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.
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Question: Abstract: The release of PRL from the pituitary of a teleost fish, the tilapia (Oreochromis mossambicus), has been previously shown to be dependent on calcium. However, the source(s) and specific action(s) of calcium in the secretory process have not been identified. Also undefined are the mechanisms by which regulators of PRL cell function may alter calcium distribution. In the present investigation, the elevation of medium K+ concentration during static incubations to a depolarizing concentration (56 mM) produced no change in cumulative PRL release over control levels during the 18-20 h of incubation. During perifusion incubation, exposure to high K+ concentrations briefly stimulated (less than or equal to 10 min) and then depressed PRL release. In contrast, reduced medium osmotic pressure elicited a rapid elevation in PRL release that was sustained for 2 h or more. D600, a calcium entry blocker, at 10(-5) M diminished the K+-induced pulses of PRL release. The same concentration, however, did not alter the release of PRL evoked by reduced osmotic pressure. In contrast, CoCl2, which blocks a range of calcium-mediated processes in addition to calcium influx, suppressed PRL release during perifusion and static incubations in hyposmotic medium. These findings suggest that while PRL secretion from the tilapia pituitary is calcium dependent, calcium entry through voltage-regulated plasmalemma channels may not be a prerequisite to the actions of reduced osmotic pressure.
Question: Does the abstract contain any numerical data?

Answer: Yes

Question: Abstract: Abnormal left ventricular diastolic performance, an early manifestation of hypertension in the heart, may precede the development of left ventricular hypertrophy. To assess effects of antihypertensive therapy on the heart, left ventricular mass (determined by echocardiography) and rapid left ventricular filling rate (determined by radionuclide ventriculography) were compared before and after 6 months of treatment of 16 patients. Nitrendipine (a dihydropyridine calcium channel blocker) was given alone or in combination with either propranolol or hydrochlorothiazide, or both, and significantly reduced blood pressure (156/103 +/- 12/7 to 137/89 +/- 10/6 mm Hg). In 6 of the 16 patients, left ventricular mass decreased by more than 10% (270 +/- 95 to 193 +/- 47 g, p less than 0.01); in the same patients, left ventricular filling rate increased (2.03 +/- 0.35 to 2.30 +/- 0.45 end-diastolic counts/s [EDC/s], p less than 0.01). In the one patient whose left ventricular mass increased (137 to 195 g), left ventricular filling rate decreased from 2.01 to 1.78 EDC/s. In the remaining nine patients who had no change in left ventricular mass, there was no significant changes in left ventricular filling. The changes in ventricular mass and filling could not be related to the extent of change in blood pressure or heart rate. These data suggest that regression of left ventricular mass during antihypertensive therapy with nitrendipine is accompanied by improved diastolic function.
Question: Does the abstract contain any numerical data?

Answer: Yes

Question: Abstract: Published normal histomorphometric data were used to derive distributions of thicknesses of trabecular plates and completed bone remodelling units (the basic multicellular unit carrying out bone remodelling, the BMU, when completed is termed a structural unit BSU). A stochastic model was set up to investigate the predictions of current BMU theory. Each of 100 trabecular "thicknesses" was drawn from the appropriate normal distribution using a pseudorandom number generator. Each day, each of its two surfaces when quiescent was assumed to have a 1:900 chance of initiating a remodelling cycle. Resorption (active, 12 days; reversal phase, 27 days) was followed by formation (94 +/- 35 days) and resulted in BMU balance when resorption depth was 36.8 +/- 9.2 micron. Fenestration (thickness less than 0) was assumed to lead to permanent loss of the trabecula. The original model unrealistically increased its mean trabecular thickness as thin trabeculae were lost. This was corrected by assuming that thin trabeculae had greater osteoblastic stimulation and a consequent tendency to thicken, perhaps due to higher mechanical loading. Over 20 years, 14% of trabeculae were lost when the BMU balance was exact and the distribution of trabecular thicknesses was unchanged. About one-half of fenestrations were due to deeper-than-average resorption cavities developing in thin trabeculae, and the remainder to coincident remodelling on both surfaces. A 10% fall in osteoblast lifespan resulted in an additional 36.7% loss of trabecular bone volume and mean trabecular thickness fell to 83.1 micron, compatible with Courpron's data. Simulating more rapid mechanisms of bone loss, approximately 50% of trabeculae could be lost after ten years by the arrest of bone formation; the doubling of resorption depth with unchanged bone formation; and a doubling in the rate of initiation of new BMUs with unchanged bone formation rate, all three followed by complete recovery of BMU balance after only two years. In each case, mean trabecular thickness fell only transiently but trabeculae continued to be lost after recovery. Prolonged osteoblast life span was the most likely explanation for the increased mean trabecular thicknesses and trabecular bone volumes seen in patients with osteoporosis, when treated with sodium fluoride plus calcium supplements or daily injections of parathyroid peptide hPTH 1-34.
Question: Does the abstract contain any numerical data?

Answer:
Yes