摘要:

ExtractThe metabolismin vitroof subcutaneous adipose tissue from human newborns of different ages was investigated and comparisons were made with material taken from healthy adult volunteers. In the first hours of life, glycerol release (micromoles glyc-erol/100 μUg DNA/90 min) by suspensions of isolated adipocytes was increased (P< 0.001), but the response to the addition of norepinephrine was minimal. The release of free fatty acids (FFA) in relation to glycerol by suspensions of free adipocytes was considerably lower in neonates than in adults. Glycogen content of the adipose tissue between 0 and 4 hr of age was significantly greater than in older neonates and adults (P< 0.01). In infants less than 4 hr of age, glycogen content of the adipose tissue was inversely correlated with the length of labor (P< 0.05). Elevated reesterification of FFA seems to be related to the higher glycogen content and breakdown in subcutaneous adipose tissue immediately after birth.SpeculationThese investigations of the subcutaneous adipose tissue from human neonates show that the two basic energy substrates (carbohydrates and lipids) are closely and reciprocally related in the first hours and days of life. The findings are compatible with a transition from predominantly carbohydrate catabolism in the first hours of life to preferential utilization lipids in older neonates. Age-dependent changes in thein vitrometabolism of the adipose tissue parallel the relative importance of carbohydrates and lipids as substrates and energy sources in the total metabolism of the newborn infant. Thus, the subcutaneous adipose tissue may serve as an easily obtainable model for the study of the metabolic adaptation of the human newborn infant to extra-uterine life.

ISSN:0031-3998    

出版商:OVID    

年代:1972

数据来源: OVID

摘要:

ExtractThe surface-active complex lining alveoli in normal lung lowers surface tension on expiration, thus preventing alveolar collapse. Surface activity follows a developmental timetable. Infants with idiopathic respiratory distress syndrome (RDS) almost exclusively are prematurely born, and their lungs lack adequate surface activity and are deficient in the principal surface-active component, lecithin. This deficiency implies that RDS is a “disease of development,” with fetal and neonatal timetables for lecithin synthesis. The biosynthesis of lung lecithin in the living human infant was studied by examining phospholipids in lung effluent (pharyngeal aspirates, mucus), which have identical phospholipids to those in lung lavage (alveolar wash). The fatty acid esters of isolated lecithin and phosphatidyl dimethylethanolamine (PDME) were examined. The β-carbonfatty acids are indicators of the primary pathways of synthesis of lecithin: (1) a preponderance of palmitic acid signifyingcytidinediphosphate choline (CDP-choline) +D-α,β-diglyceride→lecithin(choline incorporation pathway) and (2) a preponderance of myristic acid signifyingphosphatidyl ethanolamine (PE) + 2 CH3→PDME+CH3→lecithin(methylation pathway).Fetal lung of 18 and 20 weeks showed slight incorporation by CDP-choline pathway, absence of PDME, and almost no methylation. Salivary lecithin had totally different fatty acids from lecithin in aspirates. Phosphatidyl dimethylethanolamine (PDME) (therefore methylation) was identified in aspirates as early as 22–24 week-gestation. Lecithin fatty acid esters in aspirates from premature infants after birth or those with no RDS closely resembled PDME fatty acids. With RDS, PDME disappears and β-carbon palmitic acid (therefore dipalmitoyl lecithin) increases. With recovery, PDME reappears, as does the premature infant's major lecithin, palmitoylmyristoyl. Full term infants are born with more β-carbon palmitic acid (20–40%) and by 12–18 hr have equal palmitic and myristic acids, indicating function of both lecithin synthesis pathways. Stress (hypoxia acidosis, hypothermia) cause disappearance of PDME and loss of β-carbon myristic acid. Similar changes in full term infants who do

ISSN:0031-3998    

出版商:OVID    

年代:1972

数据来源: OVID

摘要:

