Search bioRxivSearch

Biology subjects

Ho, K.

Publications and source records attributed to Ho, K..

5 recordsLinked to original sources

Cleft lip/palate and educational attainment: cause, consequence, or correlation? A Mendelian randomization study

ImportancePrevious studies have found that children born with a non-syndromic form of cleft lip and/or palate have lower-than-average educational attainment. These differences could be due to a genetic predisposition to low intelligence and academic performance, factors arising due to the cleft phenotype (such as school absence, social stigmatization and impaired speech and language development), or confounding by the prenatal environment. A clearer understanding of this mechanism will inform development of interventions to improve educational attainment in individuals born with a cleft, which could have wide-ranging knock-on effects on their quality of life.\n\nObjectiveTo assess evidence for the hypothesis that common variant genetic liability to non-syndromic cleft lip with or without cleft palate (nsCL/P) influences educational attainment.\n\nDesignUsing summary data from genome-wide association studies (GWAS), we performed Linkage Disequilibrium (LD)-score regression and two-sample Mendelian randomization to evaluate the relationship between genetic liability to nsCL/P (GWAS n=3,987) and educational attainment (GWAS n=766,345), and intelligence (GWAS n=257,828).\n\nResultsThere was little evidence for shared genetic aetiology between nsCL/P and educational attainment (rg -0.03, 95% CI -0.14 to 0.08, P 0.58; {beta}MR 0.002, 95% CI -0.001 to 0.005, P 0.417) or intelligence (rg -0.01, 95% CI -0.12 to 0.10, P 0.85; {beta}MR 0.002, 95% CI -0.010 to 0.014, P 0.669).\n\nConclusions and relevanceCommon genetic variants are unlikely to predispose individuals born with nsCL/P to low educational attainment or intelligence. This information will help tailor clinical-, school-, social- and family-level interventions to improve educational attainment in this group.\n\nKey PointsO_ST_ABSQuestionC_ST_ABSDo children born with a non-syndromic cleft lip with or without palate (nsCL/P) have lower-than average academic achievement because of an underlying genetic predisposition to educational attainment and/or intelligence?\n\nFindingsThere was little evidence for shared common variant genetic correlation between nsCL/P, educational attainment and intelligence.\n\nMeaningCommon genetic variants are unlikely to predispose individuals born with nsCL/P to low educational attainment or intelligence. This information will help tailor clinical-, school-, social- and family-level interventions to improve educational attainment in this group.

genetics

Large-Scale Annotation of Histopathology Images from Social Media

Pathologists are responsible for rapidly providing a diagnosis on critical health issues. Challenging cases benefit from additional opinions of pathologist colleagues. In addition to on-site colleagues, there is an active worldwide community of pathologists on social media for complementary opinions. Such access to pathologists worldwide has the capacity to improve diagnostic accuracy and generate broader consensus on next steps in patient care. From Twitter we curate 13,626 images from 6,351 tweets from 25 pathologists from 13 countries. We supplement the Twitter data with 113,161 images from 1,074,484 PubMed articles. We develop machine learning and deep learning models to (i) accurately identify histopathology stains, (ii) discriminate between tissues, and (iii) differentiate disease states. Area Under Receiver Operating Characteristic is 0.805-0.996 for these tasks. We repurpose the disease classifier to search for similar disease states given an image and clinical covariates. We report precision@k=1 = 0.7618{+/-}0.0018 (chance 0.397{+/-}0.004, mean{+/-}stdev). The classifiers find texture and tissue are important clinico-visual features of disease. Deep features trained only on natural images (e.g. cats and dogs) substantially improved search performance, while pathology-specific deep features and cell nuclei features further improved search to a lesser extent. We implement a social media bot (@pathobot on Twitter) to use the trained classifiers to aid pathologists in obtaining real-time feedback on challenging cases. If a social media post containing pathology text and images mentions the bot, the bot generates quantitative predictions of disease state (normal/artifact/infection/injury/nontumor, pre-neoplastic/benign/ low-grade-malignant-potential, or malignant) and lists similar cases across social media and PubMed. Our project has become a globally distributed expert system that facilitates pathological diagnosis and brings expertise to underserved regions or hospitals with less expertise in a particular disease. This is the first pan-tissue pan-disease (i.e. from infection to malignancy) method for prediction and search on social media, and the first pathology study prospectively tested in public on social media. We will share data through pathobotology.org. We expect our project to cultivate a more connected world of physicians and improve patient care worldwide.

