Research Center Ste Justine

Montréal, Canada

Research Center Ste Justine

Montréal, Canada
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Feldman D.E.,University of Montréal | Feldman D.E.,McGill University | Vinet E.,McGill University | Sylvestre M.-P.,University of Montréal | And 5 more authors.
Rheumatology (United Kingdom) | Year: 2017

Objective. The aim was to evaluate the prevalence of postpartum complications, including depression, in new mothers who had juvenile idiopathic arthritis (JIA) and to assess whether these differ from mothers who never had JIA. Methods. Our cohort study used data from physician billing and hospitalizations covering Quebec, Canada. We identified females with JIA with a first-time birth between 1 January 1983 and 31 December 2010 and assembled a control cohort of first-time mothers without JIA from the same administrative data, matching 4:1 for date of first birth, maternal age and area of residence. We compared the following postpartum complications: major puerperal infection, anaesthetic complications, postpartum haemorrhage, thromboembolism, obstetrical trauma, complications of obstetrical surgical wounds and maternal depression in the first year after delivery, in the JIA vs non-JIA groups, using bivariate analysis and multiple logistic regression. Results. The mean age at delivery was 24.7 years in the JIA group (n = 1681) and 25.0 years for the non-JIA group (n = 6724). Mothers with JIA were more likely to experience complications attributable to anaesthetic [adjusted risk ratio (aRR) 2.17, 95% CI; 1.05, 4.48], postpartum haemorrhage (aRR = 2.75, 95% CI: 2.42, 3.11) and thromboembolism (aRR = 5.27, 95% CI: 1.83, 15.17) but were at lower risk for obstetrical trauma (aRR = 0.78, 95% CI: 0.64, 0.95) or newly to develop depression in the first year postpartum (aRR = 0.52, 95% CI: 0.40, 0.68).Conclusion. Mothers with JIA appear to be at higher risk for complications attributable to anaesthesia, postpartum haemorrhage and thromboembolism. Prevention strategies for postpartum haemorrhage and thromboembolism may be especially important in this population. © The Author 2017. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved.


Honore J.-C.,Research Center Ste Justine | Honore J.-C.,University of Montréal | Kooli A.,Research Center Ste Justine | Kooli A.,McGill University | And 15 more authors.
Arteriosclerosis, Thrombosis, and Vascular Biology | Year: 2013

OBJECTIVE - : Nitro-oxidative stress exerts a significant role in the genesis of hypoxic-ischemic (HI) brain injury. We previously reported that the ω-6 long chain fatty acids, transarachidonic acids (TAAs), which are nitrative stress-induced nonenzymatically generated arachidonic acid derivatives, trigger selective microvascular endothelial cell death in neonatal neural tissue. The primary molecular target of TAAs remains unidentified. GPR40 is a G protein-coupled receptor activated by long chain fatty acids, including ω-6; it is highly expressed in brain, but its functions in this tissue are largely unknown. We hypothesized that TAAs play a significant role in neonatal HI-induced cerebral microvascular degeneration through GPR40 activation. APPROACH AND RESULTS - : Within 24 hours of a HI insult to postnatal day 7 rat pups, a cerebral infarct and a 40% decrease in cerebrovascular density was observed. These effects were associated with an increase in nitrative stress markers (3-nitrotyrosine immunoreactivity and TAA levels) and were reduced by treatment with nitric oxide synthase inhibitor. GPR40 was expressed in rat pup brain microvasculature. In vitro, in GPR40-expressing human embryonic kidney (HEK)-293 cells, [C]-14E-AA (radiolabeled TAA) bound specifically, and TAA induced calcium transients, extracellular signal-regulated kinase 1/2 phosphorylation, and proapoptotic thrombospondin-1 expression. In vivo, intracerebroventricular injection of TAAs triggered thrombospondin-1 expression and cerebral microvascular degeneration in wild-type mice, but not in GPR40-null congeners. Additionally, HI-induced neurovascular degeneration and cerebral infarct were decreased in GPR40-null mice. CONCLUSIONS - : GPR40 emerges as the first identified G protein-coupled receptor conveying actions of nonenzymatically generated nitro-oxidative products, specifically TAAs, and is involved in (neonatal) HI encephalopathy. © 2013 American Heart Association, Inc.


PubMed | Research Center Ste Justine
Type: Journal Article | Journal: Arteriosclerosis, thrombosis, and vascular biology | Year: 2013

Nitro-oxidative stress exerts a significant role in the genesis of hypoxic-ischemic (HI) brain injury. We previously reported that the -6 long chain fatty acids, transarachidonic acids (TAAs), which are nitrative stress-induced nonenzymatically generated arachidonic acid derivatives, trigger selective microvascular endothelial cell death in neonatal neural tissue. The primary molecular target of TAAs remains unidentified. GPR40 is a G protein-coupled receptor activated by long chain fatty acids, including -6; it is highly expressed in brain, but its functions in this tissue are largely unknown. We hypothesized that TAAs play a significant role in neonatal HI-induced cerebral microvascular degeneration through GPR40 activation.Within 24 hours of a HI insult to postnatal day 7 rat pups, a cerebral infarct and a 40% decrease in cerebrovascular density was observed. These effects were associated with an increase in nitrative stress markers (3-nitrotyrosine immunoreactivity and TAA levels) and were reduced by treatment with nitric oxide synthase inhibitor. GPR40 was expressed in rat pup brain microvasculature. In vitro, in GPR40-expressing human embryonic kidney (HEK)-293 cells, [(14)C]-14E-AA (radiolabeled TAA) bound specifically, and TAA induced calcium transients, extracellular signal-regulated kinase 1/2 phosphorylation, and proapoptotic thrombospondin-1 expression. In vivo, intracerebroventricular injection of TAAs triggered thrombospondin-1 expression and cerebral microvascular degeneration in wild-type mice, but not in GPR40-null congeners. Additionally, HI-induced neurovascular degeneration and cerebral infarct were decreased in GPR40-null mice.GPR40 emerges as the first identified G protein-coupled receptor conveying actions of nonenzymatically generated nitro-oxidative products, specifically TAAs, and is involved in (neonatal) HI encephalopathy.

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