ExtractThe effects of phenobarbital (PB) on plasma clearance, hepatic uptake and storage, and excretion in stool and urine of131I-rose bengal (RB) were studied in seven subjects, six with a variety of hepatobiliary disorders characterized by cholestasis, and one with normal hepatic functions. In three children with patent extrahepatic biliary passages but different degrees and types of cholestasis, plasma t1/2for RB was shortened from 61.3 to 44.5 hr, from 44.5 to 24.8 hr, and from 155.5 to 96.9 hr before and during PB administration (10 mg/kg/day), respectively. The corresponding quantitative 72-hr fecal excretion of RB increased from 3.2% to 9.2%, from 9.9% to 71.0%, and from 0.3% to 10.0% of the injected dose; the normal subject excreted 78.6% before and 94.9% during PB treatment. Plasma t1/2and fecal excretion of RB were unchanged in three infants with absence of extrahepatic bile ducts who were treated with PB. Hepatic uptake and storage capacity for RB and renal excretion of RB were not affected by PB.The serum bilirubin concentration (total and direct-reacting) was lowered in patients with cholestatic jaundice not caused by biliary atresia. Interruption of drug therapy was followed by increase in the serum bilirubin to pretreatment concentrations in these patients. Phenobarbital treatment increased reduced nicotinamide adenine dinucleotide phosphate (NADPH)-cytochrome G reductase activity 30–150% in four subjects, whereas activity remained unchanged in three others. The effect of PB on microsomal reductase activity was unrelated to its ability to stimulate hepatic excretion.Phenobarbital in therapeutic dosages enhances biliary excretion of RB and conjugated bilirubin by stimulating hepatic excretory function in patients with intact extrahepatic bile ducts. Hepatic uptake, storage capacity, and NADPH-cytochrome C reductase induction do not seem to be directly involved in the acceleration of hepatic transport.SpeculationKnowledge of the kinetics of131I-RB distribution in human plasma, tissue, and excreta can serve as a basis for further studies of normal and hepatic excretory functions in man. Phenobarbital-stimulated biliary excretion of anions such as RB and conjugated bilirubin reflects patency of extrahepatic bile ducts. For this reason, PB in conjuction with131I-RB may prove to be useful agents in the diagnosis and management of various cholestatic conditions.

ISSN:0031-3998    

出版商:OVID    

年代:1972

数据来源: OVID

摘要:

ExtractMethods developed in this laboratory permit measurement of the androgens, testosterone (T), dehydroepiandrosterone (D), and androstenedione (A) on a 10-ml sample of plasma. We have determined concentrations of the unconjugated androgens (T, Δ, D) as well as of the sulfates of dehydroepiandrosterone (DS) and androsterone (AS) in the plasma of 85 healthy children of both sexes from birth through the age of 20 years. Our results are shown and summarized, along with those of other investigators.SpeculationMeasurement of the plasma androgens will aid in evaluation of children with sexual infantilism or sexual precocity. The prepubertal rise in plasma testosterone in males may be accompanied by a higher level of plasma protein binding than that which is found after puberty becomes evident.

ISSN:0031-3998    

出版商:OVID    

年代:1972

数据来源: OVID

摘要:

ExtractThe effect of zinc deficiency on the brain of the suckling rat was studied by feeding a zinc-deficient (Zn-) diet to dams from parturition and measuring thein vivouptake of3H-thymidine by brain DNA and the35S uptake by brain protein as well as the brain lipid composition of their pups. These results were compared with similar data obtained on pups nursed by pair-fed (PF) andad libitum-fed control dams which had been given zinc in addition to the diet.The specific activities (SA) of DNA and protein were decreased in the brains and livers of the pups nursed by the zinc-deficient dams compared with pups nursed by dams pair-fed with the zinc-deficient dams and hence semistarved (SA of brain DNA: Zn-= 5.90versusPF = 11.36; SA of liver DNA: Zn-= 5.16versusPF = 15.8; SA of brain protein: Zn-= 50.20versusPF = 85.30; SA of liver protein: Zn-= 56.02versusPF = 79.20). On the other hand, similar concentrations of DNA, RNA, and protein were present in their brains as well as their livers. The concentrations of total lipid were decreased in the brains of the deficient pups compared with the controls (Zn-= 0.215versusPF = 0.309 mg/mg of brain), while the concentrations of brain phospholipid and the brain fatty acid patterns were similar.Zinc deficiency has thus been shown to impair DNA and protein synthesis in brain of the suckling rat as it has previously been shown to do in other tissues including liver and epiphyseal plate.SpeculationZinc is essential for synthesis of nucleic acids and protein. In individuals with protiencalorie malnutrition, an associated zinc deficiency may compound the effects of protein deprivation by impairing utilization of the limited protein available. Zinc deficiency in the human may thus contribute to the impaired brain growth reported to occur in infants with protein-calorie malnutrition.

