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Biomedical subjects

M H Malloy

Publications and source records attributed to M H Malloy.

At least 37 records · Page 2Linked to original sources

Exposure to a chloride-deficient formula during infancy: outcome at ages 9 and 10 years.

A school-based survey of the 1978 to 1979 birth cohort of two metropolitan Washington, DC, counties was conducted to find children who had been exposed to the chloride-deficient formulas Neo-Mull-Soy and Cho-Free during infancy. Children who had ingested other soy formulas that had an adequate chloride content were also found and matched to the exposed children by sex, race, birth weight, the age of the child, the mixed feeding status of the child, and maternal education. One hundred seventy-one of the exposed children and 261 soy control children were given a battery of psychologic tests in their homes to determine whether there had been any effect on intellectual development as a result of exposure to the chloride-deficient formulas. There were no differences in scores between the groups on the Wechsler Intelligence Scale for Children-Revised, the Boston Naming Test, the Rey-Osterrieth Test, or the FAS Verbal Fluency Test. There was no correlation between duration of exclusive exposure to the chloride-deficient formulas and the Wechsler Intelligence Scale for Children-Revised Full-Scale IQ Score (Pearson product-moment r = -.0825, P = .28). These results cannot be extrapolated to exposed children with documented hypochloremic metabolic alkalosis. It is concluded that in children without documented evidence of hypochloremic metabolic alkalosis, exposure to the chloride-deficient formulas Neo-Mull-Soy or Cho-Free during infancy has not resulted in any long-term adverse effects on cognitive development.

Child↗

Increasing cesarean section rates in very low-birth weight infants. Effect on outcome.

Examination of a linked birth and death certificate file from Missouri revealed a remarkable increase in the use of cesarean section for very low-birth weight infants (500 to 1499 g) from 24% to 44% in the years 1980 to 1984. In the same years the rate for 1500- to 2499-g infants went from 21% to 26% and the rate for 2500- to 7000-g infants went from 14% to 18%. We studied first-day death rates in very low-birth weight infants as an indicator of potential benefit from this increase in cesarean sections. During the 5-year period first-day deaths averaged 10% and 22% in the cesarean and vaginal birth groups, respectively. This difference was explained almost entirely by deaths in the 500- to 740-g birth weight group, where the death rates were 33% and 59%, respectively. Although this difference remained statistically significant after adjustment for gestational age and other factors that differed between the groups, it was nullified by an excess of deaths in the succeeding 6 days of life. Overall, the odds of death in the first week in these infants weighing 500 to 749 g was 0.85 (95% confidence interval, 0.52 to 1.39) in the cesarean vs vaginal deliveries. We conclude that there is little evidence that the use of cesarean section for the delivery of very low-birth weight infants, independent of maternal or fetal compromise, improves overall survival. We were unable to find reasons to justify the sharp increase in the use of cesarean sections for these small infants.

Cesarean Section↗

Maternal smoking during pregnancy: no association with congenital malformations in Missouri 1980-83.

Using a multisource birth defects registry developed by the Missouri Center for Health Statistics for the years 1980-83, we examined the relation between maternal smoking during pregnancy and the occurrence of congenital malformations. There were 288,067 live singleton births in this data set of which 10,223 had one or more congenital malformations. When adjusted for potential confounders the odds ratio for congenital malformations in the infants of women who smoked during pregnancy was not increased (odds ratio = 0.98, 95% confidence interval = 0.94 - 1.03). We examined the relation between smoking and groups of malformations using the International Classification of Diseases, 9th Revision, as well as analyzing for certain specific malformations within each group and found no increased risk for infants of smokers.

Birth Certificates↗

Syrup of ipecac. The case for distribution from physicians' offices.

Data from a nationally representative sample of household interviews were analyzed to examine public preparedness for childhood poisoning episodes. Eighty-eight percent (61% to 77% in nonwhite groups) of respondents from households with children younger than 10 years had heard of poison control centers and 70% (50% to 57% in nonwhites) stated that they had the telephone number of such a center. In contrast only 25% stated they had syrup of ipecac in their home. Among blacks and Hispanics this proportion was 9%. To explore possible reasons for this we telephoned a sample of 65 physicians listed in the greater Washington, DC, telephone directory as providers of care for infants and children. Of the 45 (69%) who agreed to be interviewed, 73% informed their patients about poison control centers and 53% provided the appropriate telephone number. Although 78% believed parents should have ipecac in the house, only three (7%) of 45 actually dispensed ipecac to parents. We conclude that ipecac is not widely available in the homes of American children. By regularly dispensing it in the course of pediatric care, physicians could largely remedy this deficiency.

Attitude of Health Personnel↗

The association of maternal smoking with age and cause of infant death.

