TASK DEFINITION: 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.
PROBLEM: To determine whether recent reimbursement cuts have resulted in a shift of outpatient MRI from private offices to hospital outpatient departments (HOPDs); and to study office MRI utilization trends among radiologists and other specialists.', 'The Medicare Part B Physician/Supplier Procedure Summary Master Files were used. MRI codes were aggregated, and total MRI volumes from 2002 to 2012 were studied. Medicare place-of-service codes were used to identify studies performed in private offices and HOPDs and create trend lines. Specialty codes were used to categorize private office MRI users as radiologists, orthopedic surgeons, other physicians, and independent diagnostic testing facilities.', 'Medicare office and HOPD utilization of MRI (all specialties) rose rapidly from 2002 to 2006, reaching 2,727,807 in offices and 2,355,641 in HOPDs. Thereafter, office volume steadily declined, whereas HOPD volume steadily increased. By 2012, more studies were done in HOPDs than in offices. Over the entire period from 2002 and 2012, office MRI volume among radiologists increased 27%, compared with 216% among orthopedic surgeons and 124% among other physicians.

SOLUTION: Do trends in outpatient MRI seem to reflect recent reimbursement cuts?

PROBLEM: Angiotensin II (Ang II) signaling has been implicated in cardiac arrhythmogenesis, which involves induction of reactive oxygen species (ROS). It was shown that Ang II can activate Ca/Calmodulin kinase II (CaMKII) by oxidation via a NADPH oxidase 2 (NOX2)-dependent pathway leading to increased arrhythmic afterdepolarizations. Interestingly, cAMP-dependent protein kinase A (PKA) which regulates similar targets as CaMKII has recently been shown to be redox-sensitive as well.', 'This study aims to investigate the distinct molecular mechanisms underlying Ang II-related cardiac arrhythmias with an emphasis on the individual contribution of PKA vs. CaMKII.', 'Isolated ventricular cardiac myocytes from rats and mice were used. Ang II exposure resulted in increased NOX2-dependent ROS generation assessed by expression of redox-sensitive GFP and in myocytes loaded with ROS indicator MitoSOX. Whole cell patch clamp measurements showed that Ang II significantly increased peak Ca and Na current (ICa and INa) possibly by enhancing steady-state activation of ICa and INa. These effects were absent in myocytes lacking functional NOX2 (gp91phox(-/-)). In parallel experiments using PKA inhibitor H89, the Ang II effects on peak INa and ICa were also absent. In contrast, genetic knockout of CaMKIIδ (CaMKIIδ(-/-)) did not influence the Ang II-dependent increase in peak ICa and INa. On the other hand, Ang II enhanced INa inactivation, increased late INa and induced diastolic SR (sarcoplasmic reticulum) Ca leak (confocal Ca spark measurements) in a CaMKIIδ-, but not PKA-dependent manner. Surprisingly, only the increase in diastolic SR Ca leak was absent in gp91phox(-/-)myocytes suggesting that Ang II regulates INa inactivation in a manner dependent on CaMKII- but not on NOX2. Finally, we show that Ang II increased the propensity for cellular arrhythmias, for which PKA and CaMKII contribute, both dependent on NOX2.

SOLUTION: Does nADPH oxidase 2 mediate angiotensin II-dependent cellular arrhythmias via PKA and CaMKII?

PROBLEM: To test whether an acute transfusion practice of packed red blood cells (pRBC) : fresh-frozen plasma (FFP) 1 : 1 would be associated with reduced mortality in acute bleeding multiply injury.', 'Retrospective analysis using the TR-DGU database (Trauma Registry of the Deutsche Gesellschaft für Unfallchirurgie 2002-2006) on primary admissions with substantial injury (Injury Severity Score > 16) and massive transfusion (> 10 pRBCs). Seven hundred thirteen patients were divided into three groups according to the pRBC : FFP ratio transfused, that is, (i) pRBC : FFP > 1.1; (ii) pRBC : FFP 0.9-1.1 (1 : 1); and (iii) pRBC : FFP < 0.9, and mortality rates were compared.', 'Four hundred ninety-seven (69.7%) of patients were male, the mean age was 40.1 (+/- 18.3) years. Injury characteristics and pathophysiological state upon emergency room arrival were comparable between groups. Out of 713, 484 patients had undergone massive transfusion with pRBC : FFP > 1.1, 114 with pRBC : FFP 0.9-1.1 (1 : 1), and 115 with pRBC : FFP < 0.9 ratios. Acute mortality (< 6 h) rates for pRBC : FFP > 1.1, pRBC : FFP 0.9-1.1 (1 : 1), and pRBC : FFP < 0.9 ratios were 24.6, 9.6 and 3.5% (P < 0.0001), 24-h mortality rates were 32.6, 16.7 and 11.3% (P < 0.0001), and 30-day mortality rates were 45.5, 35.1 and 24.3% (P < 0.001). The frequency for septic complications and organ failure was higher in the pRBC : FFP 0.9-1.1 (1 : 1) group, ventilator days and length of stays for intensive care unit and overall in-hospital were highest in the pRBC : FFP < 0.9 ratio group (P < 0.0005).

SOLUTION:
Are red-blood-cell to plasma ratios transfused during massive transfusion associated with mortality in severe multiple injury : a retrospective analysis from the Trauma Registry of the Deutsche Gesellschaft für Unfallchirurgie?