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.

Input: Consider Input: To determine whether early enteral feeding in a septic intensive care unit (ICU) population, using a formula supplemented with arginine, mRNA, and omega-3 fatty acids from fish oil (Impact), improves clinical outcomes, when compared with a common use, high protein enteral feed without these nutrients.', 'A prospective, randomized, multicentered trial.', 'ICUs of six hospitals in Spain.', 'One hundred eighty-one septic patients (122 males, 59 females) presenting for enteral nutrition in an ICU.', 'Septic ICU patients with Acute Physiology and Chronic Health Evaluation (APACHE) II scores of > or =10 received either an enteral feed enriched with arginine, mRNA, and omega-3 fatty acids from fish oil (Impact), or a common use, high protein control feed (Precitene Hiperproteico).', 'One hundred seventy-six (89 Impact patients, 87 control subjects) were eligible for intention-to-treat analysis. The mortality rate was reduced for the treatment group compared with the control group (17 of 89 vs. 28 of 87; p < .05). Bacteremias were reduced in the treatment group (7 of 89 vs. 19 of 87; p = .01) as well as the number of patients with more than one nosocomial infection (5 of 89 vs. 17 of 87; p = .01). The benefit in mortality rate for the treatment group was more pronounced for patients with APACHE II scores between 10 and 15 (1 of 26 vs. 8 of 29; p = .02).

Output: Does an immune-enhancing enteral diet reduce mortality rate and episodes of bacteremia in septic intensive care unit patients?


Input: Consider Input: In Australia, adult immunisation coverage is primarily monitored via periodic telephone surveys that rely on self-reported immunisation status. All Australian residents are eligible for Medicare, so we examined the feasibility of using immunisation-specific Medicare Benefits Schedule (MBS) item numbers to monitor and estimate adult influenza immunisation coverage.', 'Baseline questionnaire data from 267 129 participants from the 45 and Up Study, a prospective cohort study, were linked to data containing information on individual MBS immunisation-specific items from 2006 to 2011. Temporal trends in recording of these items were examined. Self-reported influenza immunisation status obtained from a follow-up questionnaire from 27 036 participants was then compared with the MBS immunisation records.', 'From 2006 to 2011, the pattern of MBS immunisation claims was consistent with self-reported influenza immunisation trends, with annual peaks occurring from March to May. There was fair agreement between MBS immunisation records and self-reported influenza immunisation: 48.8% (95% CI 47.1, 50.4) of participants who self-reported influenza immunisation had a matching MBS record, and 79.6% (95% CI 78.8, 80.4) who reported never having influenza immunisation had no matching MBS record. However, compared with self-reported influenza vaccination for people aged ≥65 years from the 2009 Adult Immunisation Telephone Survey (74.6%), the proportion of participants aged >65 years with an MBS immunisation record was low, with an annual median of 39.3% (range 28.3%-62.1%).

Output: Do medicare Benefits Schedule data to monitor influenza immunisation in Australian adults?


Input: Consider Input: Because accumulation of extracellular matrix is a prominent characteristic of the microangiopathy that complicates long-term diabetes, a pathogenetic role for transforming growth factor beta (TGF-beta) is being considered. Having observed that glucose levels mimicking diabetic hyperglycemia induce in vitro endothelial cell overexpression of extracellular matrix molecules, decreased replication, and increased levels of TGF-beta mRNA, we have examined whether the effects of high glucose are mediated by autocrine TGF-beta.', 'TGF-beta levels were measured by bioassay in the media conditioned by human umbilical vein endothelial cells cultured in the presence of high (30 mM) or normal (5 mM) glucose concentrations. The effect of high glucose was tested on the proliferation of two epithelial cell lines, one (Mv1Lu) exquisitely sensitive to TGF-beta and the other (DR mutants) insensitive to the cytokine. To examine whether high glucose and TGF-beta affect cellular programs in a similar manner, the effects of high glucose and exogenous TGF-beta were compared on proliferation and gene expression of endothelial cells.', 'Media conditioned by endothelial cells cultured in high or normal glucose contained similar amounts of TGF-beta (4.9 +/- 3.5 and 3.7 +/- 2.5 ng/10(6) cells, respectively (mean +/- SD)), all in the latent form. The replication of parental Mv1Lu cells and their DR mutants was decreased by high glucose to the same extent. Whereas the inhibitory effect of high glucose on endothelial cell replication was reversible, that of TGF-beta was not. Both perturbations induced up-regulation of fibronectin expression, but the effects were additive. Only TGF-beta induced overexpression of Type IV collagenase.


Output: Are the effects of high glucose on human endothelial cell growth and gene expression mediated by transforming growth factor-beta?