Supplement: 9th international conference on health promoting hospitals, Copenhagen, May 16-18, 2001.
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Biomedical subjects
Publications and source records attributed to L Moller.
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This article reviews pertinent psychological theory to argue for two discrete human motivational tracts. These dual systems appear to draw from disparate constellations of emotional energies that normatively become interactive across development. The article stipulates eight premises from the accepted tenets of psychology, development, and pathology along with corroborating evidence from laterality studies, neuropsychology, and the neurosciences. These premises lead to a verifiable hypothesis reflecting Richard Leakey's proposal that H. sapiens emerged from an interpersonal shaping of adaptation across several million years of group living. The totality of the supportive evidence suggests that the flexibility, agility, and creativity of the human mind was abetted by tensions and reconciliations between two disparate hemispheric perspectives, which express as a Personal Self and a Social Self, focused by a lens molded by survival pressures.
In 3 experiments involving young children (N = 164), excellent perceptual integration of parts and wholes was revealed, unlike findings of earlier Piagetian studies (D. Elkind, R. R. Koegler, & E. Go, 1964). In Experiment 1, 5-year-olds' performance in part-whole perception was raised nearly sixfold when a multiple-choice task was substituted for the Piagetian verbal task used earlier. Performing the multiple-choice first rather than second also raised verbal scores. Experiment 2, with 3- to 5-year-olds, tested whether the children could have been confusing "whole made of parts" with "whole and parts" stimuli. Equal performance was found with 2 versions of a multiple-choice task, including either a whole and parts or a whole and different parts picture, which contradicts the confusion hypothesis. In Experiment 3, with 2- to 4-year-olds, good part-whole perception was demonstrated through the use of a 2-alternative, forced-choice procedure. The lower age bounds for this type of performance are much earlier than hitherto proposed.
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Heterocyclic aromatic amines (HAAs) are produced during cooking of proteinaceous food such as meat and fish. Humans eating a normal diet are regularly exposed to these food-borne substances. HAAs have proved to be carcinogenic in animals and to induce early lesions in the development of cancer. DNA adduct levels in mouse liver have been measured by 32P-HPLC after oral administration each of 14 different HAAs. The highest DNA adduct levels were detected for 3-amino-1-methyl-5H-pyrido[4,3-b]-indole (Trp-P-2), 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) and 2-amino-9H-pyrido[2,3-b]indole (AalphaC), respectively. To assess a relative risk in a human population, a relative risk index was calculated by combining the DNA adduct levels in mouse liver with human daily intake of heterocyclic amines in a US and in a Swedish population. Such calculations suggest that AalphaC presents the highest risk for humans, e.g. nine-fold higher compared with the most abundant amines in food, 2-amino-1-methyl-6-phenylimidazo[4,5-b]-pyridine (PhIP). Therefore, the distribution of DNA adducts in different tissues of mouse was investigated after oral administration of AalphaC. The highest AalphaC-DNA adduct levels were found in liver (137 adducts/10(8) normal nucleotides) followed by heart, kidney, lung, large intestine, small intestine, stomach and spleen, in descending order. To characterize the chemical structure of the major DNA adduct, chemical synthesis was performed. The major DNA adduct from the in vivo experiments was characterized by five different methods. On the basis of these results, the adduct was characterized as N2-(deoxyguanin-8-yl)-2-amino-9H-pyrido [2,3-b]indole. Considering the abundance of AalphaC not only in grilled meat, but also in other products like grilled chicken, vegetables and cigarette smoke and in light of the results of the present study, it is suggested that the human cancer risk for AalphaC might be underestimated.