摘要:

ExtractIntramuscular inoculation of 19-day old chickens with heterologous erythrocytes elicited significantly lower levels of agglutinins in embryonically infected birds when compared with control birds (reciprocal ha titer 10 vs. 100, respectively,P<0.01). The IgG component of this antibody was substantially less in experimental chickens, 25% vs. 70% in controls. Subsequent anamnestic antibody response in experimental birds was also significantly less than control chickens (reciprocal ha titers 25 vs. 512, respectively,P<0.02), with continued predominance of IgM antibody in experimental chickens (70% IgM-ha) vs. controls (60% IgG-ha).Induction of cell-mediated immunity by footpad inoculation of 46-day-old birds with diphtheria-tetanus toxoid in complete Freund's adjuvant failed to discern suppression of T cell function in previously infected chicks.Before hatch, the bursae of experimental and control embryos possessed a few IgM-producing lymphoid cells in equivalent numbers. There was also no difference in the relative population of IgM-producing cells in the medullary area of bursal follicles of 7-day-old hatchling chickens, approximately 70%. However, the mean density of IgG-producing cells in the bursae of experimental chickens was less than that of control chickens, 10% vs. 19%, respectively. Consistent with persistent embryonic viral infection and altered bursal function, only IgM-producing cells were detected in the spleens of 7-day-old experimental birds.These observations suggest that persistent embryonic viral infection disturbs the function of bursal-dependent immunopoiesis in the avian host.SpeculationEarly and persistent embryonic mumps virus infection in the avian host results in abnormal immunoglobulin maturation and antibody production. The following mechanisms may influence the immune response in this experimental model: viral replication may directly suppress the transition of IgM-producing cells within the embryonic and hatchling bursa at the stem cell level by altering genetic expression; infection may induce the production of a bursal repressor which disturbs the transition of immunoglobulin synthesis from IgM to IgG; growth retardation may be associated with generalized diminution of immunocellular replication and function.

ISSN:0031-3998    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

ExtractIn fetal livers of both man and rat thymidine kinase activity was 12 times higher than in the adult, glutamate dehydrogenase and arginase were present at 20–50% of their adult values, whereas alanine aminotransferase activity was only an insignificant fraction of that in the adult. Although the developmental changes for the four enzymes were quantitatively similar in both species, qualitatively there were some significant differences.In adult human liver, glutamate dehydrogenase activity was distributed almost equally between the cytosol and particles; the concentration of only the soluble enzyme increased after birth. In rat liver, glutamate dehydrogenase remained exclusively a particulate enzyme. The soluble hepatic alanine aminotransferase activity rose in both species after birth (from less than 2 U/g to 41–57 U/g, respectively). Thymidine kinase was wholly soluble in the fetal livers; only in adult human liver was additional activity (at least 50% of the total) found in the particles. Arginase isozymes, identical and apparently the same single isozyme in fetal and adult rat liver, show an ontogenetic change in man. A shift from a single form, common to human fetal liver and fetal kidney, to at least two variants in adult human liver, indicates another complexity of the fully differentiated liver in man.SpeculationIt is unlikely that the occurrence of particulate thymidine kinase and soluble glutamate dehydrogenase in man is restricted to liver. Their relatively late appearance in life suggests that their further study would be of interest to both ontogeny and phylogeny.

ISSN:0031-3998    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

ExtractThe numbers of circulating T and B lymphocytes in seven children with whooping cough due toBordetella pertussisand eight control subjects were determined. All the children with whooping cough had an absolute lymphocytosis (mean 29,142/mm3vs. 5,225/mm3) and by surface marker criteria both T cells and B cells were increased (mean T cells, whooping cough 15,794/mm3vs. 3,516/mm3controls; mean B cells, 13,393/mm3whooping cough vs. 1,706/mm3controls). However, the ratios of T cells to B cells in the whooping cough (1.4) and control group (1.9) did not differ significantly. This proportional increase in both T and B lymphocytes indicates that whatever mechanisms are responsible for lymphocytosis inB. pertussisinfection affect both populations in a similar manner.SpeculationLymphocytosis in children with whooping cough results, primarily, fromB. pertussis-induced blockage of T and B cell re-entry into lymph nodes from the blood. The profound effect ofB. pertussison lymphocyte recirculation patterns might be of value in future attempts at “immunologic engineering.”

ISSN:0031-3998    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

ExtractThe development and relative contribution of hepatic bilirubin conjugation with glucuronic acid, xylose, and glucose was studiedin vitroin newborn rats 1–20 days old. In adult control rats, 75% of the conjugates formed were with glucuronic acid, whereas in 1-day-old newborns, only 50% of the conjugates were with glucuronic acid (P<0.02) while xylose and glucose conjugates of bilirubin together were equal to that of glucuronic acid. Byday 4,total conjugating capacity increased to adult levels and a mature pattern of distribution. In response to phenobarbital treatment, xylose and glucose conjugation increased 4 days earlier than glucuronide conjugation and maximal induction occurred 8 days sooner for nonglucuronide conjugation than for glucuronide.SpeculationThe pattern of enzyme maturation and relative activities of the various bilirubin conjugating systems in newborn rats cannot be extrapolated to those in the human, but this study suggests that a similar study in the human or subhuman primate might demonstrate that glucose and xylose conjugation compensate, in part, for deficient glucuronide conjugation.

