Belief propagation or message passing on binary erasure channels (BEC) is a
low complexity decoding algorithm that allows the recovery of message symbols
based on bipartite graph prunning process. Recently, array XOR codes have
attracted attention for storage systems due to their burst error recovery
performance and easy arithmetic based on Exclusive OR (XOR)-only logic
operations. Array BP-XOR codes are a subclass of array XOR codes that can be
decoded using BP under BEC. Requiring the capability of BP-decodability in
addition to Maximum Distance Separability (MDS) constraint on the code
construction process is observed to put an upper bound on the maximum
achievable code block length, which leads to the code construction process to
become a harder problem. In this study, we introduce asymptotically MDS array
BP-XOR codes that are alternative to exact MDS array BP-XOR codes to pave the
way for easier code constructions while keeping the decoding complexity low
with an asymptotically vanishing coding overhead. We finally provide and
analyze a simple code construction method that is based on discrete geometry to
fulfill the requirements of the class of asymptotically MDS array BP-XOR codes.Comment: 8 pages, 4 figures, to be submitte

Jane Maddock (4227451)

Rebecca Hardy (188906)

Wahyu Wulaningsih (286824)

Systematic Reviews

English

arXiv

BACKGROUND: Body size, nutrition and socioeconomic position (SEP) in early life have been associated with a range of later life health outcomes. Epigenetic regulation is one mechanism through which these early life factors may impact later life health. The aim of this review protocol is to outline procedures to document the influence of body size, nutrition and SEP in early life on the epigenome. METHODS: MEDLINE, Embase and BIOSIS will be systematically searched using pre-defined keywords. Additional studies will be identified through manual searching of reference lists. Two independent researchers will assess the eligibility and quality of each study, with disagreements being resolved through discussion or a third reviewer. Studies will be included if they have epigenetic markers measured either at the same time as, or after, the early life exposure and, have a measure of body size, nutrition or SEP in early life (up to 12 years), are in the English language and are from a sample of community-dwelling participants. DISCUSSION: This protocol will be used to collate the evidence for the effect of early life factors on the epigenome. Findings will form a component of a wider research study examining epigenetic responses to exposures in early life and over the life course and its impact on healthy ageing using data from population-based cohort studies. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42016050193

