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1. Comparison of King’s clinical staging in multinational amyotrophic lateral sclerosis cohorts

Author

Balendra, R., Jones, A.R., Al Khleifat, A., Chiwera, T., Wicks, P., Young, C.A., Shaw, P.J., Turner, M.R., Leigh, P.N., and Al-Chalabi, A.

Abstract

Background: Amyotrophic lateral sclerosis (ALS) shows considerable clinical heterogeneity, which affects clinical trials. A clinical staging system has been proposed for ALS with potential applications in patient care, research, trial design and health economic analyses. The King’s system consists of five stages. We have previously shown that progressive clinical stages were reached at predictable proportions through the disease course, but this needs to be validated in other independent samples. Objectives: We aimed to compare King’s clinical staging in ALS in four patient groups, located in different regions and countries and using different health care systems from the original study population in South London. Methods: Clinical data were extracted from two European phase 3 randomized controlled trials (MitoTarget and LiCALS) and from two databases predominately from the United States: the PRO-ACT Consortium Database and a database of patients from the PatientsLikeMe website. Clinical stage was estimated using an algorithm, and standardized time to each clinical stage was calculated in deceased patients. Results: 8,796 patients were included, of whom 1,959 had died by the end of follow-up. Stages occurred in the same order as in the original study for all cohorts. Median standardized times to stages (interquartile range) were Stage 2: 0.61 (0.47–0.75), Stage 3: 0.68 (0.56–0.81), Stage 4A: 0.82 (0.71–0.91), Stage 4B: 0.82 (0.69–0.92) and Stage 4 0.80 (0.67–0.91). Discussion: Timings for all stages were similar to those reported in the original study, except Stage 2 which occurred later in the clinical trial databases due to recruitment occurring after diagnosis.

Published
2022

2. Clinical trials in pediatric ALS: a TRICALS feasibility study

Author

Kliest, T., Eijk, R.P.A. van, Al-Chalabi, A., Albanese, A., Andersen, P.M., Amador, M.D.M., BrÅthen, G., Brunaud-Danel, V., Brylev, L., Camu, W., Carvalho, M., Cereda, C., Cetin, H., Chaverri, D., Chiò, A., Corcia, P., Couratier, P., Marchi, F. De, Desnuelle, C., Es, M.A. van, Esteban, J. De, Filosto, M., Redondo, A., Grosskreutz, J., Hanemann, C.O., HolmØy, T., HØyer, H., Ingre, C., Koritnik, B., Kuzma-Kozakiewicz, M., Lambert, T., Leigh, P.N., Lunetta, C., Mandrioli, J., McDermott, C.J., Meyer, T., Mora, J.S., Petri, S., Povedano, M., Reviers, E., Riva, N., Roes, K.C.B., Rubio, Miguel, Salachas, F., Sarafov, S., SorarÙ, G., Stevic, Z., Svenstrup, K., MØller, A.T., Turner, M.R., Damme, P. van, Leeuwen, L.A.G. Van, Varona, L., Costa, J.F. VÁzquez, Weber, M., Hardiman, O., Berg, L.H. van den, Kliest, T., Eijk, R.P.A. van, Al-Chalabi, A., Albanese, A., Andersen, P.M., Amador, M.D.M., BrÅthen, G., Brunaud-Danel, V., Brylev, L., Camu, W., Carvalho, M., Cereda, C., Cetin, H., Chaverri, D., Chiò, A., Corcia, P., Couratier, P., Marchi, F. De, Desnuelle, C., Es, M.A. van, Esteban, J. De, Filosto, M., Redondo, A., Grosskreutz, J., Hanemann, C.O., HolmØy, T., HØyer, H., Ingre, C., Koritnik, B., Kuzma-Kozakiewicz, M., Lambert, T., Leigh, P.N., Lunetta, C., Mandrioli, J., McDermott, C.J., Meyer, T., Mora, J.S., Petri, S., Povedano, M., Reviers, E., Riva, N., Roes, K.C.B., Rubio, Miguel, Salachas, F., Sarafov, S., SorarÙ, G., Stevic, Z., Svenstrup, K., MØller, A.T., Turner, M.R., Damme, P. van, Leeuwen, L.A.G. Van, Varona, L., Costa, J.F. VÁzquez, Weber, M., Hardiman, O., and Berg, L.H. van den

Abstract

Item does not contain fulltext, Background: Pediatric investigation plans (PIPs) describe how adult drugs can be studied in children. In 2015, PIPs for Amyotrophic Lateral Sclerosis (ALS) became mandatory for European marketing-authorization of adult treatments, unless a waiver is granted by the European Medicines Agency (EMA).Objective: To assess the feasibility of clinical studies on the effect of therapy in children (<18 years) with ALS in Europe.Methods: The EMA database was searched for submitted PIPs in ALS. A questionnaire was sent to 58 European ALS centers to collect the prevalence of pediatric ALS during the past ten years, the recruitment potential for future pediatric trials, and opinions of ALS experts concerning a waiver for ALS.Results: Four PIPs were identified; two were waived and two are planned for the future. In total, 49 (84.5%) centers responded to the questionnaire. The diagnosis of 44,858 patients with ALS was reported by 46 sites; 39 of the patients had an onset < 18 years (prevalence of 0.008 cases per 100,000 or 0.087% of all diagnosed patients). The estimated recruitment potential (47 sites) was 26 pediatric patients within five years. A majority of ALS experts (75.5%) recommend a waiver should apply for ALS due to the low prevalence of pediatric ALS.Conclusions: ALS with an onset before 18 years is extremely rare and may be a distinct entity from adult ALS. Conducting studies on the effect of disease-modifying therapy in pediatric ALS may involve lengthy recruitment periods, high costs, ethical/legal implications, challenges in trial design and limited information.

Published
2022

4. Platform Communications: Abstract Book – 33rd International Symposium on ALS/MND (Complete printable file).

Author

Gage, F., Jones, J., Herdy, J., Mertens, J., Pupillo, E., Bianchi, E., Bendotti, C., Bonetto, V., Paganoni, S., Mazzini, L., Beghi, E., Bensimon, G., Leigh, P.N., Vucic, S., Menon, P., Huynh, W., Mahoney, C., Ho, K., Rynders, A., and Evan, J.

Subjects
AMYOTROPHIC lateral sclerosis, RILUZOLE, HEAT shock proteins
Abstract

Grey matter correlates of clinical variables in amyotrophic lateral sclerosis (ALS): a neuroimaging study of ALS motor phenotype heterogeneity and cortical focality. ALS-implicated protein TDP-43 sustains levels of STMN2, a mediator of motor neuron growth and repair. State and metropolitan area-based amyotrophic lateral sclerosis (ALS) surveillance. [Extracted from the article]

Published
2022
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5. Abnormal cortical excitability in sporadic but not homozygous D90A SOD1 ALS

Author

Turner, M.R., Osei-Lah, A.D., Hammers, A., Al-Chalabi, A., Shaw, C.E., Andersen, P.M., Brooks, D.J., Leigh, P.N., and Mills, K.R.

