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.

[Q]: Abstract: We undertook a study of the separate and combined effects of age and sex on the pulsatile pattern of GH secretion. The 24-h secretory profile of GH was generated by 20-min sampling in 10 young women (aged 18-33 yr), 10 young men (aged 18-33 yr), 8 postmenopausal women (aged greater than 55 yr), and 8 older men (aged greater than 55 yr). A computer-assisted pulse analysis program was used to assess both total GH secretion, as reflected in the 24-h integrated GH concentration (IGHC), and pulsatile secretion, as denoted by pulse frequency, duration, amplitude, and the fraction of GH secreted in pulses during the 24-h period (FGHP). IGHC was significantly greater in women than in men (P less than 0.025) and greater in the young than in the old (P less than 0.003). The mean pulse amplitude, duration, and FGHP were each greater in the young (P less than 0.006, P less than 0.03, and P less than 0.0001, respectively), but not significantly different between the sexes. The mean pulse frequency was not affected by sex or age. The serum concentration of free estradiol, but not free testosterone, correlated with IGHC (r = 0.46; P less than 0.005), pulse amplitude (r = 0.53; P less than 0.001), and FGHP (r = 0.59; P less than 0.0002). After correcting for the effects of estradiol, neither sex nor age influenced IGHC or mean pulse amplitude, while the effect of age on FGHP was reduced from 81% to 29%. Of the indices of GH secretion, FGHP had the strongest correlation (r = 0.43; P less than 0.006) with somatomedin-C. Somatomedin-C declined significantly with age in both sexes. Our results indicate that sex and age have independent and interrelated effects on GH secretion. These effects can be largely accounted for by corresponding variations in endogenous estradiol levels. These observations suggest an amplifying action of estradiol on the neuroendocrine regulation of pulsatile GH release. 
Question: Does the abstract contain any numerical data?
[A]: Yes


[Q]: Abstract: The effects of parental smoking on IgE and IgD levels in cord serum and subsequent infant allergy were investigated in an unselected series of 186 European newborn infants. Maternal smoking caused a significant rise in both IgE (p less than 0.05) and IgD (p less than 0.05), a finding that was most apparent in newborn infants with a negative biparental history of allergy (p less than 0.025 and p = 0.005, respectively). Furthermore, newborn infants of nonallergic parents had a more than threefold (p less than 0.01) higher incidence of elevated cord IgE (greater than or equal to 1.20 IU/ml) and a fourfold (p = 0.005) higher risk of developing definite or probable atopic disease before 18 months of age if the mother smoked than if she did not. Paternal smoking did not influence, in whatever the subgroup, cord IgE or subsequent infant allergy but increased cord IgD (p less than 0.001) among newborn infants with a negative family history even after controlling for maternal smoking (p less than 0.04). These results suggest that parental smoking in some way affects the fetal immune system, probably via substances in tobacco smoke. Maternal smoking in particular appears to exert a pronounced effect on the IgE system already in fetal life, predisposing even "low-risk" infants to subsequent sensitization, probably in synergy with a later acquired mucosal damage that would facilitate penetration of foreign matter. Pregnant women and mothers should be encouraged to try and give up smoking that might help to prevent allergic disease in their infants. 
Question: Does the abstract contain any numerical data?
[A]: Yes


[Q]: Abstract: We examined the activity of defensins, cysteine-rich cationic peptides that are abundant in the cytoplasmic granules of human and rabbit granulocytes, against various tumor targets. The three human defensins, HNP-1, HNP-2, and HNP-3, lysed human and murine targets in chromium release and dye exclusion assays. Defensin-mediated tumor cell lysis was concentration-dependent, inhibited by serum, and dependent on temperature-sensitive events. Lysis was first detected by three hours of incubation and it reached a plateau between eight and 14 hours. In vitro exposure of murine teratocarcinoma cells to HNP 1-3 abrogated their oncogenicity in vivo. Nonmalignant target cells were also susceptible to defensin-mediated lysis. Four rabbit granulocyte defensins exerted marked (NP-1, NP-2) or moderate (NP-3a, NP-3b) cytotoxic activity, whereas defensin NP-5 was not cytotoxic. When tumor cells were incubated with human defensins in combination with hydrogen peroxide, synergistic cytotoxicity was detected. As defensins are released from granulocytes by various stimuli, their release could contribute to extracellular cytotoxicity which is independent of reactive oxygen intermediates. 
Question: Does the abstract contain any numerical data?
[A]:
Yes


