656 research outputs found

    Formaldehyde-releasers: relationship to formaldehyde contact allergy. Contact allergy to formaldehyde and inventory of formaldehyde-releasers

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    This is one of series of review articles on formaldehyde and formaldehyde-releasers (others: formaldehyde in cosmetics, in clothes and in metalworking fluids and miscellaneous). Thirty-five chemicals were identified as being formaldehyde-releasers. Although a further seven are listed in the literature as formaldehyde-releasers, data are inadequate to consider them as such beyond doubt. Several (nomenclature) mistakes and outdated information are discussed. Formaldehyde and formaldehyde allergy are reviewed: applications, exposure scenarios, legislation, patch testing problems, frequency of sensitization, relevance of positive patch test reactions, clinical pattern of allergic contact dermatitis from formaldehyde, prognosis, threshold for elicitation of allergic contact dermatitis, analytical tests to determine formaldehyde in products and frequency of exposure to formaldehyde and releasers. The frequency of contact allergy to formaldehyde is consistently higher in the USA (8-9%) than in Europe (2-3%). Patch testing with formaldehyde is problematic; the currently used 1% solution may result in both false-positive and false-negative (up to 40%) reactions. Determining the relevance of patch test reactions is often challenging. What concentration of formaldehyde is safe for sensitive patients remains unknown. Levels of 200-300 p.p.m. free formaldehyde in cosmetic products have been shown to induce dermatitis from short-term use on normal skin

    Patch Testing with a Textile Dye Mix in a Baseline Series in Two Countries

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    Disperse dyes are the most common contact sensitizers among textile dyes. The main aim of this study was to investigate the outcome of patch testing with a textile dye mix 6.6%. A total of 2,049 patients from Sweden and 497 from Belgium were tested with the mix, consisting of Disperse (D) Blue 35, D Yellow 3, D Orange 1 and 3, D Red 1 and 17, 1.0% each, and D Blue 106 and D Blue 124, 0.3% each. Of the total number, 65 patients, 2.6%, tested positively to the mix, 4.2% of the Belgian patients and 2.1% of the Swedish patients. Patch testing with the mix 6.6% revealed significantly more patients with contact allergy compared with testing with a previous mix 3.2% (p<0.01). Contact allergy to the mix was significantly more common in the Belgian than in the Swedish patients

    BioArray Software Environment (BASE): a platform for comprehensive management and analysis of microarray data

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    The microarray technique requires the organization and analysis of vast amounts of data. These data include information about the samples hybridized, the hybridization images and their extracted data matrices, and information about the physical array, the features and reporter molecules. We present a web-based customizable bioinformatics solution called BioArray Software Environment (BASE) for the management and analysis of all areas of microarray experimentation. All software necessary to run a local server is freely available

    Expression profiling to predict outcome in breast cancer: the influence of sample selection

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    Gene expression profiling of tumors using DNA microarrays is a promising method for predicting prognosis and treatment response in cancer patients. It was recently reported that expression profiles of sporadic breast cancers could be used to predict disease recurrence better than currently available clinical and histopathological prognostic factors. Having observed an overlap in those data between the genes that predict outcome and those that predict estrogen receptor-α status, we examined their predictive power in an independent data set. We conclude that it may be important to define prognostic expression profiles separately for estrogen receptor-α-positive and estrogen receptor-α-negative tumors

    Kvinnors högre utbildning i Rwanda - En feministisk diskursanalytisk studie

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    Uppsatsen analyserar Rwandas arbete för kvinnors högre utbildning och problempresentationen bakom den rådande ojämställdheten. En kritisk feministisk diskursanalys utifrån Carols Bacchis metod ”What’s the problem represented to be?” används för att analysera två statliga utbildningsdokument från Rwanda. Bacchis metod består av sex frågor för att analysera vad det riktiga ”problemet” antas vara i dessa dokument. Uppsatsen använder en feministisk teoribildning inom genusarbete och utvecklingsstudier för att problematisera innehållet i dokumenten. Uppsatsen finner att trots att dokumenten till viss del uppmärksammar genus som en social konstruktion, grundas satsningarna i ett synsätt där genus likställs med kvinnor. Det framställs att problemet är kvinnors brist på tillgång till högre utbildning. Satsningarna motiveras genom att kvinnors utbildning anses vara viktigt för landets socioekonomiska utveckling. Vidare finner vi att satsningar på kvinnor inom högre utbildning sker inom manligt associerade utbildningar där den framtida ekonomiska vinningen för landet är stor

    Prolactin-induced mouse mammary carcinomas model estrogen resistant luminal breast cancer.

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    INTRODUCTION: Tumors that express estrogen receptor alpha (ERα+) comprise 75% of breast cancers in women. While treatments directed against this receptor have successfully lowered mortality rates, many primary tumors initially or later exhibit resistance. The paucity of murine models of this luminal tumor subtype has hindered studies of factors that promote their pathogenesis and modulate responsiveness to estrogen-directed therapeutics. Since epidemiologic studies closely link prolactin and the development of ERα+ tumors in women, we examined characteristics of the aggressive ERα+ and ERα- carcinomas which develop in response to mammary prolactin in a murine transgenic model (neu-related lipocalin- prolactin (NRL-PRL)). To evaluate their relationship to clinical tumors, we determined phenotypic relationships among these carcinomas, other murine models of breast cancer, and features of luminal tumors in women. METHODS: We examined a panel of prolactin-induced tumors for characteristics relevant to clinical tumors: histotype, ERα/progesterone receptor (PR) expression and estrogen responsiveness, Activating Protein 1 (AP-1) components, and phosphorylation of signal transducer and activator of transcription 5 (Stat5), extracellular signal regulated kinase (ERK) 1/2 and AKT. We compared levels of transcripts in the ERα-associated luminal signature that defines this subtype of tumors in women and transcripts enriched in various mammary epithelial lineages to other well-studied genetically modified murine models of breast cancer. Finally, we used microarray analyses to compare prolactin-induced ERα+ and ERα- tumors, and examined responsiveness to estrogen and the anti-estrogen, Faslodex, in vivo. RESULTS: Prolactin-induced carcinomas were markedly diverse with respect to histotype, ERα/PR expression, and activated signaling cascades. They constituted a heterogeneous, but distinct group of murine mammary tumors, with molecular features of the luminal subtype of human breast cancer. In contrast to morphologically normal and hyperplastic structures in NRL-PRL females, carcinomas were insensitive to ERα-mediated signals. These tumors were distinct from mouse mammary tumor virus (MMTV)-neu tumors, and contained elevated transcripts for factors associated with luminal/alveolar expansion and differentiation, suggesting that they arose from physiologic targets of prolactin. These features were shared by ERα+ and ERα- tumors, suggesting a common origin, although the former exhibited transcript profiles reflecting greater differentiation. CONCLUSIONS: Our studies demonstrate that prolactin can promote diverse carcinomas in mice, many of which resemble luminal breast cancers, providing a novel experimental model to examine the pathogenesis, progression and treatment responsiveness of this tumor subtype

    Recent translational research: microarray expression profiling of breast cancer – beyond classification and prognostic markers?

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    Genomic expression profiling has greatly improved our ability to subclassify human breast cancers according to shared molecular characteristics and clinical behavior. The logical next question is whether this technology will be similarly useful for identifying the dominant signaling pathways that drive tumor initiation and progression within each breast cancer subtype. A major challenge will be to integrate data generated from the experimental manipulation of model systems with expression profiles obtained from primary tumors. We highlight some recent progress and discuss several obstacles in the use of expression profiling to identify pathway signatures in human breast cancer
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