On the eve of the Civil War southern per capita real income was eighty percent of northern. Treating slaves as property, real income per free southerner was four percent greater and growing at the same rate as its northern counterpart. Southern per capita income was but fifty-one percent of the national average in 1880, and only slowly began to relatively advance after 1900.

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In this study, we examined the impact of a course, the Psychology of Homosexuality, on heterosexual students' attitudes toward and knowledge about sexual minorities (i.e., lesbians, gay men, bisexual men and women, and transgendered persons). We investigated who enrolled in a class about sexual diversity and what they most wanted to learn. Enrolled students reported increased exposure to issues of homosexuality since entering college, and many had sexual minority friends. At preclass, students were most interested in knowing why people are homosexual, whereas at postclass they were interested in supporting someone coming out. Students left the class with significantly decreased homophobia. We discuss the most effective teaching strategies and additional recommendations for discussing sexual diversity in the classroom.

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Transient transfection analysis of DNA subfragments from the distal 5-flanking region of the human plateletderived growth factor A-chain gene (؊18.3 to ؊1.8 kilobase pairs (kb)) revealed enhancer and silencer elements that contribute significantly to transcriptional regulation. Two adjacent regions (؊8.2 to ؊7.5 kb and ؊7.5 to ؊7.0 kb) enhanced transcription of both A-chain and heterologous thymidine kinase promoters, whereas repression was observed in two other nearby regions (؊9.9 to ؊8.2 kb and ؊7.0 to ؊5.9 kb). The ؊7.5 to ؊7.0-kb fragment, or J, was the strongest enhancer, and its activity was localized to a 66-base pair element (A-chain cell type-specific enhancer (ACE 66)). ACE66 activity was highly cell type-specific, with greatest activity seen in choriocarcinoma cell lines (4 -10-fold enhancement). Progressive 5-and 3-deletions of the ACE66 revealed distribution of activity across the element, with nucleotides 1-33 being critical for function. Electrophoretic mobility shift assays revealed cell type-specific patterns of high affinity protein binding to the element. Ethylation interference footprinting of JEG-3 extract localized guanine contacts on nucleotides 1-18 of both strands of the ACE element, whereas more extensive contacts were made with the phosphate backbone (nucleotides 1-32). The ACE66 element is a potent transcriptional regulator in placental cells and represents a valuable model of long distance regulation in a growth factor gene. Platelet-derived growth factor (PDGF)1 is a potent mitogen and chemoattractant for mesenchymal cells that was first purified from human platelet extracts but later shown to be expressed in a variety of normal and transformed cell types (1, 2). PDGF is a family of dimeric glycoproteins that arise from different combinations of two polypeptide chains, termed A and B, that are encoded by separate genes located on different chromosomes. The human A-chain gene contains 7 exons and is located on chromosome 7 (7pter-7q22), spanning approximately 24 kb (3, 4). Transcription of the A-chain gene is activated rapidly by a wide range of growth factors, cytokines and other mitogens (5-7), whereas complex cell type-specific patterns of A-chain transcription appear to underlie the regulation of cell proliferation during embryogenesis (8) and cellular differentiation (9). A-chain null mice exhibit abnormalities in early embryonic development and formation of lung alveolar myofibroblasts (10, 11), whereas expression of the A-chain and the PDGF ␣-receptor also appear to critical for development of the cardiovascular and nervous systems in mice (12)(13)(14). PDGF also appears to be critical for placental development, with high expression of A-chain observed in multiple cell types of the placenta including trophoblasts (2, 15), as well as extraembryonic membranes and uterine smooth muscle cells during pregnancy (15, 16). Inappropriate expression of the PDGF genes has also been implicated in many disease states involving abnormal cell proliferation, including atherosclerosis, pulmon...