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.
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Question: Inadequate response of the innate immune system to bacterial antigens present in the intestinal flora may play a role in the development of necrotizing enterocolitis (NEC). Pattern recognition receptors such as CD14, toll-like receptor (TLR) 4, and caspase-recruitment domain (CARD) 15 bind bacterial lipopolysaccharide and peptidoglycan, and their activation leads to production of inflammatory cytokines. Our aim was to evaluate whether single nucleotide polymorphisms (SNPs) of CD14, TLR4, and CARD15 are associated with the risk of NEC in very low birth weight (VLBW) infants.', 'We determined the CD14 C-260T, TLR4 A +896G, C +1196T, and CARD15 G +2722C, C +2104T, 3020insC functional SNPs in dried blood samples from 118 VLBW infants (of those, 41 developed NEC) and from 146 healthy term newborns using polymerase chain reaction and restriction fragment length polymorphism methods. We tested the association between genotype and risk of NEC.', 'No significant differences were found in the prevalence of CD14 -260T, TLR4 +896G, +1196T, and CARD15 +2722C, +2104T, 3020insC alleles between VLBW infants and healthy term newborns (P = NS). The frequencies of investigated genotypes were similar in infants with and without NEC (P = NS). Furthermore, we did not find any association between genotype and prematurity or sepsis, which are important risk factors of NEC.

Answer: Are genetic polymorphisms of CD14 , toll-like receptor 4 , and caspase-recruitment domain 15 associated with necrotizing enterocolitis in very low birth weight infants?

Question: To investigate the effects of copper on permeability and P-glycoprotein (P-gp) of Caco-2 cell monolayers.', 'The differentiated Caco-2 cell model was used in this study. Permeability of cell monolayers was reflected by monitoring transepithelial electrical resistance (TEER); distribution of tight junctional protein ZO-1 was measured by immunofluorescent staining; F actin was measured by fluorescence staining; and Activity of P-gp was reflected by changes of transcellular transport and accumulation of Rho-123 in Caco-2 cells.', "Apical treatment with copper (30 - 100 micromol/L, Hanks' buffered salt solution, up to 3 hours) induced a time- and concentration-dependent increase in permeability reflected by progressive decrease of TEER of Caco-2 cell monolayers, accompanied by deorganization of F actin, but without significant effects on tight junctional protein ZO-1; at a dose without any adverse effects on viability and permeability of Caco-2 monolayers, copper treatment (300 micromol/L, complete medium, 24 hours) decreased Papp(BL-->AP) from 7.37 +/- 0.20 x 10(-6) cm/s (controls) to (6.43 +/- 0.27) x 10(-6) cm/s, the increased Papp(AP-->BL) from (1.23 +/- 0.05) x 10(-7) cm/s (controls) to (3.41 +/- 0.08) x 10(-7) cm/s, and enhanced the intracellular Rho-123 from (0.31 +/- 0.01) nmol/filter (controls) to (0.50 +/- 0.03) nmol/filter.

Answer: Does [ Copper treatment alter the barrier functions of human intestinal Caco-2 cells ]?

Question: Systemic sclerosis (SSc) is a connective-tissue disease characterized by vascular injury, immune-system disorders, and excessive fibrosis of the skin and multiple internal organs. Recent reports found that RhoA/Rho-kinase (ROCK) pathway is implicated in various fibrogenic diseases. Intradermal injection of hypochlorous acid (HOCl)-generating solution induced inflammation, autoimmune activation, and fibrosis, mimicking the cutaneous diffuse form of SSc in humans. Our study aimed firstly to describe pulmonary inflammation and fibrosis induced by HOCl in mice, and secondly to determine whether fasudil, a selective inhibitor of ROCK, could prevent lung and skin fibroses in HOCl-injected mice.', 'Female C57BL/6 mice received daily intradermal injection of hypochlorous acid (HOCl) for 6 weeks to induce SSc, with and without daily treatment with fasudil (30mgkg(-1)day(-1)) by oral gavage.', 'HOCl intoxication induced significant lung inflammation (macrophages and neutrophils infiltration), and fibrosis. These modifications were prevented by fasudil treatment. Simultaneously, HOCl enhanced ROCK activity in lung and skin tissues. Inhibition of ROCK reduced skin fibrosis, expression of -smooth-muscle actin and 3-nitrotyrosine, as well as the activity of ROCK in the fibrotic skin of HOCl-treated mice, through inhibition of phosphorylation of Smad2/3 and ERK1/2. Fasudil significantly decreased the serum levels of anti-DNA-topoisomerase-1 antibodies in mice with HOCl-induced SSc.

Answer:
Does rhoA/Rho-kinase activation promote lung fibrosis in an animal model of systemic sclerosis?