The well-established finding that substantial confusion and misconceptions about evolution and natural selection persist after college instruction suggests that these courses neither foster accurate mental models of evolution's mechanisms nor instill an appreciation of evolution's centrality to an understanding of the living world. Our essay explores the roles that introductory biology courses and textbooks may play in reinforcing undergraduates' preexisting, faulty mental models of the place of evolution in the biological sciences. Our content analyses of the three best-selling introductory biology textbooks for majors revealed the conceptual segregation of evolutionary information. The vast majority of the evolutionary terms and concepts in each book were isolated in sections about evolution and diversity, while remarkably few were employed in other sections of the books. Standardizing the data by number of pages per unit did not alter this pattern. Students may fail to grasp that evolution is the unifying theme of biology because introductory courses and textbooks reinforce such isolation. Two goals are central to resolving this problem: the desegregation of evolution as separate ''units'' or chapters and the active integration of evolutionary concepts at all levels and across all domains of introductory biology.
In mice, the sex difference in susceptibility to hepatocarcinogenesis results from the tumor promoting activity of testosterone and from the inhibition of tumor promotion by ovarian hormones. We investigated the role of growth hormone in the sex-dependent regulation of susceptibility, because sex hormones are known to regulate the temporal pattern of growth hormone secretion and subsequent sex differences in liver gene expression. We found that in both males and females, wild-type mice developed significantly more tumors than growth hormone-deficient, C57BL/6J-lit/lit (B6-lit/lit) mutant mice following perinatal treatment with the carcinogen N,N-diethylnitrosamine (DEN). B6 wild-type males developed 36-59-fold more liver tumors per animal than age matched B6-lit/lit males and wild-type females developed 11-fold more tumors than B6-lit/lit females. We bred the little mutation onto the more susceptible C57BR/cdJ (BR) and C3H/HeJ (C3H) strains to assess the effect of growth hormone deficiency on hepatocarcinogenesis on additional genetic backgrounds. Growth hormone deficiency suppressed liver tumor development to <1% in males of each strain and in BR strain females. In B6 and C3H females, growth hormone deficiency caused 2-4-fold reductions in the volume fraction of the liver occupied by preneoplastic lesions. Furthermore, in contrast to wild-type strains, neither gonadectomy nor strain background significantly affected susceptibility in lit/lit mice, as mean liver tumor multiplicities ranged from 0 to 0.24 +/- 0.44 and the volume fraction of preneoplastic lesions ranged from 0.21 +/- 0.22 to 0.61 +/- 1.9%. These results demonstrate that both strain and sex hormonal effects on susceptibility to liver carcinogenesis are dependent on wild-type levels of growth hormone.
In order to study the interaction of genetic and hormonal factors during murine hepatocarcinogenesis, we compared the number of liver tumors induced by treatment of 12-day-old mice with N,N-diethylnitrosamine (DEN) (0.05 mumol/g body wt) in intact mice and animals gonadectomized at 8 weeks of age from the three inbred strains, C3H/HeJ (C3H), C57BL/6J (B6), and C57BR/cdJ (BR). At 50 weeks of age, the mean liver tumor multiplicity in intact BR females was 28 +/- 13, while that for intact female C3H and B6 mice was 1.4 +/- 4.7 and 0.5 +/- 1.0, respectively. In ovariectomized mice, the yield of liver tumors was approximately 8-fold higher than in intact C3H (10.3 +/- 7.5) and B6 (4.1 +/- 6.6) females. Only a slight increase (35 +/- 14) was seen in ovariectomized BR females compared to intact BR females. Castration resulted in lower mean tumor multiplicities at 32 weeks of age in the males of all three strains. Intact male C3H, B6, and BR mice had mean liver tumor multiplicities of 61 +/- 34, 7.4 +/- 13, and 26 +/- 18, respectively, while the mean tumor multiplicities in castrated C3H, B6, and BR mice were 24 +/- 14, 0.5 +/- 0.9, and 6.1 +/- 10 tumors per mouse, respectively. The apparent rate of growth of glucose-6-phosphatase-deficient, preneoplastic foci in DEN-treated BR females was significantly higher than in B6 females. The growth rates of hepatic foci in BR and B6 males were similar but foci in BR males were 5-fold more numerous than in B6 males. The high sensitivity of BR females may be due, at least in part, to the failure of ovarian hormones to inhibit the growth of preneoplastic foci and the subsequent development of liver tumors. Since BR males had a larger number of hepatic foci, it is likely that androgens increase the rate of focus formation in BR males.