ISSN:0031-3998    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

ExtractFive patients with Bartter's syndrome were investigated. Sodium restriction (<10 mEq/day for at least 5 days) showed a renal sodium wastage in only two patients(IandII)in spite of increased aldosterone secretion rate (from 151–427 to 680–842 μg/day). The effect of angiotensin II (A II) 80 ng/kg/min for 30–180 min, on plasma renin activity (PRA), plasma aldosterone, and urinary sodium excretion was compared with the effect of a previous infusion of 5% dextrose given at the same rate, 0.5 ml/min for 1 hr. A II infusion resulted in increased plasma aldosterone levels: from 236–330 pg/ml to 800–881 pg/ml in 30 min. This increase was also observed inpatient II(from 139 to 600 pg/ml). PRA was decreased by A II infusion (from 1,142–2,462 to 121–1,625 ng/liter/min). Inpatient IV,this decrease in PRA was also observed when he was on a salt-restricted diet (from 1,934 to 370 ng/liter/min); but the minimal PRA was still higher (370 ng/liter/min) than with a normal diet (121 ng/liter/min). In no case could normal PRA level be obtained. A II infusion induced an increase in urinary sodium excretion only in the two patients with renal sodium wastage (from 80–90 to 265–230 μEq/min in 30 min). Urinary sodium excretion decreased in the other patients from (37.5–213 to 4.30–46 μEq/min) and fractional sodium excretion was reduced inpatient V(from 0.56% to 0.45% at 30 min and to 0.29% at 120 min). No significant change with A II infusion was observed in patient IV when he was on a sodium-restricted diet (from 1 to 2.5 μEq/min in 30 min). Urinary potassium excretion was similar to sodium excretion. No change was observed in plasma potassium and sodium.SpeculationHypersecretion of renin is not autonomous in Bartter's syndrome. It is not explained by an insensitive feedback effect of A II on renin secretion. Hypokalemia contributes to this high level of PRA. Salt craving, which is found in 50% of the cases (ZS), is increased by A II. Nevertheless, the presence of renal sodium wastage cannot be explained only by the high A II levels which are constant in this syndrome. A deficient Na-K-ATPase activity is postulated in such cases.

ISSN:0031-3998    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

ExtractAs a prerequisite to a biochemical investigation into the role of dietary lipids in regulating perinatal fatty acid metabolism, we developed and evaluated a model in which the amount of lipid in the diet can be easily controlled from birth to at least 10 days of age. Neonatal rabbits were fed purified equicaloric diets in which lipid supplied either 14.2% or 77.6% of the total calories. Mortality due to all causes was about 40% in both groups. Some differences in physical development between the two groups were noted. Animals receiving the smaller amount of lipid (LF group) gained weight to 150% birth weight byday 10,whereas the group receiving the larger amount of lipid (HF group) did not gain. In addition, the HF group had lower body temperatures, smaller liver and kidney weights, and greater brain weights relative to body weight. These differences are discussed in relation to the composition of the HF and LF diets. The model promises to provide a direct approach to a more precise evaluation of varied dietary regimens in the neonatal period. In particular, the model lends itself to studies relating diet to developing biochemical functions. In an accompanying paper, we report the results of an investigation comparing fatty acid oxidation in heart and liver of neonates fed the HF and LF diets described here.SpeculationThe model described here overcomes many of the difficulties associated with maintaining neonates on artificial diets in a way that allows precise control of diet composition and environment for at least the first 10 postnatal days. This should provide a new approach to many old questions regarding the specific role of lipids and other dietary constituents in modulating biochemical development.

ISSN:0031-3998    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

ExtractThere is only indirect evidence to suggest that the sudden postpartum appearance of dietary lipid regulates the perinatal development of the enzyme pathways required for fatty acid oxidation. To test this idea directly, rabbit pups were maintained on diets containing lipid to equal either 14.2% (LF) or 77.6% (HF) of the total caloric intake. Palmityl coenzyme A oxidation rates in the presence of excess ADP and carnitine were measured polarographically in heart and liver homogenates. No significant difference in oxidation rates between HF and LF groups was observed even at 10 days of age. Palmityl coenzyme A oxidation in both groups was carnitine dependent and was in general the same as that of mother-fed animals. Similarly, an evaluation of cytochrome oxidase activity and glutamate + malate-supported respiration in heart and liver homogenates revealed no difference attributable to diet.To consider the possibility that fatty acid oxidation might be specifically increased or decreased over other mitochondrial respiratory activity as a function of diet, palmityl coenzyme A oxidation rates were normalized with respect to glutamate + malate oxidation rates. A similar comparison was made relative to cytochrome oxidase activity. Still no differences were observed between HF and LF groups.By studying the maximum rate of oxygen utilization in the presence of excess carnitine and palmityl-coenzyme A we would have detected any change in a rate-limiting step for fatty acid oxidation beyond acyl activation. We must conclude, therefore, that large differences in the proportion of postnatal dietary lipid do not influence the cellular capacity to oxidize palmityl coenzyme A.SpeculationWe found no evidence to support the suggestion that the ability to oxidize long chain fatty acids is influenced by the amount of lipid in the postnatal diet. It seems likely that factors other than dietary lipid may be more important in regulating perinatal oxidative energy metabolism.

