Last data update: May 06, 2024. (Total: 46732 publications since 2009)
Records 1-20 (of 20 Records) |
Query Trace: Golding H[original query] |
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STrengthening the REporting of Genetic Association studies (STREGA): an extension of the STROBE Statement.
Little J , Higgins JP , Ioannidis JP , Moher D , Gagnon F , von Elm E , Khoury MJ , Cohen B , Davey-Smith G , Grimshaw J , Scheet P , Gwinn M , Williamson RE , Zou GY , Hutchings K , Johnson CY , Tait V , Wiens M , Golding J , van Duijn C , McLaughlin J , Paterson A , Wells G , Fortier I , Freedman M , Zecevic M , King R , Infante-Rivard C , Stewart A , Birkett N . Ann Intern Med 2009 150 (3) 206-15 Making sense of rapidly evolving evidence on genetic associations is crucial to making genuine advances in human genomics and the eventual integration of this information into the practice of medicine and public health. Assessment of the strengths and weaknesses of this evidence, and hence the ability to synthesize it, has been limited by inadequate reporting of results. The STrengthening the REporting of Genetic Association studies (STREGA) initiative builds on the STrengthening the Reporting of Observational Studies in Epidemiology (STROBE) Statement and provides additions to 12 of the 22 items on the STROBE checklist. The additions concern population stratification, genotyping errors, modeling haplotype variation, Hardy-Weinberg equilibrium, replication, selection of participants, rationale for choice of genes and variants, treatment effects in studying quantitative traits, statistical methods, relatedness, reporting of descriptive and outcome data, and issues of data volume that are important to consider in genetic association studies. The STREGA recommendations do not prescribe or dictate how a genetic association study should be designed but seek to enhance the transparency of its reporting, regardless of choices made during design, conduct, or analysis. |
Strengthening the reporting of genetic association studies (STREGA): an extension of the STROBE Statement.
Little J , Higgins JP , Ioannidis JP , Moher D , Gagnon F , von Elm E , Khoury MJ , Cohen B , Davey-Smith G , Grimshaw J , Scheet P , Gwinn M , Williamson RE , Zou GY , Hutchings K , Johnson CY , Tait V , Wiens M , Golding J , van Duijn C , McLaughlin J , Paterson A , Wells G , Fortier I , Freedman M , Zecevic M , King R , Infante-Rivard C , Stewart A , Birkett N . Hum Genet 2009 125 (2) 131-51 Making sense of rapidly evolving evidence on genetic associations is crucial to making genuine advances in human genomics and the eventual integration of this information in the practice of medicine and public health. Assessment of the strengths and weaknesses of this evidence, and hence the ability to synthesize it, has been limited by inadequate reporting of results. The STrengthening the REporting of Genetic Association studies (STREGA) initiative builds on the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) Statement and provides additions to 12 of the 22 items on the STROBE checklist. The additions concern population stratification, genotyping errors, modeling haplotype variation, Hardy-Weinberg equilibrium, replication, selection of participants, rationale for choice of genes and variants, treatment effects in studying quantitative traits, statistical methods, relatedness, reporting of descriptive and outcome data, and the volume of data issues that are important to consider in genetic association studies. The STREGA recommendations do not prescribe or dictate how a genetic association study should be designed but seek to enhance the transparency of its reporting, regardless of choices made during design, conduct, or analysis. |
STrengthening the REporting of Genetic Association Studies (STREGA): an extension of the STROBE statement.
Little J , Higgins JP , Ioannidis JP , Moher D , Gagnon F , von Elm E , Khoury MJ , Cohen B , Davey-Smith G , Grimshaw J , Scheet P , Gwinn M , Williamson RE , Zou GY , Hutchings K , Johnson CY , Tait V , Wiens M , Golding J , van Duijn C , McLaughlin J , Paterson A , Wells G , Fortier I , Freedman M , Zecevic M , King R , Infante-Rivard C , Stewart A , Birkett N . PLoS Med 2009 6 (2) e22 Making sense of rapidly evolving evidence on genetic associations is crucial to making genuine advances in human genomics and the eventual integration of this information in the practice of medicine and public health. Assessment of the strengths and weaknesses of this evidence, and hence the ability to synthesize it, has been limited by inadequate reporting of results. The STrengthening the REporting of Genetic Association studies (STREGA) initiative builds on the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) Statement and provides additions to 12 of the 22 items on the STROBE checklist. The additions concern population stratification, genotyping errors, modelling haplotype variation, Hardy-Weinberg equilibrium, replication, selection of participants, rationale for choice of genes and variants, treatment effects in studying quantitative traits, statistical methods, relatedness, reporting of descriptive and outcome data, and the volume of data issues that are important to consider in genetic association studies. The STREGA recommendations do not prescribe or dictate how a genetic association study should be designed but seek to enhance the transparency of its reporting, regardless of choices made during design, conduct, or analysis. |
Strengthening the reporting of genetic association studies (STREGA): an extension of the STROBE statement.
