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: We present the case of an 11-month-old baby with a burn that healed normally over a month, but subsequently developed successive crops of blisters over the scar. There were no changes in his general condition. Clinical, immunological, histological and ultrastructural studies provided a diagnosis of mechanical dermatitis produced by microtrauma. Electron microscopy studies revealed the sub-epidermal nature of the blisters and the presence of underlying fibrin deposits.
Question: Does the abstract contain any numerical data?
[EX A]: Yes

[EX Q]: Abstract: We examined the contributions of dietary protein and mineral to fracture-healing by assessing the mechanical properties of fracture callus in rats that were fed a diet that was deficient in or enriched by these nutrients. In order to isolate the effects of diet on fracture-healing, we developed a method for producing a standard closed femoral fracture with minimum-soft-tissue injury. Three groups of animals were studied. Group I was a control group, in which the rats did not undergo an operation. The rats in Group II underwent intramedullary pinning of the right femur, but no fracture was created. The rats in Group III underwent pinning identical to that used for Group II, after which a closed, transverse femoral fracture was produced. Immediately after surgery, the animals in each group were subdivided into five diet-treatment subgroups. Subgroup A received a regular diet; Subgroup B received a protein-free diet; and Subgroup C received a mineral-free diet that was lacking in calcium, phosphorus, and vitamin D. Subgroup D received a protein-supplemented diet that was composed of three times the calculated requirement of protein, and Subgroup E received a mineral-supplemented diet that was composed of three times the calculated requirements of calcium and phosphorus as well as a therapeutic dose of vitamin D, equivalent to that used in the treatment of osteomalacia. At the end of five weeks, the animals were killed and the right femur of each one was subjected to torsion-testing to failure.(ABSTRACT TRUNCATED AT 250 WORDS)
Question: Does the abstract contain any numerical data?
[EX A]: Yes

[EX Q]: Abstract: We have previously demonstrated that T3 increases adenylate cyclase activity in rat thymocyte plasma membranes by a mechanism that is calcium dependent. In the present studies we have examined whether calmodulin participates in this response to T3. Initial experiments provided evidence that calmodulin is involved in regulating the activity of the guanyl nucleotide-dependent adenylate cyclase in this tissue. Thus, compared with findings in freshly prepared membranes, dialysis of thymocyte plasma membrane preparations for 20 h at 4 C decreased their calmodulin concentrations from an initial value of approximately 600 ng/100 micrograms protein by about 50% and decreased adenylate cyclase activity by approximately 80%. Although storage of the same preparations under comparable conditions resulted in no change in calmodulin content, it caused an approximate 30% decrease in adenylate cyclase activity. Addition of calmodulin had no effect on adenylate cyclase activity in fresh or stored membrane preparations, but produced a dose-dependent increase in enzyme activity in preparations that had been dialyzed. Further, when added to freshly isolated membranes, three calmodulin antagonists, trifluoperazine, calmidazolium, and calmodulin antibodies, all produced a concentration-dependent inhibition of adenylate cyclase activity, and this was completely reversed in all cases by the addition of high concentrations of exogenous calmodulin. The stimulation of guanyl nucleotide-dependent adenylate cyclase activity that T3 induced in fresh membrane preparations was present in membranes that had been stored, but was absent in those that had been dialyzed. In addition, the response to T3 in fresh membranes was inhibited or abolished by all three calmodulin antagonists. Both in dialyzed membranes and in the presence of antagonists, the response to T3 was restored by the addition of exogenous calmodulin. We conclude that calmodulin influences the activity of the guanyl nucleotide-dependent adenylate cyclase in rat thymocytes and ultimately mediates the stimulation of enzyme activity that T3 produces. Such mediation very likely explains the calcium-dependent nature of the stimulatory effect of T3 on thymocyte adenylate cyclase activity.
Question: Does the abstract contain any numerical data?
[EX A]:
Yes