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Notes: The changes in central venous pressure (CVP) in patients who received ergometrine, oxytocin, ergometrine with oxytocin (Syntometrine), or no oxytocic drug in the third stage of labour have been compared. The results showed that there was a significant rise in central venous pressure after the administration of ergometrine and Syntometrine. When diazepam was given late in the first stage of labour to a group of patients who received Syntometrine during the course of delivery the changes in CVP were not significantly different from those of the control group. In addition, the administration of oxytocin in the management of the third stage did not produce a significant rise in CVP. The volume of blood lost was significantly reduced in all subjects by the use of oxytocic drugs.

Notes: Abstract— Rats were undernourished by approximately halving the normal food given from the 6th day of gestation throughout lactation. Growth of the foetuses was nearly normal, in marked contrast to the severe retardation caused by undernutrition during the suckling period. In comparison with controls the size and the DNA content of the brain were permanently reduced by undernutrition during the suckling period: this effect was relatively small, approx. 15 per cent decrease at 21 and 35 days. The rate of 14C incorporation into brain DNA at 30 min after administration of [2-14C] thymidine was taken as an index of mitotic activity; compared with controls there was severe reduction in mitotic activity (maximal decrease by about 80 per cent at 6 days in the cerebrum and by 70 per cent at 10 days in the cerebellum). The rate of acquisition of cells was calculated from the slopes of the logistic curves fitted to the estimated DNA contents. In normal animals the maximal slope was attained at 2·7 days and at 12·8 days after birth in cerebrum and cerebellum respectively; the daily acquisition of cells at these times was 4·8 × 106 and 18 × 106 cells respectively. The fractional increase in cell number at the maximum was 5·4 percent per day in the cerebrum and 15·2 per cent per day in the cerebellum. The rate of acquisition of cells relative to the rate of mitotic activity was higher in the brains of undernourished animals than in controls. One of the compensatory mechanisms for the severe depression of mitotic activity in the brain of undernourished animals Seems to involve a reduction in the normal rate of cell loss.

Notes: (1) Treatment with cortisol acetate (0.2 mg daily during the first 4 days after birth) reduced the rate of growth in the rat: at 35 days of age the body weight was reduced by 50 per cent and the brain weight, depending on the region, by up to 30 per cent.(2) In the brain the normal increase in cell number was severely inhibited during the period of cortisol treatment; this resulted in a final deficit in cell number of about 20 per cent in the cerebrum and 30 per cent in the cerebellum.(3) To determine whether cortisol affected primarily cell formation or cell destruction the labelling of brain DNA was studied 1 h after a subcutaneous injection of 20 Ci/100 g [2-14C]thymidine. In the controls the amount of labelled DNA increased by a factor of two in the cerebrum and seven in the cerebellum during the period 2-13 days, and it decreased to 40 and 27 per cent of the peak values in the cerebrum and cerebellum respectively in the following 7 days. The results indicated that mitotic activity is higher in the cerebellum than in the cerebrum in the 2nd week of life. It would appear that in the cerebrum appreciable cell death accompanies new cell formation, especially during the period 13-35 days of age.(4) Cortisol treatment affected cell division rather than cell destruction in the brain since it strongly inhibited the incorporation of [2-14C]thymidine into DNA. The inhibition was severe during the period of treatment but it did not result in a lasting fall in mitotic activity. At the age of 13 days the amount of labelled DNA formed approached the normal level and it was twice that in controls at 20 days, indicating a tendency for compensating cell deficit by an accelerated mitotic activity. Nevertheless, massive cell proliferation ceased at about the same age as in normals; the labelling of DNA decreased markedly between 13 and 20 days after birth, and the DNA content did not increase after the age of 20 days.(5) In contrast to the marked effect on cell number, cortisol treatment did not influence significantly the maturational changes related to average cell size (DNA concentration) or the chemical composition of cells (RNA/DNA and protein/DNA).

