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54. Novel Association Between Immune-Mediated Susceptibility Loci and Persistent Autoantibody Positivity in Type 1 Diabetes

Author

Brorsson, C.A., Onengut, S., Chen, W.M., Wenzlau, J., Yu, L.P., Baker, P., Williams, A.J.K., Bingley, P.J., Hutton, J.C., Eisenbarth, G.S., Concannon, P., Rich, S.S., Pociot, F., and Type 1 Diabetes Genetics Consortiu

Subjects
Genotype, Endocrinology, Diabetes and Metabolism, Autoimmunity, 030209 endocrinology & metabolism, medicine.disease_cause, 03 medical and health sciences, 0302 clinical medicine, Antigen, Thyroid peroxidase, Diabetes mellitus, Internal Medicine, medicine, Humans, Genetic Predisposition to Disease, Genetic Association Studies, Autoantibodies, 030304 developmental biology, Genetic association, 0303 health sciences, Type 1 diabetes, biology, Autoantibody, Genetics/Genomes/Proteomics/Metabolomics, medicine.disease, 3. Good health, Cross-Sectional Studies, Diabetes Mellitus, Type 1, Genetic Loci, Immunology, biology.protein
Abstract

Islet autoantibodies detected at disease onset in patients with type 1 diabetes are signs of an autoimmune destruction of the insulin-producing β-cells. To further investigate the genetic determinants of autoantibody positivity, we performed dense immune-focused genotyping on the Immunochip array and tested for association with seven disease-specific autoantibodies in a large cross-sectional cohort of 6,160 type 1 diabetes–affected siblings. The genetic association with positivity for GAD autoantibodies (GADAs), IA2 antigen (IA-2A), zinc transporter 8, thyroid peroxidase, gastric parietal cells (PCAs), tissue transglutaminase, and 21-hydroxylase was tested using a linear mixed-model regression approach to simultaneously control for population structure and family relatedness. Four loci were associated with autoantibody positivity at genome-wide significance. Positivity for GADA was associated with 3q28/LPP, for IA-2A with 1q23/FCRL3 and 11q13/RELA, and for PCAs with 2q24/IFIH1. The 3q28 locus showed association after only 3 years duration and might therefore be a marker of persistent GADA positivity. The 1q23, 11q13, and 2q24 loci were associated with autoantibodies close to diabetes onset and constitute candidates for early screening. Major susceptibility loci for islet autoantibodies are separate from type 1 diabetes risk, which may have consequences for intervention strategies to reduce autoimmunity.

Published
2015

63. Second primary malignancies in multiple myeloma: An overview and IMWG consensus

Author

Musto, P. Anderson, K.C. Attal, M. Richardson, P.G. Badros, A. Hou, J. Comenzo, R. Du, J. Durie, B.G.M. San Miguel, J. Einsele, H. Chen, W.M. Garderet, L. Pietrantuono, G. Hillengass, J. Kyle, R.A. Moreau, P. Lahuerta, J.J. Landgren, O. Ludwig, H. Larocca, A. Mahindra, A. Cavo, M. Mazumder, A. McCarthy, P.L. Nouel, A. Rajkumar, S.V. Reiman, A. Riva, E. Sezer, O. Terpos, E. Turesson, I. Usmani, S. Weiss, B.M. Palumbo, A. on behalf of the International Myeloma Working Group

Abstract

Background: Therapeutic advancements following the introduction of autologous stem cell transplantation and 'novel' agents have significantly improved clinical outcomes for patients with multiple myeloma (MM). Increased life expectancy, however, has led to renewed concerns about the long-term risk of second primary malignancies (SPMs). This review outlines the most up-to-date knowledge of possible host-, disease-, and treatment-related risk factors for the development of SPMs in patients with MM, and provides practical recommendations to assist physicians. Design: A Panel of International Myeloma Working Group members reviewed the most relevant data published in the literature as full papers, or presented at meetings of the American Society of Clinical Oncology, American Society of Hematology, European Hematology Association, or International Myeloma Workshops, up to June 2016. Here, we present the recommendations of the Panel, based on this literature review. Results: Overall, the risk of SPMs in MM is low, multifactorial, and partially related to the length of patients' survival and MM intrinsic susceptibility. Studies suggest a significantly increased incidence of SPMs when lenalidomide is administered either following, or concurrently with, oral melphalan. Increased SPM incidence has also been reported with lenalidomide maintenance following high-dose melphalan, albeit to a lesser degree. In both cases, the risk of death from MM was significantly higher than the risk of death from SPMs, with lenalidomide possibly providing a survival benefit. No increase in SPM incidence was reported with lenalidomide plus dexamethasone (without melphalan), or with bortezomib plus oral melphalan, dexamethasone, or thalidomide.Conclusion: In general, the risk of SPMs should not alter the current therapeutic decision-making process in MM. However, regimens such as lenalidomide plus dexamethasone should be preferred to prolonged exposure to lenalidomide plus oral melphalan. SPM risk should be carefully discussed with the patient in the context of benefits and risks of different treatment options. © The Author 2016.

Published
2017

66. Second primary malignancies in multiple myeloma: an overview and IMWG consensus

Author

Musto, P., primary, Anderson, K.C., additional, Attal, M., additional, Richardson, P.G., additional, Badros, A., additional, Hou, J., additional, Comenzo, R., additional, Du, J., additional, Durie, B.G.M., additional, San Miguel, J., additional, Einsele, H., additional, Chen, W.M., additional, Garderet, L., additional, Pietrantuono, G., additional, Hillengass, J., additional, Kyle, R.A., additional, Moreau, P., additional, Lahuerta, J.J., additional, Landgren, O., additional, Ludwig, H., additional, Larocca, A., additional, Mahindra, A., additional, Cavo, M., additional, Mazumder, A., additional, McCarthy, P.L., additional, Nouel, A., additional, Rajkumar, S.V., additional, Reiman, A., additional, Riva, E., additional, Sezer, O., additional, Terpos, E., additional, Turesson, I., additional, Usmani, S., additional, Weiss, B.M., additional, and Palumbo, A., additional

Published
2018
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67. Dominant recombination center in electron-irradiated 3C SiC

Author

Son, N.T., Sorman, E., Chen, W.M., Singh, M., Hallin, C., Kordina, O., Monemar, B., Janzen, E., and Lindstrom, J.L.

