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.

Input: Consider Input: Context: We analyzed the involvement of thromboxane (TX) A2/prostaglandin (PG) H2 (TP) receptor in ischemia-induced neovascularization in mice.', 'Unilateral hindlimb ischemia was induced by right femoral artery ligature in male C57BL/6J mice (n=7 per group). Animals were then treated with or without TP receptor antagonist (S18886, 5 or 10 mg/kg per day; ramatroban, 10 mg/kg per day) or aspirin (30 mg/kg per day) in drinking water for 21 days. Hindlimb ischemia raised plasma level of TXB2, the stable metabolite of TXA2, by 4.7-fold. This increase was blocked by aspirin treatment whereas S18886 (5 or 10 mg/kg per day) had no effect. However, neither S 18886 nor aspirin affected postischemic neovascularization. We next assessed the putative involvement of TXA2 signaling in angiotensin II (Ang II) proangiogenic pathway. Ang II (0.3 mg/kg per day) enhanced TXB2 plasma levels by 2.6-fold over that of control (P<0.01). Ang II-induced TXB2 upregulation was reduced by cotreatment with Ang II type I receptor antagonist (candesartan, 20 mg/kg per day). Angiographic score, capillary number, and foot perfusion were improved by 1.7-, 1.7-, and 1.4-fold, respectively, in Ang II-treated mice compared with controls (P<0.05). Ang II proangiogenic effect was associated with a 1.6-fold increase in VEGF-A protein content (P<0.05) and a 1.4-fold increase in the number of Mac-3-positive cells (ie, macrophages) in ischemic areas (P<0.05). Interestingly, treatments with TP receptor antagonists or aspirin hampered the proangiogenic effects of Ang II.
Answer: Endogenous activation of TXA2 receptor by eicosanoids did not modulate spontaneous neovascularization in the setting of ischemia. Conversely, TXA2 signaling is involved in Ang II-induced AT1-dependent vessel growth.

Output: Does thromboxane A2/prostaglandin H2 receptor activation mediate angiotensin II-induced postischemic neovascularization?


Input: Consider Input: Context: Absenteeism from outpatient appointments is common. Telephone appointment-reminder calls reduce outpatient-appointment absenteeism in many clinic settings.', 'To determine if telephone appointment-reminder calls reduce outpatient absenteeism at a hospital-based pulmonary function laboratory.', 'We conducted a retrospective review of our pulmonary function laboratory\'s outpatient appointment records from April to November 2004. Data were collected from consecutive outpatient appointments, including patient age, sex, whether a telephone appointment-reminder call was successfully made, and whether the patient showed up for the scheduled test. We performed 3 analyses. Differences in absenteeism between the groups was the primary outcome measure. First, appointments were separated into 2 groups: (1) appointments for which a reminder call was attempted ("called" group) and (2) appointments for which a reminder call was not attempted ("not-called" group). The appointments were then separated into 2 further groups: (1) the reminder call was successfully achieved ("contacted" group) and (2) the patient either was not called or was called but could not be reached ("not-contacted" group). Finally, the contacted group was separated into 2 further groups: (1) reminder calls that resulted in direct conversation with an appropriate person at the patient\'s listed telephone number, and (2) reminder message left on an answering machine.', 'Data were collected from 515 consecutive outpatient appointments; 45 (8.7%) of these patients did not show up for testing. The absentee rate was 4.7% (n = 10) in the called group and 11.6% (n = 35) in the not-called group (p = 0.0066). In the called group, 6.5% (n = 14) could not be reached. The absentee rate was 4% (n = 8) in the contacted group and 11.7% (n = 37) in the not-contacted group (p = 0.0021). We found no difference in absenteeism between patients who received reminders via direct conversation (4.2%) and those who had a reminder message left on an answering machine (3.7%) (p > 0.05).
Answer: A policy of reminding outpatients of their appointments via telephone reduces absenteeism at a hospital-based pulmonary function laboratory. We found no difference in absenteeism between communicating the reminder via direct conversation versus via leaving a message on an answering machine.

Output: Does the effect of telephone appointment-reminder call on outpatient absenteeism in a pulmonary function laboratory?


Input: Consider Input: Context: Macrophage accumulation of cholesterol leads to foam cell formation which is a major pathological event of atherosclerosis. Recent studies have shown that microRNA (miR)-19b might play an important role in cholesterol metabolism and atherosclerotic diseases. Here, we have identified miR-19b binding to the 3'UTR of ATP-binding cassette transporter A1 (ABCA1) transporters, and further determined the potential roles of this novel interaction in atherogenesis.", 'To investigate the molecular mechanisms involved in a miR-19b promotion of macrophage cholesterol accumulation and the development of aortic atherosclerosis.', "We performed bioinformatics analysis using online websites, and found that miR-19b was highly conserved during evolution and directly bound to ABCA1 mRNA with very low binding free energy. Luciferase reporter assay confirmed that miR-19b bound to 3110-3116 sites within ABCA1 3'UTR. MiR-19b directly regulated the expression levels of endogenous ABCA1 in foam cells derived from human THP-1 macrophages and mouse peritoneal macrophages (MPMs) as determined by qRT-PCR and western blot. Cholesterol transport assays revealed that miR-19b dramatically suppressed apolipoprotein AI-mediated ABCA1-dependent cholesterol efflux, resulting in the increased levels of total cholesterol (TC), free cholesterol (FC) and cholesterol ester (CE) as revealed by HPLC. The excretion of (3)H-cholesterol originating from cholesterol-laden MPMs into feces was decreased in mice overexpressing miR-19b. Finally, we evaluated the proatherosclerotic role of miR-19b in apolipoprotein E deficient (apoE(-/-)) mice. Treatment with miR-19b precursor reduced plasma high-density lipoprotein (HDL) levels, but increased plasma low-density lipoprotein (LDL) levels. Consistently, miR-19b precursor treatment increased aortic plaque size and lipid content, but reduced collagen content and ABCA1 expression. In contrast, treatment with the inhibitory miR-19b antisense oligonucleotides (ASO) prevented or reversed these effects.
Answer: MiR-19b promotes macrophage cholesterol accumulation, foam cell formation and aortic atherosclerotic development by targeting ABCA1.


Output: Does microRNA-19b promote macrophage cholesterol accumulation and aortic atherosclerosis by targeting ATP-binding cassette transporter A1?