Little J , Higgins JP , Ioannidis JP , Moher D , Gagnon F , von Elm E , Khoury MJ , Cohen B , Davey-Smith G , Grimshaw J , Scheet P , Gwinn M , Williamson RE , Zou GY , Hutchings K , Johnson CY , Tait V , Wiens M , Golding J , van Duijn C , McLaughlin J , Paterson A , Wells G , Fortier I , Freedman M , Zecevic M , King R , Infante-Rivard C , Stewart A , Birkett N . Eur J Epidemiol 2009 24 (1) 37-55 Making sense of rapidly evolving evidence on genetic associations is crucial to making genuine advances in human genomics and the eventual integration of this information in the practice of medicine and public health. Assessment of the strengths and weaknesses of this evidence, and hence the ability to synthesize it, has been limited by inadequate reporting of results. The STrengthening the REporting of Genetic Association studies (STREGA) initiative builds on the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) Statement and provides additions to 12 of the 22 items on the STROBE checklist. The additions concern population stratification, genotyping errors, modeling haplotype variation, Hardy-Weinberg equilibrium, replication, selection of participants, rationale for choice of genes and variants, treatment effects in studying quantitative traits, statistical methods, relatedness, reporting of descriptive and outcome data, and the volume of data issues that are important to consider in genetic association studies. The STREGA recommendations do not prescribe or dictate how a genetic association study should be designed but seek to enhance the transparency of its reporting, regardless of choices made during design, conduct, or analysis. |
STrengthening the REporting of Genetic Association studies (STREGA)--an extension of the STROBE statement.
Little J , Higgins JP , Ioannidis JP , Moher D , Gagnon F , von Elm E , Khoury MJ , Cohen B , Davey-Smith G , Grimshaw J , Scheet P , Gwinn M , Williamson RE , Zou GY , Hutchings K , Johnson CY , Tait V , Wiens M , Golding J , van Duijn C , McLaughlin J , Paterson A , Wells G , Fortier I , Freedman M , Zecevic M , King R , Infante-Rivard C , Stewart A , Birkett N . Eur J Clin Invest 2009 39 (4) 247-66 Making sense of rapidly evolving evidence on genetic associations is crucial to making genuine advances in human genomics and the eventual integration of this information in the practice of medicine and public health. Assessment of the strengths and weaknesses of this evidence, and hence the ability to synthesize it, has been limited by inadequate reporting of results. The STrengthening the REporting of Genetic Association studies (STREGA) initiative builds on the STrengthening the Reporting of OBservational Studies in Epidemiology (STROBE) Statement and provides additions to 12 of the 22 items on the STROBE checklist. The additions concern population stratification, genotyping errors, modelling haplotype variation, Hardy-Weinberg equilibrium, replication, selection of participants, rationale for choice of genes and variants, treatment effects in studying quantitative traits, statistical methods, relatedness, reporting of descriptive and outcome data and the volume of data issues that are important to consider in genetic association studies. The STREGA recommendations do not prescribe or dictate how a genetic association study should be designed, but seek to enhance the transparency of its reporting, regardless of choices made during design, conduct or analysis. |
Strengthening the reporting of genetic association studies (STREGA): an extension of the strengthening the reporting of observational studies in epidemiology (STROBE) statement.
