This study examined witnesses' memories for an event experienced 2 years earlier. Ss in 4 age groups (6-, 8-and 10-year-olds and adults; N= 79) answered repeated questions about an ambiguous incident that occurred as part of an earlier study (D. A. Poole & L. T. White, 1991). Surprisingly, the effects of question repetition were similar to the patterns observed 2 years ago. There were important differences in the testimonies of children and adults, however, that were not observed in the initial study: Children were less consistent than adults across sessions on yes-no questions, less accurate in response to open-ended questions, and more likely to fabricate answers to a question about a man's occupation. Some children also confused the actions of 2 research assistants. These results indicate the need for additional research on qualitative and quantitative changes in children's testimonies over long delays.The literature on children's eyewitness testimony is a story of contradictions, with developmental trends in accuracy, suggestibility, and response to stress differing from study to study (see Ceci & Bruck, 1993, for a review). Discrepancies have prompted critics to argue that eyewitness research lacks theoretical cohesion and that "established theories of perception and memory are not immediately applicable" because of the influence of motivational and social factors in event reporting (Sheehy & Chapman, 1982, p. 345). In early studies, concerns about ecological validity often loomed larger than efforts to reconcile eyewitness findings with traditional concepts of memory development.Recently, lack of consensus has prompted psychologists to reconsider the extent to which information about basic cognitive processes might resolve discrepancies between studies with very different contexts, tasks, and subject characteristics (e.g., Brainerd & Ornstein, 1991). While acknowledging that memory mechanisms alone cannot explain the content of event reports (Warren-Leubecker, 1991), eyewitness researchers frequently address basic cognitive issues such as trace strength (
Control of oxidative metabolism was studied using 13C NMR spectroscopy to detect rate-limiting steps in 13C labeling of glutamate. 13C NMR spectra were acquired every 1 or 2 min from isolated rabbit hearts perfused with either 2.5 mM [2-13C]acetate or 2.5 mM [2-13C]butyrate with or without KCl arrest. Tricarboxylic acid cycle flux (VTCA) and the exchange rate between alpha-ketoglutarate and glutamate (F1) were determined by least-square fitting of a kinetic model to NMR data. Rates were compared to measured kinetics of the cardiac glutamate-oxaloacetate transaminase (GOT). Despite similar oxygen use, hearts oxidizing butyrate instead of acetate showed delayed incorporation of 13C label into glutamate and lower VTCA, because of the influence of beta-oxidation: butyrate = 7.1 +/- 0.2 mumol/min/g dry wt; acetate = 10.1 +/- 0.2; butyrate + KCl = 1.8 +/- 0.1; acetate + KCl = 3.1 +/- 0.1 (mean +/- SD). F1 ranged from a low of 4.4 +/- 1.0 mumol/min/g (butyrate + KCl) to 9.3 +/- 0.6 (acetate), at least 20-fold slower than GOT flux, and proved to be rate limiting for isotope turnover in the glutamate pool. Therefore, dynamic 13C NMR observations were sensitive not only to TCA cycle flux but also to the interconversion between TCA cycle intermediates and glutamate.
Metabolic reversal of contractile dysfunction was achieved in isolated hearts by counteracting depressed PDH activity in the postischemic myocardium. Improved cardiac performance did not result from, nor require, increased glycolysis secondary to the activation of PDH. Rather, restoring carbon flux through PDH alone was sufficient to improve mechanical work by postischemic hearts.
To test how α-ketoglutarate dehydrogenase (α-KGDH) activity influences the balance between oxidative flux and transmitochondrial metabolite exchange, we monitored these rates in isolated mitochondria and in perfused rabbit hearts at an altered kinetics ( K m) of α-KGDH for α-ketoglutarate (α-KG). In isolated mitochondria, relative K mdropped from 0.23 mM at pH = 7.2 to 0.10 mM at pH 6.8 ( P < 0.05), and α-KG efflux decreased from 126 to 95 nmol ⋅ min−1 ⋅ mg−1. In intact hearts, K m was reduced with low intracellular pH, while matching control workload and respiratory rate with increased Ca2+(pHi = 7.20, perfusate CaCl2 = 1.5 mM; pHi = 6.89, perfusate CaCl2 = 3 ± 1 mM). Sequential13C nuclear magnetic resonance spectra from hearts oxidizing [2-13C]acetate provided tricarboxylic acid cycle flux and the exchange rate between α-KG and cytosolic glutamate ( F 1). Tricarboxylic acid cycle flux was 10 μmol ⋅ min−1 ⋅ g−1in both groups, but F 1 fell from a control of 9.3 ± 0.6 to 2.8 ± 0.4 μmol ⋅ min−1 ⋅ g−1at low K m. The results indicate that increased activity of α-KGDH occurs at the expense of α-KG efflux during support of normal workloads.
