Microfiber abundance associated with coral tissue varies geographically on the Belize Mesoamerican Barrier Reef System

Ocean plastic pollution is a global problem that causes ecosystem degradation. Crucial knowledge gaps exist concerning patterns in microfiber abundance across regions and ecosystems, as well as the role of these pollutants within the environment. Here, we quantified the abundance of microfibers in coral samples collected from the Belize Mesoamerican Barrier Reef System (MBRS) using a polarized light microscope and identified a subsample of these to the polymer level using an Attenuated Total Reflectance Fourier Transform Infrared Spectroscopy microscope. Microfibers were found in all coral samples with rayon being identified as the most common microfiber, comprising 85% of quantified pollutants. We found a greater average abundance of microfibers in coral samples from the Sapodilla Cayes (296 ± SE 89) than in samples from the Drowned Cayes (75 ± SE 14), indicating spatial variation in microfiber abundance within coral tissue along the MBRS. These results demonstrate that corals on the Belize MBRS interact with microfibers and that microfiber abundance on reefs varies spatially due to point sources of pollution and local oceanography. As rayon from clothing typically enters the ocean through wastewater effluent, alterations to waste water infrastructure may prove useful in decreasing rayon pollution in coastal waters

The Two-Communities Theory and Knowledge Utilization

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66698/2/10.1177_000276427902200308.pd

An international survey of speciality training in oral and maxillofacial pathology

BACKGROUND: Speciality training in oral and maxillofacial pathology (OMFP) across the world would be aided by guidance on a generic curriculum and training programme that all countries could use as a template. In order to facilitate this, we require an understanding of the various forms which OMFP training takes across the world. METHODS: We sent a questionnaire to OMF pathologists in the 42 countries represented in the IAOP membership, via their Regional Councillor. The questionnaire included detailed demographics, entry requirements, specialty training program and facilities/ resources. RESULTS: Replies were received from 22/42 countries (52%). OMFP is a dental/dental and medical speciality in 72%, and in 92% of those, this is recognised by a licensing board. Training was undertaken in an academic environment in 85% (with many offering a further academic qualification) and the median length of training was 4 years. General/anatomical pathology training is mandated in 85% of programs and a common core of general sub-specialities was identified. An end of training assessment was conducted in 80% of programs with most including written, practical and oral elements. Training program directors and educational supervisors were in place in 12/16 programs and, in most, Quality Assurance of training was externally monitored. In only one country was the number of trainees linked to workforce planning. CONCLUSIONS: Training in OMFP varies across the world. However, we feel there is sufficient commonality for the development of an agreed indicative framework on education and training in Oral and Maxillofacial Pathology, perhaps under the auspices of the IAOP.http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1600-0714hb201

Best Practices and Joint Calling of the HumanExome BeadChip: The CHARGE Consortium

Genotyping arrays are a cost effective approach when typing previously-identified genetic polymorphisms in large numbers of samples. One limitation of genotyping arrays with rare variants (e.g., minor allele frequency [MAF] <0.01) is the difficulty that automated clustering algorithms have to accurately detect and assign genotype calls. Combining intensity data from large numbers of samples may increase the ability to accurately call the genotypes of rare variants. Approximately 62,000 ethnically diverse samples from eleve

A multi-ethnic polygenic risk score is associated with hypertension prevalence and progression throughout adulthood

In a multi-stage analysis of 52,436 individuals aged 17-90 across diverse cohorts and biobanks, we train, test, and evaluate a polygenic risk score (PRS) for hypertension risk and progression. The PRS is trained using genome-wide association studies (GWAS) for systolic, diastolic blood pressure, and hypertension, respectively. For each trait, PRS is selected by optimizing the coefficient of variation (CV) across estimated effect sizes from multiple potential PRS using the same GWAS, after which the 3 trait-specific PRSs are combined via an unweighted sum called “PRSsum”, forming the HTN-PRS. The HTN-PRS is associated with both prevalent and incident hypertension at 4-6 years of follow up. This association is further confirmed in age-stratified analysis. In an independent biobank of 40,201 individuals, the HTN-PRS is confirmed to be predictive of increased risk for coronary artery disease, ischemic stroke, type 2 diabetes, and chronic kidney disease

Meta-analysis of exome array data identifies six novel genetic loci for lung function

