instruction:
Indicate the presence of numerical data in the abstract (whether numerical data plays a key role in medical records), solely using the information from the abstract.
question:
Abstract: In search of a practical biochemical test that will reflect hepatic steatosis, we assessed the significance of serum cholinesterase activity in 48 patients with nonalcoholic fatty liver, 16 obese subjects without fatty liver, 30 cases of chronic persistent hepatitis, 38 cases of chronic active hepatitis, and 20 cases of liver cirrhosis. Increased cholinesterase activity was observed in nonobese as well as obese patients with fatty liver, whereas obese subjects without fatty liver showed levels in the upper normal range. When we set a cutoff level above the upper normal limit, half of the patients with fatty liver showed values above it, with only a few overlaps with other patients. When obese patients with fatty liver took a low-caloric diet, cholinesterase activity decreased, clearly reflecting improvement of hepatic steatosis. Thus, measurement of cholinesterase activity is of diagnostic value and an alternative to computed tomography in hepatic steatosis, and will provide a practical measure for the assessment of effects during follow-up.
Question: Does the abstract contain any numerical data?
answer:
Yes

question:
Abstract: We compared the degree of complement activation in 15 patients receiving massive blood transfusions and 21 patients with the septic syndrome and examined its association with other risk factors for adult respiratory distress syndrome (ARDS). Patients with massive transfusion (n = 8) as their only risk factor for ARDS had lower C3a levels (250 +/- 80 ng/ml) and a lower incidence of ARDS (0%) than patients with massive transfusion plus other risk factors (n = 7; C3a, 600 +/- 120 ng/ml; ARDS, 55%) or patients with the septic syndrome (n = 21; C3a, 540 +/- 80 ng/ml; ARDS, 19%). In our patients, the degree of complement activation appeared to reflect the presence of complicating clinical conditions.
Question: Does the abstract contain any numerical data?
answer:
Yes

question:
Abstract: Decreased maximal O2 uptake (VO2max) and stimulation of the sympathetic nervous system have been previously shown to occur at high altitude. We hypothesized that tachycardia mediated by beta-adrenergic stimulation acted to defend VO2max at high altitude. Propranolol treatment beginning before high-altitude (4,300 m) ascent reduced heart rate during maximal and submaximal exercise in six healthy men treated with propranolol (80 mg three times daily) compared with five healthy subjects receiving placebo (lactose). Compared with sea-level values, the VO2max fell on day 2 at high altitude, but the magnitude of fall was similar in the placebo and propranolol treatment groups (26 +/- 6 vs. 32 +/- 5%, P = NS) and VO2max remained similar at high altitude in both groups once treatment was discontinued. During 30 min of submaximal (80% of VO2max) exercise, propranolol-treated subjects maintained O2 uptake levels that were as large as those in placebo subjects. The maintenance of maximal or submaximal levels of O2 uptake in propranolol-treated subjects at 4,300 m could not be attributed to increased minute ventilation, arterial O2 saturation, or hemoglobin concentration. Rather, it appeared that propranolol-treated subjects maintained O2 uptake by transporting a greater proportion of the O2 uptake with each heartbeat. Thus, contrary to our hypothesis, beta-adrenergic blockade did not impair maximal or submaximal O2 uptake at high altitude due perhaps to compensatory mechanisms acting to maintain stroke volume and cardiac output.
Question: Does the abstract contain any numerical data?
answer:
Yes