Leadership gender disparity in the fifty highest ranking North American universities: Thematic analysis under a theoretical lens.

BACKGROUND: Despite changes in the discourse around gender distributions within academic leadership, women continue to be under-represented in academia. Our study aims to identify the extent of gender disparity in the academic leadership in the top 50 North American universities and to critically analyse the contributing factors through a comprehensive theoretical framework. METHODS: We adopted the theoretical framework of leadership continuum model. A retrospective analysis of the gender of the leadership ranks was conducted between December 2018 and March 2019 for the top 50 universities in North America (2019 Quacquarelli Symonds World University Ranking system). The leadership hierarchy was classified into six tiers. RESULTS: A total of 5806 faculty members from 45 US and five Canadian universities were included. Women were overall less likely to be in a senior leadership role than men (48.7% vs 51.3%; p value=0.05). Women accounted for fewer positions than men for resident/chancellor (23.8% vs 76.2%; p value<0.001), vice-president/vice-chancellor (36.3% vs 63.7%; p value<0.001), vice provost (42.7% vs 57.3%; p value=0.06), dean (38.5% vs 61.5%; p value<0.001) and associate dean (48.2% vs 51.8%; p-value=0.05). Women however were in a greater proportion in the assistant dean positions (63.8% vs 36.2%; p value<0.001). CONCLUSION: Leadership gender imbalance is trans-organisational and transnational within the top 50 universities of North America and progressively widens towards the top leadership pyramid. This correlates with the lack of women leadership progress and sustainability in later cycles of the leadership continuum model (beyond assistant dean).

Adherence to national paediatric bronchiolitis management guidelines and impact on emergency department resource utilization.

Objective: To evaluate the association between the use of nonrecommended pharmacology (salbutamol and corticosteroids) per national bronchiolitis guidelines, either during the index visit or at discharge, and system utilization measures (frequency of return visits [RTED] and on paediatric emergency department [PED] length of stay [LOS]). Study Design: We conducted a retrospective case control study of 185 infants (≤12 months old) who presented to the PED between December 2014 and April 2017 and discharged home with a clinical diagnosis of bronchiolitis. Inclusion criteria included ≥ 1 viral prodromal symptom and ≥ 1 physical exam finding of respiratory distress. Cases were defined as infants who had ≥ 1 RTED within 7 days of their index visit and controls were matched for age and acuity but without RTED. Logistic regression analysis and multivariable linear regression were used to assess the odds of RTED and PED LOS associated with nonadherence to pharmaceutical recommendations per AAP and CPS bronchiolitis guidelines. Results: Use of nonrecommended pharmacology per national bronchiolitis guidelines was documented among 39% of the 185 study participants. Adjusting for acuity of index visit, age, severe tachypnea, oxygen desaturation, and dehydration, use of nonrecommended pharmacology was not associated with RTED (odds ratio [OR]: 0.98, 95% confidence interval [CI]: 0.47 to 2.03). Use of salbutamol and corticosteroids, however, were each independently associated with increased PED LOS (58.3 minutes [P=0.01] and 116.7 minutes [P<0.001], respectively). Conclusion: Nonadherence to the pharmaceutical recommendations of national bronchiolitis guidelines was not associated with RTED but salbutamol and corticosteroid use increased PED LOS.

Utility of MyHEARTSMAP for Universal Psychosocial Screening in the Emergency Department.

OBJECTIVES: To evaluate the utility of universal psychosocial screening in the emergency department (ED) using MyHEARTSMAP, a digital self-assessment and management guiding tool. STUDY DESIGN: We conducted a cohort study of youth 10-17 years of age with nonmental health related presentations at 2 pediatric EDs. On randomly selected shifts (December 2017-February 2019), participants completed their psychosocial self-assessments using MyHEARTSMAP on a mobile device, then underwent a standardized clinical mental health assessment (criterion standard). We reported the sensitivity and specificity of respondents' self-assessment, against a clinician's standard emergency psychosocial assessment, and the frequency of psychosocial issues and recommended mental health resources identified by screening. RESULTS: We approached 1432 eligible youth, among which 795 youth consented to participate (55.5%). Youth and guardians' sensitivity at self-identifying psychiatric concerns was 92.7% (95% CI 89.1, 95.4%) and 93.1% (95% CI 89.5, 95.8%), respectively. In cases where clinicians had determined to be no psychiatric issues, 98.5% (95% CI 96.7, 99.4%) of youth and 98.9% (95% CI 97.3, 99.7%) of guardians identified the youth as having no or only mild issues. Screening identified 36.4% of youth as having issues in at least 1 psychosocial domain which warranted further follow-up. CONCLUSIONS: Psychosocial screening in EDs using MyHEARTSMAP can reliably be conducted using the MyHEARTSMAP self-assessment tool and over one-third of screened youth identified issues which can be directed to further care.

