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.

Let me give you an example: Context: Chronic rhinosinusitis (CRS) is a heterogeneous disease with an uncertain pathogenesis. Group 2 innate lymphoid cells (ILC2s) represent a recently discovered cell population which has been implicated in driving Th2 inflammation in CRS; however, their relationship with clinical disease characteristics has yet to be investigated. The aim of this study was to identify ILC2s in sinus mucosa in patients with CRS and controls and compare ILC2s across characteristics of disease. A cross-sectional study of patients with CRS undergoing endoscopic sinus surgery was conducted. Sinus mucosal biopsies were obtained during surgery and control tissue from patients undergoing pituitary tumour resection through transphenoidal approach. ILC2s were identified as CD45(+) Lin(-) CD127(+) CD4(-) CD8(-) CRTH2(CD294)(+) CD161(+) cells in single cell suspensions through flow cytometry. ILC2 frequencies, measured as a percentage of CD45(+) cells, were compared across CRS phenotype, endotype, inflammatory CRS subtype and other disease characteristics including blood eosinophils, serum IgE, asthma status and nasal symptom score. 35 patients (40% female, age 48 ± 17 years) including 13 with eosinophilic CRS (eCRS), 13 with non-eCRS and 9 controls were recruited. ILC2 frequencies were associated with the presence of nasal polyps (P = 0.002) as well as high tissue eosinophilia (P = 0.004) and eosinophil-dominant CRS (P = 0.001) (Mann-Whitney U). They were also associated with increased blood eosinophilia (P = 0.005). There were no significant associations found between ILC2s and serum total IgE and allergic disease. In the CRS with nasal polyps (CRSwNP) population, ILC2s were increased in patients with co-existing asthma (P = 0.03). ILC2s were also correlated with worsening nasal symptom score in CRS (P = 0.04).
Answer: As ILC2s are elevated in patients with CRSwNP, they may drive nasal polyp formation in CRS. ILC2s are also linked with high tissue and blood eosinophilia and have a potential role in the activation and survival of eosinophils during the Th2 immune response. The association of innate lymphoid cells in CRS provides insights into its pathogenesis.
The answer to this example can be: Are group 2 innate lymphoid cells ( ILC2s ) increased in chronic rhinosinusitis with nasal polyps or eosinophilia?
Here is why: The question is based on the following sentences from the two passages (i) Group 2 innate lymphoid cells (ILC2s) {ii) In the CRS with nasal polyps (CRSwNP) population, ILC2s were increased in patients with co-existing asthma (iii) As ILC2s are elevated in patients with CRSwNP, they may drive nasal polyp formation in CRS. and (iv) ILC2s are also linked with high tissue and blood eosinophilia.

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Context: Heparin is used in the treatment of venous and arterial thromboembolic events, including unstable angina. Once unfractionated heparin is discontinued during the acute phase of unstable angina, it has been demonstrated that the disease process may be reactivated within hours. It is hypothesized that this reactivation may be a result of direct platelet activation by heparin that can linger even after the drug itself has been stopped. Prior studies have shown that heparin can either increase or decrease platelet activation. More recent studies have also shown conflicting effects of unfractionated heparin on PFA-100 testing.', 'We studied the in-vitro effects of unfractionated heparin on platelet function and PFA-100 testing. Unfractionated heparin was incubated with whole blood taken from 18 healthy volunteers. Platelet activation and aggregation was assessed with and without the presence of heparin.', 'Platelet aggregation and activation were increased in the presence of heparin. Unfractionated heparin also significantly prolonged collagen/adenosine diphosphate closure time but did not affect collagen/epinephrine closure time.
Answer: Unfractionated heparin leads to direct platelet activation and increases platelet aggregation in vitro. Unfractionated heparin causes prolongation of the collagen/adenosine diphosphate closure time in PFA-100 testing, possibly as a result of direct binding to von Willebrand factor in solution and interference with von Willebrand factor-glycoprotein Ib binding.
Answer:

Show your work and conclude with the exact phrasing "Therefore, the final answer is [answer]." where [answer] is just the final number or expression that solves the problem.
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Does heparin therapy lead to platelet activation and prolongation of PFA-100 closure time?