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We propose a simple theory for the longitudinal profile of channels incised by groundwater flow. The aquifer surrounding the stream is represented in two dimensions through Darcy's law and the Dupuit approximation. The model is based on the assumption that, everywhere in the stream, the shear stress exerted on the sediment by the flow is close to the minimal intensity required to displace a sand grain. Because of the coupling of the stream discharge with the water table elevation in the neighbourhood of the channel head, the stream elevation decreases as the distance from the stream's tip with an exponent of 2/3. Field measurements of steephead ravines in the Florida Panhandle conform well to this prediction. [ABSTRACT FROM AUTHOR]

It has been recognized for many years that the metabolism of brain glutamate and gamma-aminobutyric acid (GABA), the major excitatory and inhibitory neurotransmitters, is linked to a substrate cycle between neurons and astrocytes involving glutamine. However, the quantitative significance of these fluxes in vivo was not known. Recent in vivo 13C and 15N NMR studies in rodents and 13C NMR in humans indicate that glutamine synthesis is substantial and that the total glutamate-GABA-glutamine cycling flux, necessary to replenish neurotransmitter glutamate and GABA, accounts for >80% of net glutamine synthesis. In studies of the rodent cortex, a linear relationship exists between the rate of glucose oxidation and total glutamate-GABA-glutamine cycling flux over a large range of cortical electrical activity. The molar stoichiometric relationship (approximately 1:1) found between these fluxes suggests that they share a common mechanism and that the glutamate-GABA-glutamine cycle is coupled to a major fraction of cortical glucose utilization. Thus, glutamine appears to play a central role in the normal functional energetics of the cerebral cortex. [ABSTRACT FROM AUTHOR]

Examines flux control in the rat gastrocnemius glycogen synthesis pathway by in vivo carbon-13/phosphorus-31 nuclear magnetic resonance spectroscopy. Glycogen synthesis rates and glucose plasma concentration values of subjects; Calculated values of control coefficients for glucose transport/hexokinase, glycogen synthase and glycolysis for the flux for glucose through glycogen synthesis; Effects of muscle glycolysis on the calculated control coefficients.

Natural-abundance 13C NMR spectroscopy is a non-invasive technique that enables in vivo assessments of muscle and/or liver glycogen concentrations. Over the last several years, 13C NMR has been developed and used to obtain information about human glycogen metabolism with diet and exercise. Since NMR is non-invasive, more data points are available over a specified time course, dramatically improving the time resolution. This improved time resolution has enabled the documentation of subtleties of muscle glycogen re-synthesis following severe glycogen depletion that were not previously observed. Muscle and liver glycogen concentrations have been tracked in several different human populations under conditions that include: (1) muscle glycogen recovery from intense localized exercise with normal insulin and with insulin suppressed; (2) muscle glycogen recovery in an insulin-resistant population; (3) muscle glycogen depletion during prolonged low-intensity exercise; (4) effect of a mixed meal on postprandial muscle and liver glycogen synthesis. The present review focuses on basic 13C NMR and gives results from selected studies. [ABSTRACT FROM AUTHOR]

There have been substantial changes in the pattern of pregnancies to teenagers in England and Wales in the past 25 years. The number of births and abortions to teenagers has increased until the last 2–3 years since when there has been a decline. This paper looks at the changes that have occurred in the population structure and marital patterns of teenagers during these years, and examines teenage pregnancies and their outcomes with regard to some of the medical and social factors that may have influenced these changes. [ABSTRACT FROM AUTHOR]

This study sought to determine whether the lingual ascorbic acid test (LAAT) and measurement of salivary ascorbate reflect plasma and leukocyte ascorbate levels during controlled periods of ascorbic acid depletion and supplementation. Eleven healthy non-smoking men, aged 19-28 years, ate a diet that was repeated every seven days and was adequate in all nutrients except ascorbic acid (AA). This basal diet, which provided less than 5 mg of AA per day, was supplemented with 60 mg of AA per day for two weeks, 0 mg (placebo) per day for four weeks, 600 mg per day for three weeks, and 0 mg per day for four weeks. Oral examinations, the lingual ascorbic acid test, and measurement of salivary, plasma, and leukocyte ascorbate concentrations were conducted throughout the study. Ascorbic acid concentrations in plasma and leukocytes responded rapidly to changes in vitamin C intake. LAAT-derived ascorbate values were unrelated to ascorbic acid intake and plasma and leukocyte ascorbate concentrations. Salivary ascorbate levels approached the lower limits of detection of the assay and remained constant throughout the investigation. Oral hygiene was consistently excellent, and no severe mucosal or periodontal changes were observed. It was concluded that lingual ascorbic acid test values and salivary ascorbate levels are not related to changes in ascorbic acid intake and are not consistent with plasma or leukocyte ascorbate concentrations. [ABSTRACT FROM AUTHOR]

Brain GABA levels rise and plateau following prolonged administration of the irreversible GABA-transaminase inhibitor vigabatrin (γ-vinylGABA). Recently it has been shown that increased GABA levels reduces GAD protein, one of two major isoforms of glutamic acid decarboxylase (GAD). The effects of GABA elevation on GABA synthesis were assessed in vivo usingH andC-edited NMR spectroscopy. Rates of turnover of cortical glutamate and GABA from intravenously administered [1-C]glucose were measured in α-chloralose anesthetized rats 24 hours after receiving vigabatrin (500 mg/kg, i.p.) and in non-treated controls. GABA concentration was increased 2-fold at 24 hours (from 1.3±0.4 to 2.7±0.9 μmol/g) and GABA-T activity was inhibited by 60%. Tricarboxylic acid cycle flux was not affected by vigabatrin treatment compared to non-treated rats (0.47±0.19 versus 0.52±0.18 μmol/g, respectively). GABA-C2 fractional enrichment (FE) measured in acid extracts rose more slowly in vigabatrin-treated compared to nontreated rats, reaching >90% of the glutamate FE after 3 hours. In contrast, GABA FE≥glutamate FE in non-treated rats. A metabolic model consisting of a single glutamate pool failed to account for the rapid labeling of GABA from glutamate. Metabolic modelling analysis based on two (non-communicating) glutamate pools revealed a ∼70% decrease in the rate of GABA synthesis following vigabatrin-treatment, from 0.14 (non-treated) to 0.04 μmol/g/min (vigabatrin-treated). These findings, in conjunction with the previously reported differential effects of elevated GABA on the GAD isoforms, suggests that GAD may account for a major fraction of cortical GABA synthesis in the α-chloralose anesthetized rat brain in vivo. [ABSTRACT FROM AUTHOR]