This article uses narrative, case study analysis to examine consumer leisure and travel behavior. Adopting an interpretive research paradigm, the article examines travel behavior using face-to-face interviews of traveler informants, applies the folk theory of the mind, ecological systems theory, and the fits-like-a-glove model. Findings from the investigation indicate that most individual and household leisure and travel-relating behavior results from a "causal historical wave" in which an array of events come together, interact, and cause individuals to participate in certain behaviors and that most travel behavior is the result of automatic thinking rather than a rational or constructive process.

Oral squamous cell carcinoma develops continuously out of predamaged oral mucosa. For the physician and pathologist, difficulties arise in distinguishing precancerous from cancerous lesions. MAGE-A antigens are tumor antigens that are found solely in malignant transformed cells. These antigens might be useful in distinguishing precancerous from cancerous lesions. The aim of this study was to verify this assumption by comparing MAGE-A expression in benign, precancerous, and cancerous lesions of the oral mucosa. Retrospectively, biopsies of different oral lesions were randomly selected. The lesions that were included are 64 benign oral lesions (25 traumatic lesions (oral ulcers), 13 dental follicles, and 26 epulis), 26 oral lichen planus, 123 epithelial precursor lesions (32 epithelial hyperplasia found in leukoplakias, 24 epithelial dysplasia found in leukoplakias, 26 erythroplasia with oral epithelial dysplasia, and 41 carcinomas in situ in erythroleukoplakias). The lesions were immunohistochemically stained with the poly-MAGE-A antibody 57B, and the results were compared. Biopsies of oral lichen planus, oral ulcers, dental follicles, epulis, and leukoplakia without dysplasia showed no positive staining for MAGE-A antigens. Leukoplakia with dysplasia, dysplasia, and carcinomata in situ displayed positive staining in 33%, 65%, and 56% of the cases, respectively. MAGE-A antigens were not detectable via immunohistochemistry in benign lesions of the oral mucosa. The staining rate of dysplastic precancerous lesions or malignant lesions ranged from 33% to 65%. The MAGE-A antigens might facilitate better differentiation between precancerous and cancerous lesions of the oral mucosa.

8-Aminolevulinic-acid-synthetase induction by drugs depends upon the nutritional state of the animal. I n allylisopropylacetamide-treated animals the enzyme induction is reduced in fed compared with starved rats whereas after phenobarbital treatment an induction of the enzyme seen in starved animals is not observed in fed rats. 8-Aminolevulinic-acid-synthetase induction is studied in relation to the synthesis of cytochrome P450.I n the isolated rat liver perfused with either rat blood or washed bovine erythrocytes and Eagle minimal essential medium, 8-aminolevulinic acid synthetase decreases sharply. This decrease can be prevented by the continuous addition of dexamethasone (9a-fluoro-l6a-methylpregna-1,4-diene-li,9,i7a,2l-triol-3,20-dione) or hydrocortisone (pregn-4-ene-l1,9,17a,21-triol-3,20-dione) but not by testosterone (androst-4-ene-178-01-3-one) or etiocholanolone (5P-androstan3a-ol-17-one). 8-Aminolevulinic acid synthetase cannot be significantly induced by allylisopropylacetamide unless corticoids are added to the perfusion medium. The results indicate that the synthesis of heme and, consequently, hemoproteins is controlled by corticoids or their metabolites in adult rat liver.Our interest in the mechanism(s) of cytochrome P450 induction by phenobarbital led us to the study of 8-aminolevulinic acid synthetase, because this rate limiting enzyme in heme biosynthesis is also induced rapidly and early after phenobarbital treatment [ I]. During hemoprotein formation heme and apoprotein synthesis have to be closely correlated if the intracellular heme pool is ony small. I n addition to phenobarbital, allylisopropylacetamide, the porphyria-producing moiety of the drug Sedormid, was studied as another compound affecting both enzymes-i. e. inducing d-aminolevulinic acid synthetase and, in contrast to phenobarbital, initially decreasing cytochrome P450 [2-41.I n the present study d-aminolevulinic-acid-synthetase regulation was investigated in livers in vivo and in the isolated perfused organ. The conditions for induction of the enzyme by allylisopropylacetamide and phenobarbital were first studied in intact rats.Since it was found that the induction of this enzyme by phenobarbital is a special event not seen in rats fed ad libitum, the studies in the isolated organ focusEnzyme. Tyrosine aminotransferase or L-tyrosine : 2-oxoglutarate aminotransferase (EC 2.6.1.5).Trivial Names. Etiocholanolone, 5B-androstan-3a-01-17-one; testosterone, androst-4-ene-17B-ol-3-one; hydrocortisone, pregn-4-ene-ll~,l7n,21-triol-3,20-dione; dexamethasone, 9a-fluoro-16a-methyl-pregna-1,4-diene-l1~,17a,21-triol-3,20-dione. sed on induction by allylisopropylacetamide. I n this system an induction comparable to that found in vivo could only be achieved after addition of corticoids to the perfusion medium. The dependence of8-aminolevulinic acid synthetase and consequently heme synthesis, upon corticoids will be discussed in relation to the induction of hemoproteins. I n addition, a model for 8-aminolevulinic-acid-synthetase induction by phe...