ISSN:0031-3998    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

ExtractThe primary metabolic defect in mannosidosis is the deficiency of the acidic α-mannosidase A and B activities which results in the lysosomal accumulation of mannose-rich substrates. Our studies demonstrate that the enzymatic diagnosis of suspect homozygotes can be made reliably using plasma, isolated leukocytes, or cultured skin fibroblasts assayed carefully at the appropriate acidic pH.Immunologic studies of a mannosidosis homozygote revealed significant abnormalities of neutrophil function; these included a depressed chemotactic responsiveness and impaired phagocytosis of bacteria. Lymphocyte transformation studies showed a 20% of normal response to purified phytohemagglutinin and a 25% of normal response to concanavalin A.Three major components of α-mannosidase activity in normal human liver were resolved by ion exchange chromatography on DEAE-cellulose and electrophoresis on cellulose acetate gels. Electrophoresis of the liver extract fromhomozygote 1with mannosidosis revealed only one band of activity which coelectro-phoresed with the α-mannosidase C isozyme partially purified from normal liver. However, ion exchange chromatography revealed the presence of residual hepatic acidic activities; the residual A isozyme was eluted in a position corresponding to that of normal α-mannosidase A whereas the residual B activity was eluted at a slightly more electronegative position than that of normal B isozyme.The apparent Kmvalues for α-mannosidase activity as determined from Lineweaver-Burk plots were 1.1 mM for normal liver and 0.9 mM for normal leukocytes. In contrast, the residual activity in these sources from homozygote 1 could not be saturated within the solubility range of the substrate; the apparent Kmvalue was estimated at 15.4 mM in liver extracts.Zinc significantly lowered the apparent Kmvalue of the acidic activity in normal liver (from 1.2 to 0.24 mM), whereas this metallic ion had little effect on the values for mannosidosis hepatic activity (from 15.4 to 12.3 mM). Unlike zinc, cobalt had its major effect on the acidic activity in the mannosidosis liver extract, lowering the apparent Kmfrom 15.4 to 3.9 mM, whereas the apparent Kmfot the normal activity was increased from 1.2 to 1.9 mM. The residual acidic activitieswere markedly stimulated by zinc in both leukocytes (∼300%)and plasma (∼400%)from the homozygotes and to a lesser extent in those sources from normal individuals. In contrast, cobalt enhanced the residual acidic activities in leukocytes (∼500%) and plasma (∼200%) from the homozygotes while inhibiting these acidic activities (78.9%and 47.7%, respectively) in normal individuals.SpeculationThe susceptibility of homozygotes with mannosidosis to severe recurrent infections may be the direct consequence of impaired leukocyte membrane recognition processes resulting from the defective catabolism of substrates with a-D-mannose residues. The metabolic defect in mannosidosis presumably results from a structural gene mutation which alters the kinetic and metal binding properties of the lysosomal a-mannosidase activities. Appropriate metal cation supplementation may stimulate the residual activity of the mutant isozymes and provide an effective therapeutic approach to patients with this inborn error of metabolism.

ISSN:0031-3998    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

ExtractA simple algebraic manipulation of known formulas leads to a direct expression for the specific airway resistance (SRaw) which precludes separate measurements of the airway resistance (Raw) and the thoracic gas volume (TGV). The equation is: SRaw= tg β (PBar- PH2O) e2, in which tg β stands for the relation between the plethysmographic box volume and pneumotachograph flow fluctuations; PBar- PH2Ois the barometric pressure corrected for water vapor pressure at body temperature, and e2is a calibration for graphical units. Thanks to this new formula SRawcan now be easily measured with great precision and quickly calculated, even in the case of those children (Table 1) with whom this was not previously possible. No further cooperation is needed than breathing at a normal rate through mouthpiece into a whole-body plethysmograph. The intraindividual coefficient of variation (CV) for SRawis about 8% and never exceeds 15% (Table 1).SpeculationBecause of our proposed simplification of the measurement of SRaw, the accumulation of data on bronchial obstruction and hence statistical analysis will be greatly facilitated in pediatrics. Further developments of this method should permit a comparison with previous studies in sedated children and answer the question of whether alteration in specific airway resistance is the consequence either of sedation or of some change associated with growth during the first 5 years life.

ISSN:0031-3998    

出版商:OVID    

年代:1976

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1976

数据来源: OVID