This article provides a comprehensive overview of research that has examined the content and prevalence of stereotypic media images of the poor. Research examining televised images and print media are reviewed. An analysis of media framing as well as classist, racist, and sexist imagery is provided. Additionally, to assess media depictions of the poor in the wake of welfare reform, 412 newspaper articles about poverty and welfare published during a 3-month period in 1999 were content analyzed. Although most articles were neutral in tone and portrayed the difficulties facing welfare recipients and the poor sympathetically, they did little to contextualize poverty or illuminate its causes. These findings are discussed in terms of their context and political function.The media are omnipresent in our everyday lives. Cable television provides viewers with a growing number of channels to choose from; videotapes provide easy access to films; and the Internet, newspapers, and 24-hour news radio and television programs provide round-the-clock coverage of current events. In their many forms, media have the potential to educate, raise consciousness, and shape public attitudes (Kinder, 1998).
Low-income people are stigmatized in a number of ways, including being negatively stereotyped and discriminated against both interpersonally and institutionally (see Lott & Bullock, 2007 for a comprehensive review). Yet psychologists have not focused much attention on social class in general, nor on social class-based stigma in particular. This article argues that by resolving three main problems inthe literature (the achieved/ascribed discrepancy, the complexity of operationalizing social class, and the seeming lack of identification with one's social class), psychologists are in a unique position to use their knowledge to aid practitioners and policymakers in ameliorating the consequences of poverty. Thus, this article focuses on how better to incorporate social class into the stigma literature and how this research can be linked to social policy initiatives.In the United States, income inequality stands at its highest level since 1929
We analyzed the der(11) and der(4) genomic breakpoint junctions of a t(4;11) in the leukemia of a patient previously administered etoposide and dactinomycin by molecular and biochemical approaches to gain insights about the translocation mechanism and the relevant drug exposure. The genomic breakpoint junctions were amplified by PCR. Cleavage of DNA substrates containing the normal homologues of the MLL and AF-4 translocation breakpoints was examined in vitro upon incubation with human DNA topoisomerase II␣ and etoposide, etoposide catechol, etoposide quinone, or dactinomycin. The der(11) and der(4) genomic breakpoint junctions both involved MLL intron 6 and AF-4 intron 3. Recombination was precise at the sequence level except for the overall gain of a single templated nucleotide. The translocation breakpoints in MLL and AF-4 were DNA topoisomerase II cleavage sites. Etoposide and its metabolites, but not dactinomycin, enhanced cleavage at these sites. Assuming that DNA topoisomerase II was the mediator of the breakage, processing of the staggered nicks induced by DNA topoisomerase II, including exonucleolytic deletion and templatedirected polymerization, would have been required before ligation of the ends to generate the observed genomic breakpoint junctions. These data are inconsistent with a translocation mechanism involving interchromosomal recombination by simple exchange of DNA topoisomerase II subunits and DNA-strand transfer; however, consistent with reciprocal DNA topoisomerase II cleavage events in MLL and AF-4 in which both breaks became stable, the DNA ends were processed and underwent ligation. Etoposide and͞or its metabolites, but not dactinomycin, likely were the relevant exposures in this patient. L eukemia has become an increasingly common complication of effective chemotherapy (reviewed in ref. 1). Two classes of chemotherapy are associated with leukemia-alkylating agents and DNA topoisomerase II inhibitors (reviewed in refs. 1-3). The hallmarks of leukemias associated with DNA topoisomerase II inhibitors are balanced chromosomal translocations, many of which involve the MLL gene at chromosome band 11q23 (reviewed in refs. 2, 4, and 5). It has been suggested that the MLL translocation mechanism may involve DNA topoisomerase IImediated chromosomal breakage and formation of the translocations when the breakage is repaired (2, 4, 5).DNA topoisomerase II catalyzes the relaxation of supercoiled DNA by transiently cleaving and religating both strands of the double helix (6). The DNA topoisomerase II homodimer introduces four-base staggered nicks in DNA as each subunit covalently binds and cleaves one strand (6). In the presence of ATP, the DNA open gate allows passage of a second DNA helix through the cleaved strands (6). Next, the cleaved DNA strands are religated, and after ATP hydrolysis, the enzyme homodimer attains its original conformational state to catalyze another cycle (6). DNA topoisomerase II has been implicated in MLL translocations, because several anticancer drugs interfere with its c...
We examined the MLL translocation in two cases of infant AML with X chromosome disruption. The Gbanded karyotype in the first case suggested t(X;3)(q22;p21)ins(X;11)(q22;q13q25). Southern blot analysis showed one MLL rearrangement. Panhandle PCR approaches were used to identify the MLL fusion transcript and MLL genomic breakpoint junction. SEPTIN6 from chromosome band Xq24 was the partner gene of MLL. MLL exon 7 was joined in-frame to SEPTIN6 exon 2 in the fusion transcript. The MLL genomic breakpoint was in intron 7; the SEPTIN6 genomic breakpoint was in intron 1. Spectral karyotyping revealed a complex rearrangement disrupting band 11q23. FISH with a probe for MLL confirmed MLL involvement and showed that the MLL-SEPTIN6 junction was on the der(X). The MLL genomic breakpoint was a functional DNA topoisomerase II cleavage site in an in vitro assay. In the second case, the karyotype revealed t(X;11)(q22;q23). Southern blot analysis showed two MLL rearrangements. cDNA panhandle PCR detected a transcript fusing MLL exon 8 in-frame to SEPTIN6 exon 2. MLL and SEPTIN6 are vulnerable to damage to form recurrent translocations in infant AML. Identification of SEPTIN6 and the SEPTIN family members hCDCrel and MSF as partner genes of MLL suggests a common pathway to leukaemogenesis.
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