Search PubMed⌕ Search

Biomedical subjects

Z Friedman

Publications and source records attributed to Z Friedman.

At least 73 records · Page 4Linked to original sources
PubMed1980

Neonatal sepsis due to group G streptococci.

Two cases of neonatal septicaemia due to group G streptococci (Streptococcus canis) are described. In one patient, infection coexisted with transient neonatal hyperthyroidism, while, in the other, concomitant group G streptococcal septicaemia and endometritis in the mother was seen. Group G streptococci are rare causes of infection, especially in the paediatric age group. Bacteria were identified by serological and biochemical methods. Both neonates responded well to penicillin therapy, but the maternal infection required combination therapy with penicillin G, gentamicin, and chloramphenicol. The literature on systemic group G streptococcal infection is briefly reviewed. With increasing use of serotyping in the identification of beta-haemolytic streptococci, non-group A organisms will probably be identified more frequently from neonatal and other infections.

Adolescent↗
PubMed1980

Prostaglandin synthetase in the human neonatal kidney.

Prostaglandins play an important role in renal physiology. We have studied the prostaglandin synthetase system in 10 human newborn kidneys ranging from 22 to 40 weeks of gestation who succumbed within 40 hr postnatally. Slices of medulla and cortex were incubated within 2 hr of death in a medium containing 50 microgram arachidonic acid and 50 muCi [3H]arachidonic acid. The incoroporation of [3H]AA into prostaglandin (PG)E and PGF was determined at 30-min intervals in medulla and cortex tissue and in the incubation media over 120 min and at 180 min, using silicic acid chromatography and scintillation counting. The study showed that biosynthesis of the primary prostaglandins occurs mainly in the renal medulla as early as 22 weeks of gestation, with the biosynthetic activity increasing concomitantly with advanced gestation. The ratio of PGE to PGF in the medulla and cortex was always greater than 1. The ratio was obtained in kidneys from neonates born before 28 weeks of gestation. Because prostaglandins are biosynthesized in the neonatal kidney, it is conceivable that hemodynamic and fluid and electrolyte homeostasis functions of prostaglandins may exist at this very early stage of development.

Female↗
PubMed1980

Effects of dietary variation in linoleic acid content on the major urinary metabolites of the E prostaglandins (PGE-M) in infants.

1. EFA deficiency is associated with the impairment of prostaglandin E synthesis, which is reflected by the decrease of the urinary excretion of PGE-M. 2. Excessive administration of Intralipid results in increase of the relative concentrations of linoleic acid content in plasma, RBC, and tissues with a concomitant decrease of its higher homologue, arachidonic acid. These changes are associated with diminished PGE-M excretion similar to that seen in EFA deficiency. Further investigation is needed into the pathophysiologic consequences of EFA deficiency and the excessive administration of linoleic acid since both are associated with altered prostaglandin biosynthesis and turnover in the new-born infant, particularly among those stressed low birth weight infants whose nutritional status and management are an indication for these modes of therapy.

Dietary Fats↗
PubMed1980

Prostaglandins in human milk.

Levels of prostaglandin E2 and prostaglandin F2 alpha were measured by radioimmunoassay in aliquots of foremilk and hindmilk obtained at different stages of lactation (colostrum, transitional, and mature milk) from six healthy nursing mothers who delivered at term. Immunoreactive prostaglandin E2 and prostaglandin F2 alpha were detected in all fresh human milk samples, but not in cows' milk-based formulas. Further studies are necessary to investigate the role of these hormones in the physiologic function, the extrauterine adaptation, and the cytoprotective effect on the gastrointestinal tract in the breast-fed human infant.

Breast Feeding↗
PubMed1979

Head growth in sick premature infants--a longitudinal study.

Serial weekly measurements of somatic growth and head circumference were made for ten weeks on 41 appropriately grown sick preterm infants (gestational age 28 to 32 weeks) with severe neonatal problems. Twenty-seven (66%) required prolonged assisted ventilation. During the period of acute illness, the velocity of growth for the sick infants was below that of the normal fetus, with deviation away from and below the normal fetal growth curve. During recovery, head growth paralleled that of normal fetal growth, and subsequently rapid "catch-up" growth in head circumference occurred. By comparison, six similar infants, whose head circumference followed the intrauterine growth curve, proved to have hydrocephalus. These results suggest that: (1) the brain participates in the growth retardation associated with being sick and premature and that apparently normal head growth under comparable circumstances may be associated with hydrocephalus; (2) in spite of an energy intake ranging from 80 to 120 kcal/kg/day by the end of the second postpartum week, normal growth in the sick low-birth-weight infant does not occur until their acute illness has resolved.

Female↗
PubMed1979

Familial infantile scoliosis associated with bilateral paralysis of conjugate gaze.