Maddock, J

Wulaningsih, W

Hardy, R

UCL Discovery

PROTOCOL Open AccessImpact of body size, nutrition andsocioeconomic position in early life on theepigenome: a systematic review protocolJane Maddock* , Wahyu Wulaningsih and Rebecca HardyAbstractBackground: Body size, nutrition and socioeconomic position (SEP) in early life have been associated with a rangeof later life health outcomes. Epigenetic regulation is one mechanism through which these early life factors mayimpact later life health. The aim of this review protocol is to outline procedures to document the influence of bodysize, nutrition and SEP in early life on the epigenome.Methods: MEDLINE, Embase and BIOSIS will be systematically searched using pre-defined keywords. Additionalstudies will be identified through manual searching of reference lists. Two independent researchers will assess theeligibility and quality of each study, with disagreements being resolved through discussion or a third reviewer.Studies will be included if they have epigenetic markers measured either at the same time as, or after, the early lifeexposure and, have a measure of body size, nutrition or SEP in early life (up to 12 years), are in the Englishlanguage and are from a sample of community-dwelling participants.Discussion: This protocol will be used to collate the evidence for the effect of early life factors on the epigenome.Findings will form a component of a wider research study examining epigenetic responses to exposures in early lifeand over the life course and its impact on healthy ageing using data from population-based cohort studies.Systematic review registration: PROSPERO CRD42016050193Keywords: Epigenome, Epigenetics, Early life, Body size, Growth, Nutrition, Socioeconomic positionBackgroundThe extensive growth and development that occurs inutero and childhood marks a sensitive period duringwhich external factors can elicit biological changes whichprogramme an individual’s ability to maintain health or in-crease risk of later life disease [1–3]. Body size, nutritionand socioeconomic position (SEP) at birth and duringchildhood are commonly studied characteristics whichhave been strongly linked with later life health [4–9].There are a variety of mechanisms through which theseearly life factors may impact later life health [2, 4, 7, 10].Epigenetic regulation is one such mechanism [2, 11].Epigenetics refers to alterations in gene expression.Epigenetic modifications do not alter the sequence ofDNA, but can regulate how that DNA is expressed andultimately, how the gene functions. Epigenetic modifi-cations include histone modifications and DNA methy-lation amongst others [12]. These malleable epigeneticsignals are essential for development and cell prolifera-tion but can also occur in response to environmentalstimuli [13]. Evidence from animal studies and a limitednumber of human studies suggests that early life expo-sures can modify several epigenetic signatures in amultitude of genes [11, 14].Understanding which early life exposures evoke changesin the epigenome, and identifying the genomic regions inwhich these changes are occurring will support efforts tomaintain health and prevent disease in later life. Further-more, since epigenetic changes are potentially modifiable,a greater understanding of the specific changes induced byearly life factors can elucidate potential targets for inter-vention strategies.* Correspondence: Jane.maddock@ucl.ac.ukMRC Lifelong Health and Ageing at UCL, 33 Bedford Place, LondonWC1B5JU, UK© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, andreproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link tothe Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.Maddock et al. Systematic Reviews  (2017) 6:129 DOI 10.1186/s13643-017-0521-8Since this is a relatively new area of research, most evi-dence examining the epigenetic effect of early life factorshave come from animal and exploratory studies incorporat-ing a variety of early life exposures and applying differentanalytical methods. Although there has been some review ofthe role of early life factors on the epigenome in humans[15], to the best of our knowledge, there has been no sys-tematic review of the existing literature examining body size,nutrition and social exposures in relation to epigenetic sig-nals. This review will collate human studies examining theimpact of these early life exposures on epigenetics measuredat the same time or any age subsequent to the exposure.AimThe overall aim of the review is to examine the epigeneticeffect of the following factors:i. Body size and growth in early lifeii. Nutrition during pregnancy and early lifeiii. Markers of socioeconomic position in early lifeMethods/design protocol registrationThis study protocol is registered with the PROSPEROdatabase (registration number: CRD42016050193) andhas been reported using the Preferred Reporting Itemsfor Systematic Reviews and Meta-Analyses Protocols(PRISMA-P) checklist, included as Additional file 1.Key termsFor the purposes of this review, early life is defined asthe period including prenatal, infancy, early and middlechildhood, up to 12 years to capture the pre-adolescenceperiod. Full definitions of each of each key variable usedin the review can be found in Table 1.Eligibility criteriaPapers will be included if they meet the following criteria: Original studies published in peer-reviewed journals Epigenetic markers measured either at the sametime or any age subsequent to the early life exposure(i.e. epigenetics can be measures in infancy,childhood, adolescence or adulthood) Current, prospective report or retrospective recall ofindicators of body size (see Table 1) Current, prospective report or retrospective recall ofnutrition and/or diet (see Table 1) Current, prospective report or retrospective recallSEP (see Table 1) English language Non-clinical samplesWe will not include: Studies not meeting inclusion criteria Reviews Studies based on animals Studies only assessing the effect of adulthoodexposures