Subjects
Thin films -- Evaluation, Semiconductors -- Impurity distribution, Semiconductor doping -- Analysis, Physics
Published
1996

71. Origin of n-type conductivity of low-temperature grown InP

Author

Chen, W.M., Dreszer, P., Prasad, A., Kurpiewski, A., Walukiewicz, W., Weber, E.R., Sorman, E., Monemar, B., Liang, B.W., and Tu, C.W.

Subjects
Electrical conductivity -- Analysis, Semiconductors -- Analysis, Epitaxy -- Analysis, Physics
Abstract

An experiment is performed to prove the involvement of PIn antisite as the dominating electrically active donor in the electrical properties of low-temperature InP. The n-type conductivity observed in InP, which is grown with the help of molecular beam epitaxy, is due to the PIn antisite autoionization through its first ionization stage.

Published
1994

74. Low-frequency and common genetic variation in ischemic stroke : the METASTROKE collaboration

Author

Malik, R., Traylor, M., Pulit, S.L., Bevan, S., Hopewell, J.C., Holliday, E.G., Zhao, W., Abrantes, P., Amouyel, P., Attia, J.R., Battey, T.W., Berger, K., Boncoraglio, G.B., Chauhan, G., Cheng, Y.C., Chen, W.M., Clarke, R., Cotlarciuc, I., Debette, S., Falcone, G.J., Ferro, J.M., Gamble, D.M., Ilinca, A., Kittner, S.J., Kourkoulis, C.E., Lemmens, R., Levi, C.R., Lichtner, P., Lindgren, A., Liu, J., Meschia, J.F., Mitchell, B.D., Oliveira, S.A., Pera, J., Reiner, A.P., Rothwell, P.M., Sharma, P., Slowik, A., Sudlow, C.L., Tatlisumak, T., Thijs, V., Vicente, A.M., Woo, D., Seshadri, S., Saleheen, D., Rosand, J., Markus, H.S., Worrall, B.B., Dichgans, M., ISGC Analysis Group, METASTROKE collaboration, Wellcome Trust Case Control Consortium 2 (WTCCC2), and NINDS Stroke Genetics Network (SiGN)

Subjects
0301 basic medicine, medicine.medical_specialty, Genome-wide association study, Polymorphism, Single Nucleotide, Gastroenterology, Article, Brain Ischemia, Doenças Cardio e Cérebro-vasculares, 03 medical and health sciences, 0302 clinical medicine, Missing heritability problem, Internal medicine, ABO blood group system, Genetic variation, Humans, Medicine, Cooperative Behavior, 1000 Genomes Project, Allele frequency, Stroke, Ischemic Stroke, Genetic association, Genetics, business.industry, Genetic Variation, Correction, medicine.disease, 030104 developmental biology, Case-Control Studies, Ischemic stroke, Cardiology, Neurology (clinical), business, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract

Erratum in: Low-frequency and common genetic variation in ischemic stroke: The METASTROKE collaboration. [Neurology. 2016] Objective: To investigate the influence of common and low-frequency genetic variants on the risk of ischemic stroke (all IS) and etiologic stroke subtypes. Methods: We meta-analyzed 12 individual genome-wide association studies comprising 10,307 cases and 19,326 controls imputed to the 1000 Genomes (1 KG) phase I reference panel. We selected variants showing the highest degree of association (p , 1E-5) in the discovery phase for replication in Caucasian (13,435 cases and 29,269 controls) and South Asian (2,385 cases and 5,193 controls) samples followed by a transethnic meta-analysis. We further investigated the p value distribution for different bins of allele frequencies for all IS and stroke subtypes. Results: We showed genome-wide significance for 4 loci: ABO for all IS, HDAC9 for large vessel disease (LVD), and both PITX2 and ZFHX3 for cardioembolic stroke (CE). We further refined the association peaks for ABO and PITX2. Analyzing different allele frequency bins, we showed significant enrichment in low-frequency variants (allele frequency ,5%) for both LVD and small vessel disease, and an enrichment of higher frequency variants (allele frequency 10% and 30%) for CE (all p , 1E-5). Conclusions: Our findings suggest that the missing heritability in IS subtypes can in part be attributed to low-frequency and rare variants. Larger sample sizes are needed to identify the variants associated with all IS and stroke subtypes.

Published
2016

75. International myeloma working group recommendations for the diagnosis and management of myeloma-related renal impairment