ISSN:0031-3998    

出版商:OVID    

年代:1972

数据来源: OVID

摘要:

ExtractData are provided on levels of circulating follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone in healthy male children and adolescents, and these levels are correlated with the stage of sexual maturation, bone maturation, whole body40K content, and the 24-hr excretion of creatinine, estrogens, 17-hydroxy-corticosteroids, total 17-ketosteroids, and fractionated ll-deoxy-17-ketosteroids (see Tables I and II).Before age 6 there was no significant change with age in testis size or hormone concentrations. From age 6–10 years there was a gradual rise in testis size (Fig. 1), serum FSH (Fig. 4) and serum LH (Fig. 3), but no change in plasma testosterone (Fig. 2), which remained below 40 ng/100 ml. From age 11–17 years there was a doubling of mean testis length, continued rise in serum FSH, and a steeper rise in LH; these changes were accompanied by a 20-fold increase in plasma testosterone concentration, the appearance of male secondary sexual characteristics (Figure 5), more rapid bone maturation and whole body40K accretion, and enhanced excretion of estrogens and ll-deoxy-17-ketosteroids. Mean levels of FSH in the adult range (> 10 μUg/100 ml) were achieved by age 8, and levels reached a plateau by age 15 (Fig. 6). Adult LH levels (> 2.5 μUg/100 ml) were reached by age 13 and a plateau was observed after 17 years. Plasma testosterone also ceased to rise after age 17.The data suggest that the testis may undergo progressive gonadotropin-mediated maturation in late childhood. Testosterone secretion by the Leydig cells at puberty may result from a further rise in LH levels.SpeculationPituitary secretion of gonadotropins, particularly FSH, in male children is a gradual phenomenon, antedeating by several years the release of testosterone by the testis. This gradual rise may represent a progressive reduction in hypothalamic sensitivity to feedback by testicular steroids other than testosterone. In late childhood, rising FSH and LH levels may induce increased activity of the enzymes responsible for both synthesis and catabolism of tesoterone. At puberty, an LH-mediated reduction in reductase activity might then result in testosterone accumulation and secretion.

ISSN:0031-3998    

出版商:OVID    

年代:1972

数据来源: OVID

摘要:

ExtractStudies were performed which showed that unbound unconjugated bilirubin at low concentration (0.5 mg/100 ml) causes yellow staining and aggregation of washed human platelets, whereas bilirubin bound to albumin and bilirubin altered by exposure to light have little, if any, of these effects on platelets. Less intense aggregation occurred in some but not all samples of platelet-rich plasma incubated with bilirubin and only at bilirubin levels of 10 mg/100 ml or higher. Aggregation of platelets by bilirubin showed an absolute requirement for calcium ions and this response was enhanced by potassium ions. Adenosine diphosphate and adenosine triphosphate were released from platelets with bilirubin.SpeculationIn the early accounts of human kernicterus, and in studies of experimental hyperbilirubinemia in animals, hemorrhagic complications were well known but poorly understood. The data presented suggest that bilirubin influences platelet function. It is tempting to speculate that the effect of bilirubin on platelets could play a role in producing intravascular thrombosis or hemorrhage, or both, in severe hyperbilirubinemia.

ISSN:0031-3998    

出版商:OVID    

年代:1972

数据来源: OVID

摘要:

ExtractThe spleen is essential for the formation of antibody in response to intravenously administered particulate antigen. Therefore, this splenic function was investigated in a number of children with sickle cell anemia. Following intravenous administration of 1.0 ml sheep red cells, heterophile antibody titers were determined at Q, 7, 14, and 21 days. One normal (Hgb AA), one sickle trait (Hgb AS), and two sickle-thalassemia (Hgb SSF) children had significant rises in heterophile titers with at least a 2-fold rise in 7 days and a minimum of 4-fold rise byday 14.This is comparable to responses of normal individuals previously reported. Five Hgb SS children had minimal antibody response with none having a rise in titer at 7 days. Three of these children had palpable spleens but no splenic visualization on scans. Two children received transfusions which restored splenic uptake of radiocolloid before antigenic challenge. These children also failed to form antibody. One child with sickle cell anemia received the same dose of sheep erythrocytes intramuscularly and had a significant antibody response comparable to normals.SpeculationThe defect of immunologic function in children with sickle cell anemia is similar to that described in asplenic individuals. This may be an important determinant of the increased susceptibility to infection in children with this disorder and their predisposition to overwhelming pneumococcal septicemia.

ISSN:0031-3998    

出版商:OVID    

年代:1972

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1972

数据来源: OVID