1,503 research outputs found

    A remembrance of things (best) forgotten: The 'allegorical past' and the feminist imagination

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    This is the author's PDF version of an article published in Feminist theologyΒ© 2012. The definitive version is available at http://fth.sagepub.com/This article discusses the US TV series Mad Men, which is set in an advertising agency in 1960s New York, in relation to two key elements which seem significant for a consideration of the current state of feminism in church and academy, both of which centre around what it means to remember or (not) to forget

    Females do not have more injury road accidents on Friday the 13th

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    BACKGROUND: This study reinvestigated the recent finding that females – but not males – die in traffic accidents on Friday the 13th more often than on other Fridays (NΓ€yhΓ€ S: Traffic deaths and superstition on Friday the 13th. Am J Psychiatry 2002, 159: 2110–2111). The current study used matched setting and injury accident data base that is more numerous than fatality data. If such an effect would be caused by impaired psychic and psychomotor functioning due to more frequent anxiety among women, it should also appear in injury crashes. METHODS: We used the national Finnish road accident database for 1989–2002. To control seasonal variation, 21 Fridays the 13th were compared in a matched design to previous and following Fridays, excluding all holidays, on number of accidents, male/female responsibility for accidents, and the number of dead, injured and overall number of active participants (drivers, pedestrians and bicyclists) as a consequence of the accident. RESULTS: There were no significant differences in any examined aspect of road injury accidents among the three Fridays, either in females or males. Women were not overrepresented in crashes that occurred on Fridays 13th. CONCLUSION: There is no consistent evidence for females having more road traffic crashes on Fridays the 13th, based on deaths or road accident statistics. However, this does not imply a non-existent effect of superstition related anxiety on accident risk as no exposure-to-risk data are available. People who are anxious of "Black Friday" may stay home, or at least avoid driving a car

    Does owning a pet protect older people against loneliness?

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    This article has been made available through the Brunel Open Access Publishing Fund.Pet ownership is thought to make a positive contribution to health, health behaviours and the general well-being of older people. More specifically pet ownership is often proposed as a solution to the problem of loneliness in later life and specific 'pet based' interventions have been developed to combat loneliness. However the evidence to support this relationship is slim and it is assumed that pet ownership is a protection against loneliness rather than a response to loneliness. The aim of this paper is to examine the association between pet ownership and loneliness by exploring if pet ownership is a response to, or protection against, loneliness using Waves 0-5 from the English Longitudinal Study of Ageing (ELSA)

    Blockade of insulin-like growth factors increases efficacy of paclitaxel in metastatic breast cancer.

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    Breast cancer remains the leading cause of cancer death in women owing to metastasis and the development of resistance to established therapies. Macrophages are the most abundant immune cells in the breast tumor microenvironment and can both inhibit and support cancer progression. Thus, gaining a better understanding of how macrophages support cancer could lead to the development of more effective therapies. In this study, we find that breast cancer-associated macrophages express high levels of insulin-like growth factors 1 and 2 (IGFs) and are the main source of IGFs within both primary and metastatic tumors. In total, 75% of breast cancer patients show activation of insulin/IGF-1 receptor signaling and this correlates with increased macrophage infiltration and advanced tumor stage. In patients with invasive breast cancer, activation of Insulin/IGF-1 receptors increased to 87%. Blocking IGF in combination with paclitaxel, a chemotherapeutic agent commonly used to treat breast cancer, showed a significant reduction in tumor cell proliferation and lung metastasis in pre-clinical breast cancer models compared to paclitaxel monotherapy. Our findings provide the rationale for further developing the combination of paclitaxel with IGF blockers for the treatment of invasive breast cancer, and Insulin/IGF1R activation and IGF+ stroma cells as potential biomarker candidates for further evaluation

    The glutathione biosynthetic pathway of Plasmodium is essential for mosquito transmission