Notes: 〈list xml:id="l1" style="custom"〉1The rapid and extensive conversion of glucose-carbon into amino acids is an index of the final coordination of the mechanisms underlying energy metabolism in the adult brain. This phenomenon develops in the rat during a short period extending from 10 to about 19 days after birth. The underlying factors have been analysed.〈list xml:id="l2" style="custom"〉2The development of the pattern of distribution of glucose-carbon characteristic of the adult brain was markedly influenced by the thyroid state of the animals. The age-curve for the conversion of glucose-carbon into brain amino acids was displaced to the left after treatment with thyroid hormone (T3) in infancy thus indicating an accelerated maturation. Conversely, neonatal thyroidectomy resulted in a significant retardation in the conversion of glucose-carbon into amino acids.〈list xml:id="l3" style="custom"〉3The specific radioactivity of glutamate increased five-fold in the brain of normal rats from the 10th to the 19th day of age. The values (as a percentage of those for littermate controls) were 220 in the case of the 10 day-old thyroid treated rats and about 30 for the 19 day-old thyroid deficient animals. At the age of 10 days neither treatment affected the concentration of glutamate which was also only slightly less than the control values in the brain of 19 day-old thyroid deficient animals (–17 per cent).〈list xml:id="l4" style="custom"〉4Specific pool(s) of glutamate associated with the formation of GABA can be demonstrated in the brain of 19 day-old rats after administration of [U-14C]glucose as a result of anoxia post mortem. These pools did not develop in the brain of 10 day-old animals. Neonatal thyroidectomy retarded the development of these glutamate pools.〈list xml:id="l5" style="custom"〉5Evidence is summarized which indicates that the development of the rapid conversion of glucose-carbon into amino acids reflects the enlargement, during maturation, of the metabolic compartments which are associated with neuronal processes.

Notes: Abstract— The distibution of 14C in the brains of rats that had been given [U-14C]glucose (10μCi/100g body wt.) at 10 min before death was followed for 20 min post mortem. The results indicated that the input of glucose-carbon into the tricarboxylic acid cycle stopped instantaneously after death. Although the proportion (more than 40 per cent) of tissue-14C combined in the amino acids associated with the cycle did not change significantly, there was a characteristic redistribution of 14C within the amino acid fraction after death: significantly, the 14C content of glutamate decreased andthat of GABA increased. The GABA/glutamate specific radioactivity ratio which in vivo was 0-58, increased progressively in the first 5 min after death, reaching a value of 0-93. However, by 5 min the rise in the ratio stopped abruptly, although GABA accumulation continued at about half the initial rate beyond that time. These results indicated that GA BA formation is compartmented in the brain andpermitted the evaluation of certain kinetic parameters of the two compartments which could be distinguished under the experimental conditions. One of the compartments was evidently a summation of a number of subcompartments which had certain features in common, such as a low GABA flux relative to the amount of glutamate. The properties of the other compartment were compatible with those of nerve terminals functioning with GABA as the transmitter. This compartment contained about 2 per cent of the total glutamate, but the glutamate pool was labelled about three times more than the average. Further, this compartment accounted for about 50 per cent of the total GABA formation flux andcontained GABA in high concentrations (the probable values were about seven times the mean).

Notes: Abstract— A small basic protein (mol.wt. 12,000), referred to as the P2 protein, was extracted with dilute acid from delipidated bovine root myelin and purified by ion exchange chromatography on cellulose phosphate. It appeared homogeneous on polyacrylamide gel electrophoresis. The P2 protein had a distinctly different amino acid composition than the larger basic protein (mol.wt. 18,000), referred to as the P1 protein, that is also present in peripheral nerve myelin. It contained relatively more hydrophobic residues and much less histidine and proline. The P2 protein conjugated with peroxidase was bound by lymph node cells and infiltrates in rabbits sensitized with whole bovine root myelin. No binding was evident with the bovine central nervous system myelin basic protein. Chemically and immunologically, the P2 protein appears to be specific to peripheral nervous system myelin. The isolated P2 protein produced mild clinical symptoms of experimental allergic neuritis, but no histological evidence of disease. It was suggested that the P2 protein is an important antigen for experimental allergic neuritis, and that its antigenic determinants are likely to be conformation-dependent.