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This article reconsiders the argument that 'rituals of rebellion' be seen as women's ritual response to everyday patriarchal structures – an argument originally suggested by Gluckman, but recently evoked by Spencer, the Creiders, and others – in light of recent anthropological theorizing on gender. Using as an example one such women's ritual among the Ihanzu of Tanzania, I show how this particular formulation reduces complex notions of gender and gender practices to unnuanced, monolithic, and all-encompassing gender-systems, both in everyday and ritual realms. This it does, first, by conflating gender ideals with gender behaviours and, second, by ignoring people's conflicting ideas about gender. By problematizing these contradictions, I demonstrate how Ihanzu women's rites are not about rebellion but gender complementarity, played out by women dancers embodying both genders simultaneously. Above all, this case compels us to rethink, fundamentally, 'rituals of rebellion' and 'patriarchy'.  相似文献   

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The tight junctions (TJs) of epithelia are responsible for regulating the "fence and gate" function of polarized epithelial cells. It is now well-established that dysregulation of these functions contributes to initiation and progression of cancer. Recently, it has become clear that the Claudins, members of a large family of 27 closely related transmembrane proteins, play a crucial role in formation, integrity and function of TJs, the epithelial permeability barrier and epithelial polarization. A growing body of data indicates that Claudin expression is altered in numerous epithelial cancers in a stage- and tumor-specific manner. While a single universal mechanism is still lacking, accumulating evidence supports a role for epigenetic regulation of Claudin expression in tumorgenesis, with concomitant alterations in barrier function. We review here new insights and challenges in understanding Claudin function in normal physiology and cancer.  相似文献   

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The complex interaction of genetic, microbial, and environmental factors may result in continuous activation of the mucosal immune system leading to inflammatory bowel disease (IBD). Most present treatments for IBD involve altering or suppressing the aberrant immune response; however, the role of the intestinal microbiota in the pathophysiology of IBD is becoming more evident. The epithelial layer is essential for the proper functioning of the gastrointestinal tract, and its increased permeability to the luminal antigens may lead to the inflammatory processes and mucosal damage observed in IBD. Factors affecting the efficacy of the epithelial barrier include presence of pathogenic bacteria (e.g., Helicobacter spp.), presence of probiotic bacteria, availability of selected nutrients, and others. Defective function of the mucosal barrier might facilitate the contact of bacterial antigens and adjuvants with innate and adaptive immune cells to generate prolonged inflammatory responses. This review will briefly describe the complex structure of the epithelial barrier in the context of bacterial-mucosal interactions observed in human IBD and mouse models of colitis.  相似文献   

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Garrison H  Bartholme N 《The Physiologist》2006,49(4):201, 203-201, 205
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《Bioscience Hypotheses》2008,1(5):255-257
We report an interesting finding that cellular distribution and interactions between neighboring cells modulate protein expression and localization. MCF7 breast cancer cells, which express ERb, were cultured in estrogen-free medium. ERb exhibited a unique migration pattern that was dependent on cell density and proximity. This finding attests to a novel interaction mechanism other than receptor–to–ligand. Since cells were grown in conditioned culture media, the only factor influencing protein distribution is cell–cell proximity (cell–cell interactions). Thus, hormonal receptors may function independently from their ligand. In addition, physical intercellular interactions may function as a non-molecular factor inducing gene expression and activation.  相似文献   

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R Gruneir 《CMAJ》1994,150(9):1380-1381
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Failure to eliminate abnormal proteins in the cell is associated with numerous aggregation diseases. Misfolded proteins are normally detected by protein quality control and either refolded or eliminated. The ubiquitin-proteasome system is a major pathway that degrades these unwanted proteins. Ubiquitin ligases are central to these degradation pathways as they recognize aberrant proteins and covalently attach a polyubiquitin chain to target them to the proteasome. We discovered that the Hul5 ubiquitin ligase is a major player in a novel protein quality control pathway that targets cytosolic misfolded proteins. Hul5 is required for the maintenance of cell fitness and the increased ubiquitination of low solubility proteins after heat-shock in yeast cells. We identified several low-solubility substrates of Hul5, including the prion-like protein Pin3. It is now apparent that in the cytoplasm, misfolded proteins can be targeted by multiple degradation pathways. In this review, we discuss how the Hul5 protein quality control pathway may specifically target low solubility cytosolic proteins in the cell.  相似文献   

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Phil Torres 《Bioethics》2017,31(9):691-696
In Unfit for the Future, Ingmar Persson and Julian Savulescu argue that our collective existetial predicment is unprecedentedly dangerous due to climate change and terrorism. Given these global risks to human prosperity and survival, Persson and Savulescu argue that we should explore the radical possibility of moral bioenhancement in addition to cognitive enhancement. In this article, I argue that moral bioenhancements could nontrivially exacerbate the threat posed by certain kinds of malicious agents, while reducing the threat of other kinds. This introduces a previously undiscussed complication to Persson and Savulescu's proposal. In the final section, I present a novel argument for why moral bioenhancement should either be compulsory or not be made available to the public at all.  相似文献   

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