TASK DEFINITION: Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.
PROBLEM: Previous research in fetuses with increased nuchal translucency (NT) showed abnormal lymphatic endothelial differentiation characteristics, including increased vascular endothelial growth factor (VEGF)-A expression, and aberrant smooth muscle cells (SMCs) surrounding enlarged jugular lymphatic sacs (JLS). We hypothesized that abnormal Sonic hedgehog (Shh) expression would result in altered VEGF-A signaling in the lymphatic endothelial cells of the JLS and that aberrant acquisition of SMCs could be caused by downregulation of forkhead transcription factor FOXC2 and upregulation of platelet-derived growth factor (PDGF)-B in the lymphatic endothelial cells of the JLS.', 'Five trisomy 21 fetuses and four controls were investigated using immunohistochemistry for Shh, VEGF-A, FOXC2 and PDGF-B expression in the lymphatic endothelial cells of the JLS.', 'An increased Shh, VEGF-A and PDGF-B expression, and decreased FOXC2 expression were shown in the lymphatic endothelial cells of the JLS of the trisomic fetuses.

SOLUTION: Does abnormal Shh and FOXC2 expression correlate with aberrant lymphatic development in human fetuses with increased nuchal translucency?

PROBLEM: To determine whether activin A concentrations are altered in chronic fetal hypoxemia and intrauterine fetal growth restriction (IUGR).', 'In vivo animal experimental model.', 'Department of Physiology, Monash University.', 'Chronically catherised fetal sheep in late pregnancy.', 'Chronic fetal hypoxia and IUGR were experimentally induced by single umbilical artery ligation (SUAL) in catheterised fetal sheep. Maternal and fetal blood samples and amniotic fluid (AF) samples were collected during surgery and thereafter on alternate days, until the time of delivery for analyte measurement. Fetal blood gas parameters were measured daily.', 'Plasma and AF was used to analyse activin A, prostaglandin E2 (PGE2) and cortisol and fetal blood gas analysis was undertaken in whole blood.', 'SUAL produced asymmetric IUGR and non-acidaemic chronic fetal hypoxia and resulted in preterm labour (129 [3] days). AF activin A concentrations were 10-fold higher in the SUAL group than in controls whereas levels in the fetal and maternal circulations were similar between groups.

SOLUTION: Does chronic fetal hypoxia increase activin A concentrations in the late-pregnant sheep?

PROBLEM: Preconditioning neurons with noninjurious hypoxia (hypoxic preconditioning, HPC) or the anesthetic isoflurane (APC) induces tolerance of severe ischemic stress. The mechanisms of both types of preconditioning in the hippocampus require moderate increases in intracellular Ca and activation of protein kinase signaling. The authors hypothesized that the expression of signal transduction genes would be similar after APC and HPC.', 'Hippocampal slice cultures prepared from 9-day-old rats were preconditioned with hypoxia (5 min of 95% nitrogen/5% carbon dioxide) or 1% isoflurane in air/5% carbon dioxide for 1 h. A day later, cultures were subjected to 10 min oxygen and glucose deprivation (simulated ischemia). Intracellular Ca, measured in CA1 neurons at the completion of preconditioning, and cell death in CA1, CA3, and dentate regions was assessed 48 h after simulated ischemia. Message RNA encoding 119 signal transduction genes was quantified with rat complimentary DNA microarrays from pre-oxygen-glucose deprivation samples.', 'Both APC and HPC increased intracellular Ca approximately 50 nm and decreased CA1, CA3, and dentate neuron death by about 50% after simulated ischemia. Many signaling genes were increased after preconditioning, with hypoxia increasing more apoptosis/survival genes (8 of 10) than isoflurane (0 of 10). In contrast, isoflurane increased more cell cycle/development/growth genes than did hypoxia (8 of 14 genes, vs. 1 of 14).

SOLUTION:
Does expression of signal transduction genes differ after hypoxic or isoflurane preconditioning of rat hippocampal slice cultures?