Incidence and clinical manifestation of cow's milk protein intolerance (CMPI) were studied in 1158 unselected newborn infants followed prospectively from birth to 1 year of age. No food changes were required in 914 infants who were used as healthy controls. When CMPI was suspected (211 infants), diagnostic dietary interventions according to a standard protocol were performed. After exclusion of lactose intolerance, two positive cow's milk elimination/challenge tests were considered diagnostic of CMPI. Two hundred and eleven symptomatic infants were examined for possible CMPI. A large group of 80 infants improved on a lactose reduced formula. In 87/211 infants CMPI was excluded (sick controls). Finally CMPI was proven in 26 infants. The calculated incidence rate for CMPI was 2.8%. The principal symptoms in infants with CMPI were gastrointestinal, dermatological and respiratory in 50%, 31% and 19% respectively. A positive family history for atopy (first or second degree relatives) was more frequent in either CMPI infants (65%), or sick controls (63%) when compared to either healthy controls (35%) or infants improving on a low lactose formula (51%). Differences between patients with CMPI and sick controls were only found for the presence of atopy in at least 2 first degree relatives [(5/26 in CMPI infants and 4/87 in sick controls (P < 0.05)] and for multiorgan involvement [10/26 infants with CMPI as opposed to 12/87 in the sick control group (P < 0.02)]. These statistical differences are too weak to be of clinical value.

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Nitrate reductase of Escherichia coli has been solubilized from particle fractions by a double treatment : first an alkali-acetone precipitation and then a solubilization in a buffered sodium deoxycholate. The enzyme has been purified 50-fold with a yield of 1 to 2O/,. Polyacrylamide-gel electrophoresis and ultracentrifugation show the preparation to be nearly homogeneous. The protein has a molecular weight of 320000 and an iso-electric point a t pH 4.2. The absorbance which increases continuously from 600 to 280 nm does not reveal the presence of a heme or a flavin group but the spectrum resembles that of some bacterial ferroproteins. The estimation of metals indicates 1.5 atoms Mo and 20 atoms Fe per mole. Approximately one labile sulfide is found per iron atom. It is likely that nitrate reductase A is an iron-sulfur protein containing molybdenum. The purified protein uses as substrates NO,-and C10,-and as electron donors reduced benzyl-and methyl-viologens, FMNH, and FADH, but not NADH or NADPH. It should be pointed out that the solubilization does not modify the enzymatic properties of nitrate reductase. CN-and N,-are strong inhibitors. Azide is a competitive inhibitor and the nitrate reductase affinity for this inhibitor is 1000 times greater than for nitrate. The type of inhibition observed and the metal chelating nature of the inhibitor suggest that a metal, Fe or Mo, or both, play a role in the formation of enzyme-substrate complex.Numerous bacterial strains are able to utilize nitrate as nitrogen source or as electron acceptor. In both roles nitrate, is first reduced to nitrite by nitrate reductase. This enzyme, when it is of type A [I], is localized in the cytoplasmic membrane with an electron carrier chain constituting what we call the nitrate respiratory system because of its many analogies with the system involved in aerobic respiration [2]. The membrane-bound complex thus formed has to be dissociated to allow study of its constituants. In the case of nitrate reductase, some methods of solubilization have been tried with success, as, for example, the fractionation of the particle fraction by heating employed by Tanigushi

As part of a large, prospective study we investigated the prevalence Helicobacter pylori serum antibodies in children with recurrent abdominal pain (RAP). All patients suffered from recurrent bouts of abdominal pain for at least 6 months and ranged in age from 6 to 12 years. H. pylori antibodies were detected using an enzyme-linked immunosorbent assay. The prevalence of H. pylori antibodies in the RAP group was compared to that of a control group which consisted predominantly of pre-operative children. None of the control group suffered or had suffered from RAP. Antibodies to H. pylori were found in 7 of 82 (8.5%) RAP patients and in 2 of 39 (5.1%) control children. The latter difference is not significant and suggests that RAP is only rarely caused in children by H. pylori infection.