Author

Dimopoulos, M.A. Sonneveld, P. Leung, N. Merlini, G. Ludwig, H. Kastritis, E. Goldschmidt, H. Joshua, D. Orlowski, R.Z. Powles, R. Vesole, D.H. Garderet, L. Einsele, H. Palumbo, A. Cavo, M. Richardson, P.G. Moreau, P. Miguel, J.S. Vincent Rajkumar, S. Durie, B.G.M. Terpos, E. Abildgaard, N. Abonour, R. Alsina, M. Anderson, K.C. Attal, M. Avet-Loiseau, H. Badros, A. Bahlis, N.J. Barlogie, B. Bataille, R. Beksaç, M. Belch, A. Ben-Yehuda, D. Bensinger, B. Leif Bergsagel, P. Bhutani, M. Bird, J. Bladé, J. Broijl, A. Boccadoro, M. Caers, J. Chanan-Khan, A. Chari, A. Chen, W.M. Chesi, M. Anthony Child, J. Chim, C.S. Chng, W.-J. Comenzo, R. Cook, G. Crowley, J. Crusoe, E. Dalton, W. Lee Moffitt, H. Davies, F. de la Rubia, J. de Souza, C. Delforge, M. Dhodapkar, M. Dispenzieri, A. Drach, J. Drake, M. Du, J. Dytfeld, D. Facon, T. Fantl, D. Fermand, J.-P. Fernández de Larrea, C. Fonseca, R. Gahrton, G. Garćia-Sanz, R. Gasparetto, C. Gertz, M. Ghobrial, I. Gibson, J. Gimsing, P. Giralt, S. Gu, J. Hajek, R. Hardan, I. Hari, P. Hata, H. Hattori, Y. Heffner, T. Hillengass, J. Ho, J. Hoering, A. Hoffman, J.E. Hou, J. Huang, J. Hungria, V. Ida, S. Jagannath, S. Jakubowiak, A.J. Johnsen, H.E. Jurczyszyn, A. Kaiser, M. Kaufman, J. Kawano, M. Korde, N. Kovacs, E. Krishnan, A. Kristinsson, S. Kröger, N. Kumar, S. Kyle, R.A. Kyriacou, C. Lacy, M. Lahuerta, J.J. Landgren, O. Larocca, A. Laubach, J. da Costa, F.L. Lee, J.-H. Leiba, M. Leleu, X. Lentzsch, S. Lokhorst, H. Lonial, S. Lu, J. Mahindra, A. Maiolino, A. Manasanch, E.E. Mark, T. Mateos, M.-V. Mazumder, A. McCarthy, P. Mehta, J. Mellqvist, U.-H. Mikhael, J. Morgan, G. Munshi, N. Nahi, H. Nawarawong, W. Niesvizky, R. Nouel, A. Novis, Y. Ocio, E. O'Dwyer, M. O'Gorman, P. Orfao, A. Otero, P.R. Paiva, B. Pavlovsky, S. Pilarski, L. Pratt, G. Qui, L. Raje, N. Reece, D. Reiman, A. Remaggi, G. Richter, J. Serra, E.R. Morales, A.R. Romeril, K.R. Roodman, D. Rosiñol, L. Rossi, A. Roussel, M. Russell, S. Schjesvold, F. Schots, R. Sevcikova, S. Sezer, O. Shah, J.J. Shimizu, K. Shustik, C. Siegel, D. Singhal, S. Spencer, A. Stadtmauer, E. Stewart, K. Tan, D. Terragna, C. Tosi, P. Tricot, G. Turesson, I. Usmani, S. Van Camp, B. Van de Donk, N. Van Ness, B. Van Riet, I. Broek, I.V. Vanderkerken, K. Vescio, R. Vij, R. Voorhees, P. Waage, A. Wang, M. Weber, D. Weiss, B.M. Westin, J. Wheatley, K. Zamagni, E. Zonder, J. Zweegman, S.

Abstract

Purpose: The aim of the International Myeloma Working Group was to develop practical recommendations for the diagnosis and management of multiple myeloma–related renal impairment (RI). Methods: Recommendations were based on published data through December 2015, and were developed using the system developed by the Grading of Recommendation, Assessment, Development, and Evaluation Working Group. Recommendations: All patients with myeloma at diagnosis and at disease assessment should have serum creatinine, estimated glomerular filtration rate, and electrolytes measurements as well as free light chain, if available, and urine electrophoresis of a sample from a 24-hour urine collection (grade A). The Chronic Kidney Disease Epidemiology Collaboration, preferably, or the Modification of Diet in Renal Disease formula should be used for the evaluation of estimated glomerular filtration rate in patients with stabilized serum creatinine (grade A). International Myeloma Working Group criteria for renal reversibility should be used (grade B). For the management of RI in patients with multiple myeloma, high fluid intake is indicated along with antimyeloma therapy (grade B). The use of high-cutoff hemodialysis membranes in combination with antimyeloma therapy can be considered (grade B). Bortezomib-based regimens remain the cornerstone of the management of myeloma-related RI (grade A). High-dose dexamethasone should be administered at least for the first month of therapy (grade B). Thalidomide is effective in patients with myeloma with RI, and no dose modifications are needed (grade B). Lenalidomide is effective and safe, mainly in patients with mild to moderate RI (grade B); for patients with severe RI or on dialysis, lena-lidomide should be given with close monitoring for hematologic toxicity (grade B) with dose reduction as needed. High-dose therapy with autologous stem cell transplantation (with melphalan 100 mg/m2 to 140 mg/m2) is feasible in patients with RI (grade C). Carfilzomib can be safely administered to patients with creatinine clearance > 15 mL/min, whereas ixazomib in combination with lenalidomide and dex-amethasone can be safely administered to patients with creatinine clearance > 30 mL/min (grade A). © 2016 by American Society of Clinical Oncology.

Published
2016

76. Formation of growth-in defects in molecular beam epitaxial Ga(In)NP: effects of growth conditions and postgrowth treatments

Author

Dagnelund, D., Buyanova, I.A., Wang, X.J., Chen, W.M., Utsumi, A., Furukawa, Y., Wakahara, A., and Yonezu, H.

Subjects
Crystallization -- Analysis, Gadolinium -- Thermal properties, Gadolinium -- Atomic properties, Indium -- Atomic properties, Indium -- Thermal properties, Molecular beams -- Usage, Physics
Abstract

The systematic studies on the effects of various growth parameters such as [N.sub.2] flow, growth temperature, In alloying, bombardment by N ions, and postgrowth treatment on the formation of grown-in defects in GaInNP fabricated by molecular beam epitaxy are reported. The results provide better insights into the growth and processing parameters that can suppress the formation of the grown-in defects and improve the optical properties of the alloy for device applications.

