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.

Context: To investigate the effects of quercetin, an herbal flavonoid, on LPS-induced delay in spontaneous apoptosis, adhesion molecules (CD62L, CD11b/CD18) expression of neutrophils, and superoxide (O(2)(-)) generation by LPS-primed fMLP-induced human neutrophils.', 'Neutrophils were incubated in the presence or absence of lipopolysaccharide (LPS) at a final concentration of 1 microg/ml for 24 hours. Some wells with neutrophils were pre-treated with quecetin at the final concentration ranging from 0-100 microM for 30 min and then 1 microg/ml LPS was added into the cultures for 24 hours. The apoptosis of neutrophils was evaluated by flowcytometry analysis of propidum iodide (PI)-staining of the nuclei and annexin V staining of phosphatidylserine (PS) in the cell membrane. Agarose gel electrophoresis of low molecular weight DNA was performed to analyze DNA fragmentation. The effects of quercetin on adhesion molecules were detected by using flowcytometry analysis. The generation of O(2) (-) by LPS-primed fMLP-induced neutrophils was determined by reduced cytochrome c assay.', 'LPS markedly inhibited the spontaneous apoptosis of neutrophils, but the inhibitory effect was abrogated after the pre-treatment of neutrophils with quercetin (approximately 40 microM) for 30 min. Quercetin (40 microM) also prevented LPS-induced down-regulation of CD62L expression, up-regulation of CD11b/CD18 expression, and O(2) (-) generation by fMLP-induced neutrophils.
Answer: As one of the pro-inflammatory factors, LPS aggravates inflammation through priming neutrophils to synthesize/release cytotoxic contents and prolonging functional lifespan of neutrophils by delaying the spontaneous apoptosis. Thus, our data suggest to us that quercetin might decrease the susceptibility of neutrophils to pro-inflammatory factors (e. g. LPS), which could partially explain the anti-inflammatory mechanisms of quercetin.
Does quercetin inhibit LPS-induced delay in spontaneous apoptosis and activation of neutrophils?

Context: Pulmonary vein (PV) isolation is a curative treatment for patients with atrial fibrillation. The aim of this study was to evaluate prospectively the effects of adenosine administration on the PV activity and atrio-venous conduction after PV isolation.', 'Twenty-nine patients (21 m; age: 55+/-8 years) were submitted to ostial PV isolation guided by basket catheter recordings. After successful isolation, the effects of a 12 mg intravenous bolus of adenosine were tested in 62 PVs. In 22/62 PVs (35%), left atrium (LA)-to-PV conduction was transiently (16.6+/-7.1 s, range: 3.8-27.9 s) or permanently (3 PVs) restored in response to adenosine administration. The prevalence of this phenomenon was 39% in left superior PVs, 43% in right superior PVs, and 22% in left inferior PVs (p=0.365). It occurred more frequently in the presence of dissociated PV activity (11/15 PVs, 73% vs. 11/47 PVs, 23%; p=0.002), whereas it was not influenced by the median duration of the radiofrequency current (RFC) delivery for each PV [19 (IQR: 12-26) min vs. 16 (IQR: 11-24) min: p=0.636]. A lengthening or shortening of the LA-PV conduction time was observed at LA-PV conduction appearance and disappearance in 36% and 55% of the cases, respectively. Further RFC applications (median: 5.5 min, IQR: 4-11 min) at the residual conduction breakthrough(s) indicated by the basket catheter recordings definitively eliminated adenosine-induced recovery of LA-PV conduction in all cases. Finally, when present, intrinsic PV discharge was invariably depressed by adenosine administration.
Answer: Adenosine may transiently or permanently re-establish LA-PV conduction after apparently successful PV isolation. This phenomenon is abolished by additional RFC delivery. However, its possible influence on the clinical results of PV ablation must be evaluated by properly designed, randomized studies.
Does adenosine restore atrio-venous conduction after apparently successful ostial isolation of the pulmonary veins?

Context: Inflammatory mediators released by nonparenchymal inflammatory cells in the liver have been implicated in the progression of acetaminophen (APAP) hepatotoxicity. Among hepatic nonparenchymal inflammatory cells, we examined the role of the abundant natural killer (NK) cells and NK cells with T-cell receptors (NKT cells) in APAP-induced liver injury.', 'C57BL/6 mice were administered a toxic dose of APAP intraperitoneally to cause liver injury with or without depletion of NK and NKT cells by anti-NK1.1 monoclonal antibody (MAb). Serum alanine transaminase (ALT) levels, liver histology, hepatic leukocyte accumulation, and cytokine/chemokine expression were assessed.', 'Compared with APAP-treated control mice, depletion of both NK and NKT cells by anti-NK1.1 significantly protected mice from APAP-induced liver injury, as evidenced by decreased serum ALT level, improved survival of mice, decreased hepatic necrosis, inhibition of messenger RNA (mRNA) expression for interferon-gamma (IFN-gamma), Fas ligand (FasL), and chemokines including KC (Keratinocyte-derived chemokine); MIP-1 alpha (macrophage inflammatory protein-1 alpha); MCP-1 (monocyte chemoattractant protein-1); IP-10 (interferon-inducible protein); Mig (monokine induced by IFN-gamma) and decreased neutrophil accumulation in the liver. Hepatic NK and NKT cells were identified as the major source of IFN-gamma by intracellular cytokine staining. APAP induced much less liver injury in Fas-deficient (lpr) and FasL-deficient (gld) mice compared with that in wild-type mice.
Answer: NK and NKT cells play a critical role in the progression of APAP-induced liver injury by secreting IFN-gamma, modulating chemokine production and accumulation of neutrophils, and up-regulating FasL expression in the liver, all of which may promote the inflammatory response of liver innate immune system, thus contributing to the severity and progression of liver injury downstream of the metabolism of APAP and depletion of reduced glutathione (GSH) in hepatocytes.

Does innate immune system play a critical role in determining the progression and severity of acetaminophen hepatotoxicity?