Gillian E. Hanley

Dr. Gillian E. Hanley

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Research Focus & Metrics

Academic Career Length

21Years (2006-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 May 2014 in American Journal of Obstetrics and Gynecology
Verified
Journal Article
Closed access
JMJessica N. McAlpine
Jessica N. McAlpine
GHGillian E. Hanley
Gillian E. Hanley
MWMichelle M.M. Woo
Michelle M.M. Woo
ATAlicia A. Tone
Alicia A. Tone
NRNirit Rozenberg
Nirit Rozenberg
DMDianne M. Miller
Dianne M. Miller

20 July 2011 in Pharmacoepidemiology and Drug Safety
Verified
Journal Article
Closed access
PDF file
JDJamie R. Daw
Jamie R. Daw
GHGillian E. Hanley
Gillian E. Hanley
DGDevon L. Greyson
Devon L. Greyson
SMSteven G. Morgan
Steven G. Morgan

1 March 2017 in Obstetrics & Gynecology
Verified
Journal Article
Closed access
PDF file
GHGillian E. Hanley
Gillian E. Hanley
JHJennifer A. Hutcheon
Jennifer A. Hutcheon
BKBrooke A. Kinniburgh
Brooke A. Kinniburgh
LLLily Lee
Lily Lee
OBJECTIVE: To examine the association between interpregnancy interval and maternal–neonate health when matching women to their successive pregnancies to control for differences in maternal risk factors and compare these results with traditional unmatched designs. METHODS: We conducted a retrospective cohort study of 38,178 women with three or more deliveries (two or greater interpregnancy intervals) between 2000 and 2015 in British Columbia, Canada. We examined interpregnancy interval (0–5, 6–11, 12–17, 18–23 [reference], 24–59, and 60 months or greater) in relation to neonatal outcomes (preterm birth [less than 37 weeks of gestation], small-for-gestational-age birth [less than the 10th centile], use of neonatal intensive care, low birth weight [less than 2,500 g]) and maternal outcomes (gestational diabetes, beginning the subsequent pregnancy obese [body mass index 30 or greater], and preeclampsia–eclampsia). We used conditional logistic regression to compare interpregnancy intervals within the same mother and unconditional (unmatched) logistic regression to enable comparison with prior research. RESULTS: Analyses using the traditional unmatched design showed significantly increased risks associated with short interpregnancy intervals (eg, there were 232 preterm births [12.8%] in 0–5 months compared with 501 [8.2%] in the 18–23 months reference group; adjusted odds ratio [OR] for preterm birth 1.53, 95% confidence interval [CI] 1.35–1.73). However, these risks were eliminated in within-woman matched analyses (adjusted OR for preterm birth 0.85, 95% CI 0.71–1.02). Matched results indicated that short interpregnancy intervals were significantly associated with increased risk of gestational diabetes (adjusted OR 1.35, 95% CI 1.02–1.80 for 0–5 months) and beginning the subsequent pregnancy obese (adjusted OR 1.61, 95% CI 1.05–2.45 for 0–5 months and adjusted OR 1.43, 95% CI 1.10–1.87 for 6–11 months). CONCLUSION: Previously reported associations between short interpregnancy intervals and adverse neonatal outcomes may not be causal. However, short interpregnancy interval is associated with increased risk of gestational diabetes and beginning a subsequent pregnancy obese.

9 February 2022 in JAMA Network Open
Verified
Journal Article
Open access
PDF file
GHGillian E. Hanley
Gillian E. Hanley
CPCeleste Leigh Pearce
Celeste Leigh Pearce
ATAline Talhouk
Aline Talhouk
JKJanice S. Kwon
Janice S. Kwon
SFSarah J. Finlayson
Sarah J. Finlayson
DMDianne Miller
Dianne Miller
Approximately 70% of sporadic and nearly all ovarian cancers in BRCA variant carriers are high-grade serous carcinomas (HGSCs),1 which is the most lethal of the 5 main histotypes and has a 5-year survival rate less than 50%.2 Although the general population lifetime risk of ovarian cancer is 1.4%,3 individuals with an inherited germline BRCA1 or BRCA2 variant have average cumulative risks of 40% to 75% and 8% to 34%, respectively.4 In BRCA 1/2 variant carriers, bilateral salpingo-oophorectomy is recommended, which reduces the risk of ovarian or fallopian tube cancers by 80%.5 Removal of the ovaries is not recommended for the general population because it is associated with increased total mortality, coronary heart disease, and osteoporosis.6 Thus, a different preventive strategy is needed for individuals at average risk, who account for 80% of cases of HGSCs.

