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.

[Q]: Exposure of animals for a few hours to moderate hypoxia confers relative protection against subsequent ischemic brain damage. This phenomenon, known as hypoxic preconditioning, depends on new RNA and protein synthesis, but its molecular mechanisms are poorly understood. Increased expression of IL-6 is evident, particularly in the lungs of animals subjected to hypoxic preconditioning. Stanniocalcin-1 (STC-1) is a 56-kDa homodimeric glycoprotein originally discovered in bony fish, where it regulates calcium/phosphate homeostasis and protects against toxic hypercalcemia. We originally reported expression of mammalian STC-1 in brain neurons and showed that STC-1 guards neurons against hypercalcemic and hypoxic damage.', 'We treated neural Paju cells with IL-6 and measured the induction of STC-1 mRNA. In addition, we quantified the effect of hypoxic preconditioning on Stc-1 mRNA levels in brains of wild-type and IL-6 deficient mice. Furthermore, we monitored the Stc-1 response in brains of wild-type and transgenic mice, overexpressing IL-6 in the astroglia, before and after induced brain injury.', 'Hypoxic preconditioning induced an upregulated expression of Stc-1 in brains of wild-type but not of IL-6-deficient mice. Induced brain injury elicited a stronger STC-1 response in brains of transgenic mice, with targeted astroglial IL-6 expression, than in brains of wild-type mice. Moreover, IL-6 induced STC-1 expression via MAPK signaling in neural Paju cells.
[A]: Does hypoxic preconditioning induce neuroprotective stanniocalcin-1 in brain via IL-6 signaling?


[Q]: In this study, we compared the diagnostic performance of the standard SPECT with motion-frozen (MF) myocardial perfusion SPECT (MPS) in obese patients.', 'A total of 90 consecutive obese patients (body mass index, 30.1-46.8, average, 34.3 +/- 3.6; age, 63 +/- 12 y; 30% women) underwent standard supine rest (201)Tl/stress (99m)Tc dual-isotope gated MPS and cardiac catheterization within 3 mo. MF images were obtained by nonlinear warping of cardiac phases to the end-diastolic position. Total perfusion deficit (TPD) was obtained for summed (S-TPD) and motion-frozen (MF-TPD) datasets with sex-specific standard and MF normal limits.', 'The area under the receiver-operating-characteristic (ROC) curve for detection of coronary artery disease (CAD) by MF-TPD was significantly larger than that for S-TPD (0.93 +/- 0.25 vs. 0.88 +/- 0.32, P < 0.05). MF-TPD had higher specificity (77% vs. 55%, P < 0.05) and accuracy (89% vs. 80%, P < 0.05) than did S-TPD.
[A]: Does motion-frozen myocardial perfusion SPECT improve detection of coronary artery disease in obese patients?


[Q]: Epigenetic modifications play an important role in the regulation of gene transcription and cellular function. Here, we examined if pro-inflammatory factors present in the inflamed joint of patients with rheumatoid arthritis (RA) could regulate histone deacetylase (HDAC) expression and function in fibroblast-like synoviocytes (FLS).', 'Protein acetylation in synovial tissue was assessed by immunohistochemistry. The mRNA levels of HDAC family members and inflammatory mediators in the synovial tissue and the changes in HDAC expression in RA FLS were measured by quantitative (q) PCR. FLS were either transfected with HDAC5 siRNA or transduced with adenoviral vector encoding wild-type HDAC5 and the effects of HDAC5 manipulation were examined by qPCR arrays, ELISA and ELISA-based assays.', 'Synovial class I HDAC expression was associated with local expression of tumour necrosis factor (TNF) and matrix metalloproteinase-1, while class IIa HDAC5 expression was inversely associated with parameters of disease activity (erythrocyte sedimentation rate, C-reactive protein, Disease Activity Score in 28 Joints). Interleukin (IL)-1β or TNF stimulation selectively suppressed HDAC5 expression in RA FLS, which was sufficient and required for optimal IFNB, CXCL9, CXCL10 and CXCL11 induction by IL-1β, associated with increased nuclear accumulation of the transcription factor, interferon regulatory factor 1(IRF1).
[A]:
Do inflammatory cytokines epigenetically regulate rheumatoid arthritis fibroblast-like synoviocyte activation by suppressing HDAC5 expression?