada, Tadanaga, Kawamura, Kodai, Ichikado, Kazuya, Nishiyama, Kenta, Yamasaki, Masaki, Hashimoto, Satoru, Kusaka, Yu, Ohba, Takehiko, Isogai, Susumu, Takada, Minoru, Kanda, Hidenori, Komase, Yuko, Sano, Fumiaki, Asano, Koichiro, Oguma, Tsuyoshi, Harada, Masahiro, Takahashi, Takeshi, Shibusawa, Takayuki, Abe, Shinji, Kono, Yuta, Togashi, Yuki, Izumo, Takehiro, Inomata, Minoru, Awano, Nobuyasu, Ogawa, Shinichi, Ogata, Tomouki, Ishihara, Shoichiro, Kanehiro, Arihiko, Ozaki, Shinji, Fuchimoto, Yasuko, Kitagawa, Yuichiro, Yoshida, Shozo, Ogura, Shinji, Nishiyama, Kei, Yoshida, Kousuke, Beppu, Satoru, Fukuyama, Satoru, Eriguchi, Yoshihiro, Yonekawa, Akiko, Inoue, Yoshiaki, Yamagata, Kunihiro, Chiba, Shigeru, Narumoto, Osamu, Nagai, Hideaki, Ooshima, Nobuharu, Motegi, Mitsuru, Sagara, Hironori, Tanaka, Akihiko, Ohta, Shin, Shibata, Yoko, Tanino, Yoshinori, Sato, Yuki, Yamada, Yuichiro, Hashino, Takuya, Shinoki, Masato, Iwagoe, Hajime, Imamura, Tomonori, Umeda, Akira, Shimada, Hisato, Endo, Mayu, Hayashi, Shinichi, Takahashi, Mai, Nakano, Shigefumi, Yatomi, Masakiyo, Maeno, Toshitaka, Ishii, Tomoo, Utsugi, Mitsuyoshi, Ono, Akihiro, Kanaoka, Kensuke, Ihara, Shoichi, Komuta, Kiyoshi, Boezen, Marike, Claringbould, Annique, Lopera, Esteban, Warmerdam, Robert, Vonk, Judith. M., van Blokland, Irene, Lanting, Pauline, Ori, Anil P. S., Obeidat, Ma’En, Hernández Cordero, Ana I., Sin, Don D., Bossé, Yohan, Joubert, Philippe, Hao, Ke, Nickle, David, Timens, Wim, van den Berge, Maarten, Feng, Yen-Chen Anne, Mercader, Josep, Weiss, Scott T., Karlson, Elizabeth W., Smoller, Jordan W., Murphy, Shawn N., Meigs, James B., Woolley, Ann E., Green, Robert C., Perez, Emma F., Zöllner, Sebastian, Wang, Jiongming, Beck, Andrew, Sloofman, Laura G., Ascolillo, Steven, Sebra, Robert P., Collins, Brett L., Levy, Te, Sealfon, Stuart C., Jordan, Daniel M., Thompson, Ryan C., Gettler, Kyle, Chaudhary, Kumardeep, Belbin, Gillian M., Preuss, Michael, Hoggart, Clive, Choi, Sam, Underwood, Slayton J., Salib, Irene, Britvan, Bari, Keller, Katherine, Tang, Lara, Peruggia, Michael, Hiester, Liam L., Niblo, Kristi, Aksentijevich, Alexandra, Labkowsky, Alexander, Karp, Avromie, Zlatopolsky, Menachem, Zyndorf, Marissa, Charney, Alexander W., Beckmann, Noam D., Schadt, Eric E., Abul-Husn, Noura S., Cho, Judy H., Itan, Yuval, Kenny, Eimear E., Loos, Ruth J. F., Nadkarni, Girish N., Do, Ron, O’Reilly, Paul, Huckins, Laura M., Ferreira, Manuel A. R., Abecasis, Goncalo R., Leader, Joseph B., Cantor, Michael N., Justice, Anne E., Carey, Dave J., Chittoor, Geetha, Josyula, Navya Shilpa, Kosmicki, Jack A., Horowitz, Julie E., Baras, Ari, Gass, Matthew C., Yadav, Ashish, Mirshahi, Tooraj, Jan Hottenga, Jouke, Bartels, Meike, de Geus, Eco J. C., Nivard, Michel G., Verma, Anurag, Ritchie, Marylyn D., Rader, Daniel, Li, Binglan, Verma, Shefali S., Lucas, Anastasia, Bradford, Yuki, Zara, Federico, Salpietro, Vincenzo, Scala, Marcello, Iacomino, Michele, Scudieri, Paolo, Bocciardi, Renata, Minetti, Carlo, Riva, Antonella, Vari, Maria Stella, Rahier, Jean-Françoi, Giorgio, Elisa, Carli, Diana, Louis, Edouad, Bulik, Cynthia M., Landén, Mikael, Brusco, Alfredo, Ferrero, Giovanni Battista, Madia, Francesca, Fundín, Bengt, Ismail, Said I., Saad, Chadi, Al-Sarraj, Yaser, Badji, Radja Messai, Al-Muftah, Wadha, Al Thani, Asma, Afifi, Nahla, Klovins, Jani, Rovite, Vita, Rescenko, Raimond, Peculis, Raiti, Ustinova, Monta, Zeberg, Hugo, Frithiof, Robert, Hultström, Michael, Lipcsey, Miklo, Johnson, Ruth, Geschwind, Daniel H., Freimer, Nelson, Butte, Manish J., Ding, Yi, Chiu, Alec, Chang, Timothy S., Boutros, Paul, Moutsianas, Louka, Caulfield, Mark J., Scott, Richard H., Walker, Susan, Stuckey, Alex, Odhams, Christopher A., Rhodes, Daniel, Fowler, Tom, Rendon, Augusto, Chan, Georgia, Arumugam, Prabhu, Karczewski, Konrad J., Wilson, Daniel J., Spencer, Chris A., Crook, Derrick W., Wyllie, David H., O’Connell, Anne Marie, Atkinson, Elizabeth G., Tsuo, Kristin, Baya, Nikola, Turley, Patrick, Gupta, Rahul, Walters, Raymond K., Palmer, Duncan S., Sarma, Gopal, Cheng, Nathan, Lu, Wenhan, Churchhouse, Claire, Goldstein, Jacqueline I., King, Daniel, Seed, Cotton, Daly, Mark J., Bryant, Sam, Satterstrom, F. Kyle, Band, Gavin, Earle, Sarah G., Lin, Shang-Kuan, Arning, Nicola, Armstrong, Jacob, Rudkin, Justine K., Callier, Shawneequa, Cusick, Caroline, Soranzo, Nicole, Zhao, Jing Hua, Danesh, John, Di Angelantonio, Emanuele, Butterworth, Adam S., Sun, Yan V., Huffman, Jennifer E., Cho, Kelly, O’Donnell, Christopher J., Tsao, Phil, Gaziano, J. Michael, Peloso, Gina, Ho, Yuk-Lam, Mian, Michael, Scaggiante, Federica, Chang, Xiao, Glessner, Joseph R., Hakonarson, Hakon, Mcguigan, Peter J., Prockter Moore, Luke Stephen, Vizcaychipi, Marcela Paola, Hall, Kathryn, Campbell, Andy, Nichol, Ailstair, Ward, Geraldine, Page, Valerie Joan, Semple, Malcolm G., Adeniji, Kayode, Agranoff, Daniel, Agwuh, Ken, Ail, Dhiraj, Aldera, Erin L., Alegria, Ana, Angus, Brian, Ashish, Abdul, Atkinson, Dougal, Bari, Shahedal, Barlow, Gavin, Barnass, Stella, Barrett, Nichola, Bassford, Christopher, Basude, Sneha, Baxter, David, Beadsworth, Michael, Bernatoniene, Jolanta, Berridge, John, Best, Nicola, Bothma, Pieter, Chadwick, David, Brittain-Long, Robin, Bulteel, Naomi, Burden, Tom, Burtenshaw, Andrew, Caruth, Vikki, Chambler, Duncan, Chee, Nigel, Child, Jenny, Chukkambotla, Srikanth, Clark, Tom, Collini, Paul, Cosgrove, Catherine, Cupitt, Jason, Cutino-Moguel, Maria-Teresa, Dark, Paul, Dawson, Chri, Dervisevic, Samir, Donnison, Phil, Douthwaite, Sam, Drummond, Andrew, Durand, Ingrid, Dushianthan, Ahilanadan, Dyer, Tristan, Evans, Cariad, Eziefula, Chi, Fegan, Christopher, Finn, Adam, Fullerton, Duncan, Garg, Sanjeev, Garg, Atul, Gkrania-Klotsas, Effrossyni, Godden, Jo, Goldsmith, Arthur, Graham, Clive, Hardy, Elaine, Hartshorn, Stuart, Harvey, Daniel, Havalda, Peter, Hawcutt, Daniel B., Hobrok, Maria, Hodgson, Luke, Hormis, Anil, Jacobs, Michael, Jain, Susan, Jennings, Paul, Kaliappan, Agilan, Kasipandian, Vidya, Kegg, Stephen, Kelsey, Michael, Kendall, Jason, Kerrison, Caroline, Kerslake, Ian, Koch, Oliver, Koduri, Gouri, Koshy, George, Laha, Shondipon, Laird, Steven, Larkin, Susan, Leiner, Tama, Lillie, Patrick, Limb, Jame, Linnett, Vanessa, Little, Jeff, Lyttle, Mark, Macmahon, Michael, Macnaughton, Emily, Mankregod, Ravish, Masson, Huw, Matovu, Elijah, Mccullough, Katherine, Mcewen, Ruth, Meda, Manjula, Mills, Gary H., Minton, Jane, Ward, Karl, Mirfenderesky, Mariyam, Mohandas, Kavya, Mok, Quen, Moon, Jame, Moore, Elinoor, Morgan, Patrick, Morris, Craig, Mortimore, Katherine, Moses, Samuel, Mpenge, Mbiye, Mulla, Rohinton, Murphy, Michael, Nagel, Megan, Nagarajan, Thapa, Nelson, Mark, O’Shea, Matthew K., Otahal, Igor, Ostermann, Marlie, Pais, Mark, Panchatsharam, Selva, Papakonstantinou, Danai, Paraiso, Hassan, Patel, Brij, Pattison, Natalie, Pepperell, Justin, Peters, Mark, Phull, Mandeep, Pintus, Stefania, Pooni, Jagtur Singh, Post, Frank, Price, David, Prout, Rachel, Rae, Nikola, Reschreiter, Henrik, Reynolds, Tim, Richardson, Neil, Roberts, Mark, Roberts, Devender, Rose, Alistair, Rousseau, Guy, Ryan, Brendan, Saluja, Taranprit, Shah, Aarti, Shanmuga, Prad, Sharma, Anil, Shawcross, Anna, Sizer, Jeremy, Shankar-Hari, Manu, Smith, Richard, Snelson, Catherine, Spittle, Nick, Staines, Nikki, Stambach, Tom, Stewart, Richard, Subudhi, Pradeep, Szakmany, Tama, Tatham, Kate, Thomas, Jo, Thompson, Chri, Thompson, Robert, Tridente, Ascanio, Tupper-Carey, Darell, Twagira, Mary, Ustianowski, Andrew, Vallotton, Nick, Vincent-Smith, Lisa, Visuvanathan, Shico, Vuylsteke, Alan, Waddy, Sam, Wake, Rachel, Walden, Andrew, Welters, Ingeborg, Whitehouse, Tony, Whittaker, Paul, Whittington, Ashley, Papineni, Padmasayee, Wijesinghe, Meme, Williams, Martin, Wilson, Lawrence, Cole, Sarah, Winchester, Stephen, Wiselka, Martin, Wolverson, Adam, Wooton, Daniel G., Workman, Andrew, Yates, Bryan, Young, Peter, Beale, Rupert, Bretherick, Andrew D., Clohisey, Sara, Fourman, Max Head, Furniss, Jame, Gountouna, Elvina, Grimes, Graeme, Haley, Chri, Harrison, David, Hayward, Caroline, Keating, Sean, Klaric, Lucija, Klenerman, Paul, Law, Andy, Meynert, Alison M., Millar, Jonathan, Pairo-Castineira, Erola, Parkinson, Nichola, Ponting, Chris P., Porteous, David J., Rawlik, Konrad, Richmond, Anne, Rowan, Kathy, Russell, Clark D., Shen, Xia, Shih, Barbara, Tenesa, Albert, Vitart, Veronique, Wang, Bo, Wilson, James F., Wu, Yang, Yang, Jian, Yang, Zhijian, Zechner, Marie, Zhai, Ranran, Zheng, Chenqing, Norman, Lisa, Pius, Riinu, Drake, Thomas M., Fairfield, Cameron J., Knight, Stephen R., Mclean, Kenneth A., Murphy, Derek, Shaw, Catherine A., Dalton, Jo, Girvan, Michelle, Saviciute, Egle, Roberts, Stephanie, Harrison, Janet, Marsh, Laura, Connor, Marie, Halpin, Sophie, Jackson, Clare, Gamble, Carrol, Leeming, Gary, Law, Andrew, Wham, Murray, Hendry, Ro, Scott-Brown, Jame, Begg, Colin, Hinds, Charle, Wai Ho, Antonia Ying, Horby, Peter W., Knight, Julian, Ling, Lowell, Maslove, David, Mcauley, Danny, Montgomery, Hugh, Nichol, Alistair, Openshaw, Peter J. M., Summers, Charlotte, Walsh, Timothy, Armstrong, Lisa, Bates, Hayley, Dooks, Emma, Farquhar, Fiona, Hairsine, Brigid, Mcparland, C., Packham, Sophie, Alldis, Zoe, Astin-Chamberlain, Raine, Bibi, Fatima, Biddle, Jack, Blow, Sarah, Bolton, Matthew, Borra, Catherine, Bowles, Ruth, Burton, Maudrian, Choudhury, Yasmin, Collier, David, Cox, Amber, Easthope, Amy, Ebano, Patrizia, Fotiadis, Stavro, Gurasashvili, Jana, Halls, Rosslyn, Hartridge, Pippa, Kallon, Delordson, Kassam, Jamila, Lancoma-Malcolm, Ivone, Matharu, Maninderpal, May, Peter, Mitchelmore, Oliver, Newman, Tabitha, Patel, Mital, Pheby, Jane, Pinzuti, Irene, Prime, Zoe, Prysyazhna, Oleksandra, Shiel, Julian, Taylor, Melanie, Tierney, Carey, Wood, Suzanne, Zak, Anne, Zongo, Olivier, Forsey, Miranda, Nicholson, Anne, Riches, Joanne, Vertue, Mark, Wasson, Christopher, Finn, Stephanie, Green, Jackie, Collins, Erin, King, Bernadette, Grauslyte, Lina, Hussain, Musarat, Pogreban, Tatiana, Rosaroso, Lace, Salciute, Erika, Franke, George, Wong, Joanna, George, Aparna, Akeroyd, Louise, Bano, Shereen, Bromley, Matt, Gurr, Lucy, Lawton, Tom, Morgan, Jame, Sellick, Kirsten, Warren, Deborah, Wilkinson, Brian, Mcgowan, Janet, Ledgard, Camilla, Stacey, Amelia, Pye, Kate, Bellwood, Ruth, Bentley, Michael, Loosley, Ronda, Mcguinness, Heather, Tench, Helen, Wolf-Roberts, Rebecca, Gibson, Sian, Lyle, Amanda, Mcneela, Fiona, Radhakrishnan, Jayachandran, Hughes, Alistair, Ali, Asifa, Brady, Megan, Dale, Sam, Dance, Annalisa, Gledhill, Lisa, Greig, Jill, Hanson, Kathryn, Holdroyd, Kelly, Home, Marie, Kelly, Diane, Kitson, Ro, Matapure, Lear, Melia, Deborah, Mellor, Samantha, Nortcliffe, Tonicha, Pinnell, Jez, Robinson, Matthew, Shaw, Lisa, Shaw, Ryan, Thomis, Lesley, Wilson, Alison, Wood, Tracy, Bayo, Lee-Ann, Merwaha, Ekta, Ishaq, Tahira, Hanley, Sarah, Antcliffe, David, Banach, Dorota, Brett, Stephen, Coghlan, Phoebe, Fernandez, Ziortza, Gordon, Anthony, Rojo, Roceld, Arias, Sonia Sousa, Templeton, Maie, Jha, Rajeev, Krishnamurthy, Vinodh, Lim, Lai, Bi, Rehana, Scholefield, Barney, Ashton, Lydia, Williams, Alison, Cheyne, Claire, Saunderson, Anne, Allan, Angela, Anderson, Felicity, Kaye, Callum, Liew, Jade, Medhora, Jasmine, Scott, Teresa, Trumper, Erin, Botello, Adriana, Polgarova, Petra, Stroud, Katerina, Meaney, Eoghan, Jones, Megan, Ng, Anthony, Agrawal, Shruti, Pathan, Nazima, White, Deborah, Daubney, Esther, Elston, Kay, Parker, Robert, Reddy, Amie, Turner-Bone, Ian, Wilding, Laura, Harding, Peter, Jacob, Reni, Jones, Cathy, Denmade, Craig, Croft, Maria, White, Ian, Lim, Li, Griffin, Denise, Muchenje, Nycola, Mupudzi, Mcdonald, Partridge, Richard, Conyngham, Jo-Anna, Thomas, Rachel, Wright, Mary, Corral, Maria Alvarez, Bastion, Victoria, Clarke, Daphene, David, Beena, Kent, Harriet, Lorusso, Rachel, Lubimbi, Gamu, Murdoch, Sophie, Penacerrada, Melchizedek, Thomas, Alastair, Valentine, Jennifer, Vochin, Ana, Wulandari, Retno, Djeugam, Brice, Dawson, Joy, Garrioch, Sweyn, Tolson, Melanie, Aldridge, Jonathan, de Almeida Martins, Laura Gome, Carungcong, Jaime, Beavis, Sarah, Dale, Katie, Gascoyne, Rachel, Hawes, Joanne, Pritchard, Kelly, Stevenson, Lesley, Whileman, Amanda, Cowley, Anne, Highgate, Judith, Crawley, Rikki, Crew, Abigail, Cunningham, Mishell, Daniels, Allison, Harrison, Laura, Hope, Susan, Inweregbu, Ken, Jones, Sian, Lancaster, Nicola, Matthews, Jamie, Nicholson, Alice, Wray, Gemma, Benham, Leonie, Bradshaw, Zena, Brown, Joanna, Caswell, Melanie, Melling, Sarah, Preston, Stephen, Slawson, Nicola, Stoddard, Emma, Warden, Scott, Combes, Edward, Joefield, Teishel, Monnery, Sonja, Beech, Valerie, Trotman, Sallyanne, Hopkins, Bridget, Scriven, Jame, Thrasyvoulou, Laura, Willis, Heather, Anderson, Susan, Birch, Janine, Collins, Emma, Hammerton, Kate, O’Leary, Ryan, Abernathy, Caroline, Foster, Louise, Gratrix, Andrew, Martinson, Vicky, Parkinson, Priyai, Stones, Elizabeth, Carbral-Ortega, Llucia, Kapoor, Ritoo, Loader, David, Castle, Karen, Brandwood, Craig, Smith, Lara, Clark, Richard, Birchall, Katie, Kolakaluri, Laurel, Baines, Deborah, Sukumaran, Anila, Mapfunde, Isheunesu, Meredith, Megan, Morris, Lucy, Ryan, Lucy, Clark, Amy, Sampson, Julia, Peters, Cecilia, Dent, Martin, Langley, Margaret, Ashraf, Saima, Wei, Shuying, Andrew, Angela, Chablani, Manish, Kirkby, Amy, Netherton, Kimberley, Bates, Michelle, Dasgin, Jo, Gill, Jaspret, Nilsson, Annette, Apetri, Elena, Basikolo, Cathrine, Blackledge, Bethan, Catlow, Laura, Charles, Bethan, Doonan, Reece, Harris, Jade, Harvey, Alice, Horner, Daniel, Knowles, Karen, Lee, Stephanie, Lomas, Diane, Lyons, Chloe, Marsden, Tracy, Mclaughlan, Danielle, Mcmorrow, Liam, Pendlebury, Jessica, Perez, Jane, Poulaka, Maria, Proudfoot, Nicola, Slaughter, Melanie, Slevin, Kathryn, Thomas, Vicky, Walker, Danielle, Michael, Angiy, Collis, Matthew, Clark, Martyn, Coulding, Martina, Jude, Edward, Mccormick, Jacqueline, Mercer, Oliver, Potla, Darsh, Rehman, Hafiz, Savill, Heather, Turner, Victoria, Davey, Miriam, Golden, David, Seaman, Rebecca, Hunt, Jodie, Dearden, Joy, Dobson, Emma, Mulcahy, Michelle, Munt, Sheila, O’Connor, Grainne, Philbin, Jennifer, Rishton, Chloe, Tully, Redmond, Winnard, Sarah, Cagova, Lenka, Fofano, Adama, Garner, Lucie, Holcombe, Helen, Mepham, Sue, Mitchell, Alice Michael, Mwaura, Lucy, Praman, K., Vuylsteke, Alain, Zamikula, Julie, Bercades, Georgia, Brealey, David, Hass, Ingrid, Maccallum, Niall, Martir, Glady, Raith, Eamon, Reyes, Anna, Smyth, Deborah, Taylor, Abigail, Hughes, Rachel Anne, Thomas, Helen, Rees, Alun, Duskova, Michaela, Phipps, Janet, Brooks, Suzanne, Edwards, Michelle, Alexander, Peter, Allen, Schvearn, Bradley-Potts, Joanne, Brantwood, Craig, Egan, Jasmine, Felton, Timothy, Padden, Grace, Ward, Luke, Moss, Stuart, Glasgow, Susannah, Beesley, Kate, Board, Sarah, Kubisz-Pudelko, Agnieszka, Lewis, Alison, Perry, Je, Pippard, Lucy, Wood, Di, Buckley, Clare, Brown, Alison, Gregory, Jane, O’Connell, Susan, Smith, Tim, Belagodu, Zakaula, Fuller, Bridget, Gherman, Anca, Olufuwa, Olumide, Paramsothy, Remi, Stuart, Carmel, Oakley, Naomi, Kamundi, Charlotte, Tyl, David, Collins, Katy, Silva, Pedro, Taylor, June, King, Laura, Coates, Charlotte, Crowley, Maria, Wakefield, Phillipa, Beadle, Jane, Johnson, Laura, Sargeant, Janet, Anderson, Madeleine, Jardine, Catherine, Williams, Dewi, Parris, Victoria, Quaid, Sheena, Watson, Ekaterina, Melville, Julie, Naisbitt, Jay, Joseph, Rosane, Lazo, Maria, Walton, Olivia, Neal, Alan, Hill, Michaela, Kannan, Thogulava, Wild, Laura, Allan, Elizabeth, Darlington, Kate, Davies, Ffyon, Easton, Jack, Kumar, Sumit, Lean, Richard, Menzies, Daniel, Pugh, Richard, Qiu, Xinyi, Davies, Llino, Williams, Hannah, Scanlon, Jeremy, Davies, Gwyneth, Mackay, Callum, Lewis, Joannne, Rees, Stephanie, Coetzee, Samantha, Gales, Alistair, Raj, Meena, Sell, Craig, Langton, Helen, Watters, Malcolm, Novis, Catherine, Arbane, Gill, Bociek, Aneta, Campos, Sara, Grau, Neu, Jones, Tim