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: To investigate the molecular mechanisms of CCL13/monocyte chemoattractant protein 4 (MCP-4) chemokine expression through proinflammatory cytokines in different primary human fibroblasts and the contribution of CCL13 to monocyte migration.', 'Using RNase protection assays and enzyme-linked immunosorbent assays, we quantified the expression of CCL13 compared with that of CCL2/MCP-1 in primary human fibroblasts. Boyden chamber assays were performed to determine the importance of CCL13 for migration of primary monocytes. Pharmacologic inhibitors as well as small interfering RNA knockdown approaches were used to investigate the signaling pathways regulating CCL13 expression.', 'The interleukin-6 (IL-6)-type cytokine oncostatin M (OSM) was a powerful inducer of CCL13 expression in primary synovial fibroblasts from patients with rheumatoid arthritis (RA) as well as those from healthy control subjects but not in other types of fibroblasts. Neither IL-6 nor tumor necrosis factor alpha could stimulate the expression of CCL13 in synovial fibroblasts; IL-1beta was a very weak inducer. Synovial fibroblasts from patients with RA constitutively produced low amounts of CCL13, which was partially dependent on constitutive production of OSM. By investigating the underlying molecular mechanism, we identified STAT-5, ERK-1/2, and p38 as critical factors involved in OSM-dependent transcription and messenger RNA stabilization of CCL13.

Answer: Does induction of CCL13 expression in synovial fibroblasts highlight a significant role of oncostatin M in rheumatoid arthritis?

Question: Surgery has been the gold standard in the treatment of adult pyloric stenosis (APS). The introduction of proton pump inhibitors (PPIs) in 1989 revolutionised the treatment of peptic ulcer disease and its complications.', 'We carried out a prospective study to evaluate the effectiveness of PPIs as an alternative to surgery for treatment of APS. Six consecutive patients admitted with a diagnosis of adult peptic pyloric stenosis between November 1999 and August 2002 were studied. The diagnosis was confirmed with endoscopy. All patients were commenced on a twice-daily dose of intravenous PPI. This was changed to oral treatment after 2 days. Main outcome measures evaluated were resolution of symptoms on PPIs and failure of medical therapy.', 'There were five females and one male. Median age at diagnosis was 72 years (range, 30-90 years). Median duration of symptoms was 2 weeks (range, 1-5 weeks). Of the patients, five had a history of peptic ulcer disease. Complete resolution was achieved in 5 patients (83%). Median duration for resolution of symptoms was 9 days (range, 5-14 days). All patients were changed to oral PPIs after 2 days. One patient did not respond to oral therapy and required surgical intervention (pyloroplasty). Median follow-up was 26 months (range, 6-48 months). There was no recurrence of symptoms. All patients were discharged on low-dose PPI.

Answer: Is proton pump inhibition a feasible primary alternative to surgery and balloon dilatation in adult peptic pyloric stenosis ( APS ) : report of six consecutive cases?

Question: Determination of endothelial function has emerged as a crucial factor in the assessment of individual cardiovascular risk. Sonographic measurement of flow-mediated dilation (FMD) is the most widespread technique to assess endothelial function, but analysis is very time-consuming and requires an experienced examiner. Recently, it was speculated that a reduction of small artery compliance (C2) measured by pulse wave analysis might be an indicator of endothelial dysfunction. In the present study, we investigated the correlation of pulse wave analysis parameters and endothelial function with special regard to patients who are at increased risk for endothelial dysfunction.', 'One hundred and thirty-six subjects (65 male, 71 female) were included in the study. One hundred and twenty-three probands were hypertensive. Endothelium-dependent vasodilation was assessed sonographically (flow-mediated dilation) using standard protocols and as a change of reflection index (deltaRI) after application of salbutamol by photoplethysmography. Small artery compliance, large artery compliance (C1), and systemic vascular resistance (SVR) were measured by computerized pulse wave analysis of the radial artery (CR-2000; Hypertension Diagnostics, Eagan, Minnesota, USA) and were tested for correlation with FMD.', 'Mean FMD was 6.29 +/- 2.86%. Means of pulse wave analysis-derived vascular parameters were 4.91 +/- 2.86 ml/mmHg x 100 (C2), 13.35 +/- 5.41 ml/mmHg x 10 (C1) and 1611.6 +/- 348.5 dynes x s x cm(-5) (SVR). Regression analysis excluded a significant correlation between FMD, C2, C1 and SVR (r2 < 0.05 each) both in hypertensives and normotensives. There was no significant correlation between C2 and deltaRI (r2 = 0.023).

Answer:
Is small artery elasticity assessed by pulse wave analysis no measure of endothelial dysfunction?