Subjects
Superoxide dismutase -- Physiological aspects, Amyotrophic lateral sclerosis -- Causes of, Amyotrophic lateral sclerosis -- Genetic aspects, Gene mutations -- Physiological aspects, Magnetic brain stimulation -- Research, Health, Psychology and mental health
Published
2005

7. The management of motor neurone disease

Author

Leigh, P.N., Abrahams, S., Al-Chalabi, A., Ampong, M.-A., Goldstein, L.H., Johnson, J., Lyall, R., Moxham, J., Mustfa, N., Rio, A., Shaw, C., and Willey, E.

Subjects
Psychiatric patients -- Health aspects -- Care and treatment -- Usage -- Methods -- Analysis -- Research, Neuropsychiatry -- Research -- Methods -- Analysis -- Health aspects -- Usage, Gastrostomy -- Methods -- Health aspects -- Analysis -- Usage -- Research, Mental illness -- Diagnosis, Psychiatrists -- Practice -- Analysis -- Usage -- Research -- Health aspects -- Methods, Health, Psychology and mental health, Practice, Diagnosis, Care and treatment, Usage, Analysis, Research, Methods, Health aspects
Abstract

J Neurol Neurosurg Psychiatry 2003;74(Suppl IV):iv32-iv47 The management of motor neurone disease (MND) has evolved rapidly over the last two decades. Although still incurable, MND is not untreatable. From an [...]

Published
2003

10. An estimate of amyotrophic lateral sclerosis heritability using twin data

Author

Al-Chalabi, A., Fang, F., Hanby, M.F., Leigh, P.N., Shaw, C.E., Ye, W., and Rijsdijk, F.

Subjects
Twin studies -- Analysis, Amyotrophic lateral sclerosis -- Genetic aspects, Amyotrophic lateral sclerosis -- Risk factors, Amyotrophic lateral sclerosis -- Research, Genetic susceptibility -- Research, Health, Psychology and mental health
Published
2010

11. NEK1 variants confer susceptibility to amyotrophic lateral sclerosis

Author

Kenna, K.P., van Doormaal, P.T.C., Dekker, A.M., Ticozzi, N., Kenna, B.J., Diekstra, F.P., van Rheenen, W., van Eijk, K.R., Jones, A.R., Keagle, P., Shatunov, A., Sproviero, W., Smith, B.N., van Es, M.A., Topp, S.D., Kenna, A., Miller, J.W., Fallini, C., Tiloca, C., McLaughlin, R.L., Vance, C., Troakes, C., Colombrita, C., Mora, G., Calvo, A., Verde, F., Al-Sarraj, S., King, A., Calini, D., de Belleroche, J., Baas, F., van der Kooi, A.J., de Visser, M., ten Asbroek, A.L.M.A., Sapp, P.C., McKenna-Yasek, D., Polak, M., Asress, S., Muñoz-Blanco, J.L., Strom, T.M., Meitinger, T., Morrison, K.E., D'Alfonso, S., Mazzini, L., Comi, G.P., Del Bo, R., Ceroni, M., Gagliardi, S., Querin, G., Bertolin, C., Pensato, V., Castellotti, B., Corti, S., Cereda, C., Corrado, L., Sorarù, G., Lauria, G., Williams, K.L., Leigh, P.N., Nicholson, G.A., Blair, I.P., Leblond, C.S., Dion, P.A., Rouleau, G.A., Pall, H., Shaw, P.J., Turner, M.R., Talbot, K., Taroni, F., Boylan, K.B., Van Blitterswijk, M., Rademakers, R., Esteban-Pérez, J., García-Redondo, A., Van Damme, P., Robberecht, W., Chio, A., Gellera, C., Drepper, C., Sendtner, M., Ratti, A., Glass, J.D., Mora, J.S., Basak, N.A., Hardiman, O., Ludolph, A.C., Andersen, P.M., Weishaupt, J.H., Brown, R.H., Al-Chalabi, A., Silani, V., Shaw, C.E., van den Berg, L.H., Veldink, J.H., Landers, J.E., Medical Research Council (MRC), Human Genetics, Neurology, ANS - Neurodegeneration, and SLAGEN Consortium

Subjects
0301 basic medicine, medicine.medical_specialty, Genomics, Biology, medicine.disease_cause, Article, Cohort Studies, 03 medical and health sciences, 0302 clinical medicine, Journal Article, Genetics, medicine, Humans, Comparative Study, Exome, Genetic Predisposition to Disease, SLAGEN Consortium, Risk factor, Amyotrophic lateral sclerosis, Gene, Genetic Association Studies, Netherlands, Mutation, Amyotrophic Lateral Sclerosis, Case-control study, 11 Medical And Health Sciences, 06 Biological Sciences, medicine.disease, 3. Good health, NIMA-Related Kinase 1, 030104 developmental biology, RC0346, Case-Control Studies, Medical genetics, Human medicine, 030217 neurology & neurosurgery, Developmental Biology
Abstract

To identify genetic factors contributing to amyotrophic lateral sclerosis (ALS), we conducted whole-exome analyses of 1,022 index familial ALS (FALS) cases and 7,315 controls. In a new screening strategy, we performed gene-burden analyses trained with established ALS genes and identified a significant association between loss-of-function (LOF) NEK1 variants and FALS risk. Independently, autozygosity mapping for an isolated community in the Netherlands identified a NEK1 p.Arg261His variant as a candidate risk factor. Replication analyses of sporadic ALS (SALS) cases and independent control cohorts confirmed significant disease association for both p.Arg261His (10,589 samples analyzed) and NEK1 LOF variants (3,362 samples analyzed). In total, we observed NEK1 risk variants in nearly 3% of ALS cases. NEK1 has been linked to several cellular functions, including cilia formation, DNA-damage response, microtubule stability, neuronal morphology and axonal polarity. Our results provide new and important insights into ALS etiopathogenesis and genetic etiology. ispartof: Nature Genetics vol:48 issue:9 pages:1037-+ ispartof: location:United States status: published

Published
2016
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12. Prolonged survival in motor neuron disease: a descriptive study of the King's database 1990-2002. (Short Report)

Author

Turner, M.R., Parton, M.J., Shaw, C.E., Leigh, P.N., and Al-Chalabi, A.

Subjects
Health, Psychology and mental health, Care and treatment, Prognosis
Abstract

Motor neuron disease is a clinically heterogeneous disease with significant differences in survival. The authors hove characterised a subset of long term survivors seen in a tertiary clinic over a [...]

Published
2003

13. Critical design considerations for time-to-event endpoints in amyotrophic lateral sclerosis clinical trials

Author

Eijk, R.P.A. van, Nikolakopoulos, S., Roes, K.C.B., Middelkoop, B.M., Ferguson, Tamara, Shaw, P.J., Leigh, P.N., Al-Chalabi, A., Eijkemans, M.J., Berg, L.H. van den, Eijk, R.P.A. van, Nikolakopoulos, S., Roes, K.C.B., Middelkoop, B.M., Ferguson, Tamara, Shaw, P.J., Leigh, P.N., Al-Chalabi, A., Eijkemans, M.J., and Berg, L.H. van den

Abstract

Contains fulltext : 215404.pdf (publisher's version ) (Open Access), BACKGROUND: Funding and resources for low prevalent neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS) are limited, and optimising their use is vital for efficient drug development. In this study, we review the design assumptions for pivotal ALS clinical trials with time-to-event endpoints and provide optimised settings for future trials. METHODS: We extracted design settings from 13 completed placebo-controlled trials. Optimal assumptions were estimated using parametric survival models in individual participant data (n=4991). Designs were compared in terms of sample size, trial duration, drug use and costs. RESULTS: Previous trials overestimated the hazard rate by 18.9% (95% CI 3.4% to 34.5%, p=0.021). The median expected HR was 0.56 (range 0.33-0.66). Additionally, we found evidence for an increasing mean hazard rate over time (Weibull shape parameter of 2.03, 95% CI 1.93 to 2.15, p<0.001), which affects the design and planning of future clinical trials. Incorporating accrual time and assuming an increasing hazard rate at the design stage reduced sample size by 33.2% (95% CI 27.9 to 39.4), trial duration by 17.4% (95% CI 11.6 to 23.3), drug use by 14.3% (95% CI 9.6 to 19.0) and follow-up costs by 21.2% (95% CI 15.6 to 26.8). CONCLUSIONS: Implementing distributional knowledge and incorporating accrual at the design stage could achieve large gains in the efficiency of ALS clinical trials with time-to-event endpoints. We provide an open-source platform that helps investigators to make more accurate sample size calculations and optimise the use of their available resources.