Owen, Lim, Rosario, Marotti, Martina, Whitton, Christopher, Barron, Anthony, Collins, Ciara, Kaul, Sundeep, Passmore, Heather, Prendergast, Claire, Reed, Anna, Rogers, Paula, Shokkar, Rajvinder, Woodruff, Meriel, Middleton, Hayley, Polgar, Oliver, Nolan, Claire, Thwaites, Vicky, Mahay, Kanta, Sri-Chandana, Chunda, Scherewode, Joslan, Stephenson, Lorraine, Marsh, Sarah, Bancroft, Hollie, Bellamy, Mary, Carmody, Margaret, Daglish, Jacqueline, Moore, Faye, Rhodes, Joanne, Sangombe, Mirriam, Kadiri, Salma, Ayers, Amanda, Harrison, Wendy, North, Julie, Cavazza, Anna, Cockrell, Maeve, Corcoran, Eleanor, Depante, Maria, Finney, Clare, Jerome, Ellen, Mcphail, Mark, Nayak, Monalisa, Noble, Harriet, O’Reilly, Kevin, Pappa, Evita, Saha, Rohit, Saha, Sian, Smith, John, Knighton, Abigail, Gill, Mandy, Paul, Paul, Ratnam, Valli, Shelton, Sarah, Wynter, Inez, Baptista, David, Crowe, Rebecca, Fernandes, Rita, Herdman-Grant, Rosaleen, Joseph, Anna, Loveridge, Adam, Mckenley, India, Morino, Eriko, Naranjo, Andre, Simms, Richard, Sollesta, Kathryn, Swain, Andrew, Venkatesh, Harish, Khera, Jacyntha, Fox, Jonathan, Barber, Russell, Hewitt, Claire, Hilldrith, Annette, Jackson-Lawrence, Karen, Shepardson, Sarah, Wills, Maryanne, Butler, Susan, Tavares, Silvia, Cunningham, Amy, Hindale, Julia, Arif, Sarwat, George, Linsha, Twiss, Sophie, Wright, David, Holland, Maureen, Keenan, Natalie, Lyons, Marc, Wassall, Helen, Marsh, Chri, Mahenthran, Mervin, Carter, Emma, Kong, Thoma, Adanini, Oluronke, Bhatia, Nikhil, Msiska, Maine, Mew, Louise, Mwaura, Esther, Williams, Felicity, Wren, Lynn, Sutherland, Sara-Beth, Battle, Ceri, Brinkworth, Elaine, Harford, Rachel, Murphy, Carl, Newey, Luke, Rees, Tabitha, Williams, Marie, Arnold, Sophie, Hardy, John, Houlden, Henry, Moncur, Eleanor, Tariq, Ambreen, Tucci, Arianna, Convery, Karen, Fottrell-Gould, Deirdre, Hudig, Lisa, Keshet-Price, Jocelyn, Randell, Georgina, Stammers, Katie, Abdelrazik, Marwa, Bakthavatsalam, Dhanalakshmi, Elhassan, Munzir, Ganesan, Arunkumar, Haldeos, Anne, Moreno-Cuesta, Jeronimo, Purohit, Dharam, Vincent, Rachel, Xavier, Kugan, Rohit, Kumar, Alasdair, Frater, Saleem, Malik, David, Carter, Jenkins, Samuel, Lamond, Zoe, Wall, Alanna, Reynolds, Jessica, Campbell, Helen, Thompsom, Maria, Dodds, Steve, Duffy, Stacey, Butcher, Deborah, O’Sullivan, Susie, Butterworth-Cowin, Nicola, Deacon, Bethan, Hibbert, Meg, Pothecary, Carla, Tetla, Dariusz, Woodford, Christopher, Durga, Latha, Kennard-Holden, Gareth, de Gordoa, Laura Ortiz-Ruiz, Peasgood, Emily, Phillips, Claire, Skinner, Denise, Gaylard, Jane, Mullan, Dee, Newman, Julie, Davies, Ellie, Roche, Lisa, Sathe, Sonia, Brimfield, Lutece, Daly, Zoe, Pogson, David, Rose, Steve, Collins, Amy, Khaliq, Waqa, Gude, Estefania Treu, Allen, Louise, Beranova, Eva, Crisp, Nikki, Deery, Joanne, Hazelton, Tracy, Knight, Alicia, Price, Carly, Tilbey, Sorrell, Turki, Salah, Turney, Sharon, Giles, Julian, Booth, Simon, Bell, Gillian, English, Katy, Katary, Amro, Wilcox, Louise, Campbell, Rachael, Clarke, Noreen, Whiteside, Jonathan, Mascarenhas, Mairi, Donaldson, Avril, Matheson, Joanna, Barrett, Fiona, O’Hara, Marianne, O’Keefe, Laura, Bradley, Clare, Collier, Dawn, Walker, Rachel, Maynard, Victoria, Patel, Tahera, Smith, Matthew, Kazi, Aayesha, Hartley, Janice, Dykes, Joseph, Hijazi, Muhammad, Keith, Sarah, Khan, Meherunnisa, Ryan-Smith, Janet, Springle, Philippa, Thomas, Jacqueline, Truman, Nick, Saad, Samuel, Coleman, Dabheoc, Fine, Christopher, Matt, Roseanna, Gay, Bethan, Dalziel, Jack, Ali, Syamlan, Goodchild, Drew, Harling, Rhiannan, Bhatterjee, Ravi, Goddard, Wendy, Davison, Chloe, Duberly, Stephen, Hargreaves, Jeanette, Bolton, Rachel, Verlander, Mark, Williams, Alexandra, Blackman, Helen, Creagh-Brown, Ben, Donlon, Sinead, Michalak-Glinska, Natalia, Mtuwa, Sheila, Pristopan, Veronika, Salberg, Armorel, Smith, Eleanor, Stone, Sarah, Piercy, Charle, Verula, Jerik, Burda, Dorota, Montaser, Rugia, Harden, Lesley, Mayangao, Irving, Marriott, Cheryl, Bradley, Paul, Harris, Celia, Cooper, Joshua, Finch, Cheryl, Liderth, Sarah, Quinn, Alison, Waddington, Natalia, Fidler, Katy, Tagliavini, Emma, Donnelly, Kevin, Abel, Lynn, Brett, Michael, Digby, Brian, Gemmell, Lisa, Hornsby, Jame, Macgoey, Patrick, O’Neil, Pauline, Price, Richard, Rodden, Natalie, Rooney, Kevin, Sundaram, Radha, Thomson, Nicola, Flanagan, Rebecca, Hughes, Gareth, Latham, Scott, Mckenna, Emma, Anderson, Jennifer, Hull, Robert, Rhead, Kat, Branney, Debbie, Frankham, Jordan, Pitts, Sally, White, Nigel, Cristiano, Daniele, Dormand, Natalie, Farzad, Zohreh, Gummadi, Mahitha, Liyanage, Kamal, Patel, Brijesh V., Salmi, Sara, Sloane, Geraldine, Varghese, Mathew, Zborowski, Anelise C., Bean, Sarah, Burt, Karen, Spivey, Michael, Eastgate-Jackson, Christine, Filipe, Helder, Martin, Daniel, Maharajh, Amitaa, Garcia, Sara Mingo, De Neef, Mark, Lynch, Ceri, Howe, Gwenllian Sera, Singh, Jayaprakash, Turner, Keri, Ellis, Hannah, Stroud, Natalie, Cherian, Shiney, Cutler, Sean, Heron, Anne Emma, Roynon-Reed, Anna, Williams, Gemma, Richards, Owen, Cheema, Yusuf, Ahmad, Norfaizan, Barker, Joann, Bauchmuller, Kri, Bird, Sarah, Cawthron, Kay, Harrington, Kate, Jackson, Yvonne, Kibutu, Faith, Lenagh, Becky, Masuko, Shamiso, Raithatha, Ajay, Wiles, Matthew, Willson, Jayne, Newell, Helen, Lye, Alison, Nwafor, Lorenza, Jarman, Claire, Rowland-Jones, Sarah, Foote, David, Cole, Joby, Thompson, Roger, Watson, Jame, Hesseldon, Lisa, Macharia, Irene, Chetam, Luke, Smith, Jacqui, Ford, Amber, Anderson, Samantha, Birchall, Kathryn, Housley, Kay, Walker, Sara, Milner, Leanne, Hanratty, Helena, Trower, Helen, Phillips, Patrick, Oxspring, Simon, Donne, Ben, Bevan, Emily, Martin, Jane, Trodd, Dawn, Watson, Geoff, Brown, Caroline Wrey, Bunni, Lara, Jennings, Claire, Latif, Monica, Marshall, Rebecca, Subramanian, Gayathri, Bandla, Nageswar, Gellamucho, Minnie, Davies, Michelle, Thompson, Christopher, Trim, Fiona, Eapen, Beena, Ahmed, Cecilia, Baines, Balvinder, Clamp, Sarah, Colley, Julie, Haq, Risna, Hayes, Anne, Hulme, Jonathan, Hussain, Samia, Joseph, Sibet, Kumar, Rita, Maqsood, Zahira, Purewal, Manjit, Chandler, Ben, Elliott, Kerry, Mallinson, Janine, Turnbull, Alison, Dent, Kathy, Horsley, Elizabeth, Akhtar, Muhmmad Nauman, Pearson, Sandra, Potoczna, Dorota, Spencer, Sue, Blakemore, Hayley, Borislavova, Borislava, Faulkner, Beverley, Gendall, Emma, Goff, Elizabeth, Hayes, Kati, Thomas, Matt, Worner, Ruth, Smith, Kerry, Stephens, Deanna, Delgado, Carlos Castro, Dawson, Deborah, Ding, Lijun, Durrant, Georgia, Ezeobu, Obiageri, Farnell-Ward, Sarah, Harrison, Abiola, Kanu, Rebecca, Leaver, Susannah, Maccacari, Elena, Manna, Soumendu, Saluzzio, Romina Peperman, Queiroz, Joana, Samakomva, Tinashe, Sicat, Christine, Texeira, Joana, Da Gloria, Edna Fernande, Lisboa, Ana, Rawlins, John, Mathew, Jisha, Kinch, Ashley, Hurt, William Jame, Shah, Nirav, Clark, Victoria, Thanasi, Maria, Yun, Nikki, Patel, Kamal, Crickmore, Vikki, Debreceni, Gabor, Wilkins, Joy, Nicol, Liz, Burn, Iona, Hambrook, Geraldine, Manso, Katarina, Penn, Ruth, Shanmugasundaram, Pradeep, Tebbutt, Julie, Thornton, Danielle, Rostron, Anthony, Roy, Alistair, Woods, Lindsey, Cornell, Sarah, Wakinshaw, Fiona, Rogerson, Kimberley, Jarmain, Jordan, Anderson, Peter, Archer, Katie, Austin, Karen, Davis, Caroline, Durie, Alison, Kelsall, Olivia, Thrush, Jessica, Vigurs, Charlie, Wood, Hannah-Louise, Tranter, Helen, Harrison, Alison, Cowley, Nichola, Mcalindon, Michael, Digby, Stephen, Low, Emma, Morgan, Aled, Cother, Naiara, Rankin, Tobia, Clayton, Sarah, Mccurdy, Alex, Allibone, Suzanne, Mary-Genetu, Roman, Patel, Amit, Mac, Ainhi, Murphy, Anthony, Mahjoob, Parisa, Nazari, Roonak, Worsley, Lucy, Fagan, Andrew, Mohamed Ali, Inthakab Ali, Beaumont, Karen, Blunt, Mark, Coton, Zoe, Curgenven, Hollie, Elsaadany, Mohamed, Fernandes, Kay, Ally, Sameena Mohamed, Rangarajan, Harini, Sarathy, Varun, Selvanayagam, Sivarupan, Vedage, Dave, White, Matthew, Fernandez-Roman, Jaime, Hamilton, David O., Johnson, Emily, Johnston, Brian, Martinez, Maria Lopez, Mulla, Suleman, Shaw, David, Waite, Alicia A. C., Waugh, Victoria, Welters, Ingeborg D., Williams, Karen, Bemand, Thoma, Black, Ethel, Rosa, Arnold Dela, Howle, Ryan, Jhanji, Shaman, Baikady, Ravishankar Rao, Tatham, Kate Colette, Thomas, Benjamin, Halkes, Matthew, Mercer, Pauline, Thornton, Lorraine, West, Joe, Baird, Tracy, Ruddy, Jim, Reece-Anthony, Rosie, Birt, Mark, Cowton, Amanda, Kay, Andrea, Kent, Melanie, Potts, Kathryn, Wilkinson, Ami, Naylor, Suzanne, Brown, Ellen, Clark, Michele, Purvis, Sarah, Cole, Jade, Davies, Rhy, Duffin, Donna, Hill, Helen, Player, Ben, Thomas, Emma, Williams, Angharad, Beith, Claire Marie, Black, Karen, Clements, Suzanne, Morrison, Alan, Strachan, Dominic, Taylor, Margaret, Clarkson, Michelle, D’Sylva, Stuart, Norman, Kathryn, Coventry, Tina, Fowler, Susan, Mcgregor, Amanda, Brady, Ailbhe, Chan, Rebekah, Mcivor, Shane, Prady, Helena, Whittle, Helen, Mathew, Bijoy, Clapham, Melanie, Harper, Rosemary, Poultney, Una, Rice, Polly, Mutch, Rachel, Baird, Yolanda, Butler, Aaron, Chadbourn, Indra, Folkes, Linda, Fox, Heather, Gardner, Amy, Gomez, Raquel, Hobden, Gillian, King, Kirsten, Margarson, Michael, Martindale, Tim, Meadows, Emma, Raynard, Dana, Thirlwall, Yvette, Helm, David, Margalef, Jordi, Greer, Sandra, Shuker, Karen, Smuts, Sara, Duffield, Joseph, Smith, Oliver, Mallon, Lewi, Claire, Watkin, Birkinshaw, Isobel, Carter, Joseph, Howard, Kate, Ingham, Joanne, Joy, Rosie, Pearson, Harriet, Roche, Samantha, Scott, Zoe, Knights, Ellen, Price, Alicia, Thomas, Alice, Thorpe, Chri, Abraheem, Azmerelda, Bamford, Peter, Cawley, Kathryn, Dunmore, Charlie, Faulkner, Maria, Girach, Rumanah, Jeffrey, Helen, Jones, Rhianna, London, Emily, Nagra, Imrun, Nasir, Farah, Sainsbury, Hannah, Smedley, Clare, Khade, Reena, Sundar, Ashok, Tsinaslanidis, George, Behan, Teresa, Burnett, Caroline, Hatton, Jonathan, Heeney, Elaine, Mitra, Atideb, Newton, Maria, Pollard, Rachel, Stead, Rachael, Birch, Jenny, Bough, Laura, Goodsell, Josie, Tutton, Rebecca, Williams, Patricia, Williams, Sarah, Winter-Goodwin, Barbara, Auld, Fiona, Donnachie, Joanne, Edmond, Ian, Prentice, Lynn, Runciman, Nikole, Salutous, Dario, Symon, Lesley, Todd, Anne, Turner, Patricia, Short, Abigail, Sweeney, Laura, Murdoch, Euan, Senaratne, Dhaneesha, Burns, Karen, Higham, Andrew, Anderson, Taya, Hawcutt, Dan, O’Malley, Laura, Rad, Laura, Rogers, Naomi, Saunderson, Paula, Allison, Kathryn Sian, Afolabi, Deborah, Whitbread, Jennifer, Jones, Dawn, Dore, Rachael, Lankester, Liana, Nikitas, Nikita, Wells, Colin, Stowe, Bethan, Spencer, Kayleigh, Cathcart, Susanne, Duffy, Katharine, Puxty, Alex, Puxty, Kathryn, Turner, Lynne, Ireland, Jane, Semple, Gary, Barry, Peter, Hilltout, Paula, Evitts, Jayne, Tyler, Amanda, Waldron, Joanne, Irvine, Val, Shelley, Benjamin, Akinkugbe, Olugbenga, Bamford, Alasdair, Beech, Emily, Belfield, Holly, Bell, Michael, Davies, Charlene, Jones, Gareth A. L., Mchugh, Tara, Meghari, Hamza, O’Neill, Lauran, Peters, Mark J., Ray, Samiran, Tomas, Ana Luisa, Gorman, Claire, Gupta, Abhinav, Timlick, Elizabeth, Brady, Rebecca, Bonner, Stephen, Hugill, Keith, Jones, Jessica, Liggett, Steven, Bashyal, Archana, Davidson, Neil, Hutton, Paula, Mckechnie, Stuart, Wilson, Jean, Flint, Neil, Rekha, Patel, Hales, Dawn, Cruz, Carina, Gopal, Shameer, Harris, Nichola, Lake, Victoria, Metherell, Stella, Radford, Elizabeth, Clement, Ian, Patel, Bijal, Gulati, A., Hays, Carole, Webster, K., Hudson, Anne, Webster, Andrea, Stephenson, Elaine, Mccormack, Louise, Slater, Victoria, Nixon, Rachel, Hanson, Helen, Fearby, Maggie, Kelly, Sinead, Bridgett, Victoria, Robinson, Philip, Almaden-Boyle, Christine, Austin, Pauline, Cabrelli, Louise, Cole, Stephen, Casey, Matt, Chapman, Susan, Whyte, Clare, Brayne, Adam, Fisher, Emma, Hunt, Jane, Jackson, Peter, Kaye, Duncan, Love, Nichola, Parkin, Juliet, Tuckey, Victoria, van Koutrik, Lynne, Carter, Sasha, Andrew, Benedict, Findlay, Louise, Adams, Katie, Bruce, Michelle, Connolly, Karen, Duncan, Tracy, T. -Michael, Helen, Lindergard, Gabriella, Hey, Samuel, Fox, Claire, Alfonso, Jordan, Durrans, Laura Jayne, Guerin, Jacinta, Hruska, Martin, Eltayeb, Ayaa, Lamb, Thoma, Hodgkiss, Tracey, Cooper, Lisa, Rothwell, Joanne, Dennis, Catherine, Mcgregor, Alastair, Srikaran, Sinduya, Sukha, Anisha, Davies, Kim, O’Brien, Linda, Omar, Zohra, Perkins, Emma, Lewis, Tracy, Sutherland, Isobel, Brooke, Hollie, Buckley, Sarah, Suarez, Jose Cebrian, Charlesworth, Ruth, Hansson, Karen, Norris, John, Poole, Alice, Rose, Alastair, Sandhu, Rajdeep, Sloan, Brendan, Smithson, Elizabeth, Thirumaran, Muthu, Wagstaff, Veronica, Metcalfe, Alexandra, Camsooksai, Julie, Humphrey, Charlotte, Jenkins, Sarah, Wadams, Beverley, Death, Yasmin, Adams, Colene, Agasou, Anita, Arden, Tracie, Bowes, Amy, Boyle, Pauline, Beekes, Mandy, Button, Heather, Capps, Nigel, Carnahan, Mandy, Carter, Anne, Childs, Danielle, Donaldson, Denise, Hard, Kelly, Hurford, Fran, Hussain, Yasmin, Javaid, Ayesha, Jones, Jame, Jose, Sanal, Leigh, Michael, Martin, Terry, Millward, Helen, Motherwell, Nichola, Rikunenko, Rachel, Stickley, Jo, Summers, Julie, Ting, Louise, Tivenan, Helen, Tonks, Louise, Wilcox, Rebecca, Bokhari, Maria, Lucas, Rachael, Mccormick, Wendy, Ritzema, Jenny, Sanderson, Amanda, Wild, Helen, Baxter, Nicola, Henderson, Steven, Kennedy-Hay, Sophie, Mcparland, Christopher, Rooney, Laura, Sim, Malcolm, Mccreath, Gordan, Brunton, Mark, Caterson, Je, Coles, Holly, Frise, Matthew, Rai, Sabi Gurung, Keating, Liza, Tilney, Emma, Bartley, Shauna, Bhuie, Parminder, Downes, Charlotte, Holding, Kathleen, Riches, Katie, Hilton, Mary, Hayman, Mel, Subramanian, Deepak, Daniel, Priya, Zitter, Letizia, Benyon, Sarah, Marriott, Suzie, Park, Linda, Keenan, Samantha, Gordon, Elizabeth, Quinn, Helen, Baines, Kizzy, Andrew, Gillian, Barclay, Lucy, Callaghan, Marie, Clark, Sarah, Hope, Dave, Marshall, Lucy, Mcculloch, Corrienne, Briton, Kate, Singleton, Jo, Birch, Sophie, Simpson, Kerry, Craig, Jayne, Demetriou, Carrie, Eckbad, Charlotte, Hierons, Sarah, Howie, Lucy, Mitchard, Sarah, Ramos, Lidia, Serrano-Ruiz, Alfredo, White, Katie, Kelly, Fiona, Amin, Vishal, Anastasescu, Elena, Anumakonda, Vikram, Karthik, Komala, Kausar, Rizwana, Reid, Karen, Smith, Jacqueline, Imeson-Wood, Janet, Bellini, Arianna, Bryant, Jade, Mayer, Anton, Pickard, Amy, Roe, Nichola, Sowter, Jason, Howlett, Alex, Criste, Kristine, Cusack, Rebecca, Golder, Kim, Golding, Hannah, Jones, Oliver, Leggett, Samantha, Male, Michelle, Marani, Martyna, Prager, Kirsty, Williams, Toran, Roberts, Belinda, Salmon, Karen, Gondo, Prisca, Hadebe, B., Kayani, Abdul, Masunda, Bridgett, Ahmed, Ashar, Morris, Anna, Jakkula, Sriniva, Long, Kate, Whiteley, Simon, Wilby, Elizabeth, Ogg, Bethan, Moultrie, Sam, Odam, M., Bewley, Jeremy, Garland, Zoe, Grimmer, Lisa, Gumbrill, Bethany, Johnson, Rebekah, Sweet, Katie, Webster, Denise, Efford, Georgia, Bennett, Sara, Goodwin, Emma, Jackson, Matthew, Kent, Alissa, Tibke, Clare, Woodyatt, Wiesia, Zaki, Ahmed, Daniel, Amelia, Finn, Joanne, Saha, Rajnish, Bremmer, Pamela, Allan, J., Geary, T., Houston, Gordon, Meikle, A., O’Brien, P., Bell, Dina, Boyle, Rosalind, Douglas, Katie, Glass, Lynn, Lee, Emma, Lennon, Liz, Rattray, Austin, Charnock, Rob, Mcfarland, Denise, Cosgrove, Denise, Attwood, Ben, Parsons, Penny, Carmody, Siobhain, Oblak, Metod, Popescu, Monica, Thankachen, Mini, Baruah, Rosie, Morris, Sheila, Ferguson, Susie, Shepherd, Amy, Altabaibeh, Abdelhakim, Alvaro, Ana, Gilbert, Kayleigh, Ma, Louise, Mostoles, Loreta, Parmar, Chetan, Simpson, Kathryn, Jetha, Champa, Booker, Lauren, Pratley, Anezka, Cosier, Tracey, Millen, Gemma, Schumacher, Natasha, Weston, Heather, Rand, Jame, Alex, Beatrice, Bach, Benjamin, Barclay, Wendy S., Bogaert, Debby, Chand, Meera, Cooke, Graham S., Docherty, Annemarie B., Dunning, Jake, da Silva Filipe, Ana, Fletcher, Tom, Green, Christoper A., Harrison, Ewen M., Hiscox, Julian A., Ijaz, Samreen, Khoo, Saye, Lim, Wei Shen, Mentzer, Alexander J., Merson, Laura, Noursadeghi, Mahdad, Moore, Shona C., Palmarini, Massimo, Paxton, William A., Pollakis, Georgio, Price, Nichola, Rambaut, Andrew, Robertson, David L., Sancho-Shimizu, Vanessa, Scott, Janet T., de Silva, Thushan, Sigfrid, Louise, Solomon, Tom, Sriskandan, Shiranee, Stuart, David, Tedder, Richard S., Thomson, Emma C., Roger Thompson, A. A., Thwaites, Ryan S., Turtle, Lance C. W., Gupta, Rishi K., Palmieri, Carlo, Swann, Olivia V., Zambon, Maria, Dumas, Marc-Emmanuel, Griffin, Julian L., Takats, Zoltan, Chechi, Kanta, Andrikopoulos, Petro, Osagie, Anthonia, Olanipekun, Michael, Liggi, Sonia, Lewis, Matthew R., Correia, Gonçalo dos Santo, Sands, Caroline J., Takis, Panteleimon, Maslen, Lynn, Greenhalf, William, Shaw, Victoria, Mcdonald, Sarah E., Keating, Seán, Ahmed, Katie A., Armstrong, Jane A., Ashworth, Milton, Asiimwe, Innocent G., Bakshi, Siddharth, Barlow, Samantha L., Booth, Laura, Brennan, Benjamin, Bullock, Katie, Catterall, Benjamin W. A., Clark, Jordan J., Clarke, Emily A., Cooper, Louise, Cox, Helen, Davis, Christopher, Dincarslan, Oslem, Dunn, Chri, Dyer, Philip, Elliott, Angela, Evans, Anthony, Finch, Lorna, Fisher, Lewis W. S., Foster, Terry, Garcia-Dorival, Isabel, Gunning, Philip, Hartley, Catherine, Jensen, Rebecca L., Jones, Christopher B., Jones, Trevor R., Khandaker, Shadia, King, Katharine, Kiy, Robyn T., Koukorava, Chrysa, Lake, Annette, Lant, Suzannah, Latawiec, Diane, Lavelle-Langham, Lara, Lefteri, Daniella, Lett, Lauren, Livoti, Lucia A., Mancini, Maria, Mcdonald, Sarah, Mcevoy, Laurence, Mclauchlan, John, Metelmann, Soeren, Miah, Nahida S., Middleton, Joanna, Mitchell, Joyce, Murphy, Ellen G., Penrice-Randal, Rebekah, Pilgrim, Jack, Prince, Tessa, Reynolds, Will, Ridley, P. Matthew, Sales, Debby, Shaw, Victoria E., Shears, Rebecca K., Small, Benjamin, Subramaniam, Krishanthi S., Szemiel, Agnieska, Taggart, Aislynn, Tanianis-Hughes, Jolanta, Thomas, Jordan, Trochu, Erwan, van Tonder, Libby, Wilcock, Eve, Zhang, J. Eunice, Flaherty, Lisa, Maziere, Nicole, Cass, Emily, Carracedo, Alejandra Doce, Carlucci, Nicola, Holmes, Anthony, Massey, Hannah, Murphy, Lee, Wrobel, Nicola, Mccafferty, Sarah, Morrice, Kirstie, Maclean, Alan, Armstrong, Ruth, Boz, Ceilia, Brown, Adam, Coutts, Audrey, Cullum, Louise, Day, Nicky, Donnelly, Lorna, Duncan, Esther, Fawkes, Angie, Finernan, Paul, Gilchrist, Tammy, Golightly, Ailsa, Hafezi, Katarzyna, Law, Dawn, Law, Rachel, Law, Sarah, Macgillivray, Louise, Mal, Hanning, Mcmaster, Ellie, Meikle, Jen, Oosthuyzen, Wilna, Paterson, Trevor, Stenhouse, Andrew, Swets, Maaike, Szoor-McElhinney, Helen, Taneski, Filip, Wackett, Tony, Ward, Mairi, Weaver, Jane, Coyle, Judy, Gallagher, Bernadette, Lidstone-Scott, Rebecca, Hamilton, Debbie, Schon, Katherine, Furlong, Anita, Biggs, Heather, Griffiths, Fiona, Andrews, Eleanor, Brickell, Kathy, Smyth, Michelle, Murphy, Lorna, Carson, Gail, Hardwick, Hayley, Donohue, Chloe, Pérez-Tur, Jordi [0000-0002-9111-1712], Martín, Javier [0000-0002-2202-0622], Institute for Molecular Medicine Finland [Helsinki] (FIMM), Helsinki Institute of Life Science (HiLIFE), University of Helsinki-University of Helsinki, Broad Institute of MIT and Harvard (BROAD INSTITUTE), Harvard Medical School [Boston] (HMS)-Massachusetts Institute of Technology (MIT)-Massachusetts General Hospital [Boston], Massachusetts General Hospital [Boston], A list of authors and their affiliations appears in the Supplementary Information, Helsingin yliopisto = Helsingfors universitet = University of Helsinki-Helsingin yliopisto = Helsingfors universitet = University of Helsinki, ANR-20-CO11-0001,AABIFNCOV,Bases génétiques et immunologiques des auto-anticorps contre les interférons de type I prédisposant aux formes sévères de COVID-19.