ISSN:0031-3998    

出版商:OVID    

年代:1971

数据来源: OVID

摘要:

ExtractSera of 1763 normal pregnant women were screened for antibodies against Gm (a), Gm (b), and Gm (f) factors. Twenty-eight patients (1.59%) possessed specific Gm agglutinators. Incidence of fetal death, synthesis of the incompatible genetic gamma globulin factor, and levels of gamma globulin were determined. Four infants with Gm factor fetomaternal incompatibilities whose mothers possessed isoantibodies were studied over a period of from 8 to 24 months. Serial quantitative gamma globulin determinations from the affected infants produced results which compared favorably with seven control infants and normal values cited in the literature. There appeared to be no impairment of synthesis of the specific incompatible genetic gamma globulin, expressed as a titer of hemagglutination inhibition. The development of specific genetic gamma globulin factors throughout infancy is delineated. In the patients studied, no adverse effects resulted from fetomaternal gamma globulin incompatibility.SpeculationHigh titers of maternal Gm antibody of the gamma G fraction may traverse the placenta and result in suppression of synthesis of the corresponding gamma globulin of the infant. Low titers cannot reach the fetal circulation in sufficient quantities to produce suppression. Alternatively, despite high levels of maternal antibody, no biological effects may result.

ISSN:0031-3998    

出版商:OVID    

年代:1971

数据来源: OVID

摘要:

ExtractMeasurements of thoracic gas volume and functional residual capacity were performed serially from birth on 26 premature infants to determine the presence and time course of gas trapping. Nitrogen washouts were carried out on 16 of these infants and urinary-alveolar nitrogen gradients (uADN2) were measured in 7. The infants were divided into two groups, those above and those below 1750 g birth weight. Trapped gas was documented in both groups, but in the smaller infants the condition persisted for a longer time. The mean thoracic gas volume (TGV) in infants over 1750 g birth weight was 2.0 ± 0.7 ml/cm at birth, with a mean functional residual capacity (FRC) of 1.3 ± 0.4 ml/cm; by day 9, the TGV and FRC were 1.5 ± 0.3 and 1.2 ± 0.2 ml/cm, respectively. Infants under 1750 g birth weight had a mean TGV of 1.7 ± 0.2 ml/cm at birth with an FRC of 0.9 ± 0.2 ml/cm; by week 2 of life, mean TGV and FRC were 0.9 ± 0.2 and 0.8 ± 0.2 ml/cm, respectively. When gas trapping was present, nitrogen washouts and uADN2indicated that the lung was a single well ventilated space with no evidence of an abnormal distribution of ventilation. This indicated that ventilation of the trapped areas was so small that it could not be measured. The possibility that gas trapping is related to the presence of lung fluid and very compliant airways is considered.SpeculationLow birth weight infants have been shown to have high airway resistance, compliant airways, and low lung volume. This combination of findings has been associated with airway closure in adults. The possibility arises that a volume of gas is “trapped” with each expiration until airways are sufficiently stiff and remain patent with every breath.

ISSN:0031-3998    

出版商:OVID    

年代:1971

数据来源: OVID

摘要:

ExtractBased on studies of birth weights, there has long been speculation that poverty, inadequate maternal nutrition, and race might alter prenatal growth by influencing fetal nutrition. In the present study, undernutrition was identified as the cause of low birth weight in a group of infants born to poor urban mothers in the United States. A postmortem, quantitative, morphological study of body size, organ size, and cellular structure demonstrated that the infants of 83 poor mothers had many anatomic abnormalities recognized as characteristic of undernutrition. Such abnormalities were not found in infants from 386 families with incomes above the poverty line. There were almost no differences in body or organ growth among various racial groups when the comparisons were between families of similar economic status.SpeculationIs the low birth weight in infants born to poor urban mothers due to abnormal nutrition during pregnancy, the mother's earlier development, or uterine or placental abnormalities? If maternal malnutrition is responsible, the exact nutritional deficiencies should be promptly identified so that preventive programs can be developed. There is also a pressing need to know whether or not the moderate undernutrition observed in the present study alters brain composition and subsequent mental and motor performance.

