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: Impairment of the mucosal microcirculation may contribute to ethanol-induced gastric mucosal damage. In this report, we describe diffuse and severe ultrastructural damage to the capillaries of the gastric glandular mucosa of the rat that occurred within 1 min after intragastric instillation of 100% ethanol. There was a gradient of damage in that endothelial cell structure was most severely disrupted in profiles of capillaries located close to the luminal surface but some morphologic evidence of damage was evident in the wall of capillary profiles to a mean depth of 256 micron. Capillary structure was generally normal in the deeper regions of the mucosa. Pretreatment with intragastric cysteamine, 30 mg/100 g, or intragastric prostaglandin F2 beta, 0.5 mg/100 g, significantly reduced the depth in the mucosa to which damage to capillaries extended. Pretreatment with intragastric prostaglandin F2 beta, 0.2 mg/100 g, afforded no significant protection. We conclude that a 1-min exposure to 100% ethanol induces striking damage to the microcirculation of glandular mucosa of the rat stomach with severe damage to capillary profiles near the lumen and sparing of capillary profiles near the muscularis mucosa, and pretreatment with the sulfhydryl agent, cysteamine, or with a large dose of prostaglandin F2 beta reduces the extent of but does not abolish ethanol-induced damage to gastric mucosal capillaries. 
Question: Does the abstract contain any numerical data?
[EX A]: Yes

[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: Measurement of serum angiotensin-converting enzyme (ACE) is extremely useful as an aid in the diagnosis and longitudinal evaluation of patients with sarcoidosis. We have detected a human serum ACE-inhibitor which affects the ACE level obtained by activity measurements. The effect of the inhibitor can be eliminated by a mere eight-fold dilution of the serum sample with physiologic saline. We recommend that serum ACE be performed with 1:8 dilutions of serum to eliminate the effect of the ACE inhibitor. The inhibitor has a MW above 50,000 daltons, and reversibility of inhibition by dilution appears to be ion dependent. Dialysis of an inhibitor-containing serum sample against saline causes the inhibition to become irreversible, allowing the distinction between alinearity of the assay vs an inhibitor effect when a serum has ACE activity greater than 50 units/ml. The source of the serum ACE-inhibitor remains to be determined. 
Question: Does the abstract contain any numerical data?
[EX A]:
Yes