(2020), ANR-20-COVI-0003,GENCOVID,Identification des défauts monogéniques de l'immunité responsables des formes sévères de COVID-19 chez les patients précédemment en bonne santé(2020), ANR-21-COVR-0039,GenMIS-C,Recherche 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Bocciolone, M., Miozzo, M., Chueca, N., Montano, N., Faverio, P., Preatoni, P., Bonfanti, P., Omodei, P., Castro, P., Ferrer, R., Gualtierotti, R., Gallego-Durán, R., Morilla, R., Haider, S., Marsal, S., Aneli, S., Pelusi, S., Bosari, S., Aliberti, S., Dudman, S., Zheng, T., Pumarola, T., Cejudo, T.G., Monzani, V., Friaza, V., Peter, W., Dopazo, X., May, S., Grimsrud, M.M., Gudbjartsson, D.F., Stefansson, K., Sulem, P., Sveinbjornsson, G., Melsted, P., Norddahl, G., Swerford Moore, K.H., Thorsteinsdottir, U., Holm, H., Alarcón-Riquelme, M.E., Bernardo, D., Martínez-Bueno, M., Rello, S.R., Magi, R., Milani, L., Metspalu, A., Laisk, T., Läll, K., Lepamets, M., Esko, T., Reimann, E., Naaber, P., Laane, E., Pesukova, J., Peterson, P., Kisand, K., Tabri, J., Allos, R., Hensen, K., Starkopf, J., Ringmets, I., Tamm, A., Kallaste, A., Alavere, H., Metsalu, K., Puusepp, M., Kristiansson, K., Koskelainen, S., Perola, M., Donner, K., Kivinen, K., Palotie, A., Bochud, P.Y., Boillat, N., Nussle, S.G., Albrich, W., Pagani, J.L., Zu Bentrup, F.M., Viollet, R.M., Kampouri, E.E., Meuwly, J.Y., D'Acremont, V., Younes, S.E., Albrich, W.C., O'Mahony, L., Kleger, G.R., Kahlert, C.R., Negro, T.R., Carreras, A., Galván-Femenía, I., Farré, X., Cortés, B., Mercader, J.M., Guindo-Martinez, M., Torrents, D., Garcia-Aymerich, J., Castaño-Vinyals, G., Dobaño, C., Gori, M., Mondelli, M.U., Castelli, F., Vaghi, M., Rusconi, S., Montagnani, F., Bargagli, E., Franchi, F., Mazzei, M.A., Cantarini, L., Tacconi, D., Feri, M., Scala, R., Spargi, G., Nencioni, C., Bandini, M., Caldarelli, G.P., Spagnesi, M., Canaccini, A., Ognibene, A., D'Arminio Monforte, A., Girardis, M., Antinori, A., Francisci, D., Schiaroli, E., Scotton, P.G., Panese, S., Scaggiante, R., Monica, M.D., Capasso, M., Fiorentino, G., Castori, M., Aucella, F., Di Biagio, A., Masucci, L., Valente, S., Mandalà, M., Zucchi, P., Giannattasio, F., Coviello, D.A., Mussini, C., Bosio, G., Tavecchia, L., Crotti, L., Rizzi, M., La Rovere, 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Reid, K., Imeson-Wood, J., Bellini, A., Bryant, J., Pickard, A., Roe, N., Sowter, J., Howlett, A., Criste, K., Cusack, R., Golder, K., Golding, H., Jones, O., Leggett, S., Male, M., Marani, M., Prager, K., Williams, T., Roberts, B., Salmon, K., Gondo, P., Kayani, A., Masunda, B., Ahmed, A., Morris, A., Jakkula, S., Long, K., Whiteley, S., Wilby, E., Ogg, B., Moultrie, S., Bewley, J., Garland, Z., Grimmer, L., Gumbrill, B., Sweet, K., Webster, D., Efford, G., Bennett, S., Goodwin, E., Jackson, M., Kent, A., Tibke, C., Woodyatt, W., Zaki, A., Daniel, A., Finn, J., Bremmer, P., Houston, G., O'Brien, P., Bell, D., Boyle, R., Douglas, K., Glass, L., Lee, E., Lennon, L., Rattray, A., Charnock, R., McFarland, D., Cosgrove, D., Attwood, B., Parsons, P., Carmody, S., Oblak, M., Popescu, M., Thankachen, M., Baruah, R., Morris, S., Ferguson, S., Shepherd, A., Altabaibeh, A., Alvaro, A., Gilbert, K., Ma, L., Mostoles, L., Parmar, C., Jetha, C., Booker, L., Pratley, A., Cosier, T., Millen, G., Schumacher, N., Weston, H., Rand, J., Alex, B., Bach, B., Barclay, W.S., Bogaert, D., Chand, M., Cooke, G.S., Docherty, A.B., Dunning, J., da Silva Filipe, A., Fletcher, T., Green, C.A., Harrison, E.M., Hiscox, J.A., Ijaz, S., Khoo, S., Lim, W.S., Mentzer, A.J., Merson, L., Noursadeghi, M., Moore, S.C., Palmarini, M., Paxton, W.A., Pollakis, G., Price, N., Rambaut, A., Robertson, D.L., Sancho-Shimizu, V., Scott, J.T., de Silva, T., Sigfrid, L., Solomon, T., Sriskandan, S., Stuart, D., Tedder, R.S., Thomson, E.C., Roger Thompson, A.A., Thwaites, R.S., Turtle, LCW, Gupta, R.K., Palmieri, C., Swann, O.V., Zambon, M., Dumas, M.E., Griffin, J.L., Takats, Z., Chechi, K., Andrikopoulos, P., Osagie, A., Olanipekun, M., Liggi, S., Lewis, M.R., Correia, GDS, Sands, C.J., Takis, P., Maslen, L., Greenhalf, W., Shaw, V., McDonald, S.E., Ahmed, K.A., Armstrong, J.A., Ashworth, M., Asiimwe, I.G., Bakshi, S., Barlow, S.L., Booth, L., Brennan, B., Bullock, K., Catterall, BWA, Clark, J.J., Clarke, E.A., Cox, H., Dincarslan, O., Dunn, C., Dyer, P., Elliott, A., Evans, A., Finch, L., Fisher, LWS, Foster, T., Garcia-Dorival, I., Gunning, P., Hartley, C., Jensen, R.L., Jones, C.B., Jones, T.R., Khandaker, S., Kiy, R.T., Koukorava, C., Lake, A., Lant, S., Latawiec, D., Lavelle-Langham, L., Lefteri, D., Lett, L., Livoti, L.A., Mancini, M., McDonald, S., McEvoy, L., McLauchlan, J., Metelmann, S., Miah, N.S., Middleton, J., Mitchell, J., Murphy, E.G., Penrice-Randal, R., Pilgrim, J., Prince, T., Reynolds, W., Ridley, P.M., Sales, D., Shaw, V.E., Shears, R.K., Small, B., Subramaniam, K.S., Szemiel, A., Taggart, A., Tanianis-Hughes, J., Trochu, E., van Tonder, L., Wilcock, E., Zhang, J.E., Flaherty, L., Maziere, N., Cass, E., Carracedo, A.D., Carlucci, N., Holmes, A., Massey, H., Murphy, L., Wrobel, N., McCafferty, S., Morrice, K., MacLean, A., Armstrong, R., Boz, C., Coutts, A., Cullum, L., Day, N., Donnelly, L., Duncan, E., Fawkes, A., Finernan, P., Gilchrist, T., Golightly, A., Hafezi, K., Law, D., Law, R., Law, S., Macgillivray, L., Maclean, A., Mal, H., Mcmaster, E., Meikle, J., Oosthuyzen, W., Paterson, T., Stenhouse, A., Swets, M., Szoor-McElhinney, H., Taneski, F., Wackett, T., Ward, M., Weaver, J., Coyle, J., Gallagher, B., Lidstone-Scott, R., Hamilton, D., Schon, K., Furlong, A., Biggs, H., Griffiths, F., Andrews, E., Brickell, K., Smyth, M., Carson, G., Hardwick, H., Donohue, C., Neale, Benjamin M. [0000-0003-1513-6077], Apollo - University of Cambridge Repository, Stem Cell Aging Leukemia and Lymphoma (SALL), Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), Life Course Epidemiology (LCE), Groningen Research Institute for Asthma and COPD (GRIAC), Guided Treatment in Optimal Selected Cancer Patients (GUTS), AII - Infectious diseases, Amsterdam Neuroscience - Neuroinfection & -inflammation, Neurology, Infectious diseases, Center of Experimental and Molecular Medicine, APH - Aging & Later Life, APH - Global Health, APH - Quality of Care, Amsterdam institute for Infection and Immunity, APH - Health Behaviors & Chronic Diseases, Global Health, APH - Methodology, Graduate School, ACS - Heart failure & arrhythmias, Anesthesiology, ACS - Diabetes & metabolism, APH - Digital Health, APH - Personalized Medicine, ACS - Microcirculation, Niemi, M. E. K., Liao, R. G., Neale, B. M., Pathak, G. A., Andrews, S. J., Schulte, E. C., Karim, M. A., Wendt, F. R., Kim, H. -N., Uddin, M. J., Smith, G. D., Willer, C. J., Buxbaum, J. D., Martin, A. R., Balaconis, M. K., Sankaran, V. G., Brent Richards, J., Eric Kerchberger, V., Kenneth Baillie, J., Dutta, A. K., Uddin, M. M., Perez-Tur, J., Verdugo, R. A., Zarate, R., Medina-Gomez, C., Gomez-Cabrero, D., Cadilla, C. L., Boua, P. R., Fave, M. -J., Lemacon, A., Szentpeteri, J. L., Ahmad, H. F., Kornilov, S. A., Prokic, I., Pearson, N. M., Shelton, J. F., Shastri, A. J., Weldon, C. H., Brouwer, M. C., Vlaar, A. P. J., Joost Wiersinga, W., Algera, A. G., Bogaard, H. J., Bonta, P. I., Grobusch, M. P., Hermans, S. M., Hovius, J. W., de Jong, M. D., Nossent, E. J., Prins, J. M., Schultz, M. J., Stijnis, C. S., Minnaar, R. P., van Uffelen, K. W. J., Wolterman, R. A., Ball, C. A., Mccurdy, S., Hong, E. L., Baltzell, A. H., Goffard, J. -C., Peree, H., Leonard, P., Giot, J. -B., Sauvage, A. -S., Wery, M., Morrison, D. R., Chasse, M., Kaufmann, D. E., Mark Lathrop, G., Davis, L. K., Cox, N. J., Below, J. E., Sealock, J. M., Faucon, A. B., Shuey, M. M., Polikowsky, H. G., Petty, L. E., Shaw, D. M., Chen, H. -H., Ludwig, K. U., Schroder, J., Nothen, M. M., Jensen, B. -E. O., Altmuller, J., Berger, M. M., Gogele, M., Gignoux, C. R., Wicks, S. J., Barnes, K. C., Goldstein, D. B., Reilly, M. P., Gharavi, A. G., O'Byrne, S. M., So, Y. S., Park, S. -K., Kim, H. -L., Kang, C. K., Lee, H. -J., Song, K. -H., Yoon, K. J., Paik, N. -J., Joo, E. -J., Park, W. B., Park, J. S., Park, K. U., Ham, S. Y., Kim, E. S., Kim, H. B., Caceres, M., Lenz, T. L., Julia, A., Holter, J. C., Fernandez, J., Sander, L. E., Banales, J. M., Romero-Gomez, M., Hov, J. R., Karlsen, T. H., Wacker, E. M., Elabd, H., Ruhlemann, M. C., Vadla, M. S., Lenning, O. B., Ozer, O., Kassens, J., Figuera Basso, M. E., Ortiz, A. B., Chercoles, A. G., Holten, A. R., Kildal, A. B., Gluck, A., Nolla, A. C., Dyrhol-Riise, A. M., Spinner, C. D., Hoff, D. A. L., Jimenez, D., Pestana, D., Helbig, E. T., Paraboschi, E. M., Sanchez, F. G., Hernandez, I., Galvan-Femenia, I., Badia, J. R., Muller, K. E., Gaede, K. I., Lippert, L. J., Tellez, L., Gutierrez-Stampa, M. A., Vehreschild, M. J. G. T., Marquie, M., Seilmaier, M. J., Rodriguez-Gandia, M., Ayo, N. I., Martinez, N., Cornely, O. A., Rodrigues, P. M., Espana, P. P., Garcia-Fernandez, A. -E., Fracanzani, A. L., Muniz-Diaz, E., Calderon, E. J., Solligard, E., Medrano, F. J., Muller, F., Afset, J. E., Damas, J. K., Ferrusquia-Acosta, J., Quero, J. H., Guerrero, J. M., Bettini, L. R., Gustad, L. T., Valsecchi, M. G., D'Angio, M., Gallego-Duran, R., Cejudo, T. G., Grimsrud, M. M., Gudbjartsson, D. F., Moore, K. H. S., Alarcon-Riquelme, M. E., Martinez-Bueno, M., Rello, S. R., Lall, K., Bochud, P. -Y., Nussle, S. G., Meyer zu Bentrup, F., Merlet Viollet, R., Guery, B., Hugli, O., Gonseth Nussle, S., Estoppey Younes, S., Rochat Negro, T., Mercader, J. M., Castano-Vinyals, G., Dobano, C., Mondelli, M. U., Mazzei, M. A., Caldarelli, G. P., Monforte, A. D., Scotton, P. G., Monica, M. D., Mandala, M., Coviello, D. A., La Rovere, M. T., Segala, F. V., Mencarelli, M. A., Pinto, A. M., Carriero, M. L., Ann Belli, M., Antoni, M. D., Miraglia, F. G., Parisi, S. G., Squeo, G. M., Botta, G., Hunt, K. A., Trembath, R. C., Martin, H. C., Griffiths, C. J., Curtis, C. J., Huang, Q. Q., Lee, S. H., Macarthur, D., Maclaughlin, B., Smith, A. V., Boughton, A. P., Li, K. W., Lefaive, J., Jannes, C. E., Krieger, J. E., Pereira, A. C., Lima, I. R., Tada, M. T., Mccarthy, M., Lee, J. E., Lee, H. S., Jang, H. Y., Kim, Y. -S., Kwon, K. T., Kim, S. -W., Kim, J. Y., Jang, Y. R., Kim, H., Lee, J. Y., Choe, K. -W., Kang, Y. M., Jee, S. H., Jung, K. J., Schroth, G. P., Desouza, F., Cirulli, E. T., Schiabor Barrett, K. M., Washington, N. L., Lu, J. T., Ramirez, J. M., Grzymski, J. J., Minano, J. I. E., Aguirre, L. A., Lopez-Collazo, E., Lozano-Rodriguez, R., Avendano-Ortiz, J., Arcos, V. T., Montalban-Hernandez, K. M., Quiroga, J. V., Martin-Quiros, A., Nakada, T. -A., Vonk, J. M., Ori, A. P. S., Hernandez Cordero, A. I., Sin, D. D., Bosse, Y., Feng, Y. -C. A., Weiss, S. T., Karlson, E. W., Smoller, J. W., Murphy, S. N., Meigs, J. B., Woolley, A. E., Green, R. C., Perez, E. F., Zollner, S., Sloofman, L. G., Sebra, R. P., Collins, B. L., Sealfon, S. C., Jordan, D. M., Thompson, R. C., Belbin, G. M., Underwood, S. J., Hiester, L. L., Charney, A. W., Beckmann, N. D., Schadt, E. E., Abul-Husn, N. S., Cho, J. H., Kenny, E. E., Loos, R. J. F., Nadkarni, G. N., Huckins, L. M., Ferreira, M. A. R., Abecasis, G. R., Leader, J. B., Cantor, M. N., Justice, A. E., Carey, D. J., Josyula, N. S., Kosmicki, J. A., Horowitz, J. E., Gass, M. C., Hottenga, J. J., de Geus, E. J. C., Nivard, M. G., Ritchie, M. D., Verma, S. S., Vari, M. S., Rahier, J. -F., Bulik, C. M., Landen, M., Ferrero, G. B., Fundin, B., Ismail, S. I., Badji, R. M., Hultstrom, M., Geschwind, D. H., Butte, M. J., Chang, T. S., Caulfield, M. J., Scott, R. H., Odhams, C. A., Karczewski, K. J., Wilson, D. J., Spencer, C. A., Crook, D. W., Wyllie, D. H., O'Connell, A. M., Atkinson, E. G., Walters, R. K., Palmer, D. S., Goldstein, J. I., Kyle Satterstrom, F., Earle, S. G., Lin, S. -K., Rudkin, J. K., Zhao, J. H., Butterworth, A. S., Sun, Y. V., Huffman, J. E., O'Donnell, C. J., Michael Gaziano, J., Ho, Y. -L., Glessner, J. R., Mcguigan, P. J., Moore, L. S. P., Vizcaychipi, M. P., Page, V. J., Aldera, E. L., Cutino-Moguel, M. -T., Durand, I., Hawcutt, D. B., Macmahon, M., Macnaughton, E., Mccullough, K., Mcewen, R., O'Shea, M. K., Pooni, J. S., Wooton, D. G., Bretherick, A. D., Fourman, M. H., Meynert, A. M., Ponting, C. P., Porteous, D. J., Russell, C. D., Wilson, J. F., Drake, T. M., Fairfield, C. J., Knight, S. R., Mclean, K. A., Shaw, C. A., Ho, A. Y. W., Horby, P. W., Mcauley, D., Openshaw, P. J. M., Semple, M. G., Mcgowan, J., Mcguinness, H., Mcneela, F., Bayo, L. -A., Arias, S. S., Conyngham, J. -A., Corral, M. A., de Almeida Martins, L. G., Mclaughlan, D., Mcmorrow, L., Mccormick, J., Mitchell, A. M., Maccallum, N., Hughes, R. A., Jones, T. O., Mcphail, M., Mckenley, I., Sutherland, S. -B., de Gordoa, L. O. -R., Gude, E. T., Macgoey, P., Mckenna, E., Patel, B. V., Zborowski, A. C., Garcia, S. M., Howe, G. S., Heron, A. E., Mills, G. H., Brown, C. W., Akhtar, M. N., Delgado, C. C., Saluzzio, R. P., Da Gloria, E. F., Hurt, W. J., Wood, H. -L., Mcalindon, M., Mccurdy, A., Ali, I. A. M., Ally, S. M., Hamilton, D. O., Lopez Martinez, M., Waite, A. A. C., Welters, I. D., Rosa, A. D., Baikady, R. R., Tatham, K. C., Beith, C. M., Mcgregor, A., Mcivor, S., Allison, K. S., Jones, G. A. L., Mchugh, T., Peters, M. J., Tomas, A. L., Mckechnie, S., Mccormack, L., Michael, H. T., Durrans, L. J., Suarez, J. C., Death, Y., Mccormick, W., Mccreath, G., Rai, S. G., Mcculloch, C., Mcfarland, D., Barclay, W. S., Cooke, G. S., Docherty, A. B., Green, C. A., Harrison, E. M., Hiscox, J. A., Lim, W. S., Mentzer, A. J., Paxton, W. A., Robertson, D. L., Scott, J. T., Tedder, R. S., Thomson, E. C., Thwaites, R. S., Gupta, R. K., Swann, O. V., Dumas, M. -E., Griffin, J. L., Lewis, M. R., dos Santos Correia, G., Sands, C. J., Mcdonald, S. E., Ahmed, K. A., Armstrong, J. A., Asiimwe, I. G., Barlow, S. L., Catterall, B. W. A., Clark, J. J., Clarke, E. A., Fisher, L. W. S., Jensen, R. L., Jones, C. B., Jones, T. R., Kiy, R. T., Livoti, L. A., Mcdonald, S., Mcevoy, L., Mclauchlan, J., Miah, N. S., Moore, S. C., Murphy, E. G., Matthew Ridley, P., Shaw, V. E., Shears, R. K., Subramaniam, K. S., Eunice Zhang, J., Carracedo, A. D., Mccafferty, S., Turtle, L. C. W., Data Science Genetic Epidemiology Lab, Institute for Molecular Medicine Finland, HUS Helsinki and Uusimaa Hospital District, University of Helsinki, Research Programs Unit, Doctoral Programme in Population Health, Centre of Excellence in Complex Disease Genetics, Aarno Palotie / Principal Investigator, Genomics of Neurological and Neuropsychiatric Disorders, and University of Zurich