Published
2019

14. Ubiquitin-immunoreactive intraneuronal inclusions in amyotrophic lateral sclerosis

Author

Leigh, P.N., Whitwell, H., Garofalo, O., Buller, J., Swash, M., Martin, J.E., Gallo, J.-M., Weller, R.O., and Anderton, B.H.

Subjects
Amyotrophic lateral sclerosis -- Physiological aspects, Ubiquitin -- Research, Health
Abstract

As its name implies, the protein ubiquitin is ubiquitous among cells. The protein seems to be involved in the recycling of protein structures within the living cell. Medical interest in this protein was increased when it was found that antibodies which react with ubiquitin also react with the abnormal filaments seen within some brain cells of patients with Alzheimer's disease. It has now been found that in other neurodegenerative disorders, such as Parkinson's disease and Pick's disease, the characteristic cytoplasmic inclusions react with antibodies to ubiquitin. Cytoplasmic inclusions are small structures which accumulate within the cytoplasm of abnormal cells in some conditions but not in healthy cells. While it is clear that specific cytoplasmic inclusions are often indicative of specific disease processes, the actual role of the cytoplasmic inclusion is generally not understood. The characteristic cytoplasmic inclusion found in amyotrophic lateral sclerosis (ALS) is the Bunina body, which is found in up to 70 percent of all cases. Using antibodies to ubiquitin to stain brain specimens, researchers found evidence for the presence of ubiquitin in the spinal cords from all 31 ALS patients tested and in only one of 22 patients with other neurological disorders. Similar staining with ubiquitin antibody was not observed in any of the 23 normal spinal cords tested. Furthermore, the distribution of staining cells correlated well with the distribution of cells susceptible to the ALS disease process, indicating the staining material may play a direct role in the neural degeneration. Curiously, however, the Bunina bodies themselves were only rarely stained by the ubiquitin antibodies. Bunina bodies were found in 67 percent of the ALS patients in the present study. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

17. Rare genetic variation in UNC13A may modify survival in amyotrophic lateral sclerosis

Author

Gaastra, B., Shatunov, A., Pulit, S., Jones, A.R., Sproviero, W., Gillett, A., Chen, Z., Kirby, J., Fogh, I., Powell, J.F., Leigh, P.N., Morrison, K.E., Shaw, P.J., Shaw, C.E., van den Berg, L.H., Veldink, J.H., Lewis, C.M., and Al-Chalabi, A.

Abstract

Our objective was to identify whether rare genetic variation in amyotrophic lateral sclerosis (ALS) candidate survival genes modifies ALS survival. Candidate genes were selected based on evidence for modifying ALS survival. Each tail of the extreme 1.5% of survival was selected from the UK MND DNA Bank and all samples available underwent whole genome sequencing. A replication set from the Netherlands was used for validation. Sequences of candidate survival genes were extracted and variants passing quality control with a minor allele frequency ≤0.05 were selected for association testing. Analysis was by burden testing using SKAT. Candidate survival genes UNC13A, KIFAP3, and EPHA4 were tested for association in a UK sample comprising 25 short survivors and 25 long survivors. Results showed that only SNVs in UNC13A were associated with survival (p = 6.57 × 10−3). SNV rs10419420:G > A was found exclusively in long survivors (3/25) and rs4808092:G > A exclusively in short survivors (4/25). These findings were not replicated in a Dutch sample. In conclusion, population specific rare variants of UNC13A may modulate survival in ALS.

Published
2016

18. C9orf72 and UNC13A Are Shared Risk Loci for Amyotrophic Lateral Sclerosis and Frontotemporal Dementia: A Genome-Wide Meta-Analysis

Author

Diekstra, F.P., Van Deerlin, V.M., van Swieten, J.C., Al-Chalabi, A., Ludolph, A.C., Weishaupt, J.H., Hardiman, O., Landers, J.E., Brown, R.H., Es, M.A., Pasterkamp, R.J., Koppers, M., Andersen, P.M., Estrada, K., Rivadeneira, F., Hofman, A., Uitterlinden, A. G., Van Damme, P., Melki, J., Meininger, V., Shatunov, A., Shaw, C.E., Leigh, P.N., Shaw, P.J., Morrison, K.E., Fogh, I., Chio, A., Traynor, B.J., Czell, D., Weber, M., Heutink, P., Bakker, P.I.W., Silani, V., Robberecht, W., Van den Berg, L.H., Veldink, J.H., Human genetics, Neurology, NCA - neurodegeneration, Internal Medicine, Epidemiology, and Erasmus MC other

Subjects
DNA Repeat Expansion, Pair 19, Amyotrophic Lateral Sclerosis, genetics, Chromosomes, Human, Pair 9, genetics, DNA Repeat Expansion, genetics, Frontotemporal Dementia, genetics, Genome-Wide Association Study, methods/trends, Humans, Mutation, Nerve Tissue Proteins, genetics, Polymorphism, Single Nucleotide, genetics, Proteins, genetics, Proteins, nutritional and metabolic diseases, Nerve Tissue Proteins, Chromosomes, nervous system diseases, Frontotemporal Dementia, Mutation, mental disorders, Humans, Polymorphism, methods/trends, Genome-Wide Association Study
Abstract

Objective: Substantial clinical, pathological, and genetic overlap exists between amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). TDP-43 inclusions have been found in both ALS and FTD cases (FTD-TDP). Recently, a repeat expansion in C9orf72 was identified as the causal variant in a proportion of ALS and FTD cases. We sought to identify additional evidence for a common genetic basis for the spectrum of ALS-FTD. Methods: We used published genome-wide association studies data for 4,377 ALS patients and 13,017 controls, and 435 pathology-proven FTD-TDP cases and 1,414 controls for genotype imputation. Data were analyzed in a joint meta-analysis, by replicating topmost associated hits of one disease in the other, and by using a conservative rank products analysis, allocating equal weight to ALS and FTD-TDP sample sizes. Results: Meta-analysis identified 19 genome-wide significant single nucleotide polymorphisms (SNPs) in C9orf72 on chromosome 9p21.2 (lowest p = 2.6 x 10(-12)) and 1 SNP in UNC13A on chromosome 19p13.11 (p = 1.0 x 10(-11)) as shared susceptibility loci for ALS and FTD-TDP. Conditioning on the 9p21.2 genotype increased statistical significance at UNC13A. A third signal, on chromosome 8q24.13 at the SPG8 locus coding for strumpellin (p = 3.91 x 10(-7)) was replicated in an independent cohort of 4,056 ALS patients and 3,958 controls (p = 0.026; combined analysis p = 1.01 x 10(-7)). Interpretation: We identified common genetic variants in C9orf72, but in addition in UNC13A that are shared between ALS and FTD. UNC13A provides a novel link between ALS and FTD-TDP, and identifies changes in neurotransmitter release and synaptic function as a converging mechanism in the pathogenesis of ALS and FTD-TDP.

