Achieving quality primary care data: a description of the Canadian Primary Care Sentinel Surveillance Network data capture, extraction, and processing in Alberta.

INTRODUCTION: Electronic medical record (EMR) databases have become increasingly popular for secondary purposes, such as health research. The Canadian Primary Care Sentinel Surveillance Network (CPCSSN) is the first and only pan-Canadian primary care EMR data repository, with de-identified health information for almost two million Canadians. Comprehensive and freely available documentation describing the data 'lifecycle' is important for assessing potential data quality issues and appropriate interpretation of research findings. Here, we describe the flow and transformation of CPCSSN data in the province of Alberta. APPROACH: In Alberta, the data originate from 54 publicly-funded primary care settings, including one community pediatric clinic, with 318 providers contributing de-identified EMR data for 410,951 patients (as of December 2018). Data extraction methods have been developed for five different EMR systems, and include both backend and automated frontend extractions. The raw EMR data are transformed according to specific rules, including trimming implausible values, converting values and free text to standard terminologies or classification systems, and structuring the data into a common CPCSSN format. Following local data extraction and processing, the data are transferred to a central repository and made available for research and disease surveillance. CONCLUSION: This paper aims to provide important contextual information to future CPCSSN data users.

Fused eyelids in premature infants.

The charts of 161 extremely premature newborns were reviewed to characterize and report the incidence of infants born with fused eyelids, to determine when postbirth eyelid dysjunction occurs, and to address the survivability of these infants. Logistic regression analysis was used to examine the relationship between various ophthalmic outcomes and possible predictors of these outcomes. For babies born with eyelids fused, Cox regression analysis was used to assess time to eyelid opening. From the analysis of our data, we found that the critical time for eyelid opening is between 25.5 and 26.5 weeks gestational age. If fused at birth, the average time to eyelid opening after birth was 5.5 days. Fifty-two percent of babies born with their eyelids fused survived to be discharged from the hospital, compared to 83% of those born with eyelids open. Gestational age was found to be the most important predictor of the status of the eyelids at birth, of survival, and of the presence of retinopathy of prematurity (ROP). Other variables were found to be significant, but the significance was lost once the variable was adjusted for gestational age.

The 56 kDa androgen-binding protein in human genital skin fibroblasts: its relation to the human androgen receptor.

We have recently described in genital skin fibroblasts (GSF) a relatively abundant 56 kDa protein with androgen-binding activity. This protein is missing in GSF of most patients with complete androgen insensitivity syndrome (CAI). The protein has many characteristics compatible with the androgen receptor; it has in fact been tentatively considered as a precursor or degradation form of the prototypic (approximately 100 kDa) human androgen receptor. We have prepared an antiserum to this protein, which allowed us to detect it as a direct product by in vitro translation of mRNA from GSF. It is thus very unlikely to be a degradation product of a larger precursor. Furthermore, covalent photolytic labeling of this protein with the androgen analogue [3H]mibolerone revealed a much lower affinity for this protein than is known for the androgen receptor. Finally, the GSF of two exceptional patients with complete androgen insensitivity syndrome due to negligible androgen receptor-binding activity express this protein normally, as determined on two-dimensional gels by Western blot analysis with the antiserum and by photolytic covalent labeling with androgen analogues. These data indicate that the protein is not a precursor or a degradation product of the receptor; nor is it androgen-induced. They are more compatible with the idea that the protein is another member of the steroid/thyroid/retinoic acid receptor supergene family, perhaps as an unorthodox product of the human androgen receptor gene.