Subjects
Male, 45/43, Autoimmunity, Autoimmunity/genetics, Body Mass Index, COVID-19/genetics, COVID-19/virology, Critical Illness, Female, Genetic Loci/genetics, Genetic Predisposition to Disease, Genome-Wide Association Study, Geographic Mapping, Hospitalization, Host-Pathogen Interactions/genetics, Humans, Inflammation/complications, Information Dissemination, Multifactorial Inheritance, Racial Groups/genetics, SARS-CoV-2/pathogenicity, Smoking, environmental risk factors, Q1, 631/208, 0302 clinical medicine, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Genetics, Genome-wide association studies, SARS-CoV-2, Viral infection, GWAS, Aetiology, Lung, QC, 0303 health sciences, HERITABILITY, 3. Good health, covid-19, Science & Technology - Other Topics, Identification (biology), Infection, Human, 631/208/205/2138, Settore BIO/11 - Biologia Molecolare, 03 medical and health sciences, SDG 3 - Good Health and Well-being, Clinical Research, Biodefense, Genetics, GENOME-WIDE ASSOCIATION, Medisinske Fag: 700::Basale medisinske, odontologiske og veterinærmedisinske fag: 710::Medisinsk genetikk: 714 [VDP], METAANALYSIS, 1000 Multidisciplinary, [SDV.GEN]Life Sciences [q-bio]/Genetics, Science & Technology, Prevention, Racial Groups, Pneumonia, genetic architecture, Human genetics, Genetic Loci, genetic factors, 570 Life sciences, biology, 030217 neurology & neurosurgery, Medizin, Infektionsmedicin, Genome-wide association studies, Settore BIO/12 - BIOCHIMICA CLINICA E BIOLOGIA MOLECOLARE CLINICA, Pandemic, 2.1 Biological and endogenous factors, pandemi, Multidisciplinary, article, Public Health, Global Health, Social Medicine and Epidemiology, Racial Group, 10124 Institute of Molecular Life Sciences, Host-Pathogen Interaction, Multidisciplinary Sciences, Infectious Diseases, Host-Pathogen Interactions, Critical Illne, COVID-19, GWAS, genetic factors, environmental risk factors, therapy, Infectious Medicine, Coronavirus disease 2019 (COVID-19), SUSCEPTIBILITY LOCI, General Science & Technology, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Computational biology, Biology, Vaccine Related, 692/699/255/2514, Environmental risk, Mendelian randomization, COVID-19 Host Genetics Initiative, QH426, 631/326/596/4130, 030304 developmental biology, Inflammation, therapy, SARS-CoV-2, Human Genome, COVID-19, Genetic architecture, Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi, Emerging Infectious Diseases, Good Health and Well Being, Viral infection, 3111 Biomedicine
Abstract