Published
2014
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20. Genome-wide association study identifies 19p13.3 (UNC13A) and 9p21.2 as susceptibility loci for sporadic amyotrophic lateral sclerosis

Author

Es, M.A. van, Veldink, J.H., Saris, C.G.J., Blauw, H.M., Vught, P.W. van, Birve, A., Lemmens, R., Schelhaas, H.J., Groen, E.J., Huisman, M.H., Kooi, A.J. van der, Visser, M. de, Dahlberg, C., Estrada, K., Rivadeneira, F., Hofman, A., Zwarts, M.J., Doormaal, P.T. van, Rujescu, D., Strengman, E., Giegling, I., Muglia, P., Tomik, B., Slowik, A., Uitterlinden, A.G., Hendrich, C., Waibel, S., Meyer, T., Ludolph, A.C., Glass, J.D., Purcell, S., Cichon, S., Nothen, Markus, Wichmann, H.E., Schreiber, S., Vermeulen, S., Kiemeney, L.A.L.M., Wokke, J.H.J., Cronin, S., McLaughlin, R.L., Hardiman, O., Fumoto, K., Pasterkamp, R.J., Meininger, V., Melki, J., Leigh, P.N., Shaw, C.E., Landers, J.E., Al-Chalabi, A., Brown Jr., R.H., Robberecht, W., Andersen, P.M., Ophoff, R.A., and Berg, L.H. van den

Abstract

We conducted a genome-wide association study among 2,323 individuals with sporadic amyotrophic lateral sclerosis (ALS) and 9,013 control subjects and evaluated all SNPs with P < 1.0 x 10(-4) in a second, independent cohort of 2,532 affected individuals and 5,940 controls. Analysis of the genome-wide data revealed genome-wide significance for one SNP, rs12608932, with P = 1.30 x 10(-9). This SNP showed robust replication in the second cohort (P = 1.86 x 10(-6)), and a combined analysis over the two stages yielded P = 2.53 x 10(-14). The rs12608932 SNP is located at 19p13.3 and maps to a haplotype block within the boundaries of UNC13A, which regulates the release of neurotransmitters such as glutamate at neuromuscular synapses. Follow-up of additional SNPs showed genome-wide significance for two further SNPs (rs2814707, with P = 7.45 x 10(-9), and rs3849942, with P = 1.01 x 10(-8)) in the combined analysis of both stages. These SNPs are located at chromosome 9p21.2, in a linkage region for familial ALS with frontotemporal dementia found previously in several large pedigrees.

