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Biomedical subjects

I Gross

Publications and source records attributed to I Gross.

88 records · Page 5Linked to original sources
PubMed1977

The radiographic features of early onset Group B streptococcal neonatal sepsis.

The clinical and radiographic features of 27 newborn infants with early onset Group B streptococcal infection as documented by blood culture have been reviewed. Initial chest radiographs revealed a wide spectrum of patterns. These included changes usually associated with the respiratory distress syndrome, extensive pneumonia, and small infiltrates as well as a normal appearance. Premature birth and a fatal outcome were associated with extensive radiographic changes. At autopsy some of the infants with a radiographic appearance of respiratory distress syndrome had pathologic features of Group B streptococcal infection with no apparent evidence of coexisting respiratory distress syndrome.

Humans↗
PubMed1976

Studies on pulmonary surfactant. Effects of cortisol administration to fetal rabbits on lung phospholipid content, composition and biosynthesis.

Corticosteroids are known to accelerate maturation of the fetal lung and production of surfactant. We examined the effect of cortisol administration to fetal rabbits on the phospholipid content and composition of lung lavage and lung tissue, as well as on the activities of enzymes involved in the synthesis of phosphatidylcholine and phosphatidylglycerol, the major surface-active components of surfactant. Cortisol was administered by intrauterine injection at 25 days' gestation and the fetuses were delivered at 27 days (full term, 31 days). Saline-injected fetuses, littermates of the cortisol-treated as well as non-littermates, were used as controls. The amount of phospholipid in lung lavage from the hormone-treated fetuses was almost double that of the saline-injected controls and was similar to that of an untreated fetus of more than 30 days' gestation. Similarly, the phospholipid composition of lung lavage from the hormone-treated fetuses was similar to that of an untreated fetus at a greater gestational age. These data, therefore, suggest that cortisol acts by accelerating physiological development. Cortisol administratration stimulated the activity of cholinephosphate cytidylyltransferase and lysolecithin acyltransferase to a small, but statistically significant extent. This is also consistent with an acceleration of normal development. The stimulation of lysolecithin acyltransferase is of interest, since this enzyme is believed to be involved in the synthesis of dipalmitoylglycerophosphocholine, the major surface-active species of phosphatidylcholine. Cortisol administration had no effect on the activities of pulmonary choline kinase, cholinephosphotransferase, lysophosphatidic acid acyltransferase and glycerolphosphate phosphatidyltranferase, although we have previously shown the latter enzyme to be stimulated following a longer period of exposure to the hormone. Saline injection produced some maturational effects presumably as a result of stress, which may be mediated by corticosteroids or other hormones.

1-Acylglycerophosphocholine O-Acyltransferase↗
PubMed1976

The influence of postnatal nutritional deprivation on the phospholipid content of developing rat lung.

It has been previously reported that fasting may result in decreased lung surfactant production. In order to investigate this relationship and the role of nutrition in lung phospholipid synthesis, 21-day-old rats were exposed for 60 h to one of five dietary regimens: standard rat chow (controls), fasting, pure glucose, pure fat, or pure protein. After the period of fasting there was a 33% decrease in lung protein content, but there was no change in DNA content. Exposure to any of the experimental diets resulted in a decrease in tissue total phospholipid and phosphatidylcholine content per lung, but not per unit lung protein. Similarly lung lavage phospholipid and phosphatidylcholine content was decreased by 25% after fasting when expressed per lung or per unit DNA, but not per unit protein. Pulmonary cholinephosphotransferase (EC 2.7.8.2) activity was decreased in the fasted animals and those fed the protein diet, but not in the glucose or fat-fed animals. The activities of acetyl-CoA carboxylase (EC 6.4.1.2) and microsomal fatty acid elongation were decreased in all the experimental groups except for the glucose-fed group. It is concluded that fasting results in a decrease in lung cell size but not in lung cell number. Total phospholipid and phosphatidylcholine content in lung tissue and lung lavage is decreased per cell but not per unit cell mass.

Acetyl-CoA Carboxylase↗
PubMed1976

A comparison of early-onset group B streptococcal neonatal infection and the respiratory-distress syndrome of the newborn.