Niemi, Mari E. K. et al. 39 páginas, figuras y tablas. Contiene material suplementario., The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3-7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease.

Published
2021

43. Influences of sleep and lifestyle factors on the risk for covid-19 infections, from internet survey of 10,000 Japanese business workers

Author

Masahiro, Nakashima, Ryota, Amano, Naoya, Nishino, Yasutaka, Osada, Yuriko, Watanabe, Akifumi, Miyake, Shintaro, Chiba, and Seiji, Nishino

Subjects
Male, Internet, Sleep Apnea Syndromes, Multidisciplinary, Japan, Surveys and Questionnaires, Influenza, Human, Humans, COVID-19, Female, Sleep, Life Style
Abstract

We conducted an internet survey to assess sociodemographic variables, lifestyle factors, sleep problems, and comorbidities for sleep apnea syndrome (SAS) in COVID-19 and influenza (FLU) infections. Data from 10,323 workers (50.0% male) were analyzed. COVID-19 was diagnosed in 144 subjects (COVID-19+), and 8,693 were classified as not suspected to be infected (COVID-19−). SAS had been diagnosed in 35.4% of the COVID-19+ subjects, but only 231 (2.7%) of the 8,693 COVID-19− subjects. COVID-19+ subjects were more susceptible to FLU (35.4%) compared to COVID-19− subjects (3.0%). A multivariate analysis revealed that higher risks of COVID-19+ were linked to the following factors: going out without a face mask (OR 7.05, 95% CI 4.53–11.00), FLU+ (OR 6.33, 95% CI 3.80–10.54), excessive exercise before going to sleep (OR 2.10, 95% CI 1.63–2.70), SAS+ (OR 5.08, 95% CI 2.88–8.94), younger age (OR 1.05, 95% CI 1.03–1.07), falling sleep while sitting or talking with someone (OR 3.70, 95% CI 2.30–5.95), and use of hypnotics (OR 2.28, 95% CI 1.20–4.30). Since sleep impairment played a relatively small role in COVID-19+/SAS− subjects, we assume that SAS itself was a more significant risk factor for COVID-19 infection rather than sleep impairment. A better understanding of the mechanisms that result in increased susceptibility to COVID-19 in SAS is vital for helping prevent COVID-19.

Published
2022

44. Differences between junior and senior male sprinters in physiological variables associated with sprint performance

Author

Takaya, Yoshimoto, Yohei, Takai, Hiroyasu, Tsuchie, Yoshihiro, Chiba, and Hiroaki, Kanehisa

Subjects
Male, Lower Extremity, Athletes, Multivariate Analysis, Humans, Physical Therapy, Sports Therapy and Rehabilitation, Orthopedics and Sports Medicine, Athletic Performance, Running
Abstract

The physiological variables associated with sprint performance have been extensively studied. However, little information is available on how the corresponding physiological variables differ between junior and senior sprinters. This study aimed to examine this subject.In addition to the maximal running velocity achieved while sprinting over 60-m, body composition, muscle thicknesses of the trunk and lower limbs, performance scores of four jumping tasks (countermovement, rebound, standing long, and standing five-step jumps), and 10-s maximal anaerobic pedaling power were determined in 17 junior and 22 senior male sprinters.In the junior and senior sprinters, most of the measured variables were significantly correlated with the maximal running velocity. Analysis of covariance showed that only the maximal pedaling power relative to the body mass was significantly different between the two groups in the regression equation slope of the relationship with maximal running velocity (0.20 for junior and 0.64 for senior sprinters). Additionally, multiple regression analysis revealed that while the standing five-step jump distance (40%) and the size of the psoas major muscle (23%) were selected as explanatory factors for maximal running velocity in the junior sprinters, maximal pedaling power relative to the body mass (63%) was selected in the senior sprinters.This study suggests that the following physiological factors associated with sprint running performance differ between the junior and senior sprinters: the ability of repetitive jumping in the horizontal forward direction and muscularity of hip flexors in the junior sprinters versus the anaerobic capacity in senior sprinters. Therefore, coaches and athletes need to take into consideration that the physiological variables to be focused on are different for each generation.

Published
2022

45. Intravenous Thrombolysis With Alteplase at 0.6 mg/kg in Patients With Ischemic Stroke Taking Direct Oral Anticoagulants

Author

Takashi Okada, Takeshi Yoshimoto, Shinichi Wada, Sohei Yoshimura, Tetsuya Chiba, Shuhei Egashira, Shunsuke Kimura, Masayuki Shiozawa, Manabu Inoue, Masafumi Ihara, Kazunori Toyoda, Hiroshi Takashima, and Masatoshi Koga

Subjects
Male, Anticoagulants, Dabigatran, Treatment Outcome, Rivaroxaban, Tissue Plasminogen Activator, Humans, Administration, Intravenous, Female, Thrombolytic Therapy, Cardiology and Cardiovascular Medicine, Intracranial Hemorrhages, Aged, Ischemic Stroke
Abstract

Background We elucidated the safety of treatment with alteplase at 0.6 mg/kg within 24 hours for patients on direct oral anticoagulants (DOACs) before ischemic stroke onset. Methods and Results Consecutive patients with acute ischemic stroke who underwent intravenous thrombolysis using alteplase at 0.6 mg/kg from 2011 to 2021 were enrolled from our single‐center prospective stroke registry. We compared outcomes between patients taking DOACs and those not taking oral anticoagulants within 48 hours of stroke onset. The primary safety outcome was the rate of symptomatic intracranial hemorrhage with a ≥4‐point increase on the National Institutes of Health Stroke Scale score from baseline. The efficacy outcome was defined as 3‐month modified Rankin Scale score of 0 to 2 after stroke onset. Of 915 patients with acute ischemic stroke who received intravenous thrombolysis (358 women; median age, 76 years; median National Institutes of Health Stroke Scale score, 10), 40 patients took DOACs (6 took dabigatran, 8 took rivaroxaban, 16 took apixaban, and 10 took edoxaban) within 24 hours of onset and 753 patients did not take any oral anticoagulants. The rate of symptomatic intracranial hemorrhage was comparable between patients on DOACs and those not on oral anticoagulants (2.5% versus 2.4%, P =0.95). The rate of favorable outcomes was comparable between the 2 groups (59.4% versus 58.2%, P =0.46), although the admission National Institutes of Health Stroke Scale score was higher in patients on DOACs. No significant differences showed in any intracranial hemorrhage within 36 hours or mortality at 3 months. Conclusions Intravenous thrombolysis would be safely performed for patients on DOACs following the recommendations of the Japanese guidelines. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02251665.