Published
2009

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

Author

Murray, C.J.L. (Christopher), Ortblad, K.F. (Katrina F), Guinovart, C. (Caterina), Lim, S.S. (Stephen), Wolock, T.M. (Timothy M), Roberts, D.A. (D Allen), Dansereau, E.A. (Emily A), Graetz, N. (Nicholas), Barber, R.M. (Ryan), Brown, J.C. (Jonathan C), Wang, H. (Haidong), Duber, H.C. (Herbert C), Naghavi, M. (Morteza), Dicker, D. (Daniel), Dandona, L. (Lalit), Salomon, J.A. (Joshua), Heuton, K.R. (Kyle R), Foreman, K. (Kyle), Phillips, D.E. (David E), Fleming, T.D. (Thomas D), Flaxman, A.D. (Abraham D), Phillips, B.K. (Bryan K), Johnson, E.M. (Elizabeth), Coggeshall, M.S. (Megan S), Abd-Allah, F. (Foad), Abera, S.F. (Semaw Ferede), Abraham, J.P. (Jerry), Abubakar, I. (Ibrahim), Abu-Raddad, L.J. (Laith J), Abu-Rmeileh, N.M. (Niveen Me), Achoki, T. (Tom), Adeyemo, A. (Adebowale), Adou, A.K. (Arsène Kouablan), Adsuar, J.C. (José C), Agardh, E.E. (Emilie Elisabet), Akena, D. (Dickens), Al Kahbouri, M.J. (Mazin J), Alasfoor, D. (Deena), Albittar, M.I. (Mohammed I), Alcalá-Cerra, G. (Gabriel), Alegretti, M.A. (Miguel Angel), Alemu, G. (Getnet), Alfonso-Cristancho, R. (Rafael), Alhabib, S. (Samia), Ali, R. (Raghib), Alla, F. (Francois), Allen, P.J. (Peter), Alsharif, U. (Ubai), Alvarez, E. (Elena), Alvis-Guzman, N. (Nelson), Amankwaa, A.A. (Adansi A), Amare, A.T. (Azmeraw T), Amini, H. (Hassan), Ammar, K.A., Anderson, B.O. (Benjamin), Antonio, C.A.T. (Carl Abelardo T), Anwari, P. (Palwasha), Ärnlöv, J. (Johan), Arsenijevic, V.S.A. (Valentina S Arsic), Artaman, A. (Ali), Asghar, R.J. (Rana J), Assadi, R. (Reza), Atkins, L.S. (Lydia S), Badawi, A.F. (Alaa), Banerjee, A. (Amitava), Basu, S. (Saonli), Beardsley, J. (Justin), Bekele, T. (Tolesa), Bell, M.L. (Michelle Lee), Bernabe, E. (Eduardo), Beyene, T.J. (Tariku Jibat), Bhala, N. (Neeraj), Bhalla, P.L. (Pankaj), Bhutta, Z.A. (Zulfiqar A), Abdulhak, A.B. (Aref Bin), Binagwaho, A. (Agnes), Blore, J.D. (Jed D), Bose, D. (Dipan), Brainin, M. (Michael), Breitborde, N. (Nicholas), Castañeda-Orjuela, C.A. (Carlos A), Catalá-López, F. (Ferrán), Chadha, D., Chang, J.-C. (Jung-Chen), Chiang, Y.T., Chuang, T.-W. (Ting-Wu), Colomar, M. (Mercedes), Cooper Jr., L.T. (Leslie Trumbull), Cooper, C. (Charles), Courville, K.J. (Karen J), Cowie, M.R. (Martin R.), Criqui, M. (Michael), Dandona, R. (Rakhi), Dayama, A. (Anand), Leo, D. (Diego) de, Degenhardt, F., Del Pozo-Cruz, B. (Borja), Deribe, K. (Kebede), Des Jarlais, D.C. (Don C), Dessalegn, M. (Muluken), Dharmaratne, S.D. (Samath D), Dilmen, U. (Uǧur), Ding, E.L. (Eric), Driscoll, J.M., Durrani, Z., Ellenbogen, R.G. (Richard G), Ermakov, S. (Sergey), Esteghamati, A. (Alireza), Faraon, E.J.A. (Emerito Jose A), Farzadfar, F. (Farshad), Fereshtehnejad, S.-M. (Seyed-Mohammad), Fijabi, D.O. (Daniel Obadare), Forouzanfar, M.H. (Mohammad H), Fra.Paleo, U. (Urbano), Gaffikin, L. (Lynne), Gamkrelidze, A. (Amiran), Gankpé, F.G. (Fortuné Gbètoho), Geleijnse, J.M. (Marianne), Gessner, B.D. (Bradford D), Gibney, K.B. (Katherine B), Ginawi, I.A.M. (Ibrahim Abdelmageem Mohamed), Glaser, E.L. (Elizabeth L), Gona, P. (Philimon), Goto, A. (Akimoto), Gouda, H.N. (Hebe N), Gugnani, H.C. (Harish Chander), Gupta, R. (Rajeev), Hafezi-Nejad, N. (Nima), Hamadeh, R.R. (Randah Ribhi), Hammami, M. (Mouhanad), Hankey, G.J. (Graeme), Harb, H.L. (Hilda L), Haro, J.M. (Josep Maria), Havmoeller, R. (Rasmus), Hay, S.I. (Simon I), Hedayati, M.T. (Mohammad T), Pi, I.B.H. (Ileana B Heredia), Hoek, H.W. (Hans), Hornberger, J.C. (John C), Hosgood, H.D. (H Dean), Hotez, P.J. (Peter), Hoy, D.G. (Damian G), Huang, J. (Jian), Iburg, K.M. (Kim M), Idrisov, B.T. (Bulat T), Innos, K. (Kaire), Jacobsen, K.H. (Kathryn H), Jeemon, P. (Panniyammakal), Jensen, P.N. (Paul N), Jha, V. (Vivekanand), Jiang, G. (Guohong), Jonas, J.B., Juel, K. (Knud), Kan, H. (Haidong), Kankindi, I. (Ida), Karam, V. (Vincent), Karch, F. (Francois), Karema, C.K. (Corine Kakizi), Kaul, A. (Anil), Kawakami, N. (Norito), Kazi, D.S. (Dhruv S), Kemp, A.H. (Andrew H), Kengne, A.P. (Andre Pascal), Keren, A. (Andre), Kereselidze, M. (Maia), Khader, Y.S. (Yousef Saleh), Khalifa, S.E.A.H. (Shams Eldin Ali Hassan), Khan, E.A. (Ejaz Ahmed), Khang, Y.-H. (Young-Ho), Khonelidze, I. (Irma), Kinfu, Y. (Yohannes), Kinge, J.M. (Jonas M), Knibbs, L. (Luke), Kokubo, Y. (Yoshihiro), Kosen, S. (Soewarta), Defo, B.K. (Barthelemy Kuate), Kulkarni, V.S. (Veena S), Kulkarni, C. (Chanda), Kumar, K. (Kuldeep), Kumar, R.B. (Ravi B), Kumar, G.A. (G Anil), Kwan, G.F. (Gene F), Lai, T. (Taavi), Balaji, A.L. (Arjun Lakshmana), Lam, H. (Hilton), Lan, Q. (Qing), Lansingh, V.C. (Van C), Larson, H.J. (Heidi J), Larsson, A. (Anders), Lee, J.-T. (Jong-Tae), Leigh, P.N. (Nigel), Leinsalu, M. (Mall), Leung, R. (Ricky), Li, Y. (Yichong), Li, Y. (Yongmei), Lima, G.M.F. (Graça Maria Ferreira) de, Lin, H.-H. (Hsien-Ho), Lipshultz, S.E. (Steven), Liu, S. (Simin), Liu, Y. (Yang), Lloyd, B.K. (Belinda K), Lotufo, P.A. (Paulo A), Machado, V.M.P. (Vasco Manuel Pedro), Maclachlan, J.H. (Jennifer H), Magis-Rodriguez, C. (Carlos), Majdan, M. (Marek), Mapoma, C.C. (Christopher Chabila), Marcenes, W. (Wagner), Marzan, M.B. (Melvin Barrientos), Masci, J.R. (Joseph R), Mashal, R., Mason-Jones, A.J. (Amanda J), Mayosi, B.M. (Bongani), Mazorodze, T.T. (Tasara T), Mckay, M.J. (Michael), Meaney, M.J., Mehndiratta, M.M. (Man Mohan), Mejia-Rodriguez, F. (Fabiola), Melaku, Y.A. (Yohannes Adama), Memish, Z.A. (Ziad), Mendoza, W. (Walter), Miller, T.R. (Ted R), Mills, E.J. (Edward J), Mohammad, K.A. (Karzan Abdulmuhsin), Mokdad, A.H. (Ali H), Mola, G.L. (Glen Liddell), Monasta, L. (Lorenzo), Montico, M. (Marcella), Moore, A.R. (Ami R), Mori, R. (Riccardo), Moturi, W.N. (Wilkister Nyaora), Mukaigawara, M. (Mitsuru), Murthy, A.C. (Adeline C.), Naheed, A. (Aliya), Naidoo, K.S. (Kovin S), Naldi, L. (Lucia), Nangia, M. (Monika), Narayan, K.M.V. (Venkat), Nash, J.H.E. (John), Nejjari, C. (Chakib), Nelson, R.D. (Robert), Neupane, S.P. (Sudan Prasad), Newton, C. (Cameron), Ng, M. (Marie), Nisar, M.I. (Muhammad Imran), Nolte, S. (Sandra), Norheim, O.F. (Ole F), Nowaseb, V. (Vincent), Nyakarahuka, L. (Luke), Oh, I.