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.

Q: Post-hemorrhagic shock mesenteric lymph (PHSML) has been linked with neutrophil (PMN) priming, endothelial cell (EC) activation, and acute lung injury (ALI) in rodent models. We have previously identified the lipid fraction of PHSML as containing the causative agent(s). Due to the lesson learned from the rodent gut bacterial translocation experience, we sought to confirm this phenomenon using a large animal model; hypothesizing that lymph collected from the porcine gut following ischemia/reperfusion (I/R) would cause PMN priming.', 'Mesenteric lymph was collected from adult pigs before, during, and for 2 hours after non-lethal hemorrhagic shock (mean arterial pressure = 30 mm Hg x 45 minutes). Whole lymph and the extracted lipid fractions of the lymph were then added to isolated human and porcine PMNs and superoxide production was measured by cytochrome C reduction.', 'Hemorrhagic shock profoundly affected mesenteric lymph flow from baseline (pre-shock) flow rates of 75.63 +/- 8.86 mL/hr to 49.38 +/- 5.76 mL/hr during shock and increasing to 253.38 +/- 27.62 mL/hr after 2 hours of resuscitation. Human PMNs exposed to both whole lymph (PHSML) and its extracted lipids (PHSML Lipid) collected 2 hours after shock exhibited more than a two-fold increase in superoxide release upon activation compared with pre-shock samples: PHSML- 6.27 +/- 0.83 versus 2.56 +/- 0.60 nmolO2(-)/ 3.75 cells/mL/min, respectively (p = 0.007), PHSML Lipid- 4.93 +/- 0.34 versus 2.49 +/- 0.11 nmolO2(-)/ 3.75 cells/mL/min (p < 0.001). Similarly, porcine PMNs exhibited close to a two-fold activation when exposed to the lymph and lipid fraction: PHSML- 4.51 +/- 0.42 versus 1.06 +/- 0.28 nmolO2(-)/ 3.75 cells/mL/min (p = 0.008), PHSML Lipid-4.80 +/- 0.81 versus 1.55 +/- 0.23 nmolO2(-)/ 3.75 cells/mL/min (p = 0.002).

A: Does systemic neutrophil priming by lipid mediators in post-shock mesenteric lymph exist across species?
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Q: Complement Factor I (CFI) and the CD46 complement regulator (CD46) play an important role in the complement activation pathways, which is known to affect the development of uveitis. The present study was performed to investigate the association of the CFI and CD46 genes with acute anterior uveitis (AAU).', 'A total of 600 subjects (300 patients with AAU and 300 healthy controls) were recruited for this case-control study. Six CFI single nucleotide polymorphisms (SNP) (rs7356506, rs10029485, rs11726949, rs12512308, rs7438961, rs998538) and four CD46 SNPs (rs12138764, rs2466571, rs2796278, rs7545126) were genotyped using Sequenom MassARRAY technology. Allele and genotype frequencies were compared between patients and controls using the χ(2) test. Analyses were stratified for gender, human leukocyte antigen (HLA)-B27, and ankylosing spondylitis status.', 'Rs7356506 in the CFI gene was found to be protective against AAU. There was a significant increase in the frequency of the A allele (p=0.003, pc=0.03, OR=0.684, CI 0.534 to 0.876) and AA homozygosity (p=0.004, pc=0.04, OR=0.624, CI 0.452 to 0.862) in AAU patients as compared to controls. Stratified analysis, according to gender and HLA-B27 status for AAU, also revealed the association with CFI-rs7356506. None of the tested SNPs of CD46 were associated with AAU.

A: Is cFI-rs7356506 a genetic protective factor for acute anterior uveitis in Chinese patients?
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Q: An intricate gene regulatory network drives neural crest migration and differentiation. How epigenetic regulators contribute to this process is just starting to be understood.', 'We found that mutation of med14 or brg1 in zebrafish embryos resulted in a cluster of neural crest cell-related defects. In med14 or brg1 mutants, neural crest cells that form the jaw skeleton were specified normally and migrated to target sites. However, defects in their subsequent terminal differentiation were evident. Transplantation experiments demonstrated that med14 and brg1 are required directly in neural crest cells. Analysis of med14; brg1 double mutant embryos suggested the existence of a strong genetic interaction between members of the Mediator and BAF complexes.

A:
Does med14 cooperate with brg1 in the differentiation of skeletogenic neural crest?
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