instruction:
Given a passage with a context and an answer, 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.
question:
Context: Barrett esophagus (BE) is considered precursor condition of esophageal adenocarcinoma. Its incidence and prevalence are increasing in general population. Studies reported that metabolic syndrome (MS) or diabetes mellitus (DM) is related to increased risk of BE. Current study was to assess and better understand the relationship between MS /DM and BE.', "Electronic search was conducted in the database Pubmed/Medline (-December, 2015), Embase (-December, 2015), Cochrane Library (-December, 2015), and Web of Knowledge (-December, 2015). Studies included were assessed with summary odds ratios (ORs) with 95% confidence intervals (CIs) and compared exposure group with control group. The heterogeneity was examined by the funnel plot and the Egger's test. Subgroup analyses and sensitive analyses were performed for the detection of possible heterogeneity and impact on stability of analysis results.", "Twelve publications met the criteria and included 355,311 subjects were analyzed. The pooled results showed MS was closely associated with increased risk of BE (OR\u200a=\u200a1.23; 95%CI 1.03-1.47; P\u200a=\u200a0.024), and yet DM did not significantly increase the risk of BE (OR\u200a=\u200a1.07; 95%CI 0.82-1.38; P\u200a=\u200a0.627). Substantial heterogeneities were detected. No significant publication bias was detected by Egger's test (P\u200a=\u200a0.23).
Answer: Based on the results of current meta-analysis, MS is associated with increased risk of BE. Further long-term follow-up prospective study needs to verify the current results, and definite pathophysiological mechanism needs to be further investigated and clearly elucidated.
answer:
Is metabolic syndrome associated with increased risk of Barrett esophagus : A meta-analysis?


question:
Context: Intestinal ischemia/reperfusion (I/R) injury is believed to be the major initiator of the systemic inflammatory response syndrome. As a result of intestinal I/R, the gut becomes a major source of inflammatory cytokine production. We have previously shown that heparin-binding EGF-like growth factor (HB-EGF) is cytoprotective after intestinal I/R and down-regulates pro-inflammatory cytokine production in vitro. We now examine the effects of HB-EGF on pro-inflammatory cytokine expression in vivo.', 'Rats were randomized into three groups: sham-operated, superior mesenteric artery occlusion (SMAO) for 90 min followed by 8 h of reperfusion (I/R), and I/R with intraluminal administration of HB-EGF 25 min after the initiation of ischemia (I/R + HB-EGF). Serum was drawn at 2, 4, 6, and 8 h post reperfusion for determination of cytokine protein levels using a bioplex suspension array system. Additional animals underwent the same ischemic protocol followed by 30 and 60 min of reperfusion with harvesting of ileal mucosa. Ileal pro-inflammatory cytokine gene expression was determined using reverse transcriptase polymerase chain reaction (RT-PCR) with primers specific for TNF-alpha, IL-6, and IL-1beta.', 'HB-EGF decreased TNF-alpha, IL-6, and IL-1beta serum protein levels at 4, 6, and 8 h after intestinal I/R injury. In addition, HB-EGF decreased local intestinal mucosal mRNA expression of TNF-alpha, IL-6, and IL-1beta 30 and 60 min after intestinal injury.
Answer: We conclude that pro-inflammatory cytokine expression is increased both locally and in the systemic circulation after intestinal I/R and that the administration of HB-EGF significantly reduces intestinal I/R-induced pro-inflammatory cytokine expression in vivo.
answer:
Does heparin-binding EGF-like growth factor decrease inflammatory cytokine expression after intestinal ischemia/reperfusion injury?


question:
Context: The isoflavone puerarin [7-hydroxy-3-(4-hydroxyphenyl)-1-benzopyran-4-one 8-(β-D-glucopyranoside)] possesses many biological activities. In this study, we investigated the effects of puerarin on adhesion molecules (AMs), including serum levels of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial leukocyte adhesion molecule-1 (E-selectin), and the activation of nuclear factor kappa B (NF-κB) in rabbits with experimental atherosclerosis.', 'In total, 24 rabbits were divided into control (standard diet), high-lipid diet (HLD), and PUE (HLD supplemented with puerarin) groups. At the end of weeks 0, 8, and 16, serum levels of AMs were measured. At the end of week 16, the thickness of the intima was detected. Protein and mRNA levels of AMs were checked by immunohistochemistry and RT-PCR, respectively. Protein levels of p65 NF-κB and phosphorylation of inhibitor-κB (I-κB) were investigated by Western blotting.', 'Atherosclerotic lesions in the thoracic arch were found in the HLD and PUE groups, but not in the control group. Compared with the HLD group, the thickness of the intima in the PUE group was reduced. Our results indicate that puerarin reduced the protein and mRNA levels of AMs in this rabbit model. We also found that the reduced AM levels were due to inhibition of the phosphorylation and degradation of I-κB, resulting in reduced p65 NF-κB nuclear translocation.
Answer: This study indicates that the effect of puerarin on the suppression of atherosclerosis was connected with an inhibited inflammatory response and reduced NF-κB activation.
answer:

Does puerarin inhibit the inflammatory response in atherosclerosis via modulation of the NF-κB pathway in a rabbit model?