Published
2008

78. Contrasting the Genetic Background of Type 1 Diabetes and Celiac Disease Autoimmunity

Author

Gutierrez-Achury, J., Romanos, J., Bakker, S.F., Kumar, V., Haas, E.C. de, Trynka, G., Ricano-Ponce, I., Steck, A., Chen, W.M., Onengut-Gumuscu, S., Simsek, S., Rewers, M., Mulder, C.J., Liu, E., Rich, S.S., Wijmenga, C., Type 1 Diabet Genetics Consortium, Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), Department of Health and Life Sciences, Gastroenterology and hepatology, and CCA - Immuno-pathogenesis

Subjects
Male, Endocrinology, Diabetes and Metabolism, LOCI, Autoimmunity, Genome-wide association study, CHILDREN, Disease, medicine.disease_cause, Linkage Disequilibrium, 0302 clinical medicine, Gene Frequency, HLA Antigens, Genotype, Odds Ratio, RISK VARIANTS, IMMUNE-RESPONSE, CTLA-4 Antigen, MULTIPLE COMMON, GENERAL-POPULATION, 0303 health sciences, 3. Good health, Female, Genetic Background, Risk, endocrine system, 030209 endocrinology & metabolism, Single-nucleotide polymorphism, Human leukocyte antigen, Polymorphism, Single Nucleotide, SHARED GENETICS, 03 medical and health sciences, Internal Medicine, medicine, Humans, Genetic Predisposition to Disease, GENOME-WIDE ASSOCIATION, Genetic Association Studies, METAANALYSIS, 030304 developmental biology, Advanced and Specialized Nursing, business.industry, Haplotype, fungi, CONSORTIUM, Interleukin-2 Receptor alpha Subunit, nutritional and metabolic diseases, Type 1 Diabetes Genetics Consortium (T1DGC) Autoantibody Workshop, Odds ratio, Celiac Disease, Diabetes Mellitus, Type 1, Haplotypes, Genetic Loci, Case-Control Studies, Immunology, business
Abstract

Type 1 diabetes (T1D) and celiac disease (CeD) cluster in families and can occur in the same individual. Genetic loci have been associated with susceptibility to both diseases. Our aim was to explore the genetic differences between individuals developing both these diseases (double autoimmunity) versus those with only one. We hypothesized that double autoimmunity individuals carry more of the genetic risk markers that are shared between the two diseases independently. SNPs were genotyped in loci associated with T1D (n = 42) and CeD (n = 28) in 543 subjects who developed double autoimmunity, 2,472 subjects with T1D only, and 2,223 CeD-only subjects. For identification of loci that were specifically associated with individuals developing double autoimmunity, two association analyses were conducted: double autoimmunity versus T1D and double autoimmunity versus CeD. HLA risk haplotypes were compared between the two groups. The CTLA4 and IL2RA loci were more strongly associated with double autoimmunity than with either T1D or CeD alone. HLA analyses indicated that the T1D high-risk genotype, DQ2.5/DQ8, provided the highest risk for developing double autoimmunity (odds ratio 5.22, P = 2.25 × 10−29). We identified a strong HLA risk genotype (DQ2.5/DQ8) predisposing to double autoimmunity, suggesting a dominant role for HLA. Non-HLA loci, CTLA4 and IL2RA, may also confer risk to double autoimmunity. Thus, CeD patients who carry the DQ2.5/DQ8 genotype may benefit from periodic screening of autoantibodies related to T1D.

Published
2015

79. Resonant suppression of exciton spin relaxation in Zn0.96Mn0.04Se/CdSe superlattices

Author

Buyanova, I.A., Chen, W.M., Toropov, A.A., Sorokin, S.V., Ivanov, S.V., and Kop'ev, P.S.

Subjects
Photoluminescence -- Research, Selenium compounds -- Magnetic properties, Selenium compounds -- Electric properties, Manganese -- Magnetic properties, Manganese -- Electric properties, Zinc -- Magnetic properties, Zinc -- Electric properties, Physics
Abstract

Employed hot photoluminescence combined with tunable excitation spectroscopy to analyze spin relaxation processes in the strained Zn0.96Mn0.04Se/CdSe superlattices is discussed. The observed behavior provided evidence for suprisingly strong suppression of spin relaxation from the upper lying spin-split excitons with small values of wave vector.

