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OALib Journal期刊

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The socio-cultural-symbolic nexus in the perpetuation of female genital cutting: a critical review of existing discourses
Esho, Tammary,Van Wolputte, Steven,Enzlin, Paul
Afrika Focus , 2011,
Abstract: Female Genital Cutting (FGC), also known as Female Genital Mutilation (FGM) and Female Circumcision (FC), continues to be a prevalent practice in many parts of the world and especially in Africa. This is somewhat perplexing given the concerted efforts aimed at eradicating this practice. This article argues that the perpetuation of FGC is due to the unintended effects of marginalization experienced by individuals and groups of women as a result of the approach of some of the anti-FGC global discourses and policies put forward to eradicate the practice. This, we argue, happens when the social structure that provides such groups and individuals with a sense of identity and belonging breaks down. Therefore, the attack on what practicing communities consider to be of crucial cultural value causes a re-focus on the practice resulting in a re-formulation and re-invention of these practices in a bid to counter the feelings of alienation. FGC is thus reframed and reconstructed as a reaction against these campaigns. This article intends to investigate the socio-cultural-symbolic nexus surrounding the practice of FGC, its meaning and implications with respect to its continued existence. It draws examples mainly from communities in Kenya that practice FGM as a rite of passage into adulthood. Herein, perhaps, lies the driving force behind the practice in this contemporary age: it carries a lot of significance with respect to transformational processes, and it is seen as crucial in the representation of the body, identity and belonging. The aim of this article is not to defend FGC’s continuation, but rather to explore the interplay between its changing socio-cultural dimensions as a counter-reaction to the eradication discourse and policies. In this way we will try to explore some of the factors that lay behind its perpetuation.
Mislocalization of XPF-ERCC1 Nuclease Contributes to Reduced DNA Repair in XP-F Patients
Anwaar Ahmad equal contributor,Jacqueline H. Enzlin equal contributor,Nikhil R. Bhagwat equal contributor,Nils Wijgers,Anja Raams,Esther Appledoorn,Arjan F. Theil,Jan H. J. Hoeijmakers,Wim Vermeulen,Nicolaas G. J. Jaspers,Orlando D. Sch?rer ,Laura J. Niedernhofer
PLOS Genetics , 2010, DOI: 10.1371/journal.pgen.1000871
Abstract: Xeroderma pigmentosum (XP) is caused by defects in the nucleotide excision repair (NER) pathway. NER removes helix-distorting DNA lesions, such as UV–induced photodimers, from the genome. Patients suffering from XP exhibit exquisite sun sensitivity, high incidence of skin cancer, and in some cases neurodegeneration. The severity of XP varies tremendously depending upon which NER gene is mutated and how severely the mutation affects DNA repair capacity. XPF-ERCC1 is a structure-specific endonuclease essential for incising the damaged strand of DNA in NER. Missense mutations in XPF can result not only in XP, but also XPF-ERCC1 (XFE) progeroid syndrome, a disease of accelerated aging. In an attempt to determine how mutations in XPF can lead to such diverse symptoms, the effects of a progeria-causing mutation (XPFR153P) were compared to an XP–causing mutation (XPFR799W) in vitro and in vivo. Recombinant XPF harboring either mutation was purified in a complex with ERCC1 and tested for its ability to incise a stem-loop structure in vitro. Both mutant complexes nicked the substrate indicating that neither mutation obviates catalytic activity of the nuclease. Surprisingly, differential immunostaining and fractionation of cells from an XFE progeroid patient revealed that XPF-ERCC1 is abundant in the cytoplasm. This was confirmed by fluorescent detection of XPFR153P-YFP expressed in Xpf mutant cells. In addition, microinjection of XPFR153P-ERCC1 into the nucleus of XPF–deficient human cells restored nucleotide excision repair of UV–induced DNA damage. Intriguingly, in all XPF mutant cell lines examined, XPF-ERCC1 was detected in the cytoplasm of a fraction of cells. This demonstrates that at least part of the DNA repair defect and symptoms associated with mutations in XPF are due to mislocalization of XPF-ERCC1 into the cytoplasm of cells, likely due to protein misfolding. Analysis of these patient cells therefore reveals a novel mechanism to potentially regulate a cell's capacity for DNA repair: by manipulating nuclear localization of XPF-ERCC1.
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