Published
2022

46. [Finger drop variant of Guillain-Barré syndrome: a case report]

Author

Yuki Fujii, Takamichi Kanbayashi, Shunsuke Kobayashi, Ayumi Uchibori, Atsuro Chiba, and Masahiro Sonoo

Subjects
Male, Adult, Neurologic Examination, Diagnosis, Differential, Humans, Immunoglobulins, Intravenous, Neurology (clinical), G(M1) Ganglioside, Guillain-Barre Syndrome
Abstract

We report the case of a 31-year-old man with a finger drop variant of Guillain-Barré syndrome (GBS). The patient visited a neurological clinic with complaints of difficulty in extending the fingers, which occurred seven days after he had fever and diarrhea. The physician who first saw the patient suspected posterior interosseous nerve palsy and referred him to our hospital. Neurological examination 35 days after the onset revealed distal weakness of the upper extremities, particularly in the bilateral extensor digitorum (Medical Research Council [MRC] scale 1/1 [right/left]). The left triceps surae muscle was also weak (MRC scale 5/4). Bilateral Achilles tendon reflexes were absent, but other neurological findings were normal. Cerebrospinal fluid examination showed albuminocytologic dissociation. Serum immunoglobulin G antibodies against GM1 were positive. Nerve conduction studies revealed reduced amplitude of compound muscle action potentials (CMAPs) without evidence of demyelination in the median, ulnar, radial, and tibial nerves. CMAP amplitude was most severely reduced in the radial nerve among the upper extremity nerves. We diagnosed the patient with acute motor axonal neuropathy. His symptoms gradually improved after treatment with intravenous immunoglobulin. When encountering acute finger drop, neurologists should consider the finger drop variant of GBS as a differential diagnosis.

Published
2022

47. Stroke prevention in patients from Latin American countries with non‐valvular atrial fibrillation: Insights from the GARFIELD‐AF registry

Author

Jerjes-Sanchez C., Corbalan R., Barretto A. C. P., Luciardi H. L., Allu J., Illingworth L., Pieper K. S., Kayani G., Fitzmaurice D. A., Goto S., Hacke W., Mantovani L. G., Turpie A. G. G., Gersh B. J., Gibbs H., Brodmann M., Cools F., Connolly S. J., Spyropoulos A., Eikelboom J., Hu D., Jansky P., Nielsen J. D., Ragy H., Raatikainen P., Le Heuzey J. -Y., Darius H., Keltai M., Kakkar S., Sawhney J. P. S., Agnelli G., Ambrosio G., Koretsune Y., Diaz C. J. S., ten Cate H., Atar D., Stepinska J., Panchenko E., Lim T. W., Jacobson B., Oh S., Vinolas X., Rosenqvist M., Steffel J., Angchaisuksiri P., Parkhomenko A., Al Mahmeed W., Chen K. N., Zhao Y. S., Zhang H. Q., Chen J. Z., Cao S. P., Wang D. W., Yang Y. J., Li W. H., Yin Y. H., Tao G. Z., Yang P., Chen Y. M., He S. H., Wang Y., Fu G. S., Li X., Wu T. G., Cheng X. S., Yan X. W., Zhao R. P., Chen M. S., Xiong L. G., Chen P., Jiao Y., Guo Y., Xue L., Wang F. Z., Li H., Yang Z. M., Bai C. L., Chen J., Chen J. Y., Chen X., Feng S., Fu Q. H., Gao X. J., Guo W. N., He R. H., He X. A., Hu X. S., Huang X. F., Li B., Li J., Li L., Li Y. H., Liu T. T., Liu W. L., Liu Y. Y., Lu Z. C., Luo X. L., Ma T. Y., Peng J. Q., Sheng X., Shi X. J., Sun Y. H., Tian G., Wang K., Wang L., Wu R. N., Xie Q., Xu R. Y., Yang J. S., Yang L. L., Yang Q., Ye Y., Yu H. Y., Yu J. H., Yu T., Zhai H., Zhan Q., Zhang G. S., Zhang Q., Zhang R., Zhang Y., Zheng W. Y., Zhou B., Zhou Z. H., Zhu X. Y., Jadhav P., Durgaprasad R., Ravi Shankar A. G., Rajput R. K., Bhargava K., Sarma R., Srinivas A., Roy D., Nagamalesh U. M., Chopda M., Kishore R., Kulkarni G., Chandwani P., Pothiwala R. A., Padinhare Purayil M., Shah S., Chawla K., Kothiwale V. A., Raghuraman B., Vijayaraghavan G., Vijan V. M., Bantwal G., Bisne V., Khan A., Gupta J. 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B., Yeter E., Ongen Z., Cayli M., Pekdemir H., Ozdemir M., Sucu M., Sayin T., Demir M., Yorgun H., Ersanli M., Okuyan E., Aras D., Abdelrahman H., Aktas O., Alpay D., Aras F., Bireciklioglu M. F., Budeyri S., Buyukpapuc M., Caliskan S., Esen M., Felekoglu M. A., Genc D., Ikitimur B., Karaayvaz E. B., Karatas S. K., Okutucu S., Ozcelik E., Quisi A., Sag H., Sahiner L., Sayin B. Y., Seker T., Alkan D. U., Yildirim E., Yildirim R., Yilmaz F., Yuksekdag V., Vensentini N., Ingaramo A. C., Sambadaro G. A., Caputi V. F., Berman S. G., Dragotto P., Kleiban A. J., Centurion N., Giacomi G., Guerrero R. A. A., Conde D., Zapata G., Di Paola L. A., Ramos J. L., Dran R. D., Egido J., Fernandez A. A., Fosco M. J., Sassone S., Sinisi V. A., Cartasegna L. R., Berli M. A., Vilamajo O. A. G., Ferroni F., Alaguibe E. D., D'Amelio A. A., Arabetti C., Arias L., Belardi J. A., Bergesio L., Berli F., Berli M., Borchowiec S., Buzzetti C., Cabrini R., Campisi V., Cappi A. L., Carrizo R., Berra F. 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M., Martini G., Tessitori M., Cappelli R., Poli D., Quintavalla R., Melone F., Cosmi F., Pizzini A., Piseddu G., Fanelli R., Latella C., Santi R., Pancaldi L., De Cristofaro R., Palareti G., De Blasio A., Salerno Uriarte J., Minetti F., Pogliani E. M., Lonati L. M., Accogli M., Ciampani N., Malengo S., Feola M., Raisaro A., Fattore L., Grilli P., Germini F., Settimi M., Alunni M., Duranti G., Tedeschi L., Baglioni G., Avanzino G., Berardi M., Pannacci V., Giombolini A., Nicoli S., Scarponi T., Allasia B., Ricciarini P., Nasorri R., Argena A., Bossolasco P., Ronchini P., Filippi A., Tradati F., Bulla C., Donzelli L., Foppa L., Bottarelli M. L., Tomasello A., Mauric A., Femiano C., Reggio R., Lillo F., Mariani A., Forcignano F., Volpe M., D'Avino M., Bongiorni M. 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J., Watson E., Sarai B., Ahmad N., Willcock W., Cairns J., Sathananthan S., de Kare-Silver N., Gilliland A., Strieder E., Howitt A., Vishwanathan B., Bird N., Gray D., Clark M., Bisatt J., Litchfield J., Fisher E., Fooks T., Kelsall A. R., Alborough E., Wakeling J., Parfitt M., Milne K., Rogers S., Priyadharshan R., Oliver J. L., Davies E., Abushal S., Jacobs M., Hutton C., Walls N. I., Thompson R., Chigbo C., Zaidi S. M. A., Howard M., Butter K. C., Barrow S., Little H., Haq I. U., Gibbons L., Glencross S., McLeod A. J., Poland K., Mulholland C., Warke A., Conn P., Burns G., Smith R. N., Lowe S., Kamath R., Dau H. S., Webster J., Hodgins I., Vercoe S., Roome P. C., Pinnock H., Patel J. R. A., Ali A., Hart N., Davies R., Stuart E., Neden C. A., Danielsen M., Heath R., Sharma P., Galloway S., Hawkins C., Oliver R., Aylward M., Mannion S., Braddick M., Edwards D., Rothwell A. C., Sabir A., Choudhary F., Khalaque S., Wilson A., Peters S., Coulson W., Roberts N., Heer A., Coates S., Ward B., Jackson D., Walton S., Shepherd D., Sterry M., Wong T., Boon M., Bunney R., Haria-Shah R., Baron R. T., Davies S., Schatzberger T., Hargreaves N., Stephenson T., Choi H., Batson R., Lucraft L., Myhill T., Estifano S., Geatch D., Wilkinson J., Veale R., Forshaw K., Davies T., Zaman K., Vinson P., Liley C., Bandrapalli M., McGinty P., Wastling R., McEleny P., Beattie A., Cooke P., Wong M., Gunasegaram J., Pugsley M., Ahmad S., A'Court C., Ayers J., Bennett J., Cartwright S., Dobson S., Dooldeniya C., Flynn A., Fox R., Goram J., Halpin A., Hay A., Jacobs P., Jeffers L., Lomax L., Munro I., Muvva R., Nadaph M., Powell K., Randfield S., Redpath D., Reed R., Rickenbach M., Rogers G., Saunders P. 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M., Singh R., Naguib A., Abu-Mahfouz M., Al Omairi M., Al Naeemi A., Maruthanayagam R., Bazargani N., Wassef A., Gupta R., Khan M., Subbaraman B., Abdul A., Al Mulla A., El Bardisy S., Haridas P., Jadhav S., Magdaluyo K., Makdad M., Maqsood I., Mohamed R., Sharma N., Sharma R., Thanzeel M., Canosa R., Rama P., Blumberg E., Garcia J., Mullen P., Wilson V., Quick A., Ferrick K., Kutayli W. M., Cox M., Franco M., Falkowski S., Mendelson R., Williams M., Miller S., Beach S., Alfieri A., Gutowski T., Haque I., Reddy R., Ahmed W., Delafontaine P., Diercks D., Theodoro D., Remmel K., Alberts M., Ison R., Noveck H., Duffy P., Pitta S., Nishijima D., Treasure C., Asafu-Adjaye N., Ball K., Bartlett M., Bentley M., Bowers S., Brown A., Browne A., Cameron-Watts J., Canova M., Cassidy D., Cervellione K., Congal S., DePauw J., Dickerson A., Eley M., Evans L., Felpel S., Ferdinand K., Fielder D., Gentry P., Haideri A., Hakimi F., Harbour T., Hartranft E., Hawkins B., Headlee M., Henson L., Herrick C., Hicks T., Jasinski S., Jones A., Jones L., Jones P., Karl S., Keeling M., Kerr J., Knowles P., Langdon J., Lay M., Lee J. 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P., Prieto, I., Quintern, V., Renom, R., Diaz, L. M. R., Rios, V., Sola, L. R., Rivera, R., Robiro, X. R., Roca, M., Saumell, C. R., Rodrigo, C., Rodriguez, E., Garcia, M. R., Jimenez, S. S., Calderon, P. S., Mendez, L. S., Parra, S. S., Santolaya, C., Sanz, M. R. S., Blanco, A. S., Serralvo, E., Sierra, N., Valero, C. S., Lopez, J. S., Fontanillas, M. T., Riera, M. T., Tobajas, G., Torres, C., Marques, J. T., Pastor, M. U., Wirdby, A., Linden, J., Henriksson, K., Elmersson, M., Egilsson, A., Borjesson, U., Svard, G., Liu, B., Lindh, A., Olsson, L. -B., Gustavsson, M., Andersson, L., Benson, L., Bothin, C., Hajimirsadeghi, A., Kadir, K., Ericsson, M., Ohlsson, A., Lindvall, H., Svensson, P., Thorne, K., Handel, H., Platonov, P., Eriksson, B., Timberg, I., Romberg, K., Crisby, M., Karlsson, J. -E., Jensen, S. A., Andersson, A., Malmqvist, L., Martinsson, B., Bernsten, F., Engdahl, J., Thulin, J., Hot-Bjelac, A., Stalby, P., Aaroe, H., Ahbeck, E., Ahlmark, H., Al-Khalili, F., Bonkowski, G., Dzeletovic, S., Ekstrand, A. -B., Eriksson, G. -B., Floren, K., Grassjo, C., Hahn, S., Jaensson, P., Jansson, B., Jansson, J. -H., Kangert, R. -M., Koch, A., Kusiak, D., Lettenstrom, A., Lindberg, A., Lindholm, C. -J., Mannermyr, A., Mansson, K., Millborg, M., Nilsson, C., Ohlin, A. -M., Olofsson, A., Osberg, A., Pedersen, A., Risbecker, K., Rosenberg, K., Samuelsson, J., Shayesteh, M., Skoglund, K., Stjernberg, M., Thorsen, C., Beer, J. 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S., Pickavance, G., Mcdonnell, J., Williams, A., Gooding, T., Wagner, H., Suryani, S., Singal, A., Sircar, S., Bilas, R., Hutchinson, P., Wakeman, A., Stokes, M., Paul, N., Aziz, M., Ramesh, C., Wilson, P., Franklin, S., Fairhead, S., Thompson, J., St Joseph, V., Taylor, G., Tragen, D., Seamark, D., Paul, C., Richardson, M., Jefferies, A., Sharp, H., Jones, H., Giles, C., Page, M., Oginni, O., Aldegather, J., Wetherwell, S., Lumb, W., Evans, P., Scouller, F., Macey, N., Stipp, Y., West, R., Thurston, S., Wadeson, P., Matthews, J., Pandya, P., Gallagher, A., Railton, T., Sinha, B., Russell, D., Davies, J. A., Ainsworth, P., Jones, C. P., Weeks, P., Eden, J., Kernick, D., Murdoch, W., Lumley, L., Patel, R. P., Wong, S. W., Saigol, M., Ladha, K., Douglas, K., Cumberlidge, D. F., Bradshaw, C., Van Zon, G., Jones, K. P., Thomas, M. J., Watson, E., Sarai, B., Ahmad, N., Willcock, W., Cairns, J., Sathananthan, S., de Kare-Silver, N., Gilliland, A., Strieder, E., Howitt, A., Vishwanathan, B., Bird, N., Gray, D., Clark, M., Bisatt, J., Litchfield, J., Fisher, E., Fooks, T., Kelsall, A. R., Alborough, E., Wakeling, J., Parfitt, M., Milne, K., Rogers, S., Priyadharshan, R., Oliver, J. L., Davies, E., Abushal, S., Jacobs, M., Hutton, C., Walls, N. I., Thompson, R., Chigbo, C., Zaidi, S. M. A., Howard, M., Butter, K. C., Barrow, S., Little, H., Haq, I. U., Gibbons, L., Glencross, S., Mcleod, A. J., Poland, K., Mulholland, C., Warke, A., Conn, P., Burns, G., Smith, R. N., Lowe, S., Kamath, R., Dau, H. S., Webster, J., Hodgins, I., Vercoe, S., Roome, P. C., Pinnock, H., Patel, J. R. A., Ali, A., Hart, N., Davies, R., Stuart, E., Neden, C. A., Danielsen, M., Heath, R., Sharma, P., Galloway, S., Hawkins, C., Oliver, R., Aylward, M., Mannion, S., Braddick, M., Edwards, D., Rothwell, A. C., Sabir, A., Choudhary, F., Khalaque, S., Wilson, A., Peters, S., Coulson, W., Roberts, N., Heer, A., Coates, S., Ward, B., Jackson, D., Walton, S., Shepherd, D., Sterry, M., Wong, T., Boon, M., Bunney, R., Haria-Shah, R., Baron, R. T., Davies, S., Schatzberger, T., Hargreaves, N., Stephenson, T., Choi, H., Batson, R., Lucraft, L., Myhill, T., Estifano, S., Geatch, D., Wilkinson, J., Veale, R., Forshaw, K., Davies, T., Zaman, K., Vinson, P., Liley, C., Bandrapalli, M., Mcginty, P., Wastling, R., Mceleny, P., Beattie, A., Cooke, P., Wong, M., Gunasegaram, J., Pugsley, M., Ahmad, S., A'Court, C., Ayers, J., Bennett, J., Cartwright, S., Dobson, S., Dooldeniya, C., Flynn, A., Fox, R., Goram, J., Halpin, A., Hay, A., Jacobs, P., Jeffers, L., Lomax, L., Munro, I., Muvva, R., Nadaph, M., Powell, K., Randfield, S., Redpath, D., Reed, R., Rickenbach, M., Rogers, G., Saunders, P. 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P., Hesketh, L., Hoffmann, B., Johnson, K., Juergens, C., Kassam, I., Lawlor, V., Lehman, M., Lehman, S., Leung, D., Mackay, S., Mackenzie, M., Mccarthy, C., Mcintosh, C., Mckeon, L., Morrison, H., Mussap, C., Myers, J. -D., Nagalingam, V., Oldfield, G., O'May, V., Palmer, J., Parsons, L., Patching, K., Patching, T., Paul, V., Plotz, M., Preston, S., Rashad, H., Ratcliffe, M., Raynes, S., Rose, J., Sanders, L., Seremetkoska, M., Setio, H., Shone, S., Shrestha, P., Singh, C., Singleton, C., Stoyanov, N., Sutcliffe, S., Swaraj, K., Tarrant, J., Thompson, S., Tsay, I. M., Vorster, M., Waldman, A., Wallis, L., Wilford, E., Wong, K., Luton, R., Gupta, M., Pandey, A. S., Cheung, S., Leader, R., Beaudry, P., Ayala-Paredes, F., Berlingieri, J., Heath, J., Poirier, G., Du Preez, M., Nadeau, R., Dresser, G., Dhillon, R., Hruczkowski, T., Schweitzer, B., Coutu, B., Angaran, P., Macdonald, P., Vizel, S., Fikry, S., Parkash, R., Lavoie, A., Cha, J., Ramjattan, B., Bonet, J., Ahmad, K., Aro, L., Aves, T., Beaudry, K., Bergeron, C., Bigcanoe, J., Bignell, N., Breakwell, L., Burke, E., Carroll, L., Clarke, B., Cleveland, T., Daheb, S., Dehghani, P., Denis, I., Djaidani, Z., Dorian, P., Douglass, S., Dunnigan, J., Ewert, A., Farquhar, D., Fearon, A., Ferleyko, L., Fournier, D., Fox, B., Grenier, M. -C., Gulliver, W., Haveman, K., Hines, C., Hines, K., Jackson, A. M., Jean, C., Jethoo, G., Kahlon, R., Kelly, S., Kim, R., Korley, V., Kornder, J., Kwan, L., Largy, J., Lewis, C., Lewis, S., Mangat, I., Moor, R., Navratil, J., Neas, I., Otis, J., Otis, R., Pandey, M., Petrie, F., Pinter, A., Raines, M., Roberts, P., Robinson, M., Sas, G., Schulman, S., Snell, L., Spearson, S., Stevenson, J., Trahey, T., Wong, S., Wright, D., El-Aziz, A. A., Seif, S. K. A., El Din, M. G., El Etriby, S., Elbahry, A., El-Etreby, A., Elkhadem, M., Katta, A., Khairy, T., Mowafy, A., Nawar, M., Ohanissian, A., Reda, A., Reda, M., Salem, H., Sami, N., Samir, S., Setiha, M., Sobhy, M., Soliman, A., Taha, N., Tawfik, M., Zaatout, E., Kettles, D., Bayat, J., Siebert, H., Horak, A., Kelfkens, Y., Garda, R., Pillay, T., Guerra, M., van Zyl, L., Theron, H., Murray, A., Louw, R., Greyling, D., Mntla, P., Ueckermann, V., Loghdey, R., Ismail, S., Ahmed, F., Engelbrecht, J., Ramdass, A., Maharajh, S., Oosthuysen, W., Angel, G., Bester, C., Booysen, M., Boshoff, C., Cannon, C., Cassimjee, S., Chami, C., Conway, G., Davids, A., de Meyer, L., Du Plessis, G., Ellis, T., Henley, L., Karsten, M., Loyd, E., Marks, J., Mavhusa, L., Mostert, M., Page, A., Rikhotso, L., Salie, M., Sasto, J., Shaik, F., Skein, A., Smith, L., Tarr, G., Tau, T., van Zyl, F., Yousef, G., Agrawal, A., Nathani, M., Ibrahim, M., Esheiba, E. M., Singh, R., Naguib, A., Abu-Mahfouz, M., Al Omairi, M., Al Naeemi, A., Maruthanayagam, R., Bazargani, N., Wassef, A., Gupta, R., Khan, M., Subbaraman, B., Abdul, A., Al Mulla, A., El Bardisy, S., Haridas, P., Jadhav, S., Magdaluyo, K., Makdad, M., Maqsood, I., Mohamed, R., Sharma, N., Sharma, R., Thanzeel, M., Canosa, R., Rama, P., Blumberg, E., Garcia, J., Mullen, P., Wilson, V., Quick, A., Ferrick, K., Kutayli, W. M., Cox, M., Franco, M., Falkowski, S., Mendelson, R., Williams, M., Miller, S., Beach, S., Alfieri, A., Gutowski, T., Haque, I., Reddy, R., Ahmed, W., Delafontaine, P., Diercks, D., Theodoro, D., Remmel, K., Alberts, M., Ison, R., Noveck, H., Duffy, P., Pitta, S., Nishijima, D., Treasure, C., Asafu-Adjaye, N., Ball, K., Bartlett, M., Bentley, M., Bowers, S., Brown, A., Browne, A., Cameron-Watts, J., Canova, M., Cassidy, D., Cervellione, K., Congal, S., Depauw, J., Dickerson, A., Eley, M., Evans, L., Felpel, S., Ferdinand, K., Fielder, D., Gentry, P., Haideri, A., Hakimi, F., Harbour, T., Hartranft, E., Hawkins, B., Headlee, M., Henson, L., Herrick, C., Hicks, T., Jasinski, S., Jones, A., Jones, L., Jones, P., Karl, S., Keeling, M., Kerr, J., Knowles, P., Langdon, J., Lay, M., Lee, J. A., Lincoln, T., Malone, E., Merliss, A., Merritt, D., Minardo, J., Mooso, B., Orosco, C., Palumbo, V., Parker, M., Parrott, T., Paserchia, S., Pearl, G., Peterson, J., Pickelsimer, N., Purcell, T., Raynor, J., Raziano, S., Richard, C., Richardson, T., Robertson, C., Sage, A., Sanghera, T., Shaw, P., Shoemaker, J., Smith, K., Stephanie, B., Thatcher, A., Theobald, H., Thompson, N., Treasure, L., Tripti, T., Verdi, C., and Worthy, V.

