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.
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Question: Changes of volume status can be readily inferred from variations in diameter of the inferior vena cava (IVC) measured by ultrasound. However the effect of IVC changes following acute blood loss are not fully established. In this study, three different approaches to measuring IVC variables were compared in healthy blood donors, as a model of acute volume depletion, in order to establish their relative ability to detect acute blood loss.', 'Inspiratory and expiratory IVC diameters were measured before and after blood donation in hepatic long axis, hepatic short axis and renal short axis views using a 2-5\xa0MHz curvilinear probe. All measurements were recorded and examined in real-time and post-processing sessions.', 'All windows performed satisfactorily but the renal window approach was feasible in only 30 out of 47 subjects. After blood donation, IVC diameters decreased in hepatic long axis, hepatic short axis and renal short axis (expiratory: -19.9, -18.0, -26.5\xa0%; CI 95\xa0%: 14.5-24.1; 13.1-22.9; 16.0-35.9, respectively) (inspiratory: -31.1, -31.6, -36.5\xa0%; CI 95\xa0%: 21.3-40.1; 18.8-45.2; 23.4-46.0, respectively), whereas the IVC collapsibility index increased by 21.6, 22.6 and 19.3\xa0% (CI 95\xa0%: 11.6-42.9; 18.5-39.5; 7.7-30.0). IVC diameters appeared to return to pre-donation values within 20\xa0min but this was only detected by the hepatic long axis view.

Answer: Do inferior vena cava diameters and collapsibility index reveal early volume depletion in a blood donor model?


Question: 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%).

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


Question: Aging and obesity are associated with elevated pro-inflammatory cytokines such as monocyte chemoattractant protein (MCP)-1 and tumor necrosis factor (TNF)α, which are linked to insulin resistance. Anti-inflammatory agents have marginal effect in improving insulin resistance. Hence, agents are needed to improve glycemic control despite the inflammation. Ad36, a human adenovirus, increases TNFα and MCP1 mRNA in adipose tissue, yet improves glycemic control in mice. Ad36 via its E4orf1 gene, up-regulates AKT/glucose transporter (Glut)-4 signaling to enhance cellular glucose uptake.', 'Directly test a role of Ad36, or E4orf1 in enhancing cellular glucose uptake in presence of inflammatory cytokines.', 'Experiment 1: 3T3-L1 preadipocytes were treated with 0, 10 or 100\xa0ng/mL lipopolysaccharides (LPS), and infected with 0 or 5 plaque forming units (PFU) of Ad36/cell. 3T3-L1 cells that stably and inducibly express E4orf1 or a null vector (pTRE-E4orf1 or pTRE-null cells), were similarly treated with LPS and then with doxycycline, to induce E4orf1. Experiment 2: 3T3L1 preadipocytes were treated with 25\xa0nM MCP1 or 20\xa0nM TNFα for 16\xa0h, followed by infection with 0 or 5\xa0PFU of Ad36/cell. Experiment 3: pTRE-E4orf1 or -null cells were similarly treated with MCP1 or TNFα followed by doxycycline to induce E4orf1. Cellular glucose uptake and cellular signaling were determined 72\xa0h post-Ad36 infection or E4orf1-induction, in continued presence of MCP1 or TNFα.', 'In 3T3-L1 preadipocytes, Ad36, but not E4orf1, increased MCP1 and TNFα mRNA, in presence of LPS stimulation. Ad36 or E4orf1 up-regulated AKT-phosphorylation and Glut4 and increased glucose uptake (P\xa0<\xa00.05) in the presence of MCP1 or TNFα.

Answer:
Do human adenovirus Ad36 and its E4orf1 gene enhance cellular glucose uptake even in the presence of inflammatory cytokines?