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.

[EX Q]: Abstract: Although an action of corticosteroids to inhibit glucose transport is well known, the mechanism by which this is brought about has been unclear. Some evidence has suggested an action on insulin receptors, but a postbinding or postreceptor effect has also been reported. As hydrogen peroxide acts at a postbinding site to stimulate glucose transport, studies were carried out in 3T3-L1 fibroblasts to determine whether corticosteroids would inhibit hydrogen peroxide-induced glucose transport. In this cell type, both insulin and hydrogen peroxide produced a marked increase in glucose transport after a 30-min incubation. The increase produced by hydrogen peroxide, as well as insulin, was inhibited by previous incubation of the cells with dexamethasone. These findings give further support to the conclusion that dexamethasone has effects on glucose transport at a postbinding site. As changes in membrane lipids influence the movement and/or activity of glucose transporters, and dexamethasone alters membrane lipids, dexamethasone-induced changes in the lipids of the plasma membrane may be important in the mediation of the steroid effect upon glucose transport.
Question: Does the abstract contain any numerical data?
[EX A]: Yes

[EX Q]: Abstract: In patients with primary pulmonary hypertension, competition between the right and left ventricles for the limited pericardial space results in distortion of left ventricular geometry reflected in displacement of the ventricular septum toward the left ventricular cavity. Left ventricular shape is most dramatically deranged at end-systole and early diastole, suggesting the possibility that the distribution of left ventricular diastolic filling might be altered. To investigate this hypothesis, nine patients with primary pulmonary hypertension and nine normal individuals were studied with echocardiographic techniques. Left ventricular isovolumic relaxation time was significantly prolonged in patients with primary pulmonary hypertension by comparison with normal individuals (129 +/- 36 versus 53 +/- 9 ms, p less than 0.005) and the fraction of the transmitral flow velocity integral occurring in the first half of diastole was significantly less than in normal individuals (38 +/- 14% versus 70 +/- 9%, p less than 0.005). Measurement of fractional changes in short-axis left ventricular cavity area similarly demonstrated that in patients with primary pulmonary hypertension fractional early diastolic cavity expansion (32 +/- 11%) was significantly less than in normal individuals (78 +/- 9%, p less than 0.005). In patients with primary pulmonary hypertension, the ventricular septum was abnormally flattened toward the left ventricular cavity at end-systole (normalized septal curvature 0.04 +/- 0.19) and remained that way throughout early diastolic filling but returned toward normal at end-diastole (normalized septal curvature 0.68 +/- 0.19, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
Question: Does the abstract contain any numerical data?
[EX A]: Yes

[EX Q]: Abstract: Little is known about the reflex effect on airway caliber evoked by stimulation of phrenic afferents. Therefore, in chloralose-anesthetized, paralyzed dogs, we recorded airflow, airway pressure, arterial pressure, and heart rate while electrically stimulating a phrenic nerve. Total lung resistance was calculated breath by breath. The phrenic nerve was stimulated at 3, 5, 20, 70, 140, and 200 times motor threshold and the compound action potential was recorded. Stimulation of the phrenic nerve at three and five times threshold, which activated groups I, II, and a few group III fibers, had no effect on any of the variables measured. Stimulation at 20 times threshold, which activated many group III fibers and groups I and II fibers, reflexly decreased resistance. Stimulation at 70, 140, and 200 times threshold, which activated groups I-IV fibers, evoked progressively greater decreases in lung resistance. The reflex bronchodilation evoked by phrenic nerve stimulation was unaffected by propranolol or phentolamine but was abolished by atropine. We conclude that activation of groups III and IV phrenic nerve afferents reflexly decreased total lung resistance by withdrawing cholinergic tone to airway smooth muscle.
Question: Does the abstract contain any numerical data?
[EX A]:
Yes