on epigenetic markers Studies assessing the effect of epigenetic markersbefore early life exposures Samples with a specific clinical conditionSearch strategyUsing OvidSP as the database interface, a joint electronicsearch on MEDLINE and Embase will be conducted. TheBIOSIS database will be searched using ISI Web of Sci-ence. The search will use free-text search terms (Table 2)with truncations to allow for different spellings, proximityoperators (‘adj’ in OvidSP, ‘NEAR’ in ISI Web of Science)and joined using Boolean logic (“AND”, “OR”). The refer-ence lists’ of relevant reviews, all included papers and theirISI citation index (via Web of Science) will be searched forstudies meeting inclusion criteria. Eligible studies identifiedwill be combined with the electronic search results.Study selectionResults of the searches will be merged and stored in thereference manager, EndNote. All duplicate citations willbe removed. All abstracts will be screened for eligibilityby two independent researchers (from JM, WW andRH). The full text of all potentially eligible papers willthen also be double screened and reasons for theirTable 1 Definitions of key variables included in reviewTerm DescriptionEpigenetics Any recognised indicator of DNA methylation or histone modification, measured in any tissueBody size Any measure of body size including: weight, height, BMI, head circumference and growth(or change) in any of these measurements at birth and in early lifeNutrition Any measure of maternal nutrition, supplement use and/or diet during pregnancy, breastfeeding/formula, weaning practices and nutrition/diet of the child in early life measured using dietaryquestionnaires and/or objectively measured nutritional biomarkersSocioeconomic position (SEP) Any recognised indicator of SEP within society, including occupation, education, income, occupationalor social class, poverty and household overcrowding, as defined in reference [16], measured duringearly lifeMaddock et al. Systematic Reviews  (2017) 6:129 Page 2 of 4exclusion will be documented. Disagreements about thepaper’s eligibility will be resolved through discussion andif necessary, a third reviewer.Data extractionEach reviewer will extract the relevant information usingthe data extraction form (Additional file 2).The followinginformation will be extracted from selected papers:citation details, study details including design, country/region and sample size; participant details including ageand sex; and exposure and outcome details, includingdetails on methods used. A free-text box for recordingmain findings will be used because of the expectedheterogeneous methods that will have been used.Quality assessmentVarious tools for assessing the quality of observationalstudies such as the Downs and Black checklist [16] andNewcastle-Ottawa Scale [17] are available. However,these are not suitable for assessing the quality of epi-genetic studies. The following aspects of the paperwhich may relate to the quality of each study will beextracted and discussed; study design, methods used tomeasure epigenetics, statistical analysis includingadjustment of relevant confounders, recall bias, i.e. pro-spective or retrospective measures of early life factorsand generalisability [18].SynthesisDescriptive tables will be used to outline the includedstudies in the systematic review. Results will be groupedunder the following thematic groups: (1) body size inearly life; (2) nutrition in early life; 3) SEP in early life. Ifthere is more than one exposure assessed in an individ-ual study, they will be discussed separately where prac-tical. If feasible, the effects of similar epigenetic analysesmethods, e.g. epigenome-wide association studies/locus-specific studies and the age at which epigenetic markerswere identified will also be grouped within each theme.Due to the expected diversity in eligible studies, interms of methods used, a meta-analysis will not be con-ducted [18]. Therefore, a narrative synthesis will beundertaken. The structure of the narrative synthesis willbe based on guidance from Economic and SocialResearch Council Methods Programme [19]. This willinvolve preliminary synthesis, exploring relationshipsbetween and within studies, with particular focus onsources of heterogeneity in study design and characteris-tics between studies, and assessing the robustness of thesynthesis, i.e. assessing the strength of the evidencegiven the methodological quality and generalisability ofincluded papers [18, 19].Table 2 Search termsEpigenetics1 (epigen* )2 (EWAS)3 (Methylation)4 (DNA adj5 methyl*)5 (differential adj1 methylation)6 (global adj1 methylation)7 (DNA adj5 hypermethyl*)8 (DNA adj5 hypomethyl*)9 (gene* adj5 methyl*)10 Gene Expression Regulation11 (methyl* adj5 region)12 (histone adj1 modif*)13 1 OR 2 OR 3 OR 4 OR 5 OR 6 OR 7 OR 8 OR 9 OR 10 OR 11 OR 12Body size/ growth14 ((premature or pre-mature or preterm or pre-term) adj2 (birth or infant*or child* or neonat*))15 (gestation* adj2 age)16 (weight or body-size or bmi or height or length or head-circumference)17 ((grow*) adj3 (fet* or neonat* or prenatal* or pre-natal* or intrauterine or in-utero or postnatal or post-natal or birth* or infant* or child* orearly-life or earlylife))18 (fet* or neonat* or prenatal* or pre-natal* or intrauterine or in-uteroor postnatal or post-natal or birth* or infant* or child* or early-life)19 16 OR 1720 18 AND 1921 14 OR 15 OR 20Nutrition22 (nutrition adj3 (maternal or mother* or pregn* or fet* or neonat* orprenatal* or pre-natal* or intrauterine or in-utero))23 ((nutrition or diet or wean*) adj3 (postnatal or post-natal or infant* orchild* or early-life))24 (breastfe* or breast-fe*)25 (formula adj3 (infant* or child* or early-life))26 22 OR 23 OR 24 OR 25Socioeconomic position27 ((occupation* or education*) adj3 (father* or mother* or parent*))28 ((income or manual) adj3 (father* or mother* or parent*))29 ((social class or social status) adj3 (father* or mother* or parent* orchild* or early-life))30 ((socioeconomic