Little J , Higgins JP , Ioannidis JP , Moher D , Gagnon F , von Elm E , Khoury MJ , Cohen B , Davey-Smith G , Grimshaw J , Scheet P , Gwinn M , Williamson RE , Zou GY , Hutchings K , Johnson CY , Tait V , Wiens M , Golding J , van Duijn C , McLaughlin J , Paterson A , Wells G , Fortier I , Freedman M , Zecevic M , King R , Infante-Rivard C , Stewart AF , Birkett N . J Clin Epidemiol 2009 62 (6) 597-608.e4 Making sense of rapidly evolving evidence on genetic associations is crucial to making genuine advances in human genomics and the eventual integration of this information in the practice of medicine and public health. Assessment of the strengths and weaknesses of this evidence, and hence, the ability to synthesize it, has been limited by inadequate reporting of results. The STrengthening the REporting of Genetic Association (STREGA) studies initiative builds on the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) statement and provides additions to 12 of the 22 items on the STROBE checklist. The additions concern population stratification, genotyping errors, modeling haplotype variation, Hardy-Weinberg equilibrium, replication, selection of participants, rationale for choice of genes and variants, treatment effects in studying quantitative traits, statistical methods, relatedness, reporting of descriptive and outcome data, and the volume of data issues that are important to consider in genetic association studies. The STREGA recommendations do not prescribe or dictate how a genetic association study should be designed, but seek to enhance the transparency of its reporting, regardless of choices made during design, conduct, or analysis. |
Innovations in public health surveillance: updates from a forum convened by the WHO Hub for Pandemic and Epidemic Intelligence, 2 and 3 February 2022.
Morgan Oliver , Redies Isabel , Beatriz Leiva Rioja Zoila , Brownstein John , George Dylan , Golding Josie , Hanefeld Johanna , Horby Peter , Lee Christopher , Mikhailov Danil , Philip Wolfgang , Scarpino Samuel , Kifle Tessema Sofonias , Ihekweazu Chikwe . Euro Surveill 2022 27 (15) In the 2 years since the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) there has been an unprecedented collective effort from the academic, public, and private sectors to advance surveillance for pandemic preparedness and response. The coronavirus disease (COVID-19) pandemic has created momentum that will define the future of public health intelligence. On 2 and 3 February 2022, the World Health Organization (WHO) Hub for Pandemic and Epidemic Intelligence convened a meeting of a small group of surveillance innovators to share insights and approaches about their initiatives and future directions. The meeting served as an opportunity for participants to share updates about their work, to explore potential for collaboration, exchange ideas, cross-fertilise our work and discuss challenges in the field of surveillance. Although the group of attendees was not geographically representative of the global surveillance community, the meeting was the first in a planned series of exchanges convened by the WHO Pandemic Hub that will generate dialogue among global thought leaders and new voices in the surveillance community. In this first convening we discussed several themes, including what is meaningful collaboration for success; how to bring the public back into public health; what are individual-centred approaches; how new kinds of data have new privacy concerns; how government structures affect the functioning of surveillance systems; how to inform the decisionmaking process; cross-scaling and down-scaling tools and technologies; investing in human talent and future practitioners; and achieving sustainability into surveillance. In this meeting report, we summarise the discussions on innovations in public health surveillance and provide a list with references and links to the organisations and initiatives represented at the meeting. |
A Research and Development (R&D) roadmap for influenza vaccines: Looking toward the future
Moore KA , Ostrowsky JT , Kraigsley AM , Mehr AJ , Bresee JS , Friede MH , Gellin BG , Golding JP , Hart PJ , Moen A , Weller CL , Osterholm MT . Vaccine 2021 39 (45) 6573-6584 Improved influenza vaccines are urgently needed to reduce the burden of seasonal influenza and to ensure a rapid and effective public-health response to future influenza pandemics. The Influenza Vaccines Research and Development (R&D) Roadmap (IVR) was created, through an extensive international stakeholder engagement process, to promote influenza vaccine R&D. The roadmap covers a 10-year timeframe and is organized into six sections: virology; immunology; vaccinology for seasonal influenza vaccines; vaccinology for universal influenza vaccines; animal and human influenza virus infection models; and policy, finance, and regulation. Each section identifies barriers, gaps, strategic goals, milestones, and additional R&D priorities germane to that area. The roadmap includes 113 specific R&D milestones, 37 of which have been designated high priority by the IVR expert taskforce. This report summarizes the major issues and priority areas of research outlined in the IVR. By identifying the key issues and steps to address them, the roadmap not only encourages research aimed at new solutions, but also provides guidance on the use of innovative tools to drive breakthroughs in influenza vaccine R&D. |
The origins and genomic diversity of American Civil War Era smallpox vaccine strains.
