16 research outputs found
'I act this way because why?' Prior knowledges, teaching for change, imagining new masculinities
This article begins by outlining some of the prior knowledges brought by
undergraduate students to an introduction to gender studies class in the Women's
and Gender Studies Department at the University of the Western Cape, South Africa. I
show that, at the beginning of the course, students clearly understand gender to refer to
women and femininity, imagining femininity (but not masculinity) to be responsive to
social change. I suggest that, in the face of these prior knowledges, it is important to
focus on masculinity as performance, as a cultural artefact and one that is deeply
harmful to South African men. Student experiences of this teaching and learning
suggest that it offers possibilities for imagining men as allies and beneficiaries - rather
than enemies - in the struggle for gender equity
Contribution of CgPDR1-Regulated Genes in Enhanced Virulence of Azole-Resistant Candida glabrata
In Candida glabrata, the transcription factor CgPdr1 is involved
in resistance to azole antifungals via upregulation of ATP binding cassette
(ABC)-transporter genes including at least CgCDR1,
CgCDR2 and CgSNQ2. A high diversity of GOF
(gain-of-function) mutations in CgPDR1 exists for the
upregulation of ABC-transporters. These mutations enhance C.
glabrata virulence in animal models, thus indicating that
CgPDR1 might regulate the expression of yet unidentified
virulence factors. We hypothesized that CgPdr1-dependent virulence factor(s)
should be commonly regulated by all GOF mutations in CgPDR1. As
deduced from transcript profiling with microarrays, a high number of genes (up
to 385) were differentially regulated by a selected number (7) of GOF mutations
expressed in the same genetic background. Surprisingly, the transcriptional
profiles resulting from expression of GOF mutations showed minimal overlap in
co-regulated genes. Only two genes, CgCDR1 and
PUP1 (for PDR1
upregulated and encoding a mitochondrial protein), were
commonly upregulated by all tested GOFs. While both genes mediated azole
resistance, although to different extents, their deletions in an azole-resistant
isolate led to a reduction of virulence and decreased tissue burden as compared
to clinical parents. As expected from their role in C. glabrata
virulence, the two genes were expressed as well in vitro and
in vivo. The individual overexpression of these two genes
in a CgPDR1-independent manner could partially restore
phenotypes obtained in clinical isolates. These data therefore demonstrate that
at least these two CgPDR1-dependent and -upregulated genes
contribute to the enhanced virulence of C. glabrata that
acquired azole resistance
Candida glabrata : a review of its features and resistance
Candida species belong to the normal microbiota of the oral cavity and gastrointestinal and vaginal tracts, and are responsible for several clinical manifestations, from mucocutaneous overgrowth to bloodstream infections. Once believed to be non-pathogenic, Candida glabrata was rapidly blamable for many human diseases. Year after year, these pathological circumstances are more recurrent and problematic to treat, especially when patients reveal any level of immunosuppression. These difficulties arise from the capacity of C. glabrata to form biofilms and also from its high resistance to traditional antifungal therapies. Thus, this review intends to present an excerpt of the biology, epidemiology, and pathology of C. glabrata, and detail an approach to its resistance mechanisms based on studies carried out up to the present.The authors are grateful to strategic project PTDC/SAU-MIC/119069/2010 for the financial support to the research center and for Celia F. Rodrigues' grant