A family with two sibs suffering from idiopathic infantile scoliosis associated with bilateral paralysis of conjugate gaze is reported. Although the parental consanguinity and the involvement of patients of both sexes in this family are suggestive of an autosomal recessive mode of inheritance, a dominant or multifactorial pattern remains a possibility.

Child, Preschool↗
PubMed1979

Intravenous alimentation and insensible water loss in low-birth-weight infants.

Insensible water loss (IWL) was measured in six premature infants, between 4 and 21 days of age, by continuous weight monitoring on an electronic balance inside an incubator. Multiple measurements of IWL were made during the sequential infusion of 10% dextrose in 0.225% NaCl, 10% dextrose-amino acid solution, or 10% dextrose-amino acid and a commercial intravenous fat emulsion. Each solution was administered for three hours by constant infusion through a scalp vein needle. The order of the infusion was random and a 30- to 60-minute infusion with 5% dextrose water was given between each solution. During the infusion of 10% dextrose in 0.225% NaCl and 10% dextrose + amino acid solution, IWL was 1.0 +/- 0.8 gm/kg/hr and 1.1 +/- 0.8 gm/kg/hr, respectively. In contrast, IWL increased significantly to 1.6 +/- 0.7 gm/kg/hr when additional calories were given using the 10% dextrose-amino acid with the intravenous fat emulsion (P less than .005). There was a positive correlation between calorie intake and IWL. These data suggest that parenteral nutrition solutions with intravenous fat emulsion are rapidly metabolized and the increase in IWL is probably secondary to an increase in thermogenesis.

Enterocolitis, Pseudomembranous↗
PubMed1979

Polyunsaturated fatty acids in the low-birth-weight infant.

The essentiality of certain PUFAs is related to their capability to be incorporated into lipids and to act as precursor in the formation of prostaglandins. Via phospholipids the EFA's influence the physico-chemical characteristics of biomembranes. EFAs are metabolized differently from nonessential PUFAs. While the nonessential fatty acids are metabolized rapidly, the organism tends to conserve the stores of EFAs. Inhibitions and competitions among the EFAs of the three series (oleic, linoleic, and alpha-linolenic) have been demonstrated. Apparently, for any given chain length the more unsaturated fatty acid has a greater affinity for the enzyme system responsible for further elongation and desaturation. EFAs are also necessary for the proper utilization of the saturated fatty acids. Vitamin E and pyridoxine seem to be involved in EFA metabolism. Normal growth of infants is dependent upon an adequate supply of EFA. The human fetus, like the adult, is unable to synthesize the EFAs, which must therefore be derived from the maternal circulation and pass through the placenta. In the fetus, increased concentration of the polyenoic fatty acids with advanced gestational age may result from increased activity of the fetomaternal unit by preferential transfer of these FAs. Enzymatic activity in the placenta or the fetus may also be responsible for desaturation and elongation of these EFAs. Several clinical manifestations have been ascribed in the human infant to prolonged EFA deficiency; however, none of these findings was noted in a group of sick newborn infants with very rapid onset of deficiency. Platelet dysfunction, decreased prostaglandin biosynthesis and turnover and altered pulmonary surfactant are among the effects of EFA deficiency on infants. Supplementation of the EFAs by the diet, parenterally or by the inunction of oil rich in linoleic acid, were reported to alleviate the symptoms of EFA deficiency. The minimal estimated requirement of linoleic acid is 1% of calories and 4% is an optimal intake. Most diets, including human breast milk, infant formulas and parenteral fat emulsions, far exceed the optimal intake of linoleic acid. Relatively little is known about the possible effects of high levels of linoleate in the diet; however, early studies suggest an adverse effect on platelet function, prostaglandin biosynthesis, pulmonary gas exchange and immune function.

Adult↗
PubMed1979

Abnormal lung surfactant related to essential fatty acid deficiency in a neonate.

A low-birth-weight infant, suffering from chronic bronchopulmonary dysplasia following hyaline membrane disease and recurrent episodes of necrotizing enterocolitis, developed biochemical evidence of essential fatty acid (EFA) deficiency in the plasma. Fatty acid composition of phosphatidylcholine and phosphatidylglycerol in the lung lavage fluid was abnormal. Plasma changes included a decrease in the level of linoleic acid and an increased level of palmitic, palmitoleic, oleic, and 5,8,11-eicosatrienoic acid to arachidonic acid being greater than 0.4:1. A lower than normal level of palmitic acid and an increased level of palmitoleic and oleic acids were seen in pulmonary sufactant phospholipid components. Upon treatment and recovery from EFA deficiency, the fatty acid pattern both in plasma and surfactant phospholipids returned to normal along with clinical improvement. An association between EFA deficiency and altered fatty acid composition of pulmonary surfactant phospholipids is suggested.

Arachidonic Acids↗