Duggan AT , Klunk J , Porter AF , Dhody AN , Hicks R , Smith GL , Humphreys M , McCollum AM , Davidson WB , Wilkins K , Li Y , Burke A , Polasky H , Flanders L , Poinar D , Raphenya AR , Lau TTY , Alcock B , McArthur AG , Golding GB , Holmes EC , Poinar HN . Genome Biol 2020 21 (1) 175 Vaccination has transformed public health, most notably including the eradication of smallpox. Despite its profound historical importance, little is known of the origins and diversity of the viruses used in smallpox vaccination. Prior to the twentieth century, the method, source and origin of smallpox vaccinations remained unstandardised and opaque. We reconstruct and analyse viral vaccine genomes associated with smallpox vaccination from historical artefacts. Significantly, we recover viral molecules through non-destructive sampling of historical materials lacking signs of biological residues. We use the authenticated ancient genomes to reveal the evolutionary relationships of smallpox vaccination viruses within the poxviruses as a whole. |
Preexisting immunity not frailty phenotype predicts influenza post vaccination titers among older veterans
Van Epps P , Tumpey T , Pearce MB , Golding H , Higgins P , Hornick T , Burant C , Wilson BM , Banks R , Gravenstein S , Canaday DH . Clin Vaccine Immunol 2017 24 (3) Both preexisting immunity to influenza and age have been shown to be a correlate of influenza vaccine response. Frailty, an indicator of functional impairment in older adults, has also been shown in one study to predict lower influenza vaccine responses among non-veterans. In the current study we aimed to determine the association between frailty, preexisting immunity and immune response to influenza vaccine in older veterans. We analyzed 117 subjects (age range 62-95 years; median 81) divided into 3 cohorts based on the Fried frailty test: non-frail (NF: N=23; median age 68), pre-frail (PF: N=50; median age 80) and frail (F:N=44; median age 82) during the 2010-2011 and 11-12 influenza seasons. Subjects received the seasonal trivalent inactivated influenza vaccine and baseline and post-vaccination samples were obtained. Anti-influenza humoral immunity as measured by hemagglutinin inhibition (HI) and microneutralization (MN) assays were measured for influenza B, A(H1N1)pdm09 and A(H3N2) viruses. Post vaccination-titers to Influenza vaccine were not different between frail and NF subjects overall in this older subset of veterans. However, preexisting HI titers strongly correlated with post-vaccination titers among all functional status groups. When microneutralization titers are compared, the association between preexisting immunity and vaccine response varies by frailty status with the highest correlation observed in the NF subjects. In conclusion, preexisting immunity rather than frailty appear to predict post-influenza vaccine titer in this older veteran cohort. |
Spread of yellow fever virus outbreak in Angola and the Democratic Republic of the Congo 2015-16: a modelling study
Kraemer MU , Faria NR , Reiner RC Jr , Golding N , Nikolay B , Stasse S , Johansson MA , Salje H , Faye O , Wint GRW , Niedrig M , Shearer FM , Hill SC , Thompson RN , Bisanzio D , Taveira N , Nax HH , Pradelski BSR , Nsoesie EO , Murphy NR , Bogoch II , Khan K , Brownstein JS , Tatem AJ , de Oliveira T , Smith DL , Sall AA , Pybus OG , Hay SI , Cauchemez S . Lancet Infect Dis 2016 17 (3) 330-338 BACKGROUND: Since late 2015, an epidemic of yellow fever has caused more than 7334 suspected cases in Angola and the Democratic Republic of the Congo, including 393 deaths. We sought to understand the spatial spread of this outbreak to optimise the use of the limited available vaccine stock. METHODS: We jointly analysed datasets describing the epidemic of yellow fever, vector suitability, human demography, and mobility in central Africa to understand and predict the spread of yellow fever virus. We used a standard logistic model to infer the district-specific yellow fever virus infection risk during the course of the epidemic in the region. FINDINGS: The early spread of yellow fever virus was characterised by fast exponential growth (doubling time of 5-7 days) and fast spatial expansion (49 districts reported cases after only 3 months) from Luanda, the capital of Angola. Early invasion was positively correlated with high population density (Pearson's r 0.52, 95% CI 0.34-0.66). The further away locations were from Luanda, the later the date of invasion (Pearson's r 0.60, 95% CI 0.52-0.66). In a Cox model, we noted that districts with higher population densities also had higher risks of sustained transmission (the hazard ratio for cases ceasing was 0.74, 95% CI 0.13-0.92 per log-unit increase in the population size of a district). A model that captured human mobility and vector suitability successfully discriminated districts with high risk of invasion from others with a lower risk (area under the curve 0.94, 95% CI 0.92-0.97). If at the start of the epidemic, sufficient vaccines had been available to target 50 out of 313 districts in the area, our model would have correctly identified 27 (84%) of the 32 districts that were eventually affected. INTERPRETATION: Our findings show the contributions of ecological and demographic factors to the ongoing spread of the yellow fever outbreak and provide estimates of the areas that could be prioritised for vaccination, although other constraints such as vaccine supply and delivery need to be accounted for before such insights can be translated into policy. FUNDING: Wellcome Trust. |
Global distribution and environmental suitability for chikungunya virus, 1952 to 2015.