Published
2003

80. Genetic associations at 53 loci highlight cell types and biological pathways relevant for kidney function.

Author

ICBP Consortium, AGEN Consortium, CHARGe-Heart Failure Group, ECHOGen Consortium, CARDIOGRAM, Abecasis, GR., Adair, LS., Alexander, M., Altshuler, D., Amin, N., Arking, DE., Arora, P., Aulchenko, Y., Bakker, SJ., Bandinelli, S., Barroso, I., Beckmann, JS., Beilby, JP., Bergman, RN., Bergmann, S., Bis, JC., Boehnke, M., Bonnycastle, LL., Bornstein, SR., Bots, ML., Bragg-Gresham, JL., Brand, SM., Brand, E., Braund, PS., Brown, MJ., Burton, PR., Casas, JP., Caulfield, MJ., Chakravarti, A., Chambers, JC., Chandak, GR., Chang, YP., Charchar, FJ., Chaturvedi, N., Shin Cho, Y., Clarke, R., Collins, FS., Collins, R., Connell, JM., Cooper, JA., Cooper, MN., Cooper, RS., Corsi, AM., Dörr, M., Dahgam, S., Danesh, J., Davey Smith, G., Day, IN., Deloukas, P., Denniff, M., Dominiczak, AF., Dong, Y., Doumatey, A., Elliott, P., Elosua, R., Erdmann, J., Eyheramendy, S., Farrall, M., Fava, C., Forrester, T., Fowkes, FG., Fox, ER., Frayling, TM., Galan, P., Ganesh, SK., Garcia, M., Gaunt, TR., Glazer, NL., Go, MJ., Goel, A., Grässler, J., Grobbee, DE., Groop, L., Guarrera, S., Guo, X., Hadley, D., Hamsten, A., Han, BG., Hardy, R., Hartikainen, AL., Heath, S., Heckbert, SR., Hedblad, B., Hercberg, S., Hernandez, D., Hicks, AA., Hilton, G., Hingorani, AD., Bolton, JA., Hopewell, JC., Howard, P., Humphries, SE., Hunt, SC., Hveem, K., Ikram, MA., Islam, M., Iwai, N., Jarvelin, MR., Jackson, AU., Jafar, TH., Janipalli, CS., Johnson, T., Kathiresan, S., Khaw, KT., Kim, HL., Kinra, S., Kita, Y., Kivimaki, M., Kooner, JS., Kumar, MJ., Kuh, D., Kulkarni, SR., Kumari, M., Kuusisto, J., Kuznetsova, T., Laakso, M., Laan, M., Laitinen, J., Lakatta, EG., Langefeld, CD., Larson, MG., Lathrop, M., Lawlor, DA., Lawrence, RW., Lee, JY., Lee, NR., Levy, D., Li, Y., Longstreth, WT., Luan£££Jian'an£££ J., Lucas, G., Ludwig, B., Mangino, M., Mani, KR., Marmot, MG., Mattace-Raso, FU., Matullo, G., McArdle, WL., McKenzie, CA., Meitinger, T., Melander, O., Meneton, P., Meschia, JF., Miki, T., Milaneschi, Y., Mohlke, KL., Mooser, V., Morken, MA., Morris, RW., Mosley, TH., Najjar, S., Narisu, N., Newton-Cheh, C., Nguyen, KD., Nilsson, P., Nyberg, F., O'Donnell, CJ., Ogihara, T., Ohkubo, T., Okamura, T., Ong, RT., Ongen, H., Onland-Moret, NC., O'Reilly, PF., Org, E., Orru, M., Palmas, W., Palmen, J., Palmer, LJ., Palmer, ND., Parker, AN., Peden, JF., Peltonen, L., Perola, M., Pihur, V., Platou, CG., Plump, A., Prabhakaran, D., Psaty, BM., Raffel, LJ., Rao, DC., Rasheed, A., Ricceri, F., Rice, KM., Rosengren, A., Rotter, JI., Rudock, ME., Sõber, S., Salako, T., Saleheen, D., Salomaa, V., Samani, NJ., Schwartz, SM., Schwarz, PE., Scott, LJ., Scott, J., Scuteri, A., Sehmi, JS., Seielstad, M., Seshadri, S., Sharma, P., Shaw-Hawkins, S., Shi, G., Shrine, NR., Sijbrands, EJ., Sim, X., Singleton, A., Sjögren, M., Smith, NL., Soler Artigas, M., Spector, TD., Staessen, JA., Stancakova, A., Steinle, NI., Strachan, DP., Stringham, HM., Sun, YV., Swift, AJ., Tabara, Y., Tai, ES., Talmud, PJ., Taylor, A., Terzic, J., Thelle, DS., Tobin, MD., Tomaszewski, M., Tripathy, V., Tuomilehto, J., Tzoulaki, I., Uda, M., Ueshima, H., Uiterwaal, CS., Umemura, S., van der Harst, P., van der Schouw YT., van Gilst WH., Vartiainen, E., Vasan, RS., Veldre, G., Verwoert, GC., Viigimaa, M., Vinay, DG., Vineis, P., Voight, BF., Vollenweider, P., Wagenknecht, LE., Wain, LV., Wang, X., Wang, TJ., Wareham, NJ., Watkins, H., Weder, AB., Whincup, PH., Wiggins, KL., Witteman, JC., Wong, A., Wu, Y., Yajnik, CS., Yao, J., Young, JH., Zelenika, D., Zhai, G., Zhang, W., Zhang, F., Zhao, JH., Zhu, H., Zhu, X., Zitting, P., Zukowska-Szczechowska, E., Okada, Y., Wu, JY., Gu, D., Takeuchi, F., Takahashi, A., Maeda, S., Tsunoda, T., Chen, P., Lim, SC., Wong, TY., Liu, J., Young, TL., Aung, T., Teo, YY., Kim, YJ., Kang, D., Chen, CH., Tsai, FJ., Chang, LC., Fann, SJ., Mei, H., Hixson, JE., Chen, S., Katsuya, T., Isono, M., Albrecht, E., Yamamoto, K., Kubo, M., Nakamura, Y., Kamatani, N., Kato, N., He, J., Chen, YT., Tanaka, T., Reilly, MP., Schunkert, H., Assimes, TL., Hall, A., Hengstenberg, C., König, IR., Laaksonen, R., McPherson, R., Thompson, JR., Thorsteinsdottir, U., Ziegler, A., Absher, D., Chen, L., Cupples, LA., Halperin, E., Li, M., Musunuru, K., Preuss, M., Schillert, A., Thorleifsson, G., Wells, GA., Holm, H., Roberts, R., Stewart, AF., Fortmann, S., Go, A., Hlatky, M., Iribarren, C., Knowles, J., Myers, R., Quertermous, T., Sidney, S., Risch, N., Tang, H., Blankenberg, S., Schnabel, R., Sinning, C., Lackner, KJ., Tiret, L., Nicaud, V., Cambien, F., Bickel, C., Rupprecht, HJ., Perret, C., Proust, C., Münzel, TF., Barbalic, M., Chen, IY., Demissie-Banjaw, S., Folsom, A., Lumley, T., Marciante, K., Taylor, KD., Volcik, K., Gretarsdottir, S., Gulcher, JR., Kong, A., Stefansson, K., Thorgeirsson, G., Andersen, K., Fischer, M., Grosshennig, A., Linsel-Nitschke, P., Stark, K., Schreiber, S., Aherrahrou, Z., Bruse, P., Doering, A., Klopp, N., Diemert, P., Loley, C., Medack, A., Nahrstedt, 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Seielstad, M., Seshadri, S., Sharma, P., Shaw-Hawkins, S., Shi, G., Shrine, NR., Sijbrands, EJ., Sim, X., Singleton, A., Sjögren, M., Smith, NL., Soler