-H. (In-Hwan), Ohkubo, T. (Takayoshi), Olusanya, B.O. (Bolajoko O), Omer, S.B. (Saad B), Opio, J.N. (John Nelson), Orisakwe, O.E. (Orish Ebere), Pandian, N.G. (Natesa), Papachristou, C., Caicedo, M.S. (Marco), Patten, J., Paul, V.K. (Vinod K), Pavlin, B.I. (Boris Igor), Pearce, N. (Neil), Pereira, D.M. (David M), Pervaiz, Z. (Zahid), Pesudovs, K. (Konrad), Petzold, M. (Max), Pourmalek, F. (Farshad), Qato, D. (Dima), Quezada, A.D. (Amado D), Quistberg, D.A. (D Alex), Rafay, A. (Anwar), Rahimi, K. (Kazem), Rahimi-Movaghar, V. (Vafa), Rahman, S.U. (Sajjad Ur), Raju, M. (Murugesan), Rana, S.M. (Saleem M), Razavi, H. (Homie), Reilly, R.Q. (Robert Quentin), Remuzzi, G. (Giuseppe), Richardus, J.H. (Jan Hendrik), Ronfani, L. (Luca), Roy, N. (Nadine) van, Sabin, M.L. (Miriam Lewis), Saeedi, M.Y. (Mohammad Yahya), Sahraian, M.A. (Mohammad Ali), Samonte, G.M.J. (Genesis May J), Sawhney, M.S. (Monika), Schneider, I.J.C. (Ione J C), Schwebel, D.C. (David C), Seedat, S. (Soraya), Sepanlou, S.G. (Sadaf G), Servan-Mori, E.E. (Edson E), Sheikhbahaei, S. (Sara), Shibuya, K. (Kenji), Shin, H.H. (Hwashin Hyun), Shiue, I. (Ivy), Shivakoti, R. (Rupak), Sigfusdottir, I.D. (Inga Dora), Silberberg, D.H. (Donald H), Silva, A.P. (Andrea P), Simard, J. (Jacques), Singh, J.A. (Jasvinder), Skirbekk, V. (Vegard), Sliwa, K. (Karen), Soneji, S. (Samir), Soshnikov, S.S. (Sergey S), Sreeramareddy, C.T. (Chandrashekhar T), Stathopoulou, V.K. (Vasiliki Kalliopi), Stroumpoulis, K. (Konstantinos), Swaminathan, S., Sykes, B.C. (Bryan), Tabb, K.M. (Karen M), Talongwa, R.T. (Roberto Tchio), Tenkorang, E.Y. (Eric Yeboah), Terkawi, A.S. (Abdullah Sulieman), Thomson, A.J. (Alan J), Thorne-Lyman, A.L. (Andrew L), Towbin, J.A. (Jeffrey A), Traebert, J. (Jefferson), Tran, B.X. (Bach X), Dimbuene, Z.T. (Zacharie Tsala), Tsilimbaris, M. (Miltiadis), Uchendu, U.S. (Uche S), Ukwaja, K.N. (Kingsley N), Vallely, S.R. (Stephen), Vasankari, T.J. (Tommi J), Venketasubramanian, N. (Narayanaswamy), Violante, F.S. (Francesco S), Vlassov, V.V. (Vasiliy Victorovich), Waller, P. (Patrick), Wallin, M.T. (Mitchell T), Wang, L. (Linhong), Wang, S.X., Wang, Y. (Yanping), Weichenthal, S. (Scott), Weiderpass, E. (Elisabete), Weintraub, R.G. (Robert G), Westerman, R. (Ronny), White, R.G. (Richard), Wilkinson, J.D. (James D), Williams, T.N. (Thomas Neil), Woldeyohannes, S.M. (Solomon Meseret), Wong, J.B. (John), Xu, G. (Gelin), Yang, Y.C. (Yang C), Yano, K.-I., Yip, P. (Paul), Yonemoto, N. (Naohiro), Yoon, S.-J. (Seok-Jun), Younis, M. (Mustafa), Yu, C. (Chuanhua), Jin, K.Y. (Kim Yun), El Sayed Zaki, M. (Maysaa), Zhao, Y. (Yong), Zheng, Y. (Yuhui), Balakrishnan, K. (Kalpana), Zhou, M. (Ming), Zhu, J. (Jun), Zou, X.N. (Xiao Nong), Lopez, A.D. (Alan D), Vos, T. (Theo), Murray, C.J.L. (Christopher), Ortblad, K.F. (Katrina F), Guinovart, C. (Caterina), Lim, S.S. (Stephen), Wolock, T.M. (Timothy M), Roberts, D.A. (D Allen), Dansereau, E.A. (Emily A), Graetz, N. (Nicholas), Barber, R.M. (Ryan), Brown, J.C. (Jonathan C), Wang, H. (Haidong), Duber, H.C. (Herbert C), Naghavi, M. (Morteza), Dicker, D. (Daniel), Dandona, L. (Lalit), Salomon, J.A. (Joshua), Heuton, K.R. (Kyle R), Foreman, K. (Kyle), Phillips, D.E. (David E), Fleming, T.D. (Thomas D), Flaxman, A.D. (Abraham D), Phillips, B.K. (Bryan K), Johnson, E.M. (Elizabeth), Coggeshall, M.S. (Megan S), Abd-Allah, F. (Foad), Abera, S.F. (Semaw Ferede), Abraham, J.P. (Jerry), Abubakar, I. (Ibrahim), Abu-Raddad, L.J. (Laith J), Abu-Rmeileh, N.M. (Niveen Me), Achoki, T. (Tom), Adeyemo, A. (Adebowale), Adou, A.K. (Arsène Kouablan), Adsuar, J.C. (José C), Agardh, E.E. (Emilie Elisabet), Akena, D. (Dickens), Al Kahbouri, M.J. (Mazin J), Alasfoor, D. (Deena), Albittar, M.I. (Mohammed I), Alcalá-Cerra, G. (Gabriel), Alegretti, M.A. (Miguel Angel), Alemu, G. (Getnet), Alfonso-Cristancho, R. (Rafael), Alhabib, S. (Samia), Ali, R. (Raghib), Alla, F. (Francois), Allen, P.J. (Peter), Alsharif, U. (Ubai), Alvarez, E. (Elena), Alvis-Guzman, N. (Nelson), Amankwaa, A.A. (Adansi A), Amare, A.T. (Azmeraw T), Amini, H. (Hassan), Ammar, K.A., Anderson, B.O. (Benjamin), Antonio, C.A.T. (Carl Abelardo T), Anwari, P. (Palwasha), Ärnlöv, J. (Johan), Arsenijevic, V.S.A. (Valentina S Arsic), Artaman, A. (Ali), Asghar, R.J. (Rana J), Assadi, R. (Reza), Atkins, L.S. (Lydia S), Badawi, A.F. (Alaa), Banerjee, A. (Amitava), Basu, S. (Saonli), Beardsley, J. (Justin), Bekele, T. (Tolesa), Bell, M.L. (Michelle Lee), Bernabe, E. (Eduardo), Beyene, T.J. (Tariku Jibat), Bhala, N. (Neeraj), Bhalla, P.L. (Pankaj), Bhutta, Z.A. (Zulfiqar A), Abdulhak, A.B. (Aref Bin), Binagwaho, A. (Agnes), Blore, J.D. (Jed D), Bose, D. (Dipan), Brainin, M. (Michael), Breitborde, N. (Nicholas), Castañeda-Orjuela, C.A. (Carlos A), Catalá-López, F. (Ferrán), Chadha, D., Chang, J.-C. (Jung-Chen), Chiang, Y.T., Chuang, T.-W. (Ting-Wu), Colomar, M. (Mercedes), Cooper Jr., L.T. (Leslie Trumbull), Cooper, C. (Charles), Courville, K.J. (Karen J), Cowie, M.R. (Martin R.), Criqui, M. (Michael), Dandona, R. (Rakhi), Dayama, A. (Anand), Leo, D. (Diego) de, Degenhardt, F., Del Pozo-Cruz, B. (Borja), Deribe, K. (Kebede), Des Jarlais, D.C. (Don C), Dessalegn, M. (Muluken), Dharmaratne, S.D. (Samath D), Dilmen, U. (Uǧur), Ding, E.L. (Eric), Driscoll, J.M., Durrani, Z., Ellenbogen, R.G. (Richard G), Ermakov, S. (Sergey), Esteghamati, A. (Alireza), Faraon, E.J.A. (Emerito Jose A), Farzadfar, F. (Farshad), Fereshtehnejad, S.