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.

Ex Input:
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.

Ex Output:
Does hypoxic preconditioning induce neuroprotective stanniocalcin-1 in brain via IL-6 signaling?


Ex Input:
A significant proportion of school-aged children experience special health care needs (SCHN) and seek care from pediatricians with a wide range of condition types and severity levels. This study examines the learning pathways of children with established (already diagnosed at school entry) and emerging (teacher identified) SHCN from school entry through the elementary school years.', 'The Longitudinal Study of Australian Children (LSAC) is a nationally representative clustered cross-sequential sample of 2 cohorts of Australian children which commenced in May 2004. Data were analyzed from the LSAC kindergarten cohort (n\xa0=\xa04,983), as well as a subsample of 720 children for whom teachers also completed the Australian Early Development Index checklist, a measure of early childhood development at school entry that includes SHCN.', 'Latent class analysis was utilized to establish 3 academic trajectories from 4-5 to 10-11 years: high (24.3%), average (49.8%), and low (23.6%). Descriptive statistics revealed a trend for both children with established and emerging SHCN to fall into weaker performing learning pathways. Multinomial logistic regression focusing on those children with emerging SHCN confirmed this pattern of results, even after adjustment for covariates (relative risk 3.06, 95% confidence interval 1.03-9.10). Children who additionally had low socioeconomic standing were particularly at risk.

Ex Output:
Does learning trajectories of children with special health care need across the severity spectrum?


Ex Input:
The persistence of human immunodeficiency virus (HIV) type 1 within resting CD4+ T cells poses a daunting therapeutic challenge. Histone deacetylase (HDAC)-1, a chromatin-remodeling enzyme that can mediate gene silencing, is recruited to the HIV-1 long terminal repeat by the host transcription factor LSF. Pyrrole-imidazole polyamides, small molecules that target specific DNA sequences, can access the nucleus of cells and specifically block transcription-factor binding.', 'We used polyamides to directly test the role of chromatin remodeling in HIV quiescence in primary resting CD4+ T cells obtained from HIV-infected patients.', "After exposure to any of 4 different polyamides that specifically block HDAC-1 recruitment by LSF to the HIV promoter, replication-competent HIV was recovered from cultures of resting CD4+ T cells in 6 of 8 HIV-infected patients whose viremia had been suppressed by therapy. In comparison, HIV was not recovered after exposure to control, mismatched polyamides but was recovered from 7 of 8 of these patients' samples after the activation of T cells.

Ex Output:

Do polyamides reveal a role for repression in latency within resting T cells of HIV-infected donors?