or socio-economic) adj3 (father* or mother* or parent*or child* or early-life))31 ((deprivation or poverty) adj3 (child* or early-life))32 ((overcrowding) adj3 (child* or early-life))33 27 OR 28 OR 29 OR 30 OR 31 OR 32Combining results34 21 OR 26 OR 3335 13 AND 33Maddock et al. Systematic Reviews  (2017) 6:129 Page 3 of 4ReportingThe findings of this systematic review will be reported inaccordance with the Preferred Reporting Items for System-atic Reviews and Meta-Analyses Protocols (PRISMA-P)guidelines [20].DiscussionThis study will systematically review the literature exam-ining the effect of body size and growth, nutrition andsocioeconomic position in early life on the epigenome.The relationship between different early life exposuresand epigenetics as well as other sources of between-study heterogeneity will be explored. The strengths andlimitations, and therefore potential for bias, of individualstudies will be considered. Since this is a relatively newfield, we anticipate that there will be a small number ofstudies and considerable between-study heterogeneity interms of study design and characteristics. In addition tocollating existing evidence of the effects of early life onthe epigenome, this review will form a significant com-ponent of a wider research study examining epigeneticresponses to exposures in early life and over the lifecourse and its impact on healthy ageing.Additional filesAdditional file 1: PRISMA. PRISMA-P 2015 Checklist. Preferred ReportingItems for Systematic Reviews and Meta-Analyses Protocols (PRISMA-P)guidelines. (PDF 222 kb)Additional file 2: Data extraction. Data extraction form. Template forextracting data from selected papers. (DOCX 25 kb)AbbreviationsBMI: Body mass index; PRISMA: Preferred Reporting Items for SystematicReviews and Meta-Analyses; SEP: Socioeconomic positionAcknowledgementsThis work is supported by the ESRC and BBSRC [ES/N000404/1] and theMedical Research Council [MC_UU_12019/1, MC_UU_ 12019/2 ]. Fundershad no role in developing the protocol.Availability of data and materialsNot applicableAuthors’ contributionsRH and JM designed the study and developed the review questions. WWreviewed and commented on the protocol. JM registered the protocol withPROSPERO and drafted the manuscript. All authors read and approved thefinal version of the manuscript.Competing interestsThe authors declare that they have no competing interests.Consent for publicationNot applicable.Ethics approval and consent to participateNot applicable.Publisher’s NoteSpringer Nature remains neutral with regard to jurisdictional claims inpublished maps and institutional affiliations.Received: 25 January 2017 Accepted: 16 June 2017References1. Ben-Shlomo Y, Kuh D. A life course approach to chronic diseaseepidemiology: conceptual models, empirical challenges and interdisciplinaryperspectives. Int J Epidemiol. 2002;31:285–93.2. Gluckman PD, Hanson MA, Cooper C, Thornburg KL. Effect of in utero andearly-life conditions on adult health and disease. N Engl J Med. 2008;359:61–73.3. Kuh D, Cooper R, Hardy R, Richards M, Ben-Schlomo Y. A life courseapproach to healthy ageing. Oxford: Oxford University Press; 2014.4. Lucas A, Fewtrell M, Cole T. Fetal origins of adult disease—the hypothesisrevisited. Br Med J. 1999;319:245.5. Barker DJ. Maternal nutrition, fetal nutrition, and disease in later life.Nutrition. 1997;13:807–13.6. Lucas A. Long-term programming effects of early nutrition—implications forthe preterm infant. J Perinatol. 2005;25:S2–6.7. Galobardes B, Lynch JW, Smith GD. Childhood socioeconomiccircumstances and cause-specific mortality in adulthood: systematic reviewand interpretation. Epidemiol Rev. 2004;26:7–21.8. Galobardes B, Smith GD, Lynch JW. Systematic review of the influence ofchildhood socioeconomic circumstances on risk for cardiovascular diseasein adulthood. Ann Epidemiol. 2006;16:91–104.9. Hertzman C, Boyce T. How experience gets under the skin to creategradients in developmental health. Annu Rev Public Health. 2010;31:329–47.10. Power C, Hertzman C. Social and biological pathways linking early life andadult disease. Br Med Bull. 1997;53:210–21.11. Mitchell C, Schneper LM, Notterman DA. DNA methylation, early lifeenvironment, and health outcomes. Pediatr Res. 2015;79:212–9.12. Bernstein BE, Meissner A, Lander ES. The mammalian epigenome. Cell. 2007;128:669–81.13. Jaenisch R, Bird A. Epigenetic regulation of gene expression: how thegenome integrates intrinsic and environmental signals. Nat Genet. 2003;33:245–54.14. Feil R, Fraga MF. Epigenetics and the environment: emerging patterns andimplications. Nat Rev Genet. 2012;13:97–109.15. Demetriou CA, van Veldhoven K, Relton C, Stringhini S, Kyriacou K, Vineis P.Biological embedding of early-life exposures and disease risk in humans: arole for DNA methylation. Eur J Clin Invest. 2015;45:303–32.16. Downs SH, Black N. The feasibility of creating a checklist for theassessment of the methodological quality both of randomised andnon-randomised studies of health care interventions. J EpidemiolCommunity Health. 1998;52:377–84.17. Wells G, Shea B, O’connell D, Peterson J, Welch V, Losos M, Tugwell P.Ottawa: The Newcastle-Ottawa Scale (NOS) for assessing the quality ofnonrandomised studies in meta-analyses. 2000.18. Centre for Reviews and Dissemination. Systematic reviews: CRD’s guidancefor undertaking reviews in health care. York: University of York; 2009.19. Popay J, Roberts H, Sowden A, Petticrew M, Arai L, Rodgers M, BrittenN, Roen K, Duffy S: Guidance on the conduct of narrative synthesis insystematic reviews. A product from the ESRC methods programmeVersion. Lancaster: Lancaster University; 2006;1:b92.20. Moher D, Liberati A, Tetzlaff J, Altman DG. Preferred reporting items forsystematic reviews and meta-analyses: the PRISMA statement. Ann InternMed. 2009;151:264–9.Maddock et al. 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Impact of body size, nutrition and socioeconomic position in early life on the epigenome: a systematic review protocol