Artigas, M., Spector, TD., Staessen, JA., Stancakova, A., Steinle, NI., Strachan, DP., Stringham, HM., Sun, YV., Swift, AJ., Tabara, Y., Tai, ES., Talmud, PJ., Taylor, A., Terzic, J., Thelle, DS., Tobin, MD., Tomaszewski, M., Tripathy, V., Tuomilehto, J., Tzoulaki, I., Uda, M., Ueshima, H., Uiterwaal, CS., Umemura, S., van der Harst, P., van der Schouw YT., van Gilst WH., Vartiainen, E., Vasan, RS., Veldre, G., Verwoert, GC., Viigimaa, M., Vinay, DG., Vineis, P., Voight, BF., Vollenweider, P., Wagenknecht, LE., Wain, LV., Wang, X., Wang, TJ., Wareham, NJ., Watkins, H., Weder, AB., Whincup, PH., Wiggins, KL., Witteman, JC., Wong, A., Wu, Y., Yajnik, CS., Yao, J., Young, JH., Zelenika, D., Zhai, G., Zhang, W., Zhang, F., Zhao, JH., Zhu, H., Zhu, X., Zitting, P., Zukowska-Szczechowska, E., Okada, Y., Wu, JY., Gu, D., Takeuchi, F., Takahashi, A., Maeda, S., Tsunoda, T., Chen, P., Lim, SC., Wong, TY., Liu, J., Young, TL., Aung, T., Teo, YY., Kim, YJ., Kang, D., Chen, CH., Tsai, FJ., Chang, LC., Fann, SJ., Mei, H., Hixson, JE., Chen, S., Katsuya, T., Isono, M., Albrecht, E., Yamamoto, K., Kubo, M., Nakamura, Y., Kamatani, N., Kato, N., He, J., Chen, YT., Tanaka, T., Reilly, MP., Schunkert, H., Assimes, TL., Hall, A., Hengstenberg, C., König, IR., Laaksonen, R., McPherson, R., Thompson, JR., Thorsteinsdottir, U., Ziegler, A., Absher, D., Chen, L., Cupples, LA., Halperin, E., Li, M., Musunuru, K., Preuss, M., Schillert, A., Thorleifsson, G., Wells, GA., Holm, H., Roberts, R., Stewart, AF., Fortmann, S., Go, A., Hlatky, M., Iribarren, C., Knowles, J., Myers, R., Quertermous, T., Sidney, S., Risch, N., Tang, H., Blankenberg, S., Schnabel, R., Sinning, C., Lackner, KJ., Tiret, L., Nicaud, V., Cambien, F., Bickel, C., Rupprecht, HJ., Perret, C., Proust, C., Münzel, TF., Barbalic, M., Chen, IY., Demissie-Banjaw, S., Folsom, A., Lumley, T., Marciante, K., Taylor, KD., Volcik, K., Gretarsdottir, S., Gulcher, JR., Kong, A., Stefansson, K., Thorgeirsson, G., Andersen, K., Fischer, M., Grosshennig, A., Linsel-Nitschke, P., Stark, K., Schreiber, S., Aherrahrou, Z., Bruse, P., Doering, A., Klopp, N., Diemert, P., Loley, C., Medack, A., Nahrstedt, J., Peters, A., Wagner, AK., Willenborg, C., Böhm, BO., Dobnig, H., Grammer, TB., Hoffmann, MM., Meinitzer, A., Winkelmann, BR., Pilz, S., Renner, W., Scharnagl, H., Stojakovic, T., Tomaschitz, A., Winkler, K., Guiducci, C., Burtt, N., Gabriel, SB., Dandona, S., Jarinova, O., Qu, L., Wilensky, R., Matthai, W., Hakonarson, HH., Devaney, J., Burnett, MS., Pichard, AD., Kent, KM., Satler, L., Lindsay, JM., Waksman, R., Knouff, CW., Waterworth, DM., Walker, MC., Epstein, SE., Rader, DJ., Nelson, CP., Wright, BJ., Balmforth, AJ., Ball, SG., Loehr, LR., Rosamond, WD., Benjamin, E., Haritunians, T., Couper, D., Murabito, J., Wang, YA., Stricker, BH., Chang, PP., Willerson, JT., Felix, SB., Watzinger, N., Aragam, J., Zweiker, R., Lind, L., Rodeheffer, RJ., Greiser, KH., Deckers, JW., Stritzke, J., Ingelsson, E., Kullo, I., Haerting, J., Reffelmann, T., Redfield, MM., Werdan, K., Mitchell, GF., Arnett, DK., Gottdiener, JS., Blettner, M., Friedrich, N., Pattaro, C., Teumer, A., Gorski, M., Chu, A.Y., Mijatovic, V., Garnaas, M., Tin, A., Sorice, R., Taliun, D., Olden, M., Foster, M., Yang, Q., Chen, M.H., Pers, T.H., Johnson, A.D., Ko, Y.A., Fuchsberger, C., Tayo, B., Nalls, M., Feitosa, M.F., Isaacs, A., Dehghan, A., d'Adamo, P., Adeyemo, A., Dieffenbach, A.K., Zonderman, A.B., Nolte, I.M., van der Most, P.J., Wright, A.F., Shuldiner, A.R., Morrison, A.C., Hofman, A., Smith, A.V., Dreisbach, A.W., Franke, A., Uitterlinden, A.G., Metspalu, A., Tonjes, A., Lupo, A., Robino, A., Johansson, Å., Demirkan, A., Kollerits, B., Freedman, B.I., Ponte, B., Oostra, B.A., Paulweber, B., Krämer, B.K., Mitchell, B.D., Buckley, B.M., Peralta, C.A., Hayward, C., 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Whitfield, J.B., Chalmers, J., Viikari, J., Coresh, J., Denny, J.C., Karjalainen, J., Fernandes, J.K., Endlich, K., Butterbach, K., Keene, K.L., Lohman, K., Portas, L., Launer, L.J., Lyytikäinen, L.P., Yengo, L., Franke, L., Ferrucci, L., Rose, L.M., Kedenko, L., Rao, M., Struchalin, M., Kleber, M.E., Cavalieri, M., Haun, M., Cornelis, M.C., Ciullo, M., Pirastu, M., de Andrade, M., McEvoy, M.A., Woodward, M., Adam, M., Cocca, M., Nauck, M., Imboden, M., Waldenberger, M., Pruijm, M., Metzger, M., Stumvoll, M., Evans, M.K., Sale, M.M., Kähönen, M., Boban, M., Bochud, M., Rheinberger, M., Verweij, N., Bouatia-Naji, N., Martin, N.G., Hastie, N., Probst-Hensch, N., Soranzo, N., Devuyst, O., Raitakari, O., Gottesman, O., Franco, O.H., Polasek, O., Gasparini, P., Munroe, P.B., Ridker, P.M., Mitchell, P., Muntner, P., Meisinger, C., Smit, J.H., Kovacs, P., Wild, P.S., Froguel, P., Rettig, R., Mägi, R., Biffar, R., Schmidt, R., Middelberg, R.P., Carroll, R.J., Penninx, B.W., Scott, R.J., Katz, R., Sedaghat, S., Wild, S.H., Kardia, S.L., Ulivi, S., Hwang, S.J., Enroth, S., Kloiber, S., Trompet, S., Stengel, B., Hancock, S.J., Turner, S.T., Rosas, S.E., Stracke, S., Harris, T.B., Zeller, T., Zemunik, T., Lehtimäki, T., Illig, T., Aspelund, T., Nikopensius, T., Esko, T., Gyllensten, U., Völker, U., Emilsson, V., Vitart, V., Aalto, V., Gudnason, V., Chouraki, V., Chen, W.M., Igl, W., März, W., Koenig, W., Lieb, W., Loos, R.J., Liu, Y., Snieder, H., Pramstaller, P.P., Parsa, A., O'Connell, J.R., Susztak, K., Hamet, P., Tremblay, J., de Boer, I.H., Böger, C.A., Goessling, W., Chasman, D.I., Köttgen, A., Kao, W.H., and Fox, C.S.