Nsoesie EO , Kraemer MU , Golding N , Pigott DM , Brady OJ , Moyes CL , Johansson MA , Gething PW , Velayudhan R , Khan K , Hay SI , Brownstein JS . Euro Surveill 2016 21 (20) Chikungunya fever is an acute febrile illness caused by the chikungunya virus (CHIKV), which is transmitted to humans by Aedes mosquitoes. Although chikungunya fever is rarely fatal, patients can experience debilitating symptoms that last from months to years. Here we comprehensively assess the global distribution of chikungunya and produce high-resolution maps, using an established modelling framework that combines a comprehensive occurrence database with bespoke environmental correlates, including up-to-date Aedes distribution maps. This enables estimation of the current total population-at-risk of CHIKV transmission and identification of areas where the virus may spread to in the future. We identified 94 countries with good evidence for current CHIKV presence and a set of countries in the New and Old World with potential for future CHIKV establishment, demonstrated by high environmental suitability for transmission and in some cases previous sporadic reports. Aedes aegypti presence was identified as one of the major contributing factors to CHIKV transmission but significant geographical heterogeneity exists. We estimated 1.3 billion people are living in areas at-risk of CHIKV transmission. These maps provide a baseline for identifying areas where prevention and control efforts should be prioritised and can be used to guide estimation of the global burden of CHIKV. |
A simple flow-cytometric method measuring B cell surface immunoglobulin avidity enables characterization of affinity maturation to influenza A virus
Frank GM , Angeletti D , Ince WL , Gibbs JS , Khurana S , Wheatley AK , Max EE , McDermott AB , Golding H , Stevens J , Bennink JR , Yewdell JW . mBio 2015 6 (4) e01156 Antibody (Ab) affinity maturation enables an individual to maintain immunity to an increasing number of pathogens within the limits of a total Ig production threshold. A better understanding of this process is critical for designing vaccines that generate optimal Ab responses to pathogens. Our study describes a simple flow-cytometric method that enumerates virus-specific germinal center (GC) B cells as well as their AC50, a measure of Ab avidity, defined as the antigen concentration required to detect 50% of specific B cells. Using a model of mouse Ab responses to the influenza A virus hemagglutinin (IAV HA), we obtained data indicating that AC50 decreases with time postinfection in an affinity maturation-dependent process. As proof of principle of the utility of the method, our data clearly show that relative to intranasal IAV infection, intramuscular immunization against inactivated IAV in adjuvant results in a diminished GC HA B cell response, with increased AC50 correlating with an increased serum Ab off-rate. Enabling simultaneous interrogation of both GC HA B cell quantity and quality, this technique should facilitate study of affinity maturation and rational vaccine design. IMPORTANCE: Though it was first described 50 years ago, little is known about how antibody affinity maturation contributes to immunity. This question is particularly relevant to developing more effective vaccines for influenza A virus (IAV) and other viruses that are difficult vaccine targets. Limitations in methods for characterizing antigen-specific B cells have impeded progress in characterizing the quality of immune responses to vaccine and natural immunogens. In this work, we describe a simple flow cytometry-based approach that measures both the number and affinity of IAV-binding germinal center B cells specific for the IAV HA, the major target of IAV-neutralizing antibodies. Using this method, we showed that the route and form of immunization significantly impacts the quality and quantity of B cell antibody responses. This method provides a relatively simple yet powerful tool for better understanding the contribution of affinity maturation to viral immunity. |
Fish consumption and blood mercury levels: Golding et al. respond
