The aim of this study was to investigate the developmental change of gastric myoelectrical activity in humans. Five groups of healthy subjects were studied, including 10 preterm newborns, 8 full-term newborns, 8 full-term infants (ages 2-6 mo), 9 children (ages 4-11 yr), and 9 adults. Gastric myoelectrical activity was recorded using surface electrogastrography for 30 min before and 30 min after a test meal in each subject. Spectral analysis methods were applied to compute the parameters of the electrogastrogram (EGG). The results showed that the percentage of 2- to-4-cycles/min (cpm) slow waves was 26.6 +/- 3.9% in the preterm newborns, 30.0 +/- 4.0% in full-term newborns, 70 +/- 6.1% in 2- to 6-mo-old infants (P < 0.001 compared with newborns), 84.6 +/- 3.2% in 4- to 11-yr-old children (P < 0.03 compared with infants), and 88.9 +/- 2.2% in the adults (P > 0.05 compared with children). In conclusion, gastric slow waves are absent at birth, and there is a maturing process after birth. Age-matched controls are necessary for the interpretation of EGG data from neonates and infants, whereas EGG data in children are the same as in adults.

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I n Eseheriehia coli there is one binding site per ribosome for lincomycin, chloramphenicol and erythromycin.These antibiotics act a t closely related sites on the 50-5 subunit. There are, however, some interesting differences in the properties of the three sites, such as: (a) the apparent possibility of obstructing the lincomycin site without closing the chloramphenicol site, (b) asymmetry of competition effects between chloramphenicol and erythromycin, (c) differential responses to ethanol and (d) differential responses to other antibiotics (puromycin, macrolides, streptogramins A and B and others also acting on the larger ribosome subunit).Chloramphenicol binds to ribosomes from bacteria [1,2], chloroplast and blue-green algae [3,4] a t a site located on the 50-S subunit [5,6]. Chloramphenicol-binding is inhibited by a number of other antibiotic inhibitors of protein synthesis, including members of the lincomycin, streptogramin-A and macrolide groups, thus suggesting that all of these compounds interact with the 50-S subunit a t related sites [6]. Binding to the 50-S subunit has been directly confirmed in the cases of lincomycin [7 -91, members of the streptogramin-A group [lo -121, and the macrolides erythromycin [13-151 and spiramycin [ l l , 161.By use of the experimental system known as the "fragment reaction", the above antibiotics have been shown to act on the peptidyl-transferase centre of the 50 S subunit [17]. We have been investigating relationships between the substrate and antibioticbinding sites on this centre [IS, 211. The present paper reports further studies into the nature of the chloramphenicol, lincomycin and erythromycin sites. MATERIALS AND METHODSRibosomes and ribosomal subunits were prepared from log phase Escheriehia coli MRE 600 following methods previously described 1221. The S-30 extract of cells was incubated a t 37 "C for 15 min with 0.i mM puromycin. The antibiotic was removed during purification of the ribosomes. Estimations on the calculations of ribosome concentrations were carried out on the basis that I mglml70 S or 50 S has an absorbance of 15 units a t 260 nm and that the molecular weight of 7 0 s = 2.65 x 106and of50S = 1.55+106 [23].Abbreviation. Ka, dissociation constant.

The generally accepted concept that metabolic acidosis in infant diarrhea results from the loss of buffer base in the stool has been based on the common observation that inorganic cations predominate over inorganic anions in diarrheal stools (1)(2)(3)(4)(5). This predominant loss of inorganic cations has been taken as evidence of loss of bicarbonate. On the other hand, Teree, Mirabal-Font, Ortiz, and Wallace (6) have shown by direct measurements that the pH of the stool water in infant diarrhea is frequently acidic (almost always below the pH of the blood) and that HCO3-is very low or absent. On the basis of the observed differences between Na+ + Ki and Cl-, these authors have suggested that there is a high concentration of organic anions in diarrheal stools of infants and have advanced several hypotheses to explain the origin of these substances (7).The effect of fecal loss of organic anion on acidbase balance will depend upon several factors. These include the origin of the organic anions (i.e., whether ingested preformed, or generated within the body) and the nature of, the cations accompanying them (8). Those organic acids generated in the intestinal lumen or elsewhere in the body change the H+ concentration of the body fluids, depending upon the degree of ionization of

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