Abstract

Reduced glomerular filtration rate defines chronic kidney disease and is associated with cardiovascular and all-cause mortality. We conducted a meta-analysis of genome-wide association studies for estimated glomerular filtration rate (eGFR), combining data across 133,413 individuals with replication in up to 42,166 individuals. We identify 24 new and confirm 29 previously identified loci. Of these 53 loci, 19 associate with eGFR among individuals with diabetes. Using bioinformatics, we show that identified genes at eGFR loci are enriched for expression in kidney tissues and in pathways relevant for kidney development and transmembrane transporter activity, kidney structure, and regulation of glucose metabolism. Chromatin state mapping and DNase I hypersensitivity analyses across adult tissues demonstrate preferential mapping of associated variants to regulatory regions in kidney but not extra-renal tissues. These findings suggest that genetic determinants of eGFR are mediated largely through direct effects within the kidney and highlight important cell types and biological pathways.

Published
2016

81. Burkholderia dipogonis sp. nov., isolated from root nodules of Dipogon lignosus in New Zealand and Western Australia

Author

Sheu, S-Y, Chen, M-H, Liu, W.Y.Y., Andrews, M., James, E.K., Ardley, J.K., De Meyer, S.E., James, T.K., Howieson, J.G., Coutinho, B.G., Chen, W.M, Sheu, S-Y, Chen, M-H, Liu, W.Y.Y., Andrews, M., James, E.K., Ardley, J.K., De Meyer, S.E., James, T.K., Howieson, J.G., Coutinho, B.G., and Chen, W.M

