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The differences between open-book, cheat sheet, and closed-book exams were examined in two different types of psychology courses. A total of 297 students enrolled in eight sections of Introductory Psychology and 99 students enrolled in four sections of Statistics participated in this study. Exam types were counterbalanced across sections of the same course. Students were given either open-book, cheat sheet, or closed-book exams, took a surprise quiz two weeks after the exams to measure retention of course material, completed a preference questionnaire, and took a pre-test measure of test anxiety on open-book and cheat sheet tests. While students did slightly better on open-book exam than on closed-book exams, they also much preferred open-book and cheat sheet exams over closed-book exams, and had lower levels of anxiety when taking open-book exams compared to cheat sheet exams. Based on these results, open-book exams may be a superior style of examination for a variety of psychology courses. (Contains 2 tables and 2 figures.) [This research was supported in part by an Academic Excellence Grant from Dominican University of California.]

A mouse model with compromised mitochondrial fatty acid synthesis has been engineered in order to assess the role of this pathway in mitochondrial function and overall health. Reduction in the expression of mitochondrial malonyl CoA-acyl carrier protein transacylase, a key enzyme in the pathway encoded by the nuclear Mcat gene, was achieved to varying extents in all examined tissues employing tamoxifen-inducible Cre-lox technology. Although affected mice consumed more food than control animals, they failed to gain weight, were less physically active, suffered from loss of white adipose tissue, reduced muscle strength, kyphosis, alopecia, hypothermia and shortened lifespan. The Mcat-deficient phenotype is attributed primarily to reduced synthesis, in several tissues, of the octanoyl precursors required for the posttranslational lipoylation of pyruvate and α-ketoglutarate dehydrogenase complexes, resulting in diminished capacity of the citric acid cycle and disruption of energy metabolism. The presence of an alternative lipoylation pathway that utilizes exogenous free lipoate appears restricted to liver and alone is insufficient for preservation of normal energy metabolism. Thus, de novo synthesis of precursors for the protein lipoylation pathway plays a vital role in maintenance of mitochondrial function and overall vigor.

Two bar-press experiments with rats tested the role that reducing expectation of reward increases the variation from which reward selects. Experiment 1 used a discrete-trial random-interval schedule, with trials signaled by light or sound. One signal always ended with reward; the other signal ended with reward less often. The 2 signals were randomly mixed. Bar-press duration (how long the bar was held down) varied more during the signal with the lower probability of reward. Experiment 2 closely resembled Experiment 1 but used a random-ratio schedule rather than a random-interval schedule. Again, bar-press duration varied more during the signal with the lower probability of reward. The results support the role--the first well-controlled comparisons to do so.

Accumulation of oxidative damage to mitochondria, protein, and nucleic acid in the brain may lead to neuronal and cognitive dysfunction. The effects on cognitive function, brain mitochondrial structure, and biomarkers of oxidative damage were studied after feeding old rats two mitochondrial metabolites, acetyl-L-carnitine (ALCAR) [0.5% or 0.2% (wt/vol) in drinking water], and/or R-[alpha]-lipoic acid (LA) [0.2% or 0.1% (wt/wt) in diet]. Spatial memory was assessed by using the Morris water maze; temporal memory was tested by using the peak procedure (a time-discrimination procedure). Dietary supplementation with ALCAR and/or LA improved memory, the combination being the most effective for two different tests of spatial memory (P < 0.05; P < 0.01) and for temporal memory (P < 0.05). Immunohistochemical analysis showed that oxidative damage to nucleic acids (8-hydroxyguanosine and 8-hydroxy-2'-deoxyguanosine) increased with age in the hippocampus, a region important for memory. Oxidative damage to nucleic acids occurred predominantly in RNA. Dietary administration of ALCAR and/or LA significantly reduced the extent of oxidized RNA, the combination being the most effective. Electron microscopic studies in the hippocampus showed that ALCAR and/or LA reversed age-associated mitochondrial structural decay. These results suggest that feeding ALCAR and LA to old rats improves performance on memory tasks by lowering oxidative damage and improving mitochondrial function.

Examines the relationship between memory loss in old rats and brain mitochondrial decay and RNA/DNA oxidation. Effects accumulation of oxidative damage in the brain; Improvement of memory with dietary supplementation of acetyl-L-carnitine and/or R-alpha-lipoic acid; Occurrence of oxidative damage to nucleic acids in the RNA.