ISSN:0031-3998    

出版商:OVID    

年代:1971

数据来源: OVID

摘要:

ExtractLiver biopsy specimens from four patients with homocystinuria were examined by electron microscopy before and after treatment with massive doses of pyridoxine. The chief abnormalities found were as follows: unusually shaped mitochondria, hypertrophy of the smooth endoplasmic reticulum, and numerous pericanalicular lysosomes.Several of the mitochondria in each cell in the various zones of the liver lobule had narrow projections and breaks in the outer mitochondrial membrane. Mitochondria were normal in size, but the mitochondrial dark granules appeared larger than normal.Two patients responded biochemically to treatment by disappearance of hyper-methioninemia and homocystinemia. No recognizable differences in hepatocellular structure resulted from treatment in any of the patients.SpeculationPatients with homocystinuria who respond to pyridoxine treatment by disappearance of hypermethioninemia and homocystinemia exhibit no change in ultrastructural aberrations following treatment. This suggests that “toxic” accumulation of metabolites proximal to an enzymatic block may not account for all the phenotypical manifestations of inborn errors of the metabolism of amino acids.

ISSN:0031-3998    

出版商:OVID    

年代:1971

数据来源: OVID

摘要:

ExtractThe interrelations of plasma levels of glucose, free fatty acids (FFA), α-amino nitrogen (α-aaN), insulin, and growth hormone (GH) were studied in 26 malnourished infants shortly after admission to the hospital and again several weeks later when they had recovered. In the sick children (SC) fasting levels of FFA and GH were high, and insulin and α-aaN were low; with recovery FFA, α-aaN and insulin levels became normal, and GH levels fell. No change occurred in glucose levels.Ten infants were given glucose (0.5 g/kg body weight) intravenously on the 1st or 2nd day after admission and again 6–12 weeks later. Glucose tolerance was impaired in the sick group and, although improved, was not normal when the children had recovered from the nutritional insult. Insulin secretion was stimulated by glucose in those that had recovered (RC), but not in the SC. No significant change occurred in either FFA or α-aaN levels in these groups.Nine infants received glucagon (0.1 mg/kg body weight) intravenously on the 2nd to 6th day after admission and again 6–12 weeks later. Glucagon caused a rise in glucose levels that were greater in RC than in SC but did not cause a significant change in insulin levels in either group. Free fatty acid levels were higher in SC throughout the test, but in both groups FFA levels responded similarly to glucagon administration, falling 10 and 60 min after the injection.Changes in GH levels in plasma after glucose or glucagon administration were compared with the changes caused by five venepunctures in RC. Venepunctures and glucose caused similar rises in GH levels, but glucagon caused a greater rise than either. It was concluded that the stress of repeated venepunctures caused a rise in GH levels in plasma in all three tests, but that, independent of this, glucagon stimulated GH secretion.SpeculationInsulin secretion is impaired in infantile malnutrition and does not improve at the same rate as clinical recovery occurs, suggesting that normal β cell function is not essential for rapid growth. The role of growth hormone in malnutrition is not clear, but it appears to be involved more in the metabolic adaptation to malnutrition than in the control of growth.

ISSN:0031-3998    

出版商:OVID    

年代:1971

数据来源: OVID

摘要:

ExtractIn order to determine the effect of vitamin D on tubular reabsorption of phosphate, micropuncture studies were performed in the proximal convolution of normal rats, of parathyroidectomized rats, and of rats with rickets. The studies showed that vitamin D exerted a direct effect on transtubular reabsorption of phosphate that was independent of parathyroid function. The glomerular filtration rate was not affected by vitamin D. The reabsorption of phosphate of normal rats was 13.51 μmoles/min per kg. This corresponds to a fractional reabsorption of 73%. With vitamin D the fractional reabsorption increased to 86%. Despite continuous infusion of vitamin D, the phosphate reabsorption decreased to 13.95 μmoles/min/kg (fractional reabsorption 74%) after 180–240 min. Parathyroidectomized rats also showed a decreased trans-tubular reabsorption of phosphate during vitamin D infusion. In animals under a phosphate load who suffered from rickets, it was possible to normalize the decreased rate of reabsorption of phosphate (fractional reabsorption 59%) by the administration of vitamin D (fractional reabsorption 78%).SpeculationWe were unable to determine why, despite continuous infusion of vitamin D and independent of the dosage, a decrease occurred in the increased reabsorption after 90–120 min and why after 180–240 min this function returned to the starting value. Since at this latter time toxic renal damage is unlikely and renal function was controlled during the whole experiment, the question arises whether inadequate activation, reactive breakdown of vitamin D, or development of resistance to the physiological activity of the vitamin is involved.

ISSN:0031-3998    

出版商:OVID    

年代:1971

数据来源: OVID