-M. (Seyed-Mohammad), Fijabi, D.O. (Daniel Obadare), Forouzanfar, M.H. (Mohammad H), Fra.Paleo, U. (Urbano), Gaffikin, L. (Lynne), Gamkrelidze, A. (Amiran), Gankpé, F.G. (Fortuné Gbètoho), Geleijnse, J.M. (Marianne), Gessner, B.D. (Bradford D), Gibney, K.B. (Katherine B), Ginawi, I.A.M. (Ibrahim Abdelmageem Mohamed), Glaser, E.L. (Elizabeth L), Gona, P. (Philimon), Goto, A. (Akimoto), Gouda, H.N. (Hebe N), Gugnani, H.C. (Harish Chander), Gupta, R. (Rajeev), Hafezi-Nejad, N. (Nima), Hamadeh, R.R. (Randah Ribhi), Hammami, M. (Mouhanad), Hankey, G.J. (Graeme), Harb, H.L. (Hilda L), Haro, J.M. (Josep Maria), Havmoeller, R. (Rasmus), Hay, S.I. (Simon I), Hedayati, M.T. (Mohammad T), Pi, I.B.H. (Ileana B Heredia), Hoek, H.W. (Hans), Hornberger, J.C. (John C), Hosgood, H.D. (H Dean), Hotez, P.J. (Peter), Hoy, D.G. (Damian G), Huang, J. (Jian), Iburg, K.M. (Kim M), Idrisov, B.T. (Bulat T), Innos, K. (Kaire), Jacobsen, K.H. (Kathryn H), Jeemon, P. (Panniyammakal), Jensen, P.N. (Paul N), Jha, V. (Vivekanand), Jiang, G. (Guohong), Jonas, J.B., Juel, K. (Knud), Kan, H. (Haidong), Kankindi, I. (Ida), Karam, V. (Vincent), Karch, F. (Francois), Karema, C.K. (Corine Kakizi), Kaul, A. (Anil), Kawakami, N. (Norito), Kazi, D.S. (Dhruv S), Kemp, A.H. (Andrew H), Kengne, A.P. (Andre Pascal), Keren, A. (Andre), Kereselidze, M. (Maia), Khader, Y.S. (Yousef Saleh), Khalifa, S.E.A.H. (Shams Eldin Ali Hassan), Khan, E.A. (Ejaz Ahmed), Khang, Y.-H. (Young-Ho), Khonelidze, I. (Irma), Kinfu, Y. (Yohannes), Kinge, J.M. (Jonas M), Knibbs, L. (Luke), Kokubo, Y. (Yoshihiro), Kosen, S. (Soewarta), Defo, B.K. (Barthelemy Kuate), Kulkarni, V.S. (Veena S), Kulkarni, C. (Chanda), Kumar, K. (Kuldeep), Kumar, R.B. (Ravi B), Kumar, G.A. (G Anil), Kwan, G.F. (Gene F), Lai, T. (Taavi), Balaji, A.L. (Arjun Lakshmana), Lam, H. (Hilton), Lan, Q. (Qing), Lansingh, V.C. (Van C), Larson, H.J. (Heidi J), Larsson, A. (Anders), Lee, J.-T. (Jong-Tae), Leigh, P.N. (Nigel), Leinsalu, M. (Mall), Leung, R. (Ricky), Li, Y. (Yichong), Li, Y. (Yongmei), Lima, G.M.F. (Graça Maria Ferreira) de, Lin, H.-H. (Hsien-Ho), Lipshultz, S.E. (Steven), Liu, S. (Simin), Liu, Y. (Yang), Lloyd, B.K. (Belinda K), Lotufo, P.A. (Paulo A), Machado, V.M.P. (Vasco Manuel Pedro), Maclachlan, J.H. (Jennifer H), Magis-Rodriguez, C. (Carlos), Majdan, M. (Marek), Mapoma, C.C. (Christopher Chabila), Marcenes, W. (Wagner), Marzan, M.B. (Melvin Barrientos), Masci, J.R. (Joseph R), Mashal, R., Mason-Jones, A.J. (Amanda J), Mayosi, B.M. (Bongani), Mazorodze, T.T. (Tasara T), Mckay, M.J. (Michael), Meaney, M.J., Mehndiratta, M.M. (Man Mohan), Mejia-Rodriguez, F. (Fabiola), Melaku, Y.A. (Yohannes Adama), Memish, Z.A. (Ziad), Mendoza, W. (Walter), Miller, T.R. (Ted R), Mills, E.J. (Edward J), Mohammad, K.A. (Karzan Abdulmuhsin), Mokdad, A.H. (Ali H), Mola, G.L. (Glen Liddell), Monasta, L. (Lorenzo), Montico, M. (Marcella), Moore, A.R. (Ami R), Mori, R. (Riccardo), Moturi, W.N. (Wilkister Nyaora), Mukaigawara, M. (Mitsuru), Murthy, A.C. (Adeline C.), Naheed, A. (Aliya), Naidoo, K.S. (Kovin S), Naldi, L. (Lucia), Nangia, M. (Monika), Narayan, K.M.V. (Venkat), Nash, J.H.E. (John), Nejjari, C. (Chakib), Nelson, R.D. (Robert), Neupane, S.P. (Sudan Prasad), Newton, C. (Cameron), Ng, M. (Marie), Nisar, M.I. (Muhammad Imran), Nolte, S. (Sandra), Norheim, O.F. (Ole F), Nowaseb, V. (Vincent), Nyakarahuka, L. (Luke), Oh, I.-H. (In-Hwan), Ohkubo, T. (Takayoshi), Olusanya, B.O. (Bolajoko O), Omer, S.B. (Saad B), Opio, J.N. (John Nelson), Orisakwe, O.E. (Orish Ebere), Pandian, N.G. (Natesa), Papachristou, C., Caicedo, M.S. (Marco), Patten, J., Paul, V.K. (Vinod K), Pavlin, B.I. (Boris Igor), Pearce, N. (Neil), Pereira, D.M. (David M), Pervaiz, Z. (Zahid), Pesudovs, K. (Konrad), Petzold, M. (Max), Pourmalek, F. (Farshad), Qato, D. (Dima), Quezada, A.D. (Amado D), Quistberg, D.A. (D Alex), Rafay, A. (Anwar), Rahimi, K. (Kazem), Rahimi-Movaghar, V. (Vafa), Rahman, S.U. (Sajjad Ur), Raju, M. (Murugesan), Rana, S.M. (Saleem M), Razavi, H. (Homie), Reilly, R.Q. (Robert Quentin), Remuzzi, G. (Giuseppe), Richardus, J.H. (Jan Hendrik), Ronfani, L. (Luca), Roy, N. (Nadine) van, Sabin, M.L. (Miriam Lewis), Saeedi, M.Y. (Mohammad Yahya), Sahraian, M.A. (Mohammad Ali), Samonte, G.M.J. (Genesis May J), Sawhney, M.S. (Monika), Schneider, I.J.C. (Ione J C), Schwebel, D.C. (David C), Seedat, S. (Soraya), Sepanlou, S.G. (Sadaf G), Servan-Mori, E.E. (Edson E), Sheikhbahaei, S. (Sara), Shibuya, K. (Kenji), Shin, H.H. (Hwashin Hyun), Shiue, I. (Ivy), Shivakoti, R. (Rupak), Sigfusdottir, I.D. (Inga Dora), Silberberg, D.H. (Donald H), Silva, A.P. (Andrea P), Simard, J. (Jacques), Singh, J.A. (Jasvinder), Skirbekk, V. (Vegard), Sliwa, K. (Karen), Soneji, S. (Samir), Soshnikov, S.S. (Sergey S), Sreeramareddy, C.T. (Chandrashekhar T), Stathopoulou, V.K. (Vasiliki Kalliopi), Stroumpoulis, K. (Konstantinos), Swaminathan, S., Sykes, B.C. (Bryan), Tabb, K.M. (Karen M), Talongwa, R.T. (Roberto Tchio), Tenkorang, E.Y. (Eric Yeboah), Terkawi, A.S. (Abdullah Sulieman), Thomson, A.J. (Alan J), Thorne-Lyman, A.L. (Andrew L), Towbin, J.A. (Jeffrey A), Traebert, J. (Jefferson), Tran, B.X. (Bach X), Dimbuene, Z.T. (Zacharie Tsala), Tsilimbaris, M. (Miltiadis), Uchendu, U.S. (Uche S), Ukwaja, K.N. (Kingsley N), Vallely, S.R. (Stephen), Vasankari, T.J. (Tommi J), Venketasubramanian, N. (Narayanaswamy), Violante, F.S. (Francesco S), Vlassov, V.V. (Vasiliy Victorovich), Waller, P. (Patrick), Wallin, M.T. (Mitchell T), Wang, L. (Linhong), Wang, S.X., Wang, Y. (Yanping), Weichenthal, S. (Scott), Weiderpass, E. (Elisabete), Weintraub, R.G. (Robert G), Westerman, R. (Ronny), White, R.G. (Richard), Wilkinson, J.D. (James D), Williams, T.N. (Thomas Neil), Woldeyohannes, S.M. (Solomon Meseret), Wong, J.B. (John), Xu, G. (Gelin), Yang, Y.C. (Yang C), Yano, K.-I., Yip, P. (Paul), Yonemoto, N. (Naohiro), Yoon, S.-J. (Seok-Jun), Younis, M. (Mustafa), Yu, C. (Chuanhua), Jin, K.Y. (Kim Yun), El Sayed Zaki, M. (Maysaa), Zhao, Y. (Yong), Zheng, Y. (Yuhui), Balakrishnan, K. (Kalpana), Zhou, M. (Ming), Zhu, J. (Jun), Zou, X.N. (Xiao Nong), Lopez, A.D. (Alan D), and Vos, T. (Theo)

