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.

Example Input: Context: An association between mitral valvar prolapse and low body mass index has been proposed. The goal of this study was to evaluate this suggested association using two independent and large databases. For comparison, we evaluated the association, if any, between bicuspid aortic valve and low body mass index.', 'We retrospectively analyzed, using uni- and multivariate analysis, 1742 echocardiograms that were performed as a part of a cardiac screening of teenage athletes and 24,265 echocardiograms performed between 1984 and 1998 for various clinical indications.', 'The first database included a total of 12,926 (53%) female and 11,339 (47%) male patients. The second database included a total of 1172 male (67%) and 570 female (33%) high school athletes. Mitral valvar prolapse was independently associated with low body mass index in addition to mitral regurgitation in both data bases. An index less than 30 occurred in 78 of 13,874 (0.6%) as opposed to 7 of 3236 (0.2%) in the echo data base, p equal to 0.03, odds ratio: 2.4 confidence intervals: 1.1-5.2, and an index less than 20 occurred in 7 of 354 (2%) as opposed to 6 of 944 (0.6%) in the athletic data base, p equal to 0.03, odds ratio: 3.2 confidence intervals: 1.05-9.5. The finding of a bicuspid aortic valve did not have any association with low body mass index.\Question: Is mitral valvar prolapse significantly associated with low body mass index in addition to mitral and tricuspid regurgitation?
Example Output: In our two independent databases, mitral valvar prolapse was independently associated with low body mass index in addition to mitral and tricuspid regurgitation. The cause of this association remains unknown.

Example Input: Context: Allogeneic mesenchymal stem cells (MSCs) exhibit therapeutic effects in human autoimmune diseases such as systemic lupus erythematosus (SLE), but the underlying mechanisms remain largely unknown. The aim of this study was to investigate how allogeneic MSCs mediate immunosuppression in lupus patients.', 'The effects of allogeneic umbilical cord-derived MSCs (UC-MSCs) on inhibition of T cell proliferation were determined. MSC functional molecules were stimulated with peripheral blood mononuclear cells from healthy controls and SLE patients and examined by real-time polymerase chain reaction. CD4+ and CD8+ T cells were purified using microbeads to stimulate MSCs in order to determine cytokine expression by MSCs and to further determine which cell subset(s) or which molecule(s) is involved in inhibition of MSC-mediated T cell proliferation. The related signaling pathways were assessed. We determined levels of serum cytokines in lupus patients before and after UC-MSC transplantation.', 'Allogeneic UC-MSCs suppressed T cell proliferation in lupus patients by secreting large amounts of indoleamine 2,3-dioxygenase (IDO). We further found that interferon-γ (IFNγ), which is produced predominantly by lupus CD8+ T cells, is the key factor that enhances IDO activity in allogeneic MSCs and that it is associated with IFNGR1/JAK-2/STAT signaling pathways. Intriguingly, bone marrow-derived MSCs from patients with active lupus demonstrated defective IDO production in response to IFNγ and allogeneic CD8+ T cell stimulation. After allogeneic UC-MSC transplantation, serum IDO activity increased in lupus patients.\Question: Is a CD8 T cell/indoleamine 2,3-dioxygenase axis required for mesenchymal stem cell suppression of human systemic lupus erythematosus?
Example Output: We found a previously unrecognized CD8+ T cell/IFNγ/IDO axis that mediates the therapeutic effects of allogeneic MSCs in lupus patients.

Example Input: Context: A number of distinct stress signaling pathways in myocardium cause cardiac hypertrophy and heart failure. Class II histone deacetylases (HDACs) antagonize several stress-induced pathways and hypertrophy. However, cardiac hypertrophy induced by transgenic overexpression of the homeodomain only protein, HOP, can be prevented by the nonspecific HDAC inhibitors trichostatin A and valproic acid, suggesting that alternate targets that oppose class II HDAC function might exist in myocardium. We tested the effects of several HDAC inhibitors, including a class I HDAC-selective inhibitor, SK-7041, on cardiac hypertrophy induced by angiotensin II (Ang II) treatment or aortic banding (AB).', 'Cardiac hypertrophy was induced by chronic infusion of Ang II or by AB in mice or rats and evaluated by determining the ratio of heart weight to body weight or to tibia length, cross-sectional area, or echocardiogram. Cardiac hypertrophy induced by Ang II or AB for 2 weeks was significantly reduced by simultaneous administration of trichostatin A, valproic acid, or SK-7041. Echocardiogram revealed that exaggerated left ventricular systolic dimensions were relieved by HDAC inhibitors. HDAC inhibitors partially reversed preestablished cardiac hypertrophy and improved survival of AB mice. The expressions of atrial natriuretic factor, alpha-tubulin, beta-myosin heavy chain, and interstitial fibrosis were reduced by HDAC inhibition.\Question: Does inhibition of histone deacetylation block cardiac hypertrophy induced by angiotensin II infusion and aortic banding?
Example Output:
These results suggest that the predominant effect of HDAC inhibition, mainly mediated by class I HDACs, is to prevent cardiac hypertrophy in response to a broad range of agonist and stretch stimuli.