Abstract

Seven strains, ICMP 19430T, ICMP 19429, ICMP 19431, WSM4637, WSM4638, WSM4639 and WSM4640, were isolated from nitrogen-fixing nodules on roots of the invasive South African legume Dipogon lignosus (subfamily Papilionoideae, tribe Phaseoleae) in New Zealand and Western Australia, and their taxonomic positions were investigated by using a polyphasic approach. All seven strains grew at 10–37 °C (optimum, 25–30 °C), at pH 4.0–9.0 (optimum, pH 6.0–7.0) and with 0–2 % (w/v) NaCl (optimum growth in the absence of NaCl). On the basis of 16S rRNA gene sequence analysis, the strains showed 99.0–99.5 % sequence similarity to the closest type strain, Burkholderia phytofirmans PsJNT, and 98.4–99.7 % sequence similarity to Burkholderia caledonica LMG 19076T. The predominant fatty acids were C18 : 1ω7c (21.0 % of the total fatty acids in strain ICMP 19430T), C16 : 0 (19.1 %), C17 : 0 cyclo (18.9 %), summed feature 3 (C16 : 1ω7c and/or C16 : 1ω6c; 10.7 %) and C19 : 0 cyclo ω8c (7.5 %). The polar lipid profile consisted of a mixture of phosphatidylethanolamine, phosphatidylglycerol, diphosphatidylglycerol and several uncharacterized aminophospholipids and phospholipids. The major isoprenoid quinone was Q-8 and the DNA G+C content of strain ICMP 19430T was 63.2 mol%. The DNA–DNA relatedness of the novel strains with respect to the closest neighbouring members of the genus Burkholderia was 55 % or less. On the basis of 16S rRNA and recA gene sequence similarities and chemotaxonomic and phenotypic data, these strains represent a novel symbiotic species in the genus Burkholderia, for which the name Burkholderia dipogonis sp. Nov. is proposed, with the type strain ICMP 19430T (=LMG 2841T =HAMBI 3637T).

Published
2015

86. Optically detected magnetic resonance studies of point defects in Ga(Al)NAs

Author

Vorona, I.P., Mchedlidze, T., Dagnelund, D., Buyanova, I.A., Chen, W.M., Köhler, K., and Publica

Subjects
optische Spektroskopie, Materialeigenschaft, III-V Halbleiter, optical spectroscopy, material property, III-V semiconductor
Abstract

An optically detected magnetic resonance (ODMR) study of Ga(Al)NAs alloys grown by molecular beam epitaxy on GaAs substrates is presented. A number of grown-in defects were observed which act as nonradiative recombination centers. A detailed analysis of experimental data using a spin Hamiltonian leads to the identification of two Gai defects. A comparison with similar defects in other phosphide-based diluted nitride III-V compounds, such as GaAlNP and GaInNP, allows us to obtain additional information about the nearest surrounding of the defects. A discussion of possible models for other defects observed in the experiments is also presented.

Published
2006

88. ImmunoChip Study Implicates Antigen Presentation to T Cells in Narcolepsy

Author

Faraco, J., Lin, L., Kornum, B.R., Kenny, E.E., Trynka, G., Einen, M., Rico, T.J., Lichtner, P., Dauvilliers, Y., Arnulf, I., Lecendreux, M., Javidi, S., Geisler, P., Mayer, G., Pizza, F., Poli, F., Plazzi, G., Overeem, S., Lammers, G.J., Kemlink, D., Sonka, K., Nevsimalova, S., Rouleau, G., Desautels, A., Montplaisir, J., Frauscher, B., Ehrmann, L., Hogl, B., Jennum, P., Bourgin, P., Peraita-Adrados, R., Iranzo, A., Bassetti, C., Chen, W.M., Concannon, P., Thompson, S.D., Damotte, V., Fontaine, B., Breban, M., Gieger, C., Klopp, N., Deloukas, P., Wijmenga, C., Hallmayer, J., Onengut-Gumuscu, S., Rich, S.S., Winkelmann, J., Mignot, E., Faraco, J., Lin, L., Kornum, B.R., Kenny, E.E., Trynka, G., Einen, M., Rico, T.J., Lichtner, P., Dauvilliers, Y., Arnulf, I., Lecendreux, M., Javidi, S., Geisler, P., Mayer, G., Pizza, F., Poli, F., Plazzi, G., Overeem, S., Lammers, G.J., Kemlink, D., Sonka, K., Nevsimalova, S., Rouleau, G., Desautels, A., Montplaisir, J., Frauscher, B., Ehrmann, L., Hogl, B., Jennum, P., Bourgin, P., Peraita-Adrados, R., Iranzo, A., Bassetti, C., Chen, W.M., Concannon, P., Thompson, S.D., Damotte, V., Fontaine, B., Breban, M., Gieger, C., Klopp, N., Deloukas, P., Wijmenga, C., Hallmayer, J., Onengut-Gumuscu, S., Rich, S.S., Winkelmann, J., and Mignot, E.

Abstract

Contains fulltext : 118596.pdf (publisher's version ) (Open Access), Recent advances in the identification of susceptibility genes and environmental exposures provide broad support for a post-infectious autoimmune basis for narcolepsy/hypocretin (orexin) deficiency. We genotyped loci associated with other autoimmune and inflammatory diseases in 1,886 individuals with hypocretin-deficient narcolepsy and 10,421 controls, all of European ancestry, using a custom genotyping array (ImmunoChip). Three loci located outside the Human Leukocyte Antigen (HLA) region on chromosome 6 were significantly associated with disease risk. In addition to a strong signal in the T cell receptor alpha (TRA@), variants in two additional narcolepsy loci, Cathepsin H () and Tumor necrosis factor (ligand) superfamily member 4 (, also called ), attained genome-wide significance. These findings underline the importance of antigen presentation by HLA Class II to T cells in the pathophysiology of this autoimmune disease.

Published
2013

95. A human type 1 diabetes susceptibility locus maps to chromosome 21q22.3

Author

Concannon, P., Onengut-Gumuscu, S., Todd, J.A., Smyth, D.J., Pociot, F., Bergholdt, R., Akolkar, B., Erlich, H.A., Hilner, J.E., Julier, C., Morahan, G., Nerup, J., Nierras, C.R., Chen, W.M., Rich, S.S., Concannon, P., Onengut-Gumuscu, S., Todd, J.A., Smyth, D.J., Pociot, F., Bergholdt, R., Akolkar, B., Erlich, H.A., Hilner, J.E., Julier, C., Morahan, G., Nerup, J., Nierras, C.R., Chen, W.M., and Rich, S.S.

Abstract

Udgivelsesdato: 2008

Published
2008

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