pathology

Spontaneous resistance to phage NPV1 confers increased daptomycin susceptibility in Enterococcus faecalis OG1RF

Enterococcus faecalis is a Gram-positive opportunistic pathogen that inhabits the human gastrointestinal tract. Because of the high frequency of antibiotic resistance among Enterococcus clinical isolates, interest in using phage to treat enterococcal infections and to decolonize high-risk patients for antibiotic-resistant Enterococcus is rising. Bacteria can evolve phage resistance, but there is little published information on these mechanisms in E. faecalis. In this report, we identified genetic determinants of E. faecalis resistance to {phi}NPV1. We found that loss-of-function mutations in epaR confer {phi}NPV1 resistance by blocking phage adsorption. We attribute the inability of the phage to adsorb to the modification or loss of an extracellular polymer in strains with inactivated epaR. Phage-resistant epaR mutants exhibited increased daptomycin and osmotic stress susceptibilities. Our results demonstrate that in vitro spontaneous resistance to {phi}NPV1 comes at a cost in E. faecalis OG1RF.

microbiology

Distinct Blood DNA Methylation Profiles In Subtypes Of Orofacial Cleft

BackgroundThere is evidence that different subtypes of orofacial cleft have distinct aetiologies, although the precise molecular mechanisms underlying these are unknown. Given the key role of epigenetic processes such as DNA methylation in embryonic development, it is likely that aberrant DNA methylation may also play a part in the development of orofacial clefts.\n\nMethodsIn this study, we explored whether blood samples from children with different cleft subtypes showed distinct DNA methylation profiles.\n\nIn whole blood samples from 150 children from the Cleft Collective cohort study, we measured DNA methylation at over 450,000 sites on the genome. We then carried out epigenome-wide association studies (EWAS) to test the association between methylation at each site and cleft subtype (cleft lip only CLO n=50; cleft palate only CPO n=50; cleft lip and palate CLP n=50).\n\nResultsWe found four genomic regions differentially methylated in CLO compared to CLP, 17 in CPO compared to CLP and 294 in CPO compared to CLO. These regions included several mapping to genes that have previously been implicated in the development of orofacial clefts (for example, TBX1, COL11A2, HOXA2, PDGFRA) and over 250 novel associations.\n\nConclusionOur finding of distinct methylation profiles in different cleft subtypes might reflect differences in their aetiologies, with DNA methylation either playing a causal role in development of OFC subtypes or reflecting causal genetic or environmental factors.

epidemiology

Analytical and Clinical Validity Study of FirstStepDx PLUS: A Chromosomal Microarray Optimized for Patients with Neurodevelopmental Conditions