Linked birth certificate and infant death certificate data from Missouri for 1979-1983 were used to explore the association of maternal smoking with age and cause of infant death. The data included 305,730 singleton white livebirths, of which 2,720 resulted in infant deaths. Using multiple logistic regression to control for the confounding effects of maternal age, parity, marital status, and education, the authors found that smoking was associated with both neonatal and post-neonatal mortality and with each cause of death except congenital anomalies. The adjusted odds ratio for smoking was higher for postneonatal deaths than neonatal deaths and was particularly high for two causes: respiratory disease (odds ratio = 3.4) and sudden infant death syndrome (odds ratio = 1.9). A moderate odds ratio (about 1.4) was found for causes attributed to the International Classification of Diseases, 9th Revision Perinatal Conditions Chapter. Although the associations for neonatal deaths and perinatal conditions were partially attributable to the effect of maternal smoking in lowering birth weight, virtually none of the excess respiratory mortality and sudden infant death syndrome mortality among the offspring of smokers was attributable to birth weight differences between the infants of smokers and nonsmokers. This suggests that respiratory deaths and sudden infant death syndrome deaths may be related to the effect of passive exposure of the infant to smoke after birth.

Adolescent↗

Trends in mortality caused by respiratory distress syndrome in the United States, 1969-83.

Using United States vital statistical data we examined trends in infant deaths from Respiratory Distress Syndrome/Hyaline Membrane Disease (RDS/HMD) for 1969 to 1983, by race and age at death. In order to improve comparability of diagnosis across two revisions of the International Classification of Diseases, deaths from RDS/HMD were ascertained using both underlying and associated causes of death. These data document a 2 per cent per year increase in infant mortality attributed to RDS/HMD for all races during interval I (1969-73) followed by 9 per cent per year decreases during intervals II (1974-78) and III (1979-83). However, there was a marked difference between Whites and Blacks in these trends. In the White population, RDS/HMD infant mortality increased by 2.2 per cent per year in interval I but then decreased by 10.5 per cent per year in interval II and 8.9 per cent per year in interval III. Among Blacks, on the other hand, the initial increase in RDS/HMD mortality was steeper (5.2 per cent per year) and the subsequent decreases were less (6.3 per cent per year and 8.0 per cent per year). As a result, the Black-White ratio in infant mortality attributed to RDS/HMD increased from 1.32 in 1969-73, to 1.59 in 1974-78 and to 1.72 in 1979-83. The proportion of RDS/HMD deaths that occurred in the postneonatal period increased from 1.1 per cent in interval I to 3.6 per cent in interval II to 5.0 per cent in interval III.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

Cysteine supplementation of total parenteral nutrition: the effect in beagle pups.

Total parenteral nutrition solutions supplemented with cysteine-HCl (S-TPN, 0.8 mmol/kg/day) were infused into beagle pups from day 10 of life to day 20 (n = 6). Another group of pups received unsupplemented TPN solutions (US-TPN) (n = 6). Fluid, protein, and energy intake from nonprotein sources were similar in both groups. Data from these two groups were compared and similar measurements in normally suckled pups were also compared with the two TPN groups (n = 6). There were significant differences in the rate of weight gain between the pups that received TPN and the pups that were suckled (P less than 0.01). Weight gain, hepatic DNA and protein concentrations, and cerebral DNA and protein concentrations in the pups that received TPN supplemented with cysteine were not different from similar measurements in pups that received unsupplemented TPN. Plasma total cyst(e)ine (Cyst(e)ine refers to the mixture in any proportion of the sulfhydryl (cysteine) and the disulfide (cystine) forms of this compound) concentrations in the cysteine-supplemented pups (7.9 +/- 1.2 mumol/DL, X +/- SD) were significantly greater than in the unsupplemented pups (4.9 +/- 1.8 mumol/DL). Hepatic glutathione concentrations in the supplemented pups (583 +/- 85 mumol/100 g liver) were also significantly greater than in the unsupplemented pups (392 +/- 113 mumol/100 g liver). These data suggest that the supplementation of TPN solutions with cysteine, even in an animal enzymatically capable of cysteine synthesis, has significant effects on glutathione synthesis.

Amino Acids↗

Total parenteral nutrition in sick preterm infants: effects of cysteine supplementation with nitrogen intakes of 240 and 400 mg/kg/day.

The effects of supplementing total parenteral nutrition (TPN) solutions with cysteine were assessed at two different levels of nitrogen intake by determining nitrogen retention, sulfate excretion, and sulfur-containing amino acid concentrations. Ten infants received 72 mg/kg/day of cysteine-HCl in a TPN solution for a period of 6 days. Five of these infants received 251 +/- 48 (mean +/- SD) mg/kg/day of nitrogen, and five received 403 +/- 45 mg/kg/day of nitrogen. Two other groups of five infants each received unsupplemented TPN at nitrogen intakes of 235 +/- 48 and 412 +/- 54 mg/kg/day, respectively. Fluid and nonprotein caloric intakes were similar for all four groups. Cysteine supplementation increased plasma and urine free cyst(e)ine concentrations and enhanced total sulfur retention, but did not enhance nitrogen retention. [Cyst(e)ine refers to the mixture in any proportion of the sulfhydryl (cysteine) and the disulfide (cystine) forms of this compound.] Nitrogen retention, sulfate excretion, cyst(e)ine excretion, and plasma taurine concentrations increased as the result of the increase in nitrogen intake.