Ascertainment Bias in the Association Between Elevated Lipoprotein(a) and Familial Hypercholesterolemia.

BACKGROUND: Lipoprotein(a) is an atherogenic low-density lipoprotein-like particle and circulating levels are largely determined by genetics. Patients with familial hypercholesterolemia (FH) have elevated lipoprotein(a); however, it remains unclear why. OBJECTIVES: This study compared the levels of lipoprotein(a) and associated genetic factors between individuals that were ascertained for FH clinically versus genetically. METHODS: We investigated causes of elevated lipoprotein(a) in individuals with clinically diagnosed FH (FH cohort, n = 391) and in individuals with genetically diagnosed FH from the general population (UK Biobank; n = 37,486). RESULTS: Patients in the FH cohort had significantly greater lipoprotein(a) levels than either the general population or non-FH dyslipidemic patients. This was accounted for by increased frequency of the rs10455872-G LPA risk allele (15.1% vs. 8.8%; p < 0.05). However, within the FH cohort, lipoprotein(a) levels did not differ based on the presence or absence of an FH-causing variant (means = 1.43 log mg/dl vs. 1.42 log mg/dl; p = 0.97). Lipoprotein(a) levels were also not statistically different between individuals with and without an FH-causing variant in the UK Biobank cohort, which represents a population sample not biased to cardiovascular ascertainment (n = 221 vs. 37,486). We performed a phenome-wide association study between LPA genotypes and 19,202 phenotypes to demonstrate that elevated lipoprotein(a) is associated with increased low-density lipoprotein cholesterol, a family history of cardiovascular disease, premature coronary artery disease, and a diagnosis of FH. CONCLUSIONS: These results suggest that FH does not cause elevated lipoprotein(a), but that elevated lipoprotein(a) increases the likelihood that an individual with genetic FH will be clinically recognized.

Risk of Premature Atherosclerotic Disease in Patients With Monogenic Versus Polygenic Familial Hypercholesterolemia.

BACKGROUND: A pathogenic variant in LDLR, APOB, or PCSK9 can be identified in 30% to 80% of patients with clinically-diagnosed familial hypercholesterolemia (FH). Alternatively, ∼20% of clinical FH is thought to have a polygenic cause. The cardiovascular disease (CVD) risk associated with polygenic versus monogenic FH is unclear. OBJECTIVES: This study evaluated the effect of monogenic and polygenic causes of FH on premature (age <55 years) CVD events in patients with clinically diagnosed FH. METHODS: Targeted sequencing of genes known to cause FH as well as common genetic variants was performed to calculate polygenic scores in patients with "possible," "probable," or "definite" FH, according to Dutch Lipid Clinic Network Criteria (n = 626). Patients with a polygenic score ≥80th percentile were considered to have polygenic FH. We examined the risk of unstable angina, myocardial infarction, coronary revascularization, or stoke. RESULTS: A monogenic cause of FH was associated with significantly greater risk of CVD (adjusted hazard ratio: 1.96; 95% confidence interval: 1.24 to 3.12; p = 0.004), whereas the risk of CVD in patients with polygenic FH was not significantly different compared with patients in whom no genetic cause of FH was identified. However, the presence of an elevated low-density lipoprotein cholesterol (LDL-C) polygenic risk score further increased CVD risk in patients with monogenic FH (adjusted hazard ratio: 3.06; 95% confidence interval: 1.56 to 5.99; p = 0.001). CONCLUSIONS: Patients with monogenic FH and superimposed elevated LDL-C polygenic risk scores have the greatest risk of premature CVD. Genetic testing for FH provides important prognostic information that is independent of LDL-C levels.