The coordination of long chain fatty acid (LCFA) transport across the mitochondrial membrane (V(PAL)) with subsequent oxidation rate through beta-oxidation and the tricarboxylic acid (TCA) cycle (V(tca)) has been difficult to characterize in the intact heart. Kinetic analysis of dynamic (13)C-NMR distinguished these flux rates in isolated rabbit hearts. Hearts were perfused in a 9.4 T magnet with either 0.5 mM [2,4,6,8,10,12,14,16-(13)C(8)] palmitate (n = 4), or 0.5 mM (13)C-labeled palmitate plus 0.08 mM unlabeled butyrate (n = 4). Butyrate is a short chain fatty acid (SCFA) that bypasses the LCFA transporters of mitochondria. In hearts oxidizing palmitate alone, the ratio of V(TCA) to V(PAL) was 8:1. This is consistent with one molecule of palmitate yielding eight molecules of acetyl-CoA for the subsequent oxidation through the TCA cycle. Addition of butyrate elevated this ratio; V(TCA)/V(PAL) = 12:1 due to an SCFA-induced increase in V(TCA) of 43% (p < 0.05). However, SCFA oxidation did not significantly reduce palmitate transport into the mitochondria: V(PAL) = 1.0 +/- 0.2 micromol/min/g dw with palmitate alone versus 0.9 +/- 0.1 with palmitate plus butyrate. Thus, the products of beta-oxidation are preferentially channeled to the TCA cycle, away from mitochondrial efflux via carnitine acetyltransferase.
University students (N = 301) in Estonia, Morocco, and the United States read scenarios about various scheduled appointments and indicated the time at which a person arriving would be inappropriately early or inappropriately late. Participants also completed measures of time orientation, collectivism, and personality. Definitions of "on time" varied substantially across countries and across individuals but interacted in a regular fashion with specific features of appointments (e.g., the purpose of an appointment or the status of persons involved). Flexible definitions of "on time" were associated with youth, collectivist values, and a fatalistic orientation toward the present. Finally, definitions of "on time" were largely independent of personality traits. Taken as a whole, personal standards of punctuality appear to be best understood within a situational and sociocultural-rather than dispositional-framework.
For the first time, 13C NMR signals are shown from 13C-enriched, low-level tricarboxylic acid (TCA) cycle intermediates from extracts of normal cardiac tissue. As the low tissue content of the key intermediates alpha-ketoglutarate (alpha-KG) and succinate (SUC) in normal, well perfused tissues has until now precluded direct NMR detection from intact tissues and tissue extracts, 13C NMR signal from glutamate has generally been used to infer the isotopomer patterns of intermediates that are in chemical exchange with glutamate. However, the required assumptions regarding intracellular compartmentation for such indirect analysis have not been previously tested, as glutamate is largely cytosolic while the TCA cycle enzymes are located in the mitochondria. Chromatographic isolation of alpha-KG and SUC from heart tissue extracts allowed isotopomer analysis to be performed for comparison with that of glutamate. At steady state, a direct relationship between glutamate and alpha-ketoglutarate isotopomers was found, but succinate isotopomers matched those of glutamate only in hearts that displayed negligible contributions from the oxidation of unlabeled endogenous carbon sources.
To examine metabolic regulation in postischemic hearts, we examined oxidative recycling of 13C within the glutamate pool (GLU) of intact rabbit hearts. Isolated hearts oxidized 2.5 mmol/L [2-13C]acetate during normal conditions (n = 6) or during reperfusion after 10 minutes of ischemia (n = 5). 13C-Nuclear magnetic resonance spectra were acquired every 1 minute. Kinetic analysis of 13C incorporation into GLU provided both tricarboxylic acid (TCA) cycle flux and the interconversion rate (F1) between the TCA cycle intermediate, alpha-ketoglutarate (alpha-KG), and the largely cytosolic GLU. The rate-pressure product in postischemic hearts was 46% of normal (P < .05). No difference in substrate utilization occurred between groups, with acetate accounting for 92% of the carbon units entering the TCA cycle at the citrate synthase step. TCA cycle flux in postischemic hearts was normal (normal hearts, 10.7 mumol.min-1.g-1; postischemic hearts, 9.4 mumol.min-1.g-1), whereas F1 was 72% lower at 2.9 +/- 0.4 versus 10.2 +/- 2.5 mumol.min-1.g-1 (mean +/- SE) in normal hearts (P < .05). From additional hearts perfused with 2.5 mmol/L [2-13C]acetate plus supplemental 5 mmol/L glucose, any potential differences in endogenous carbohydrate availability were proved not to account for the reduced rate alpha-KG and GLU exchange, which remained depressed in postischemic hearts. However, specific activities of the transaminase enzyme, catalyzing chemical exchange of alpha-KG and GLU, were the same, and transaminase flux was 100 mumol.min-1.g-1 in postischemic hearts versus 68 mumol.min-1.g-1 in normal hearts. Normal transaminase activity and the increased flux in postischemic hearts are contrary to the reduced F1. The findings indicate reduced metabolite transport rates across the mitochondrial membranes of stunned myocardium, particularly through the reversible alpha-KG-malate carrier.
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