Cysteine↗

Cyst(e)ine measurements during total parenteral nutrition.

Using a method that measures plasma protein-bound 1/2 cystine, plasma free cyst(e)ine, and urine free cyst(e)ine, we have observed that infants receiving total parenteral nutrition supplemented with cysteine-HCl have significantly higher plasma and urine free cyst(e)ine concentrations (11.3 +/- 3.4 microns/dl and 47.2 +/- 24.0 microns/dl, means +/- SD) than when 1/2 cystine concentrations are measured by automated amino acid analysis (7.4 +/- 2.0 microns/dl, plasma and 25.0 +/- 7.0 microns/dl, urine). These data suggest that both the sulfhydryl and disulfide form of cyst(e)ine must be measured to assess the effect of cysteine-HCl supplemented total parenteral nutrition.

Chemistry, Organic↗

Maternal-fetal cyst(e)ine transfer.

In order to investigate the mechanisms by which cyst(e)ine (referring in the following to the mixture, in any proportion, of the sulfhydryl form of this compound - cysteine - and the disulfide form - cystine) transfer across the placenta to the fetus might be limited we first assessed the original observation that cyst(e)ine concentrations in fetal plasma are less than or equal to maternal cyst(e)ine concentrations. Second, we determined the capacity of the placenta to concentrate cyst(e)ine. And third, using an animal model, we determined the effects of providing excess cysteine to maternal rats on maternal-fetal cyst(e)ine transfer. Our data confirm (1) that cyst(e)ine is present in concentrations in human cord plasma that are equal to maternal plasma cyst(e)ine concentrations; (2) establish that cyst(e)ine is concentrated in the placenta, and (3) suggest that the incorporation of cyst(e)ine into glutathione in the placenta may limit the transfer of cyst(e)ine to the fetus.

Animals↗

Plasma cyst(e)ine in homocyst(e)inemia.

Using a method developed to measure plasma protein-bound 1/2-cystine, we have observed that the metabolic state can affect the distribution of plasma cyst(e)ine between the bound and the free form. In five patients with homocyst(e)inemia, 1/2-homocystine was found to have replaced virtually all the cysteine normally present on sulfhydryl-binding sites of plasma proteins. The majority of the cyst(e)ine measured in the plasma of these patients (6.9 +/- 2.4 mumol/dl, mean +/- SD) was present in the form of a mixed disulfide with 1/2-homocystine (5.4 +/- 0.9 mumol/dl) rather than being free in the plasma or bound to plasma proteins.

Blood Proteins↗

Development of taurine metabolism in beagle pups: effects of taurine-free total parenteral nutrition.

In beagle pups (from 5 to 84 days of age), plasma taurine concentration decreased between 5 and 21 days of age with no change thereafer; cerebral taurine concentration decreased throughout the period of study but cerebral taurine content increased between 5 and 21 days of age; hepatic taurine content (but not concentration) increased throughout. Both hepatic cysteinesulfinic acid decarboxylase (CSAD) activity and the concentration of taurine-conjugated bile acid of gallbladder bile increased during the period of study. Plasma and cerebral taurine pools were not affected by taurine-free total parenteral nutrition (TPN). Hepatic taurine content was also not affected, but taurine concentration decreased; however, this change resulted from an increase in hepatic size. Hepatic CSAD activity of animals that received TPN was greater than that of 35-day control animals while the concentration of taurine-conjugated bile acids in the gallbladder bile was less. Although plasma taurine concentration was not affected by intravenous glucose therapy, both the hepatic taurine concentration and content of these animals were less than those of 35-day control animals. Cerebral taurine concentration of these animals, on the other hand, were greater. Hepatic CSAD activity of the animals that received only intravenous glucose was similar to that of controls, but the taurine-conjugated bile acid concentration in the gallbladder bile, like that of animals that received TPN, was less than that observed in 35-day control animals.

Aging↗

Neonatal gastric motility in dogs: maturation and response to pentagastrin.

Postnatal changes in the pH of gastric secretions, gastric motility, serum gastrin concentration, and response of the stomach to pentagastrin administration were studied in 15 beagle puppies from birth to 5 wk of age. Motility was monitored manometrically via twin-lumen catheters 3--6 h postprandially. Mean gastric pH was stable at 5.85 until the 7th postnatal day when pH decreased to 3.45; pH then increased to a mean value of 4.95 through the 18th day. Antral contractions increased from 0.2 contractions per min on the day of birth to a maximum 2.3 contractions per min on the 11th day and then gradually declined. Pentagastrin (8.0 microgram/kg sc) had no effect on gastric pH or motility until the 2nd postnatal wk. Pentagastrin inhibited the rate and peak pressure of antral contractions from the 2nd through the 5th wk. Mean serum gastrin concentrations in six puppies were greater than values for adult dogs, attaining a preweaning maximum on the 9th day.

Aging↗