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.

[EX Q]: Context: In atherogenesis, dendritic cells, beside presenting antigens, may be sources of tumour necrosis factor (TNF)alpha and nitric oxide (NO), together with mast cells and smooth muscle cells.', 'We have looked at the expression of TNFalpha and inducible NO synthase (iNOs) by these cells by affinity cytochemistry in autoptical specimens from normal carotid arteries and not ruptured, hemorrhagic or calcified atheromata.', 'Round to dendritic, major histocompatibility complex class II molecules (MHC-II+) cells and avidin-labeled mast cells were rare in normal arteries and significantly more numerous in atheromata. Many MHC-II+ cells expressed S-100 antigen; while a few were positive for phalloidin; appreciable fractions of these cells were immunoreactive for TNFalpha and iNOs, both in control specimens and atheromata. The fraction of mast cells labeled for iNOs was significantly lower in atheromata than in controls. Phalloidin positive cells were the most abundant cell type in the normal intima and atheromata; the fractions of these cells labeled for TNFalpha and iNOs were significantly higher in atheromata than in controls. Very few of these cells were also labeled for MHC-II. Computerized image analysis confirmed that the amounts of iNOs and TNFalpha were higher in atheromata than in controls. The increase in TNFalpha in atheromata was also confirmed by western blot.
Answer: Dendritic cells and mast cells can participate to the generation of TNFalpha and NO in the normal arterial wall and in atheromata, but myointimal cells are candidates as major sources of these molecules.
[EX A]: Are smooth muscle cells , dendritic cells and mast cells sources of TNFalpha and nitric oxide in human carotid artery atherosclerosis?

[EX Q]: Context: We hypothesized that self-reported pad use per day (PPD) after pubovaginal sling (PVS) correlated with postoperative quality of life (QOL) scores.', 'Two hundred fifteen women completed the incontinence impact questionnaire 7 (IIQ-7) and urogenital distress inventory 6 (UDI-6) before PVS and during follow-up. Starting 3 days before a visit, women recorded the number of protective urinary pad changes per day. Analysis of variance and Pearson correlation tests were used to determine if women reporting zero, one, or greater than or equal to two urinary pads per day after PVS had significantly different changes in baseline QOL scores.', 'Over a mean 8.5 months follow-up after PVS, 131, 56, and 28 women reported zero, one, and greater than or equal to two pad changes/day. Each pad group showed progressively less improvement from baseline IIQ-7 and UDI-6 scores after PVS. Change in IIQ-7 and UDI-6 scores negatively correlated with PPD (p < 0.0001).
Answer: Self-reported PPD after PVS reflects patient perception of urinary-specific QOL.
[EX A]: Does self-reported pad use per day reflect patient quality of life after pubovaginal sling surgery?

[EX Q]: Context: We have reported that triptolide can inhibit airway remodeling in a murine model of asthma via TGF-1/Smad signaling. In the present study, we aimed to investigate the effect of triptolide on airway smooth muscle cells (ASMCs) proliferation and the possible mechanism.', 'Rat airway smooth muscle cells were cultured and made synchronized, then pretreated with different concentration of triptolide before stimulated by TGF-1. Cell proliferation was evaluated by MTT assay. Flow cytometry was used to study the influence of triptolide on cell cycle and apoptosis. Signal proteins (Smad2, Smad3 and Smad7) were detected by western blotting analysis.', 'Triptolide significantly inhibited TGF-1-induced ASMC proliferation (P<0.05). The cell cycle was blocked at G1/S-interphase by triptolide dose dependently. No pro-apoptotic effects were detected under the concentration of triptolide we used. Western blotting analysis showed TGF-1 induced Smad2 and Smad3 phosphorylation was inhibited by triptolide pretreatment, and the level of Smad7 was increased by triptolide pretreatment.
Answer: Triptolide may function as an inhibitor of asthma airway remodeling by suppressing ASMCs proliferation via negative regulation of Smad signaling pathway.
[EX A]:
Does triptolide inhibit TGF-1-induced cell proliferation in rat airway smooth muscle cells by suppressing Smad signaling?