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Notes: The dissociation of CH4 physisorbed on Ni(111) at 46 K is observed to be induced by the impact of incident inert gas atoms. The dynamics and mechanism of this new process, collision induced dissociative chemisorption, are studied by molecular beam techniques coupled with ultrahigh vacuum electron spectroscopies. The absolute cross section for collision induced dissociation is measured over a wide range of kinetic energies (28–109 kcal/mol) and incident angles of Ne, Ar, and Kr atom beams. The cross section displays a complex dependence on the energy of the impinging inert gas atom characteristic of neither total nor normal energy scaling. Quantitative reproduction of the complex dependence of the cross section on the Ar and Ne incident energy by a two-step, dynamical model establishes the mechanism for collision induced dissociation. Collision induced dissociation occurs by the impulsive transfer of kinetic energy upon collision of Ar or Ne with CH4, followed by the translationally activated dissociative chemisorption of the CH4 upon its subsequent collision with the Ni surface. The dependence of the probability of activated dissociation on the resultant CH4 normal energy derived from the fit of the model to the experimental cross section is in excellent agreement with the results of a previous study of the translationally activated dissociative chemisorption of CH4 on Ni(111). Collision induced activation and translational activation are shown to be consistent mechanisms for providing energy to CH4 to surmount the barrier to dissociative chemisorption.

Notes: —The effect of 1-hydroxy-3-aminopyrrolidone-2(HA-966), a CNS depressant, was studied on the metabolism of [14C]glucose and [3H]acetate in the brain in mice. HA-966 had a marked effect on glucose metabolism. The conversion of glucose carbon into amino acids associated with the tricarboxylic acid cycle (‘cycle’) was severely reduced, while the concentration of brain glucose was approximately doubled. Relative to the specific radioactivity of glucose in the brain, the specific radioactivity of alanine was 60–70 per cent of the control, indicating a reduction in the rate of glycolysis, and those of the‘cycle’amino acids were also lowered. A reduction in‘cycle’flux of 30–35 per cent was estimated. It was established that the depressed glucose utilization flux was not due to either impaired uptake of glucose from blood to brain or to hypothermia. In contrast to [14C]glucose, there was no change in the labelling of the amino acid fraction from [3H]acetate, which is preferentially metabolized in the 'small’compartment believed to be associated with glia. Thus it seems that CNS depression caused by HA-966 resulted in a selective decrease in energy production in the‘large’metabolic compartment where glucose is oxidized preferentially and which is believed to be associated with neuronal structures.The results also suggested that communication between the metabolic compartments mediated via glutamine and GABA was reduced, since the labelling from [3H]acetate of glutamine was increased and that of GABA decreased by HA-966.

Notes: Abstract— Thiamine deficiency produced by administration of pyrithiamine to rats maintained on a thiamine-deficient diet resulted in a marked disturbance in amino acid and glucose levels of the brain.In the two pyrithiamine-treated groups of rats (Expt. A and Expt. B) there was a significant decrease in the levels of glutamate (23%, 9%) and aspartate (42%, 57%), and an increase in the levels of glycine (26%, 27%) in the brain, irrespective of whether the animals showed signs of paralysis (Expt. A) or not (Expt. B). as a result of thiamine deficiency. A significant decrease in the levels of γ-aminobutyrate (22%) and serine (28%) in the brain was also observed in those pyrithiamine-treated rats which showed signs of paralysis (Expt. A). Threonine content increased by 57% in Expt. A and 40% in Expt. B in the brain of pyrithiamine-treated rats, but these changes were not statistically significant.The utilization of [U-14C]glucose into amino acids decreased and accumulation of glucose and [U-14C]glucose increased significantly in the brain after injection of [U-14C]glucose to pyrithiamine-treated rats which showed abnormal neurological symptoms (Expt. A). The decrease in 14C-content of amino acids was due to decreased conversion of [U-14C]glucose into alanine, glutamate, glutamine, aspartate and γ-aminobutyrate. The flux of [14C]glutamate into glutamine and γ-aminobutyrate also decreased significantly only in the brain of animals paralysed on treatment with pyrithiamine.The decrease in the labelling of, amino acids was attributed to a decrease in the activities of pyruvate dehydrogenase and α-oxoglutarate dehydrogenase in the brain of pyrithiamine-treated rats. The measurement of specific radioactivity of glucose, glucose-6-phosphate and lactate also indicated a decrease in the activities of glycolytic enzymes in the brain of pyrithiamine-treated animals in Expt. A only. It was suggested that an alteration in the rate of oxidation in vivo of pyruvate in the brain of thiamine-deficient rats is controlled by the glycolytic enzymes, probably at the hexokinase level.The lack of neurotoxic effect and absence of significant decrease in the metabolism of [U-14C]glucose in the brain of pyrithiamine-treated animals in Expt. B were probably due to the fact that animals in Expt. B were older and weighed more than those in Expt. A, both at the start and the termination of the experiments.

Notes: Kaposi's sarcoma is associated with an increased frequency of HLA-DR5. The hypothesized model of a susceptibility gene in linkage disequilibrium with DR5 may be tested by haplotype analysis in familial Kaposi's sarcoma. Our finding of no common haplotype among afflicted members of a family provides evidence against the hypothesized linkage.

Notes: Summary This study was set up to compare the frequency of health, educational and behavioural problems in a geographically defined birth cohort of 7-year-old children grouped by weight at birth. The study design was based on a multi-stage postal survey, with sampling stratified by birthweight. It took place in the four counties of Oxfordshire, Buckinghamshire, Berkshire and Northamptonshire which make up the former Oxford region. We studied 1319 live births to women resident in the former Oxford region in1985, including all those with birthweights under 1500 g, or whose weight was not recorded, and a sample of those who weighed 1500–2499 g, and of those who weighed 2500 g or more at birth. The children in the sample were traced through the National Health Service Central Register (NHSCR) and self-administered questionnaires were sent to their parents, general practitioners (GP) and teachers. Of the 1169 children who were alive at the age of 7 years and were successfully traced, 805 (75%) were followed up by postal survey. The use of health services, and of additional educational support was higher, and school performance was poorer among children who had weighed less than 1500 g at birth than among children who had weighed 2500 g or more, with the rates for children who had weighed 1500–2499 g falling in between. This survey method identifies the higher rate of health and educational problems in children weighing under 2500 g at birth, particularly those with birthweight under 1500 g, compared with other children. The method could be developed to provide a way of monitoring any changes over time in the prevalence of these problems. This information can be used to assess the health and educational needs of 7-year-old children in the population.