Validation of self-reported weights and heights in the avoiding diabetes after pregnancy trial (ADAPT)

Background: Randomized controlled trials that test the effectiveness of mobile health-based weight loss programs are attractive to participants, funders, and researchers because of the low implementation cost, minimal participant burden, and the ability to recruit participants from longer distances. Collecting weight data from geographically dispersed participants is a challenge. Relying on participant self-report is one approach to data collection, but epidemiologic studies indicate that self-reported anthropometric data may be inaccurate. Methods: We provided women enrolled in a randomized controlled trial (RCT) of postpartum weight loss after gestational diabetes with a digital scale and training to collect and report weight via a web-based survey. To validate self-reported weights and heights, we visited 30 randomly selected women in their homes, with a reference scale and stadiometer, a mean of 34 days after the self-report. We ran linear regression models to identify characteristics that were associated with underreporting or overreporting of anthropometric measures. Results: Of the 30 women we visited, 11 women (37%) were assigned to the weight loss intervention group and 19 women (63%) were in the control group. Mean age was 38.5 years (SD 4.5). The overall mean difference between participants’ self-reported weights and the weights obtained at their home visit was 0.70 kg (+1.92). Women assigned to the intervention group underreported their weight in comparison with the control group by 1.29 kg (95% CI −2.52, −0.06). The overall difference in collected to self-reported height was −0.56 cm (±1.91). No characteristics were associated with underreporting or overreporting of height. Conclusions: Our research suggests that by providing a digital scale and developing a weight collection protocol, researchers can train women to collect and record their own study weights with reasonable validity. To achieve the level of validity required for clinical trials, researchers should consider additional strategies to assure the validity of the data. Trial registration NCT01923350

Erratum: Author Correction: Identification of genes required for eye development by high-throughput screening of mouse knockouts.

[This corrects the article DOI: 10.1038/s42003-018-0226-0.]

Identification of genes required for eye development by high-throughput screening of mouse knockouts.

Despite advances in next generation sequencing technologies, determining the genetic basis of ocular disease remains a major challenge due to the limited access and prohibitive cost of human forward genetics. Thus, less than 4,000 genes currently have available phenotype information for any organ system. Here we report the ophthalmic findings from the International Mouse Phenotyping Consortium, a large-scale functional genetic screen with the goal of generating and phenotyping a null mutant for every mouse gene. Of 4364 genes evaluated, 347 were identified to influence ocular phenotypes, 75% of which are entirely novel in ocular pathology. This discovery greatly increases the current number of genes known to contribute to ophthalmic disease, and it is likely that many of the genes will subsequently prove to be important in human ocular development and disease

Identification of genes required for eye development by high-throughput screening of mouse knockouts

International audienc

Identification of genes required for eye development by high-throughput screening of mouse knockouts.

Despite advances in next generation sequencing technologies, determining the genetic basis of ocular disease remains a major challenge due to the limited access and prohibitive cost of human forward genetics. Thus, less than 4,000 genes currently have available phenotype information for any organ system. Here we report the ophthalmic findings from the International Mouse Phenotyping Consortium, a large-scale functional genetic screen with the goal of generating and phenotyping a null mutant for every mouse gene. Of 4364 genes evaluated, 347 were identified to influence ocular phenotypes, 75% of which are entirely novel in ocular pathology. This discovery greatly increases the current number of genes known to contribute to ophthalmic disease, and it is likely that many of the genes will subsequently prove to be important in human ocular development and disease

Erratum: Author Correction: Identification of genes required for eye development by high-throughput screening of mouse knockouts.

[This corrects the article DOI: 10.1038/s42003-018-0226-0.]