Golding J , Steer CD , Lowery T , Jones R , Hibbeln JR . Environ Health Perspect 2014 122 (5) A120-1 Obviously our article (Golding et al. 2013) must have been less than clear in leading Groth to assume findings that we had not claimed. For example, he states both that “there was no strong correlation between fish consumption and blood mercury levels” and that we “observed no association between fish intake and blood mercury.” Neither statement is true. We did show that the R2 for total blood mercury associated with seafood consumption was 8.75%, implying a correlation coefficient of about 0.3. The relationship between fish intake and blood mercury was highly significant (p < 0.0001). | The point that we were making in the article was that seafood did contribute to the total blood mercury levels, but that many other dietary items did so as well. The other studies quoted by Groth did not investigate other sources of mercury. However, two studies in the United Kingdom have shown that seafood provides only 25–33% of dietary mercury (Ysart et al. 1999, 2000); although we did not distinguish between types of fish, these authors assayed the mercury content of 500 different samples of seafood, typical of a normal UK diet. | In conclusion we do not disagree with Groth that excessive consumption of fish with high mercury content should be avoided, but would emphasize the overall beneficial effects of fish in general. |
Modelling adult Aedes aegypti and Aedes albopictus survival at different temperatures in laboratory and field settings
Brady OJ , Johansson MA , Guerra CA , Bhatt S , Golding N , Pigott DM , Delatte H , Grech MG , Leisnham PT , Maciel-de-Freitas R , Styer LM , Smith DL , Scott TW , Gething PW , Hay SI . Parasit Vectors 2013 6 (1) 351 BACKGROUND: The survival of adult female Aedes mosquitoes is a critical component of their ability to transmit pathogens such as dengue viruses. One of the principal determinants of Aedes survival is temperature, which has been associated with seasonal changes in Aedes populations and limits their geographical distribution. The effects of temperature and other sources of mortality have been studied in the field, often via mark-release-recapture experiments, and under controlled conditions in the laboratory. Survival results differ and reconciling predictions between the two settings has been hindered by variable measurements from different experimental protocols, lack of precision in measuring survival of free-ranging mosquitoes, and uncertainty about the role of age-dependent mortality in the field. METHODS: Here we apply generalised additive models to data from 351 published adult Ae. aegypti and Ae. albopictus survival experiments in the laboratory to create survival models for each species across their range of viable temperatures. These models are then adjusted to estimate survival at different temperatures in the field using data from 59 Ae. aegypti and Ae. albopictus field survivorship experiments. The uncertainty at each stage of the modelling process is propagated through to provide confidence intervals around our predictions. RESULTS: Our results indicate that adult Ae. albopictus has higher survival than Ae. aegypti in the laboratory and field, however, Ae. aegypti can tolerate a wider range of temperatures. A full breakdown of survival by age and temperature is given for both species. The differences between laboratory and field models also give insight into the relative contributions to mortality from temperature, other environmental factors, and senescence and over what ranges these factors can be important. CONCLUSIONS: Our results support the importance of producing site-specific mosquito survival estimates. By including fluctuating temperature regimes, our models provide insight into seasonal patterns of Ae. aegypti and Ae. albopictus population dynamics that may be relevant to seasonal changes in dengue virus transmission. Our models can be integrated with Aedes and dengue modelling efforts to guide and evaluate vector control, better map the distribution of disease and produce early warning systems for dengue epidemics. |
Dietary predictors of maternal prenatal blood mercury levels in the ALSPAC Birth Cohort Study
Golding Jean , Steer Colin D , Hibbeln Joseph R , Emmett Pauline M , Lowery Tony , Jones Robert . Environ Health Perspect 2013 121 (10) 1214-1218 BACKGROUND: Very high levels of prenatal maternal mercury have adverse effects on the developing fetal brain. It has been suggested that all possible sources of mercury should be avoided. However, although seafood is a known source of mercury, little is known about other dietary components that contribute to the overall levels of blood mercury. OBJECTIVE: Our goal was to quantify the contribution of components of maternal diet to prenatal blood mercury level. Methods: Whole blood samples and information on diet and sociodemographic factors were colÂlected from pregnant women (n = 4,484) enrolled in the Avon Longitudinal Study of Parents and Children (ALSPAC). The blood samples were assayed for total mercury using inductively coupled plasma dynamic reaction cell mass spectrometry. Linear regression was used to estimate the relative contributions of 103 dietary variables and 6 sociodemographic characteristics to whole blood total mercury levels (TBM; untransformed and log-transformed) based on R2 values. RESULTS: We estimated that maternal diet accounted for 19.8% of the total variation in ln-TBM, with 44% of diet-associated variability (8.75% of the total variation) associated with seafood consumption (white fish, oily fish, and shellfish). Other dietary components positively associated with TBM included wine and herbal teas, and components with significant negative associations included white bread, meat pies or pasties, and french fries. CONCLUSIONS: Although seafood is a source of dietary mercury, seafood appeared to explain a relaÂtively small proportion of the variation in TBM in our UK study population. Our findings require confirmation, but suggest that limiting seafood intake during pregnancy may have a limited impact on prenatal blood mercury levels. |