PRISMA. PRISMA-P 2015 Checklist. Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocols (PRISMA-P) guidelines. (PDF 222Â kb

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Additional file 1: of Impact of body size, nutrition and socioeconomic position in early life on the epigenome: a systematic review protocol

Abstract Background Body size, nutrition and socioeconomic position (SEP) in early life have been associated with a range of later life health outcomes. Epigenetic regulation is one mechanism through which these early life factors may impact later life health. The aim of this review protocol is to outline procedures to document the influence of body size, nutrition and SEP in early life on the epigenome. Methods MEDLINE, Embase and BIOSIS will be systematically searched using pre-defined keywords. Additional studies will be identified through manual searching of reference lists. Two independent researchers will assess the eligibility and quality of each study, with disagreements being resolved through discussion or a third reviewer. Studies will be included if they have epigenetic markers measured either at the same time as, or after, the early life exposure and, have a measure of body size, nutrition or SEP in early life (up to 12 years), are in the English language and are from a sample of community-dwelling participants. Discussion This protocol will be used to collate the evidence for the effect of early life factors on the epigenome. Findings will form a component of a wider research study examining epigenetic responses to exposures in early life and over the life course and its impact on healthy ageing using data from population-based cohort studies. Systematic review registration PROSPERO CRD4201605019

Asymptotically MDS Array BP-XOR Codes

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