Subjects
Registrie, Male, Latin Americans, 030204 cardiovascular system & hematology, outcomes, 0302 clinical medicine, Drug Prescription, Retrospective Studie, Risk Factors, Atrial Fibrillation, Antithrombotic, Prospective Studies, Registries, 030212 general & internal medicine, Practice Patterns, Physicians', Stroke, Anticoagulant, Atrial fibrillation, General Medicine, Middle Aged, Treatment Outcome, Stroke prevention, outcome, Female, medicine.symptom, Cardiology and Cardiovascular Medicine, Human, medicine.medical_specialty, medicine.drug_class, Clinical Investigations, Hemorrhage, antithrombotic treatment, Drug Prescriptions, 03 medical and health sciences, Internal medicine, medicine, Humans, Mexico, Aged, Retrospective Studies, Fibrillation, business.industry, Risk Factor, Anticoagulants, South America, medicine.disease, Drug Utilization, Clinical trial, Prospective Studie, Latin American, antithrombotic treatment, atrial fibrillation, Latin American, outcomes, business
Abstract

Author(s): Jerjes-Sanchez, Carlos; Corbalan, Ramon; Barretto, Antonio CP; Luciardi, Hector L; Allu, Jagan; Illingworth, Laura; Pieper, Karen S; Kayani, Gloria; GARFIELD-AF Investigators | Abstract: BackgroundAtrial fibrillation (AF) is an important preventable cause of stroke. Anticoagulation (AC) therapy can reduce this risk. However, prescribing patterns and outcomes in patients with non-valvular AF (NVAF) from Latin American countries are poorly described.MethodsUsing data from the Global Anticoagulant Registry in the FIELD-AF (GARFIELD-AF), we examined the stroke prevention strategies and the 1-year outcomes in patients from four Latin American countries: Argentina, Brazil, Chile, and Mexico.ResultsA total of 4162 patients (2010-2014) were included in this analysis. At the time of AF diagnosis, 39.9% of patients were prescribed vitamin K antagonists (VKA) ± antiplatelet (AP) therapy, 21.8% non-VKA oral anticoagulant (NOAC) ± AP, 24.1% AP only and 14.1% no antithrombotic treatment. The proportion of moderate-high risk patients receiving no AC therapy at participating centers was highest in Mexico (46.4%) and lowest in Chile (14.3%). During 1-year follow-up, the rates of all-cause mortality, stroke/SE and major bleeding were: 5.77 (95% CI) (5.06-6.56), 1.58 (1.23-2.02), and 0.99 (0.72-1.36) and per 100 person-years, respectively, which are higher than the global rates across all countries in GARFIELD-AF. Unadjusted rates of all-cause mortality were highest in Argentina, 6.95 (5.43-8.90), and lowest in Chile, 4.01 (2.92-5.52).ConclusionsGARFIELD-AF results describes the marked variation in the baseline characteristics and patterns of antithrombotic treatments in patients with NVAF in four Latin American countries. Over one-third of patients with a moderate-to-high risk of stroke received no AC therapy, highlighting the need for improved management of patients according to national guideline. CLINICAL TRIAL REGISTRATION-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01090362.

Published
2019

48. Etrolizumab as induction and maintenance therapy for ulcerative colitis in patients previously treated with tumour necrosis factor inhibitors (HICKORY): a phase 3, randomised, controlled trial