Timing of maturation and predictors of Tanner stage transitions in boys enrolled in a contemporary British cohort
Monteilh C , Kieszak S , Flanders WD , Maisonet M , Rubin C , Holmes AK , Heron J , Golding J , McGeehin MA , Marcus M . Paediatr Perinat Epidemiol 2011 25 (1) 75-87 This study describes the timing of puberty in 8- to 14-year-old boys enrolled in the Avon Longitudinal Study of Parents and Children (ALSPAC) and identifies factors associated with earlier achievement of advanced pubic hair stages. Women were enrolled during pregnancy and their offspring were followed prospectively. We analysed self-reported pubic hair Tanner staging collected annually. We used survival models to estimate median age of attainment of pubic hair stage >1, stage >2 and stage >3 of pubic hair development. We also constructed multivariable logistic regression models to identify factors associated with earlier achievement of pubic hair stages. Approximately 5% of the boys reported Tanner pubic hair stage >1 at age 8; 99% of boys were at stage >1 by age 14. The estimated median ages of entry into stages of pubic hair development were 11.4 years [95% confidence interval (CI) 11.3, 11.4] for stage >1, 12.7 years [95% CI 12.7, 12.8] for stage >2 and 13.5 years [95% CI 13.5, 13.6] for stage >3. Predictors of younger age at Tanner stage >1 included low birthweight, younger maternal age at delivery and being taller at age 8. Associations were found between younger age at attainment of stage >2 and gestational diabetes and taller or heavier body size at age 8. Being taller or heavier at age 8 also predicted younger age at Tanner stage >3. The results give added support to the strong influence of pre-adolescent body size on male pubertal development; the tallest and heaviest boys at 8 years achieved each stage earlier and the shortest boys later. Age at attainment of pubic hair Tanner stages in the ALSPAC cohort are similar to ages reported in other European studies that were conducted during overlapping time periods. This cohort will continue to be followed for maturational information until age 17. |
Role of prenatal characteristics and early growth on pubertal attainment of British girls
Maisonet M , Christensen KY , Rubin C , Holmes A , Flanders WD , Heron J , Ong KK , Golding J , McGeehin MA , Marcus M . Pediatrics 2010 126 (3) e591-600 OBJECTIVES: The objective of this study was to explore the influence of maternal prenatal characteristics and behaviors and of weight and BMI gain during early childhood on the timing of various puberty outcomes in girls who were enrolled in the Avon Longitudinal Study of Parents and Children. METHODS: Repeated self-assessments of pubertal development were obtained from approximately 4000 girls between the ages of 8 and 14. Data on prenatal characteristics and weight at birth and 2, 9, and 20 months of age were obtained from questionnaires, birth records, and clinic visits. Infants' weights were converted to weight-for-age and BMI SD scores (SDSs; z scores), and change values were obtained for the 0- to 20-month and other intervals within that age range. We used parametric survival models to estimate associations with age of entry into Tanner stages of breast and pubic hair and menarche. RESULTS: Maternal initiation of menarche at age <12, smoking during pregnancy, and primiparity were associated with earlier puberty. A 1-unit increase in the weight SDS change values for the 0- to 20-month age interval was associated with earlier ages of entry into pubertal outcomes (0.19-0.31 years). Increases in the BMI SDS change values were also associated with earlier entry into pubertal outcomes (0.07-0.11 years). CONCLUSIONS: Many of the maternal prenatal characteristics and weight and BMI gain during infancy seemed to have similar influences across different puberty outcomes. Either such early factors have comparable influences on each of the hormonal processes involved in puberty, or processes are linked and awakening of 1 aspect triggers the others. |
STrengthening the REporting of Genetic Association Studies (STREGA)--an extension of the STROBE statement.
