5 research outputs found
From Periphery to Core (and Back)? Political, Journalistic, and Academic Perceptions of Celtic Tiger- and post-Celtic Tiger-Ireland
<div class="page" title="Page 115"><div class="section"><div class="layoutArea"><div class="column"><p><span>Since the Celtic Tiger, the concept of periphery has been an integral part of the debates on Ireland’s role in the world economy, on its <br />position in the European Union, on its relationship with Great Britain and on internal regional disparities. Whereas Ireland has universally been perceived as being at the core of the European integration project, there is no consensus whether Celtic Tiger-Ireland eventually managed to leave the economic periphery or semi-periphery as defined in the World-Systems Analysis. Additionally, the Celtic Tiger did not manage to reduce regional disparity within Ireland – a fact that resulted in an increased focus on the internal periphery and core. The current recession negatively influences the perceptions of Ireland’s economic development and of its role in the European Union. </span></p></div></div></div></div
Uterine rupture in a primigravid patient with an unscarred bicornuate uterus at term
Background: Uterine rupture of an unscarred primigravid uterus is an exceedingly rare event. Cases of spontaneous rupture of an unscarred bicornuate uterus have been reported, but typically occur in the first or second trimester.
Case: A 28-year-old primigravida at 37Â weeks gestation with a known bicornuate uterus and no prior surgery underwent an emergent cesarean section after presenting with severe abdominal pain and signs of fetal compromise. She was found to have a uterine rupture with the fetus free in the abdomen accompanied by a large hemoperitoneum. Both mother and baby did well postoperatively.
Conclusion: Bicornuate uterus may be an independent risk factor for uterine rupture, which can occur in primigravid patients and at any gestation
Endothelial S1P 1 Signaling Counteracts Infarct Expansion in Ischemic Stroke
International audienceRationale: Cerebrovascular function is critical for brain health, and endogenous vascular protective pathways may provide therapeutic targets for neurological disorders. S1P (Sphingosine 1-phosphate) signaling coordinates vascular functions in other organs, and S1P 1 (S1P receptor-1) modulators including fingolimod show promise for the treatment of ischemic and hemorrhagic stroke. However, S1P 1 also coordinates lymphocyte trafficking, and lymphocytes are currently viewed as the principal therapeutic target for S1P 1 modulation in stroke. Objective: To address roles and mechanisms of engagement of endothelial cell S1P 1 in the naive and ischemic brain and its potential as a target for cerebrovascular therapy. Methods and Results: Using spatial modulation of S1P provision and signaling, we demonstrate a critical vascular protective role for endothelial S1P 1 in the mouse brain. With an S1P 1 signaling reporter, we reveal that abluminal polarization shields S1P 1 from circulating endogenous and synthetic ligands after maturation of the blood-neural barrier, restricting homeostatic signaling to a subset of arteriolar endothelial cells. S1P 1 signaling sustains hallmark endothelial functions in the naive brain and expands during ischemia by engagement of cell-autonomous S1P provision. Disrupting this pathway by endothelial cell-selective deficiency in S1P production, export, or the S1P 1 receptor substantially exacerbates brain injury in permanent and transient models of ischemic stroke. By contrast, profound lymphopenia induced by loss of lymphocyte S1P 1 provides modest protection only in the context of reperfusion. In the ischemic brain, endothelial cell S1P 1 supports blood-brain barrier function, microvascular patency, and the rerouting of blood to hypoperfused brain tissue through collateral anastomoses. Boosting these functions by supplemental pharmacological engagement of the endothelial receptor pool with a blood-brain barrier penetrating S1P 1 -selective agonist can further reduce cortical infarct expansion in a therapeutically relevant time frame and independent of reperfusion. Conclusions: This study provides genetic evidence to support a pivotal role for the endothelium in maintaining perfusion and microvascular patency in the ischemic penumbra that is coordinated by S1P signaling and can be harnessed for neuroprotection with blood-brain barrier-penetrating S1P 1 agonists