IntroductionChromosomal microarray analysis (CMA) is recognized as the first-tier test in the genetic evaluation of children with developmental delays, intellectual disabilities, congenital anomalies and autism spectrum disorders of unknown etiology.\n\nArray DesignTo optimize detection of clinically relevant copy number variants associated with these conditions, we designed a whole-genome microarray, FirstStepDx PLUS (FSDX). A set of 88,435 custom probes was added to the Affymetrix CytoScanHD platform targeting genomic regions strongly associated with these conditions. This combination of 2,784,985 total probes results in the highest probe coverage and clinical yield for these disorders.\n\nResults and DiscussionClinical testing of this patient population is validated on DNA from either non-invasive buccal swabs or traditional blood samples. In this report we provide data demonstrating the analytic and clinical validity of FSDX and provide an overview of results from the first 7,570 consecutive patients tested clinically. We further demonstrate that buccal sampling is an effective method of obtaining DNA samples, which may provide improved results compared to traditional blood sampling for patients with neurodevelopmental disorders who exhibit somatic mosaicism.\n\nClinical scenarioNeurodevelopmental disabilities, including developmental delays (DD), intellectual disabilities (ID), and autism spectrum disorders (ASD), affect up to 15% of children (1). In the majority of cases, a childs clinical presentation does not allow for a definitive etiological diagnosis. In such cases, CMA is recommended as the first-tier test that should be used to evaluate for a potential genetic etiology (2-7). A definitive genetic diagnosis allows patients to more often receive appropriate medical care tailored to their condition, as reflected by medical management changes and improved access to necessary support and educational services (8-13).\n\nTest descriptionFirstStepDx PLUS (FSDX) is an optimized clinical microarray test provided in the context of a comprehensive clinical service. Testing starts with either a non-invasive buccal swab sample or traditional blood sample from which DNA extraction using a Gentra Puregene(R) kit specific to the sample type (Qiagen, Inc., Valencia, CA) is performed in one of several contracted CLIA/CAP credentialed laboratories according to manufacturers protocols. High quality genomic DNA is fragmented, labeled and hybridized to FSDX arrays using reagents, equipment and methodology as specified by by the manufacturer (Affymetrix, Inc., Santa Clara, CA)(14). Washed arrays are scanned and raw data files are processed to CYCHP files using a reference file comprising at least 100 samples with normal array findings. Data analysis is performed using Chromosome Analysis Suite software version 2.0.1 (Affymetrix). Hybridization of patient DNA to oligonucleotide and SNP probes is independently compared against a previously analyzed cohort of normal samples to call CNVs and allele genotypes. The percentage mosaicism of whole-chromosome aneuploidies is determined using the average log2 ratio of the entire chromosome (14).\n\nMicroarray designFSDX was optimized by the addition of 88,435 custom probes targeting genomic regions strongly associated with ID/DD/ASD (15-24). This was effected, under GMP by Affymetrix, to the CytoScanHD platform using their microarray design process specifications which have been previously described (14). This is consistent with the ACMG recommendation of \"enrichment of probes targeting dosage-sensitive genes known to result in phenotypes consistent with common indications for a genomic screen\" (25). Critical regions that did not meet a desired probe density [≥]1 probe/1000 bp on the CytoScanHD were supplemented with additional probe content to allow for improved detection of smaller deletions and duplications in these critical regions. Finally, additional probes were added to improve detection of CNVs encompassing genes involved in other well-characterized neurodevelopmental disorders, for example GAMT (26) and GATM (27). All incremental probes were added in substitution for probes deemed sub-optimal by Affymetrix and previously masked, bringing FSDX to a grand total of 2,784,985 probes. Custom SNP probes (n =416) on FSDX are targeted by 12 oligonucleotides, three for each strand of each allele, which is approximately double the typical probe coverage for SNPs.\n\nTest interpretationCYCHP files are evaluated by ABMG certified cytogeneticists. Determination of CNVs is consistent with established cytogenetic standards. A minimum of 25-consecutive impacted probes is the baseline determinant for deletions and 50 probes for duplications independent of variant size. Rare CNVs are determined to be \"pathogenic\" if there is sufficient evidence published (at least two independent publications) to indicate that haploinsufficiency or triplosensitivity of the region or gene(s) involved is causative of clinical features or of sufficient overall size (28). If however, there is insufficient but at least preliminary evidence for a causative role for the region or gene(s) therein they are classified as variants of unknown significance (VOUS) independent of CNV size. Areas of absence of heterozygosity (AOH) are also classed as VOUS if of sufficient size and location to increase the risk for conditions with autosomal recessive inheritance or conditions with parent-of-origin/imprinting effects. Other CNVs are typically not reported after determination that they most likely represent normal common population variants and are contained in databases documenting presumptively benign CNVs, e.g., the Database of Genomic Variants (DGV) (29). These parameters were standard independent of the microarray used for analysis in comparative studies.\n\nPublic health importanceA definitive genetic diagnosis facilitates patient access to appropriate and necessary medical and support services. Defining the underlying genetic cause of DD/ID/ASD and/or multiple congenital anomalies (MCA) in each unique patient is vital to understanding etiology, prognosis, and course. It informs physicians of potential comorbid conditions for which a patient should be evaluated and treated proactively and optimally. Improved understandings of the appropriate therapeutic and behavioral approaches to that patient are also enabled. Genetic testing is best provided in the context of an integrated service (30), so FSDX provides comprehensive, clear, readable, and personalized reports for the healthcare provider and a family-friendly section to facilitate understanding of the often-complex results. The report is complemented by availability of pre- and post-test genetic counseling and technical support to providers. Moreover, FSDX includes personalized insurance pre-authorization and appeals assistance to overcome barriers encountered by both providers and families that, in many circumstances, prevent access to crucial genetic testing services (10-11).\n\nPublished reviews, recommendations and guidelinesThe American College of Medical Genetics (ACMG) (2,3), the American Academy of Child and Adolescent Psychiatry (4,7), the American Academy of Pediatrics (5), and the American Academy of Neurology/Child Neurology Society (6) recommend CMA as the first-tier test in the genetic evaluation of children with unexplained DD, ID, or ASD. Considerable data supporting these guidelines are documented in numerous reviews and publications (31-36). The ACMG has also published guidelines on both array design (25) and the validation of arrays, including validation of a new version of a platform in use by the laboratory from the same manufacturer, and of additional sample types (28).

genomics