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: Epinephrine commonly is added to epidural opioids and local anesthetics, however, little is known about the fate of epidurally administered epinephrine. Studies have identified the epinephrine metabolizing enzyme, catechol-O-methyl transferase (COMT), in the cranial meninges of several species. The purpose of this study was to determine whether the spinal meninges also contain COMT and are capable of metabolizing epinephrine. If so, then the spinal meninges may have an important impact in limiting the bioavailability of epinephrine in both the spinal cord and epidural space.', 'Spinal meningeal specimens measuring 4 cm2 were obtained from monkeys (M. nemestrina) and farm-bred pigs and were incubated in bicarbonate-buffered mock cerebrospinal fluid. Epinephrine (200 micrograms base) was added at t = 0, and 200 min later, the mock cerebrospinal fluid was collected for metanephrine analysis. In separate experiments, pig meningeal specimens were separated into dura mater, pia-arachnoid mater, and pia mater, and the experiments were repeated to determine which meninx had the greatest COMT activity.', 'Metanephrine was produced by monkey meninges at the rate of 0.47 ng.min-1.cm-2 and by pig meninges at the rate of 0.23 ng.min-1.cm-2 (P > 0.05). The pia-arachnoid meninx produced metanephrine at a greater rate (4.48 +/- 0.46 ng.min-1.mg-1 tissue) than did the pia mater (1.3 +/- 0.15 ng.min-1.mg-1 tissue) or dura mater alone (1.82 +/- 0.23 ng.min-1.mg-1 tissue).

SOLUTION: Is epinephrine metabolized by the spinal meninges of monkeys and pigs?

PROBLEM: Pulmonary artery hypertension (PAH) is characterized by vascular remodeling, high pulmonary blood pressure, and right ventricular hypertrophy. Oxidative stress, inflammation and pulmonary artery remodeling are important components in PAH. Ellagic acid (EA) is a phenolic compound with anti-oxidative, anti-inflammatory, and anti-proliferative properties. This study aimed to investigate whether EA could prevent the development of monocrotaline (MCT)-induced PAH in rats.', 'Male Sprague-Dawley rats received EA (30 and 50mg/kg/day) or vehicle one day after a single-dose of monocrotaline (MCT, 60mg/kg). Hemodynamic changes, right ventricular hypertrophy, and lung morphological features were assessed 4weeks later. Activation of the NLRP3 (NACHT, LRR, and PYD domain-containing protein 3) inflammasome pathway in the lungs was assessed using Western blot analysis.', 'MCT induced PAH, oxidative stress, and NLRP3 inflammasome activation in vehicle-treated rats. EA reduced the right ventricle systolic pressure, the right ventricular hypertrophy and the wall thickness/external diameter ratio of the pulmonary arteries compared with vehicle. EA also inhibited the MCT-induced elevation of oxidative stress, NLRP3, and caspase-1, IL-β in the lungs and the elevated levels of brain natriuretic peptide (BNP) and inflammatory cytokines in serum.

SOLUTION: Does ellagic acid prevent monocrotaline-induced pulmonary artery hypertension via inhibiting NLRP3 inflammasome activation in rats?

PROBLEM: Restoration of posterior condylar offset during TKA is believed to be important to improving knee kinematics, maximizing ROM, and minimizing flexion instability. However, controversy exists regarding whether there are important anatomic differences between sexes and whether a unisex knee prosthesis can restore the anatomy of knees in males and females.', 'The purposes of our study were to determine if sex differences exist in (1) absolute posterior condylar offset size, (2) relative posterior condylar offset size in relation to total condylar height, and (3) posterior condylar articular cartilage thickness.', 'We identified 100 patients (50 men and 50 women) without a history of arthritis, deformity, dysplasia, osteochondral defect, fracture, or surgery about the knee who had MRI of the knee performed. All MR images were ordered by primary care medical physicians for evaluation of nonspecific knee pain. Using a previously described three-dimensional MRI protocol, we measured posterior condylar offset, total condylar height, and articular cartilage thickness at the medial and lateral femoral condyles and compared values to evaluate for potential sex differences. We performed an a priori power calculation using a 2-mm posterior condylar offset difference as the minimum clinically important difference; with 2n = 100, our power to detect such a difference was 99.8%.', 'Compared with females, males had greater medial posterior condylar offset (30 mm [95% CI, 29.3-30.7 mm; SD, 2.5 mm] vs 28 mm [95% CI, 27.0-28.5 mm; SD, 2.7 mm]), lateral posterior condylar offset (27 mm [95% CI, 26.2-27.3 mm; SD, 2.0 mm] vs 25 mm [95% CI, 24.2-25.4 mm; SD, 2.0 mm]), medial condylar height (63 mm [SD, 3.2 mm] vs 57 mm [SD, 4.4 mm]), and lateral condylar height (71 mm [SD, 5.2 mm] vs 65 mm [SD: 4.0 mm]) (all p values < 0.001). However, the mean ratio of medial posterior condylar offset to medial condylar height (0.48 [SD, 0.04] vs 0.49 [SD, 0.05]) and the mean ratio of lateral posterior condylar offset to lateral condylar height (0.38 [SD, 0.05] vs 0.38 [SD, 0.03]) were not different between sexes (p = 0.08 and p = 0.8, respectively). There also was no sex difference in mean articular cartilage thickness at either condyle (medial condyle: 2.7 mm [SD, 0.5 mm] vs 2.5 mm [SD, 0.7 mm]; lateral condyle: 2.6 mm [SD, 0.6 mm] vs 2.5 mm [SD, 0.8 mm]) (both p values ≥ 0.1).

SOLUTION:
Do no sex differences exist in posterior condylar offsets of the knee?