Hormonal and genetic factors strongly influence the susceptibility of inbred mice to hepatocarcinogenesis. Female C57BR/cdJ (BR) 12) were 5.4-and 4.3-fold more sensitive than mice homozygous for B6 alleles at both loci (6.5 ± 5.4).The risk for liver cancer development is sex-dependent in both humans and mice. The incidence of primary hepatocellular carcinoma (HCC) is 2-to 5-fold higher in men than in women (1-4). At present, it is not known whether this sex difference results from differences in the exposure of men and women to risk factors, such as hepatitis B virus (3, 5), aflatoxin B1 (6), alcohol consumption (1), or from hormonal effects on the pathogenesis of liver cancer (4-6). Sensitivity to hepatocarcinogenesis in mice is highly sexually dimorphic. Male mice have a higher incidence of spontaneous liver tumors than females (7, 8) and are more susceptible to hepatocarcinogenesis following perinatal treatment with a variety of carcinogens (9-11). The sexual dimorphism in murine hepatocarcinogenesis results from the contrasting effects of androgens and ovarian hormones on liver tumor induction; androgens promote hepatocarcinogenesis whereas ovarian hormones inhibit the development of liver tumors (11-13). Thus, castration of male mice results in a decreased yield of liver tumors, whereas ovariectomy of females increases liver tumor multiplicity relative to intact animals (12)(13)(14).One exception to this strong, sex-dependent effect on liver tumor induction in mice is the response of the C57BR/cdJ (BR) inbred strain. Whereas BR males are intermediateThe publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact. among inbred strains in sensitivity to hepatocarcinogenesis, the mean tumor multiplicity following perinatal carcinogen treatment in BR females is 15-30 times higher than that observed in the females of other inbred strains (10). The unusual susceptibility of the BR female is characterized by its insensitivity to the suppressing effects of ovarian hormones. In most strains, ovariectomized mice are significantly more susceptible than intact females to liver tumor induction (11, 12) but ovariectomized and intact BR females have similar mean tumor multiplicities (14, 15). In contrast, the responsiveness of BR male mice to the promotion of hepatocarcinogenesis by androgens is similar to that observed in other strains (14, 15).There are large differences among inbred strains in the sensitivity of male mice to hepatocarcinogenesis (7, 9, 10). Analysis of segregating crosses between strains that vary widely in their susceptibility provides a means for mapping genes that contribute to the sensitivity to liver tumor induction. Our laboratory and others have been successful in identifying loci that influence the development of liver tumors in the males of sensitive strains, such as C3H/HeJ (C3H) and DBA/2J (D2), using linkage analysis. Dragani and cow...
Evaluation of a Keller Type Course in Organic ChemistryA modified Keller course has been developed and used since 1972 to teach organic chemistry to first year undergraduates in the Chemistry Department at Surrey University. The need for innovation in teaching arose initially as a result of service teaching to biochemists. These students did consistently badly and worse then chemists, who followed the same lecture course, in the final examinations. This was due not to the biochemists' lower ability but to their lower motivation.The Keller Plan was imported into England in 1971 by physicists and was believed to be particularly suitable for conceptual subjects and not factual ones.1 Keller Plan is valuable for learning in discrete steps which take place in a prescribed order. Concepts in science are developed from experimental facts and facts must be considered as essential steps in the learning of systematic organic chemistry based on modern electronic theory. One doubts whether heterocyclic
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