Background: Over 90 regions of the genome have been associated with lung function to date, many of which have also been implicated in chronic obstructive pulmonary disease. Methods: We carried out meta-analyses of exome array data and three lung function measures: forced expiratory volume in one second (FEV1), forced vital capacity (FVC) and the ratio of FEV1 to FVC (FEV1/FVC). These analyses by the SpiroMeta and CHARGE consortia included 60,749 individuals of European ancestry from 23 studies, and 7,721 individuals of African Ancestry from 5 studies in the discovery stage, with follow-up in up to 111,556 independent individuals. Results: We identified significant (P<2·8x10-7) associations with six SNPs: a nonsynonymous variant in RPAP1, which is predicted to be damaging, three intronic SNPs (SEC24C, CASC17 and UQCC1) and two intergenic SNPs near to LY86 and FGF10. Expression quantitative trait loci analyses found evidence for regulation of gene expression at three signals and implicated several genes, including TYRO3 and PLAU. Conclusions: Further interrogation of these loci could provide greater understanding of the determinants of lung function and pulmonary disease

Multiethnic meta-analysis identifies ancestry-specific and cross-ancestry loci for pulmonary function

Nearly 100 loci have been identified for pulmonary function, almost exclusively in studies of European ancestry populations. We extend previous research by meta-analyzing genome-wide association studies of 1000 Genomes imputed variants in relation to pulmonary function in a multiethnic population of 90,715 individuals of European (N = 60,552), African (N = 8429), Asian (N = 9959), and Hispanic/Latino (N = 11,775) ethnicities. We identify over 50 additional loci at genome-wide significance in ancestry-specific or multiethnic meta-analyses. Using recent fine-mapping methods incorporating functional annotation, gene expression, and differences in linkage disequilibrium between ethnicities, we further shed light on potential causal variants and genes at known and newly identified loci. Several of the novel genes encode proteins with predicted or established drug targets, including KCNK2 and CDK12. Our study highlights the utility of multiethnic and integrative genomics approaches to extend existing knowledge of the genetics of l

Clonal hematopoiesis associated with epigenetic aging and clinical outcomes

Clonal hematopoiesis of indeterminate potential (CHIP) is a common precursor state for blood cancers that most frequently occurs due to mutations in the DNA-methylation modifying enzymes DNMT3A or TET2. We used DNA-methylation array and whole-genome sequencing data from four cohorts together comprising 5522 persons to study the association between CHIP, epigenetic clocks, and health outcomes. CHIP was strongly associated with epigenetic age acceleration, defined as the residual after regressing epigenetic clock age on chronological age, in several clocks, ranging from 1.31 years (GrimAge, p &lt; 8.6 × 10−7) to 3.08 years (EEAA, p &lt; 3.7 × 10−18). Mutations in most CHIP genes except DNA-damage response genes were associated with increases in several measures of age acceleration. CHIP carriers with mutations in multiple genes had the largest increases in age acceleration and decrease in estimated telomere length. Finally, we found that ~40% of CHIP carriers had acceleration &gt;0 in both Hannum and GrimAge (referred to as AgeAccelHG+). This group was at high risk of all-cause mortality (hazard ratio 2.90, p &lt; 4.1 × 10−8) and coronary heart disease (CHD) (hazard ratio 3.24, p &lt; 9.3 × 10−6) compared to those who were CHIP−/AgeAccelHG−. In contrast, the other ~60% of CHIP carriers who were AgeAccelHG− were not at increased risk of these outcomes. In summary, CHIP is strongly linked to age acceleration in multiple clocks, and the combination of CHIP and epigenetic aging may be used to identify a population at high risk for adverse outcomes and who may be a target for clinical interventions

Comparison of Proteomic Assessment Methods in Multiple Cohort Studies

Novel proteomics platforms, such as the aptamer-based SOMAscan platform, can quantify large numbers of proteins efficiently and cost-effectively and are rapidly growing in popularity. However, comparisons to conventional immunoassays remain underexplored, leaving investigators unsure when cross-assay comparisons are appropriate. The correlation of results from immunoassays with relative protein quantification is explored by SOMAscan. For 63 proteins assessed in two chronic obstructive pulmonary disease (COPD) cohorts, subpopulations and intermediate outcome measures in COPD Study (SPIROMICS), and COPDGene, using myriad rules based medicine multiplex immunoassays and SOMAscan, Spearman correlation coefficients range from −0.13 to 0.97, with a median correlation coefficient of ≈0.5 and consistent results across cohorts. A similar range is observed for immunoassays in the population-based Multi-Ethnic Study of Atherosclerosis and for other assays in COPDGene and SPIROMICS. Comparisons of relative quantification from the antibody-based Olink platform and SOMAscan in a small cohort of myocardial infarction patients also show a wide correlation range. Finally, cis pQTL data, mass spectrometry aptamer confirmation, and other publicly available data are integrated to assess relationships with observed correlations. Correlation between proteomics assays shows a wide range and should be carefully considered when comparing and meta-analyzing proteomics data across assays and studies