Author

Laurent Peyrin-Biroulet, Ailsa Hart, Peter Bossuyt, Millie Long, Matthieu Allez, Pascal Juillerat, Alessandro Armuzzi, Edward V Loftus, Elham Ostad-Saffari, Astrid Scalori, Young S Oh, Swati Tole, Akiko Chai, Jennifer Pulley, Stuart Lacey, William J Sandborn, Humberto Aguilar, Tariq Ahmad, Evangelos Akriviadis, Xavier Aldeguer Mante, Istvan Altorjay, Ashwin Ananthakrishnan, Vibeke Andersen, Montserrat Andreu Garcia, Guy Aumais, Irit Avni-Biron, Jeffrey Axler, Kamran Ayub, Filip Baert, Mauro Bafutto, George Bamias, Isaac Bassan, Curtis Baum, Laurent Beaugerie, Brian Behm, Pradeep Bekal, Michael Bennett, Fernando Bermejo San Jose, Charles Bernstein, Dominik Bettenworth, Sudhir Bhaskar, Livia Biancone, Bahri Bilir, Michael Blaeker, Stuart Bloom, Verle Bohman, Francisco Javier Bosques Padilla, Yoram Bouhnik, Gerd Bouma, Raymond Bourdages, Stephan Brand, Brian Bressler, Markus Brückner, Carsten Buening, Franck Carbonnel, Thomas Caves, Jonathon Chapman, Jae Hee Cheon, Naoki Chiba, Camelia Chioncel, Dimitrios Christodoulou, Martin Clodi, Albert Cohen, Gino Roberto Corazza, Richard Corlin, Rocco Cosintino, Fraser Cummings, Robin Dalal, Silvio Danese, Marc De Maeyer, Carlos Fernando De Magalhães Francesconi, Aminda De Silva, Henry Debinski, Pierre Desreumaux, Olivier Dewit, Geert D'Haens, Sandra Di Felice Boratto, John Nik Ding, Tyler Dixon, Gerald Dryden, George Aaron Du Vall, Matthias Ebert, Ana Echarri Piudo, Robert Ehehalt, Magdy Elkhashab, Craig Ennis, Jason Etzel, Jan Fallingborg, Brian Feagan, Roland Fejes, Daniel Ferraz de Campos Mazo, Valéria Ferreira de Almeida Borges, Andreas Fischer, Alan Fixelle, Mark Fleisher, Sharyle Fowler, Bradley Freilich, Keith Friedenberg, Walter Fries, Csaba Fulop, Mathurin Fumery, Sergio Fuster, Gyula G Kiss, Santiago Garcia Lopez, Sonja Gassner, Kanwar Gill, Cyrielle Gilletta de Saint Joseph, Philip Ginsburg, Paolo Gionchetti, Eran Goldin, Adrian-Eugen Goldis, Hector Alejandro Gomez Jaramillo, Maciej Gonciarz, Glenn Gordon, Daniel Green, Jean-Charles Grimaud, Rogelio Guajardo Rodriguez, Zoltan Gurzo, Alexandra Gutierrez, Tibor Gyökeres, Ki Baik Hahm, Stephen Hanauer, John Hanson, William Harlan III, Peter Hasselblatt, Buhussain Hayee, Xavier Hebuterne, Peter Hendy, Melvin Heyman, Peter Higgins, Raouf Hilal, Pieter Hindryckx, Frank Hoentjen, Peter Hoffmann, Frank Holtkamp-Endemann, Gerald Holtmann, Gyula Horvat, Stefanie Howaldt, Samuel Huber, Ikechukwu Ibegbu, Maria Isabel Iborra Colomino, Peter Irving, Kim Isaacs, Kiran Jagarlamudi, Rajesh Jain, Sender Jankiel Miszputen, Jeroen Jansen, Jennifer Jones, John Karagiannis, Nicholas Karyotakis, Arthur Kaser, Lior Katz, Seymour Katz, Leo Katz, Nirmal Kaur, Edita Kazenaite, Reena Khanna, Sunil Khurana, Joo Sung Kim, Young-Ho Kim, Sung Kook Kim, Dongwoo Kim, Jochen Klaus, Dariusz Kleczkowski, Pavel Kohout, Bartosz Korczowski, Georgios Kouklakis, Ioannis Koutroubakis, Richard Krause, Tunde Kristof, Ian Kronborg, Annette Krummenerl, Limas Kupcinskas, Jorge Laborda Molteni, David Laharie, Adi Lahat-zok, Jonghun Lee, Kang-Moon Lee, Rupert Leong, Henry Levine, Jimmy Limdi, James Lindsay, Nilesh Lodhia, Edward Loftus, Randy Longman, Pilar Lopez Serrano, Edouard Louis, Maria Helena Louzada Pereira, John Lowe, Stefan Lueth, Milan Lukas, Giovanni Maconi, Finlay Macrae, Laszlo Madi-Szabo, Uma Mahadevan-Velayos, Everson Fernando Malluta, Fazia Mana, Peter Mannon, Gerasimos Mantzaris, Ignacio Marin Jimenez, Maria Dolores Martin Arranz, Radu-Bogdan Mateescu, Felipe Mazzoleni, Agnieszka Meder, Ehud Melzer, Jessica Mertens, Konstantinos Mimidis, Brent Mitchell, Tamas Molnar, Gregory Moore, Luis Alonso Morales Garza, Reme Mountifield, Vinciane Muls, Charles Murray, Bela Nagy, Markus Neurath, Augustin Nguyen, Remo Panaccione, William Pandak, Julian Panes Diaz, Jihye Park, Luca Pastorelli, Bhaktasharan Patel, Markus Peck-Radosavljevic, Gyula Pecsi, Farhad Peerani, Javier Perez Gisbert, Martin Pesta, Robert Petryka, Raymond Phillips, Marieke Pierik, Vijayalakshmi Pratha, Vlastimil Prochazka, Istvan Racz, Graham Radford-Smith, Daniel Ramos Castañeda, Odery Ramos Júnior, Jaroslaw Regula, Jean-Marie Reimund, Bryan Robbins, Xavier Roblin, Francesca Rogai, Gerhard Rogler, Jerzy Rozciecha, David Rubin, Azalia Yuriria Ruiz Flores, Maciej Rupinski, Grazyna Rydzewska, Sumona Saha, Simone Saibeni, Agnes Salamon, Zoltan Sallo, Bruce Salzberg, Douglas Samuel, Sunil Samuel, William Sandborn, Edoardo Vincenzo Savarino, Anja Schirbel, Robert Schnabel, Stefan Schreiber, John Scott, Shahriar Sedghi, Frank Seibold, Jakob Seidelin, Ursula Seidler, Ahmad Shaban, Ira Shafran, Aasim Sheikh, Alex Sherman, Haim Shirin, Patryk Smolinski, Geun Am Song, Konstantinos Soufleris, Alexander Speight, Dirk Staessen, Andreas Stallmach, Michael Staun, Daniel Stein, Hillary Steinhart, Jonathas Stifft, David Stokesberry, Andreas Sturm, Keith Sultan, Gyorgy Szekely, Kuldeep Tagore, Hugo Tanno, Lena Thin, Syed Thiwan, Carlton Thomas, Michal Tichy, Gabor Tamas Toth, Zsolt Tulassay, Jan Ulbrych, John Valentine, Marta Varga, Eduardo Vasconcellos, Byron Vaughn, Brenda Velasco, Francisco Velazquez, Severine Vermeire, Erica Villa, Aron Vincze, Harald Vogelsang, Miroslava Volfova, Lucine Vuitton, Petr Vyhnalek, Peter Wahab, Jens Walldorf, Mattitiahu Waterman, John Weber, L. Michael Weiss, Anna Wiechowska-Kozlowska, Elise Wiesner, Thomas Witthoeft, Robert Wohlman, Barbara Wozniak-Stolarska, Bruce Yacyshyn, Byong-Duk Ye, Ziad Younes, Lígia Yukie Sassaki, Cyrla Zaltman, Stefan Zeuzem, Neurosurgery, ANS - Neurovascular Disorders, Gastroenterology and Hepatology, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, Peyrin-Biroulet L., Hart A., Bossuyt P., Long M., Allez M., Juillerat P., Armuzzi A., Loftus E.V., Ostad-Saffari E., Scalori A., Oh Y.S., Tole S., Chai A., Pulley J., Lacey S., Sandborn W.J., Aguilar H., Ahmad T., Akriviadis E., Aldeguer Mante X., Altorjay I., Ananthakrishnan A., Andersen V., Andreu Garcia M., Aumais G., Avni-Biron I., Axler J., Ayub K., Baert F., Bafutto M., Bamias G., Bassan I., Baum C., Beaugerie L., Behm B., Bekal P., Bennett M., Bermejo San Jose F., Bernstein C., Bettenworth D., Bhaskar S., Biancone L., Bilir B., Blaeker M., Bloom S., Bohman V., Bosques Padilla F.J., Bouhnik Y., Bouma G., Bourdages R., Brand S., Bressler B., Bruckner M., Buening C., Carbonnel F., Caves T., Chapman J., Cheon J.H., Chiba N., Chioncel C., Christodoulou D., Clodi M., Cohen A., Corazza G.R., Corlin R., Cosintino R., Cummings F., Dalal R., Danese S., De Maeyer M., De Magalhaes Francesconi C.F., De Silva A., Debinski H., Desreumaux P., Dewit O., D'Haens G., Di Felice Boratto S., Ding J.N., Dixon T., Dryden G., Du Vall G.A., Ebert M., Echarri Piudo A., Ehehalt R., Elkhashab M., Ennis C., Etzel J., Fallingborg J., Feagan B., Fejes R., Ferraz de Campos Mazo D., Ferreira de Almeida Borges V., Fischer A., Fixelle A., Fleisher M., Fowler S., Freilich B., Friedenberg K., Fries W., Fulop C., Fumery M., Fuster S., G Kiss G., Garcia Lopez S., Gassner S., Gill K., Gilletta de Saint Joseph C., Ginsburg P., Gionchetti P., Goldin E., Goldis A.-E., Gomez Jaramillo H.A., Gonciarz M., Gordon G., Green D., Grimaud J.-C., Guajardo Rodriguez R., Gurzo Z., Gutierrez A., Gyokeres T., Hahm K.B., Hanauer S., Hanson J., Harlan III W., Hasselblatt P., Hayee B., Hebuterne X., Hendy P., Heyman M., Higgins P., Hilal R., Hindryckx P., Hoentjen F., Hoffmann P., Holtkamp-Endemann F., Holtmann G., Horvat G., Howaldt S., Huber S., Ibegbu I., Iborra Colomino M.I., Irving P., Isaacs K., Jagarlamudi K., Jain R., Jankiel Miszputen S., Jansen J., Jones J., Karagiannis J., Karyotakis N., Kaser A., Katz L., Katz S., Kaur N., Kazenaite E., Khanna R., Khurana S., Kim J.S., Kim Y.-H., Kim S.K., Kim D., Klaus J., Kleczkowski D., Kohout P., Korczowski B., Kouklakis G., Koutroubakis I., Krause R., Kristof T., Kronborg I., Krummenerl A., Kupcinskas L., Laborda Molteni J., Laharie D., Lahat-zok A., Lee J., Lee K.-M., Leong R., Levine H., Limdi J., Lindsay J., Lodhia N., Loftus E., Longman R., Lopez Serrano P., Louis E., Louzada Pereira M.H., Lowe J., Lueth S., Lukas M., Maconi G., Macrae F., Madi-Szabo L., Mahadevan-Velayos U., Malluta E.F., Mana F., Mannon P., Mantzaris G., Marin Jimenez I., Martin Arranz M.D., Mateescu R.-B., Mazzoleni F., Meder A., Melzer E., Mertens J., Mimidis K., Mitchell B., Molnar T., Moore G., Morales Garza L.A., Mountifield R., Muls V., Murray C., Nagy B., Neurath M., Nguyen A., Panaccione R., Pandak W., Panes Diaz J., Park J., Pastorelli L., Patel B., Peck-Radosavljevic M., Pecsi G., Peerani F., Perez Gisbert J., Pesta M., Petryka R., Phillips R., Pierik M., Pratha V., Prochazka V., Racz I., Radford-Smith G., Ramos Castaneda D., Ramos Junior O., Regula J., Reimund J.-M., Robbins B., Roblin X., Rogai F., Rogler G., Rozciecha J., Rubin D., Ruiz Flores A.Y., Rupinski M., Rydzewska G., Saha S., Saibeni S., Salamon A., Sallo Z., Salzberg B., Samuel D., Samuel S., Sandborn W., Savarino E.V., Schirbel A., Schnabel R., Schreiber S., Scott J., Sedghi S., Seibold F., Seidelin J., Seidler U., Shaban A., Shafran I., Sheikh A., Sherman A., Shirin H., Smolinski P., Song G.A., Soufleris K., Speight A., Staessen D., Stallmach A., Staun M., Stein D., Steinhart H., Stifft J., Stokesberry D., Sturm A., Sultan K., Szekely G., Tagore K., Tanno H., Thin L., Thiwan S., Thomas C., Tichy M., Toth G.T., Tulassay Z., Ulbrych J., Valentine J., Varga M., Vasconcellos E., Vaughn B., Velasco B., Velazquez F., Vermeire S., Villa E., Vincze A., Vogelsang H., Volfova M., Vuitton L., Vyhnalek P., Wahab P., Walldorf J., Waterman M., Weber J., Weiss L.M., Wiechowska-Kozlowska A., Wiesner E., Witthoeft T., Wohlman R., Wozniak-Stolarska B., Yacyshyn B., Ye B.-D., Younes Z., Yukie Sassaki L., Zaltman C., and Zeuzem S.

Subjects
Adult, Male, Ulcerative Colitis Flare, medicine.medical_specialty, Asia, Adolescent, Oceania, Population, Antibodies, Monoclonal, Humanized, Injections, Subcutaneou, Placebo, Severity of Illness Index, law.invention, Middle East, Young Adult, Maintenance therapy, Randomized controlled trial, law, Internal medicine, Gastrointestinal Agent, medicine, Adverse effect, education, Aged, Aged, 80 and over, Tumor Necrosis Factor Inhibitor, education.field_of_study, Hepatology, business.industry, Remission Induction, Gastroenterology, Middle Aged, South America, medicine.disease, Ulcerative colitis, Europe, Treatment Outcome, Etrolizumab, North America, Colitis, Ulcerative, Female, business, Inflammatory diseases Radboud Institute for Molecular Life Sciences [Radboudumc 5], Human
Abstract

Summary Background Etrolizumab is a gut-targeted, anti-β7 integrin, monoclonal antibody. In an earlier phase 2 induction study, etrolizumab significantly improved clinical remission compared with placebo in patients with moderately to severely active ulcerative colitis. We aimed to evaluate the efficacy and safety of etrolizumab in patients with moderately to severely active ulcerative colitis who had been previously treated with anti-tumour necrosis factor (TNF) agents. Methods HICKORY was a multicentre, phase 3, double-blind, placebo-controlled study in adult (18–80 years) patients with moderately to severely active ulcerative colitis (Mayo Clinic total score [MCS] of 6–12 with an endoscopic subscore of ≥2, a rectal bleeding subscore of ≥1, and a stool frequency subscore of ≥1) previously treated with TNF inhibitors. Patients were recruited from 184 treatment centres across 24 countries in North America, South America, Europe, Asia, Oceania, and the Middle East. Patients needed to have an established diagnosis of ulcerative colitis for at least 3 months, corroborated by both clinical and endoscopic evidence, and evidence of disease extending at least 20 cm from the anal verge. In cohort 1, patients received open-label etrolizumab 105 mg every 4 weeks for a 14-week induction period. In cohort 2, patients were randomly assigned (4:1) to receive subcutaneous etrolizumab 105 mg or placebo every 4 weeks for the 14-week induction phase. Patients in either cohort achieving clinical response to etrolizumab induction were eligible for the maintenance phase, in which they were randomly assigned (1:1) to receive subcutaneous etrolizumab 105 mg or placebo every 4 weeks through to week 66. Randomisation was stratified by baseline concomitant treatment with corticosteroids, concomitant treatment with immunosuppressants (induction randomisation only), baseline disease activity, week 14 MCS remission status (maintenance randomisation only), and induction cohort (maintenance randomisation only). All patients and study site personnel were masked to treatment assignment. Primary endpoints were remission (Mayo Clinic total score [MCS] ≤2, with individual subscores of ≤1 and a rectal bleeding subscore of 0) at week 14, and remission at week 66 among patients with a clinical response (MCS with ≥3-point decrease and ≥30% reduction from baseline, plus ≥1 point decrease in rectal bleeding subscore or absolute rectal bleeding score of 0 or 1) at week 14. Efficacy was analysed using a modified intent-to-treat population. Safety analyses included all patients who received at least one dose of study drug during the induction phase. This study is registered at ClinicalTrials.gov , NCT02100696 . Findings HICKORY was conducted from May 21, 2014, to April 16, 2020, during which time 1081 patients were screened, and 609 deemed eligible for inclusion. 130 patients were included in cohort 1. In cohort 2,479 patients were randomly assigned to the induction phase (etrolizumab n=384, placebo n=95). 232 patients were randomly assigned to the maintenance phase (etrolizumab to etrolizumab n=117, etrolizumab to placebo n=115). At week 14, 71 (18·5%) of 384 patients in the etrolizumab group and six (6·3%) of 95 patients in the placebo group achieved the primary induction endpoint of remission (p=0·0033). No significant difference between etrolizumab and placebo was observed for the primary maintenance endpoint of remission at week 66 among patients with a clinical response at week 14 (27 [24·1%] of 112 vs 23 [20·2%] of 114; p=0·50). Four patients in the etrolizumab group reported treatment-related adverse events leading to treatment discontinuation. The proportion of patients reporting at least adverse event was similar between treatment groups for induction (etrolizumab 253 [66%] of 384; placebo 63 [66%] of 95) and maintenance (etrolizumab to etrolizumab 98 [88%] of 112; etrolizumab to placebo 97 [85%] of 114). The most common adverse event in both groups was ulcerative colitis flare. Most adverse events were mild or moderate. During induction, the most common serious adverse event was ulcerative colitis flare (etrolizumab ten [3%] of 384; placebo: two [2%] of 95). During maintenance, the most common serious adverse event in the etrolizumab to etrolizumab group was appendicitis (two [2%] of 112) and the most common serious adverse events in the etrolizumab to placebo group were ulcerative colitis flare (two [2%] of 114) and anaemia (two [2%] of 114). Interpretation HICKORY demonstrated that a significantly higher proportion of patients with moderately to severely active ulcerative colitis who had been previously treated with anti-TNF agent were able to achieve remission at week 14 when treated with etrolizumab compared with placebo; however, there was no significant difference between groups in remission at week 66 among patients with a clinical response at week 14. Funding F Hoffmann-La Roche.

Published
2022

49. Fatal bilateral pneumothoraces after electroacupuncture treatment: A case report and literature review

Author

Hirotaro Iwase, Yuko Kihara, Yohsuke Makino, Fumiko Chiba, Suguru Torimitsu, and Rutsuko Yamaguchi

Subjects
Lung Diseases, Male, medicine.medical_specialty, Forensic pathology, Lung, business.industry, Electroacupuncture, medicine.medical_treatment, Pneumothorax, Autopsy, Acupuncture treatment, medicine.disease, Pathology and Forensic Medicine, Surgery, medicine.anatomical_structure, Genetics, medicine, Acupuncture, Humans, Gold, business, Adverse effect
Abstract

Acupuncture is practiced as a complementary medicine worldwide. Although it is considered a safe practice, pneumothorax is one of its most common serious complications. However, there have been few reports of deaths due to pneumothorax after acupuncture treatment, especially focused on electroacupuncture. We report an autopsy case of a man in his 60s who went into cardiopulmonary arrest and died immediately after receiving electroacupuncture. Postmortem computed tomography (PMCT) showed bilateral pneumothoraces, as well as the presence of numerous gold threads embedded subcutaneously. An autopsy revealed two ecchymoses in the right thoracic cavity and a pinhole injury on the lower lobe of the right lung, suggesting that the needles had penetrated the lung. There were marked emphysematous changes in the lung, suggesting that rupture of bullae might also have contributed to bilateral pneumothoraces and fatal outcome. The acupuncture needles may have been drawn deeper into the body than at the time of insertion due to electrical pulses and muscle contraction, indicating the need for careful determination of treatment indications and technical safety measures, such as fail-safe mechanisms. This is the first case report of fatal bilateral pneumothoraces after electroacupuncture reported in the English literature. This case sheds light on the safety of electroacupuncture and the need for special care when administering it to patients with pulmonary disease who may be at a higher risk of pneumothorax. This is also the first report of three-dimensional reconstructed PMCT images showing the whole-body distribution of embedded gold acupuncture threads, which is unusual.

Published
2021

50. Detection and Structural Characterization of SFAHFA Homologous Series in Mouse Colon Contents by LTQ-Orbitrap-MS and Their Implication in Influenza Virus Infection

Author

Marumi Ohno, Chongsheng Liang, Hitoshi Chiba, Shu-Ping Hui, Divyavani Gowda, and Siddabasave Gowda B. Gowda

Subjects
Male, Colon, Endogeny, 010402 general chemistry, Mass spectrometry, 01 natural sciences, Mass Spectrometry, Virus, Homologous series, chemistry.chemical_compound, Influenza A Virus, H1N1 Subtype, Orthomyxoviridae Infections, Structural Biology, Animals, Spectroscopy, chemistry.chemical_classification, Chemistry, 010401 analytical chemistry, Fatty acid, Esters, Metabolism, Fatty Acids, Volatile, 0104 chemical sciences, Chlorobenzoates, Mice, Inbred C57BL, Mouse Colon, Biochemistry, Multivariate Analysis, Epoxy Compounds, Function (biology)
Abstract

Fatty acid esters of hydroxy fatty acids (FAHFAs) are a new class of endogenous lipids with promising physiological functions in mammals. We previously introduced a new type of lipids to this family called short-chain fatty acid esters of hydroxy fatty acids (SFAHFAs), branching specific to the C2 carbon of a long-chain fatty acid (≥C20). In this study, we discovered a homologous series of SFAHFAs comprising C16-C26 hydroxy fatty acids esterified with short-chain fatty acids (C2-C5) in mouse colon contents. The detected SFAHFAs were characterized by high-resolution mass spectrometry with MSn analysis. The double-bond position of monounsaturated SFAHFAs was determined by the epoxidation reaction of samples with m-chloroperoxybenzoic acid and their MSn analysis. Further, the measurement of SFAHFA concentration in the colon contents of mice infected with influenza A/Puerto Rico/8/34 (H1N1; PR8) virus revealed a significant increase in their levels compared to native control. A strong correlation was observed between hydroxy fatty acid and SFAHFAs. Detection, characterization, and profiling of these new SFAHFA levels in relation with pandemic H1N1; PR8 influenza virus will contribute to the in-depth study of their function and metabolism.

Published
2021

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