Abstract

__Abstract__ Background: The Millennium Declaration in 2000 brought special global attention to HIV, tuberculosis, and malaria through the formulation of Millennium Development Goal (MDG) 6. The Global Burden of Disease 2013 study provides a consistent and comprehensive approach to disease estimation for between 1990 and 2013, and an opportunity to assess whether accelerated progress has occured since the Millennium Declaration. Methods: To estimate incidence and mortality for HIV, we used the UNAIDS Spectrum model appropriately modified based on a systematic review of available studies of mortality with and without antiretroviral therapy (ART). For concentrated epidemics, we calibrated Spectrum models to fit vital registration data corrected for misclassification of HIV deaths. In generalised epidemics, we minimised a loss function to select epidemic curves most consistent with prevalence data and demographic data for all-cause mortality. We analysed counterfactual scenarios for HIV to assess years of life saved through prevention of mother-to-child transmission (PMTCT) and ART. For tuberculosis, we analysed vital registration and verbal autopsy data to estimate mortality using cause of death ensemble modelling. We analysed data for corrected case-notifications, expert opinions on the case-detection rate, prevalence surveys, and estimated cause-specific mortality using Bayesian meta-regression to generate consistent trends in all parameters. We analysed malaria mortality and incidence using an updated cause of death database, a systematic analysis of verbal autopsy validation studies for malaria, and recent studies (2010-13) of incidence, drug resistance, and coverage of insecticide-treated bednets. Findings: Globally in 2013, there were 1·8 million new HIV infections (95% uncertainty interval 1·7 million to 2·1 million), 29·2 million prevalent HIV cases (28·1 to 31·7), and 1·3 million HIV deaths (1·3 to 1·5). At the peak of the epidemic in 2005, HIV caused 1·7 mil

Published
2014
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23. Mapping of gene expression reveals CYP27A1 as a susceptibility gene for sporadic ALS

Author

Diekstra, F.P. (Frank), Saris, C.G.J. (Christiaan), Rheenen, W. (Wouter) van, Franke, L. (Lude), Jansen, R.C. (Ritsert), Es, M.A. (Michael) van, Estrada Gil, K. (Karol), Vught, P.W.J. (Paul) van, Blauw, H.M. (Hylke), Groen, E.J.N. (Ewout), Horvath, S. (Steve), Rivadeneira Ramirez, F. (Fernando), Hofman, A. (Albert), Uitterlinden, A.G. (André), Robberecht, W. (Wim), Andersen, P.M. (Peter), Melki, J. (Judith), Meininger, V. (Vincent), Hardiman, O. (Orla), Landers, J.E. (John), Brown, R.H. (Robert), Shatunov, A. (Aleksey), Shaw, C.E. (Christopher), Leigh, P.N. (Nigel), Al-Chalabi, A. (Ammar), Ophoff, R.A. (Roel), Berg, L.H. (Leonard) van den, Veldink, J.H. (Jan), Diekstra, F.P. (Frank), Saris, C.G.J. (Christiaan), Rheenen, W. (Wouter) van, Franke, L. (Lude), Jansen, R.C. (Ritsert), Es, M.A. (Michael) van, Estrada Gil, K. (Karol), Vught, P.W.J. (Paul) van, Blauw, H.M. (Hylke), Groen, E.J.N. (Ewout), Horvath, S. (Steve), Rivadeneira Ramirez, F. (Fernando), Hofman, A. (Albert), Uitterlinden, A.G. (André), Robberecht, W. (Wim), Andersen, P.M. (Peter), Melki, J. (Judith), Meininger, V. (Vincent), Hardiman, O. (Orla), Landers, J.E. (John), Brown, R.H. (Robert), Shatunov, A. (Aleksey), Shaw, C.E. (Christopher), Leigh, P.N. (Nigel), Al-Chalabi, A. (Ammar), Ophoff, R.A. (Roel), Berg, L.H. (Leonard) van den, and Veldink, J.H. (Jan)

Abstract

Amyotrophic lateral sclerosis (ALS) is a progressive, neurodegenerative disease characterized by loss of upper and lower motor neurons. ALS is considered to be a complex trait and genome-wide association studies (GWAS) have implicated a few susceptibility loci. However, many more causal loci remain to be discovered. Since it has been shown that genetic variants associated with complex traits are more likely to be eQTLs than frequency-matched variants from GWAS platforms, we conducted a two-stage genome-wide screening for eQTLs associated with ALS. In addition, we applied an eQTL analysis to finemap association loci. Expression profiles using peripheral blood of 323 sporadic ALS patients and 413 controls were mapped to genome-wide genotyping data. Subsequently, data from a two-stage GWAS (3,568 patients and 10,163 controls) were used to prioritize eQTLs identified in the first stage (162 ALS, 207 controls). These prioritized eQTLs were carried

Published
2012
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44. Regional changes of ciliary neurotrophic factor and nerve growth factor levels in post mortem spinal cord and cerebral cortex from patients with motor disease

Author

Anand, P., primary, Parrett, A., additional, Martin, J., additional, Zeman, S., additional, Foley, P., additional, Swash, M., additional, Leigh, P.N., additional, Cedarbaum, J.M., additional, Lindsay, R.M., additional, Williams-Chestnut, R.E., additional, and Sinicropi, D.V., additional

Published
1995
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