Little J , Higgins JP , Ioannidis JP , Moher D , Gagnon F , von Elm E , Khoury MJ , Cohen B , Davey-Smith G , Grimshaw J , Scheet P , Gwinn M , Williamson RE , Zou GY , Hutchings K , Johnson CY , Tait V , Wiens M , Golding J , van Duijn C , McLaughlin J , Paterson A , Wells G , Fortier I , Freedman M , Zecevic M , King R , Infante-Rivard C , Stewart A , Birkett N . Genet Epidemiol 2009 33 (7) 581-98 Making sense of rapidly evolving evidence on genetic associations is crucial to making genuine advances in human genomics and the eventual integration of this information in the practice of medicine and public health. Assessment of the strengths and weaknesses of this evidence, and hence the ability to synthesize it, has been limited by inadequate reporting of results. The STrengthening the REporting of Genetic Association studies (STREGA) initiative builds on the STrengthening the Reporting of OBservational Studies in Epidemiology (STROBE) Statement and provides additions to 12 of the 22 items on the STROBE checklist. The additions concern population stratification, genotyping errors, modelling haplotype variation, Hardy-Weinberg equilibrium, replication, selection of participants, rationale for choice of genes and variants, treatment effects in studying quantitative traits, statistical methods, relatedness, reporting of descriptive and outcome data, and the volume of data issues that are important to consider in genetic association studies. The STREGA recommendations do not prescribe or dictate how a genetic association study should be designed but seek to enhance the transparency of its reporting, regardless of choices made during design, conduct, or analysis. |
Timing of maturation and predictors of menarche in girls enrolled in a contemporary British cohort
Rubin C , Maisonet M , Kieszak S , Monteilh C , Holmes A , Flanders D , Heron J , Golding J , McGeehin M , Marcus M . Paediatr Perinat Epidemiol 2009 23 (5) 492-504 This study describes the timing of puberty in 8- to 13-year-old girls enrolled in the Avon Longitudinal Study of Parents and Children (ALSPAC) and identifies factors associated with earlier achievement of menarche. Women were enrolled during pregnancy and their offspring were followed prospectively. We analysed self-reported Tanner staging and menstrual status information collected annually from daughters up to age 13. We used survival models to estimate median age of attainment of stage >1 and stage >2 of breast and pubic hair development and of menarche. We also constructed multivariable logistic regression models to identify factors associated with earlier achievement of menarche. About 12% of girls reported Tanner breast stage >1 at age 8; 98% of girls were above stage 1 by age 13. For pubic hair, 5% and 95% of girls had attained a stage >1 by 8 and 13 years, respectively. The estimated median age of entry into stage >1 of breast development was 10.14 years (95% confidence interval [CI], 10.08, 10.19), and for pubic hair development the median age was 10.92 years [95% CI, 10.87, 10.97]. One girl (out of 2953) had attained menarche by age 8; 60% had attained menarche by age 13. The estimated median age at menarche was 12.93 years [95% CI, 12.89, 12.98]. Prenatal predictors of menarche by age 11 (12% of girls) included earlier maternal age at menarche, high maternal pre-pregnancy body mass index, smoking during the third trimester, and non-white race; the single postnatal predictor was the girl's body size at 8 years. Age at attainment of breast and pubic hair Tanner stage and age at menarche in the ALSPAC cohort are similar to ages reported in other European studies that were conducted during overlapping time periods. The results also give added support to the strong influence of maternal maturation, pre-adolescent body size and race on the timing of a girl's menarche. This cohort will continue to be followed for maturational information until age 17. |
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