In attempting to differentiate early-onset Group B streptococcal infection from hyaline-membrane disease we found features of severe Group B infection to be rupture of the membranes for more than 12 hours before delivery (four or eight versus one of nine), gram-positive cocci in the gastric aspirate (four or four versus none of one), apnea and shock in the first 24 hours of life (seven of eight versus none of nine), and the generation of lower peak inspiratory pressures on avolume-cycled respirator (mean of 36.5 +/- 2.8 versus 63.9 +/- 6.2 cm of water; P = 0.005). In eight fatal cases of Group B infection, four patients had radiographic features indistinguishable from hyaline-membrane disease whereas the other cases were consistent with neonatal pneumonia. Seven of the eight infected infants had no histologic evidence of coexisting hyaline-membrane disease. Microscopical features of Group B infection included cocci in unevenly distributed hyaline membranes and minimal atelectasis. Group B streptococcal infection differs clinically and pathologically from hyaline-membrane disease. Differentiating clinical features include early apnea and shock and lower inspiratory pressures on mechanical ventilation.

Diagnosis, Differential↗
PubMed1975

Stimualtion of glycerolphosphate phosphatidyltransferase activity in fetal rabbit lung by cortisol administration.

Phosphatidylglycerol is an important component of pulmonary surfactant. Previous studies have shown that direct administration of corticosteroids of thyroxine to the fetus during the latter part of gestation results in accelerated lung maturation with increased surfactant production. We have shown that administration of cortisol to fetal rabbits at 24 days' gestation results 3 days later in a significant increase in the activity of pulmonary glycerolphosphate phosphatidyltransferase, an enzyme involved in the synthesis of phosphatidylglycerol. The activity of the liver enzyme was not affected. Choline phosphotransferase, CDPdiglyceride-inositol phosphatidyltransferase, lysophosphatidic acid acyltransferase and lysolecithin acyltransferase activities were not altered significantly by cortisol treatment. Thyroxine treatment had no effect on any of the enzymes of phospholipid or fatty acid biosynthesis studied.

Animals↗
PubMed1975

Blood platelet response to plasma from patients with ischemic heart disease.

Blood platelets change shape (from small round spheres to larger spread forms) as they participate in thrombosis. Using an electron microscopic technique, we surveyed 14 patients with both acute and chronic ischemic heart disease; each had increased spread platelet forms (69 plus and minus 22.2 [standard deviation] percent) when compared with 14 asymptomatic control subjects (P less than 0.001). When platelets from these 14 control subjects were exposed to plasma from the patients with ischemic heart disease, spread forms increased from 13.4 plus and minus 9.1 to 44.5 plus and minus 15.5 percent (P less than 0.001). There was no significant increase in spread platelets in these control subjects when their blood was mixed with plasma from another control group. Similar studies were performed in seriously ill noncardiac patients: 9 of 13 had increased spread platelet forms when compared with control subjects, but plasma from only 5 of these 9 subjects caused increased spread forms when mixed with platelets from normal subjects (P less than 0.05). Thus a factor existed in the plasma of these patients with ischemic heart disease that caused normal platelets to become spread. Similarly the plasma of some patients with serious noncardiac disease had a comparable effect on normal platelets. Although the identity of this factor is unknown, it is probably unrelated to hormonal or therapeutic influences occurring either during acute infarction or during the stress of serious illness because (1) the effect of the plasma from patients with acute ischemic heart disease was identical to that of patients with chronic ischemic heart disease, and (2) the effect was not present in all patients with serious noncardiac disease.

Acidosis↗
PubMed1975

The influence of cortisol on the enzymes of fatty acid synthesis in developing mammalian lung and brain.

Administration of cortisol to fetal rabbits resulted in a 42% inhibition of pulmonary de novo fatty acid synthesis from acetyl coenzyme A (CoA) (P = less than 0.025). This was associated with inhibition of acetyl-CoA carboxylase (EC. 6.4.1.2.) activity (P = less than 0.01) and a tendency towards decreased activity of fatty acid synthetase. There was no effect on pulmonary microsomal fatty acid elongation activity. Light and electron microscopic examination of the apex of the right lung of control and cortisol-treated animals revealed changes consistent with accelerated lung maturation in the treated animals. The in vitro activities of acetyl-CoA carboxylase and fatty acid synthetase were similar in rabbit lung and thus acetyl-CoA carboxylase activity does not appear to be rate limiting for de novo fatty acid synthesis in lung. No significant change in the activity of enzymes associated with de novo fatty acid synthesis of microsomal fatty acid elongation was found in fetal brain after cortisol exposure. However, in a parallel study on fatty acid synthesis in fetal liver, cortisol administration resulted in a 30% increase in fatty acid synthetase activity (P less than 0.025). The finding of cortisol-induced inhibition of de novo fatty acid synthesis in fetal rabbit lung may be related to the known inhibitory effect of cortisol on lung growth in the fetus.

Acetyl Coenzyme A↗