2 April 2016 in BMC Pregnancy and Childbirth
Verified
Journal Article
Open access
PDF file
GHGillian E. Hanley
Gillian E. Hanley
SMSarah Munro
Sarah Munro
DGDevon Greyson
Devon Greyson
MGMechthild M. Gross
Mechthild M. Gross
VHVanora Hundley
Vanora Hundley
PJPatricia A. Janssen
Patricia A. Janssen
The diagnosis of labor onset has been described as one of the most important judgments in maternity care. There is compelling evidence that the duration of both latent and active phase labor are clinically important and require consistent approaches to measurement. In order to measure the duration of labor phases systematically, we need standard definitions of their onset. We reviewed the literature to examine definitions of labor onset and the evidentiary basis provided for these definitions. Five electronic databases were searched using predefined search terms. We included English, French and German language studies published between January 1978 and March 2014 defining the onset of latent labor and/or active labor in a population of healthy women with term births. Studies focusing exclusively on induced labor were excluded. We included 62 studies. Four ‘types’ of labor onset were defined: latent phase, active phase, first stage and unspecified. Labor onset was most commonly defined through the presence of regular painful contractions (71 % of studies) and/or some measure of cervical dilatation (68 % of studies). However, there was considerable discrepancy about what constituted onset of labor even within ‘type’ of labor onset. The majority of studies did not provide evidentiary support for their choice of definition of labor onset. There is little consensus regarding definitions of labor onset in the research literature. In order to avoid misdiagnosis of the onset of labor and identify departures from normal labor trajectories, a consistent and measurable definition of labor onset for each phase and stage is essential. In choosing standard definitions, the consequences of their use on rates of maternal and fetal morbidity must also be examined.

1 January 2019 in JAMA Pediatrics
Verified
Journal Article
Closed access
PDF file
LPLief Pagalan
Lief Pagalan
CBCeleste Bickford
Celeste Bickford
WWWhitney Weikum
Whitney Weikum
BLBruce Lanphear
Bruce Lanphear
MBMichael Brauer
Michael Brauer
MWMeghan Winters
Meghan Winters
Importance The etiology of autism spectrum disorder (ASD) is poorly understood, but prior studies suggest associations with airborne pollutants. Objective To evaluate the association between prenatal exposures to airborne pollutants and ASD in a large population-based cohort. Design, Setting, and Participants This population-based cohort encompassed nearly all births in Metro Vancouver, British Columbia, Canada, from 2004 through 2009, with follow-up through 2014. Children were diagnosed with ASD using a standardized assessment with the Autism Diagnostic Interview–Revised and Autism Diagnostic Observation Schedule. Monthly mean exposures to particulate matter with a diameter less than 2.5 µm (PM2.5), nitric oxide (NO), and nitrogen dioxide (NO2) at the maternal residence during pregnancy were estimated with temporally adjusted, high-resolution land use regression models. The association between prenatal air pollution exposures and the odds of developing ASD was evaluated using logistic regression adjusted for child sex, birth month, birth year, maternal age, maternal birthplace, and neighborhood-level urbanicity and income band. Data analysis occurred from June 2016 to May 2018. Exposures Mean monthly concentrations of ambient PM2.5, NO, and NO2at the maternal residence during pregnancy, calculated retrospectively using temporally adjusted, high-resolution land use regression models. Main Outcomes and Measures Autism spectrum disorder diagnoses based on standardized assessment of the Autism Diagnostic Interview–Revised and Autism Diagnostic Observation Schedule. The hypothesis being tested was formulated during data collection. Results In a cohort of 132 256 births, 1307 children (1.0%) were diagnosed with ASD by the age of 5 years. The final sample size for the PM2.5-adjusted model was 129 439 children, and for NO and NO2, it was 129 436 children; of these, 1276 (1.0%) were diagnosed with ASD. Adjusted odds ratios for ASD per interquartile range (IQR) were not significant for exposure to PM2.5during pregnancy (1.04 [95% CI, 0.98-1.10] per 1.5 μg/m3increase [IQR] in PM2.5) or NO2(1.06 [95% CI, 0.99-1.12] per 4.8 ppb [IQR] increase in NO2) but the odds ratio was significant for NO (1.07 [95% CI, 1.01-1.13] per 10.7 ppb [IQR] increase in NO). Odds ratios for male children were 1.04 (95% CI, 0.98-1.10) for PM2.5; 1.09 (95% CI, 1.02-1.15) for NO; and 1.07 (95% CI, 1.00-1.13) for NO2. For female children, they were for 1.03 (95% CI, 0.90-1.18) for PM2.5; 0.98 (95% CI, 0.83-1.13) for NO; and 1.00 (95% CI, 0.86-1.16) for NO2. Conclusions and Relevance In a population-based birth cohort, we detected an association between exposure to NO and ASD but no significant association with PM2.5and NO2.