In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Q: Context: The purpose of this study was to examine the effectiveness of ankle bracing and taping in preventing recurrencess of ankle sprains, specifically in female athletes.', "Varsity soccer players' medical records over a five-year period were retrospectively reviewed at a Division III women's college. Data were extracted regarding any history of ankle sprain(s), type of intervention used as prophylaxis after the ankle sprain, number of exposures, and any incidence of recurrence.", 'All collegiate varsity soccer players who had suffered a previous sprain to either one or both ankles (38 players) were identified as subjects.', 'Each previously injured ankle (n = 56) was considered as a case for the analysis. Ankles that had a previous sprain received one of four interventions: 1) a canvas, laced ankle brace (n = 19), 2) taping (n = 12), 3) a combination of taping and ankle bracing (n = 8), or 4) no treatment (n = 17).', 'The four intervention groups had a total of 1717 practice exposures and 650 competitive game exposures; exposures did not differ among the 4 groups. Ankle sprain recurrence frequency was 0%, 25%, 25%, and 35% for the braced, taped, combination, and untreated groups, respectively. The recurrence incidence for the braced group was significantly lower than that of the other three groups. The ankle sprain recurrence frequency did not differ among the taped, combination, and no treatment groups.\Question: Does ankle brace effectively reduce recurrence of ankle sprains in female soccer players?

A: We suggest that prophylactic ankle bracing is effective in reducing the incidence of ankle sprains in female soccer players with a previous history of ankle sprains.
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Q: Context: Staphylococcus aureus sepsis is associated with significant myocardial dysfunction. Toll-like receptor 2 (TLR2) mediates the inflammatory response to S aureus and may trigger an innate immune response in the heart. We hypothesized that a TLR2 deficiency would attenuate S aureus-induced cardiac proinflammatory mediator production and the development of cardiac dysfunction.', 'Wild-type and TLR2-deficient (TLR2D) mice were studied. S aureus challenge significantly increased tumor necrosis factor, interleukin-1beta, and nitric oxide expression in hearts of wild-type mice. This response was significantly blunted in TLR2D mice. Hearts from TLR2D mice had impaired S aureus-induced activation of interleukin-1 receptor-associated kinase, c-Jun NH2 terminal kinase, nuclear factor-kappaB, and activator protein-1. Moreover, hearts from TLR2D mice were protected against S aureus-induced contractile dysfunction.\Question: Does toll-like receptor 2 mediate Staphylococcus aureus-induced myocardial dysfunction and cytokine production in the heart?

A: These results show for the first time that TLR2 signaling contributes to the loss of myocardial contractility and cytokine production in the heart during S aureus sepsis.
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Q: Context: In the present study, we made an attempt to elucidate the role of oversecretion of interleukin-4 (IL-4) in cancer stem cells (CSCs) of head and neck squamous cell carcinoma (HNSCC).', 'HNSCC samples were analyzed for the presence of CSCs by flow cytometry. In addition, we have performed drug and apoptosis resistance assays to determine the role of IL-4 in CSCs.', 'HNSCC samples contained 3.3% of CD133+ cancer stem like side population (SP) cells in HNSCC which displayed infinite cell proliferation and they had high self-renewal capacity. These CD133+ cells displayed enhanced expression of IL-4, which promoted multidrug and apoptosis resistance. After neutralizing IL-4, the CD133+ SP cells became more sensitive to drug treatment and apoptosis.\Question: Does constitutive secretion of Interleukin-4 dictate CD133+ side population cells to resist drug treatment and cell death?

A:
Our data suggest that the autocrine secretion of IL-4 is a potential target for the development of novel anticancer drugs to prevent the CSCs-mediated therapy failure and tumorigenesis.
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