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    1Infection of red blood cells (RBC) subjects the malaria parasite to oxidative stress. Therefore, efficient antioxidant and redox systems are required to prevent damage by reactive oxygen species. Plasmodium spp. have thioredoxin and glutathione (GSH) systems that are thought to play a major role as antioxidants during blood stage infection. In this report, we analyzed a critical component of the GSH biosynthesis pathway using reverse genetics. Plasmodium berghei parasites lacking expression of gamma-glutamylcysteine synthetase (Ξ³-GCS), the rate limiting enzyme in de novo synthesis of GSH, were generated through targeted gene disruption thus demonstrating, quite unexpectedly, that Ξ³-GCS is not essential for blood stage development. Despite a significant reduction in GSH levels, blood stage forms of pbggcsβˆ’ parasites showed only a defect in growth as compared to wild type. In contrast, a dramatic effect on development of the parasites in the mosquito was observed. Infection of mosquitoes with pbggcsβˆ’ parasites resulted in reduced numbers of stunted oocysts that did not produce sporozoites. These results have important implications for the design of drugs aiming at interfering with the GSH redox-system in blood stages and demonstrate that de novo synthesis of GSH is pivotal for development of Plasmodium in the mosquito

    A Context-Specific Role for Retinoblastoma Protein-Dependent Negative Growth Control in Suppressing Mammary Tumorigenesis

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    The ability to respond to anti-growth signals is critical to maintain tissue homeostasis and loss of this negative growth control safeguard is considered a hallmark of cancer. Negative growth regulation generally occurs during the G0/G1 phase of the cell cycle, yet the redundancy and complexity among components of this regulatory network has made it difficult to discern how negative growth cues protect cells from aberrant proliferation.The retinoblastoma protein (pRB) acts as the final barrier to prevent cells from entering into the cell cycle. By introducing subtle changes in the endogenous mouse Rb1 gene (Rb1(Ξ”L)), we have previously shown that interactions at the LXCXE binding cleft are necessary for the proper response to anti-growth signals such as DNA damage and TGF-Ξ², with minimal effects on overall development. This disrupts the balance of pro- and anti-growth signals in mammary epithelium of Rb1(Ξ”L/Ξ”L) mice. Here we show that Rb1(Ξ”L/Ξ”L) mice are more prone to mammary tumors in the Wap-p53(R172H) transgenic background indicating that negative growth regulation is important for tumor suppression in these mice. In contrast, the same defect in anti-growth control has no impact on Neu-induced mammary tumorigenesis.Our work demonstrates that negative growth control by pRB acts as a crucial barrier against oncogenic transformation. Strikingly, our data also reveals that this tumor suppressive effect is context-dependent

    Association Analysis of 94 Candidate Genes and Schizophrenia-Related Endophenotypes

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    While it is clear that schizophrenia is highly heritable, the genetic basis of this heritability is complex. Human genetic, brain imaging, and model organism studies have met with only modest gains. A complementary research tactic is to evaluate the genetic substrates of quantitative endophenotypes with demonstrated deficits in schizophrenia patients. We used an Illumina custom 1,536-SNP array to interrogate 94 functionally relevant candidate genes for schizophrenia and evaluate association with both the qualitative diagnosis of schizophrenia and quantitative endophenotypes for schizophrenia. Subjects included 219 schizophrenia patients and normal comparison subjects of European ancestry and 76 schizophrenia patients and normal comparison subjects of African ancestry, all ascertained by the UCSD Schizophrenia Research Program. Six neurophysiological and neurocognitive endophenotype test paradigms were assessed: prepulse inhibition (PPI), P50 suppression, the antisaccade oculomotor task, the Letter-Number Span Test, the California Verbal Learning Test-II, and the Wisconsin Card Sorting Test-64 Card Version. These endophenotype test paradigms yielded six primary endophenotypes with prior evidence of heritability and demonstrated schizophrenia-related impairments, as well as eight secondary measures investigated as candidate endophenotypes. Schizophrenia patients showed significant deficits on ten of the endophenotypic measures, replicating prior studies and facilitating genetic analyses of these phenotypes. A total of 38 genes were found to be associated with at least one endophenotypic measure or schizophrenia with an empirical p-value<0.01. Many of these genes have been shown to interact on a molecular level, and eleven genes displayed evidence for pleiotropy, revealing associations with three or more endophenotypic measures. Among these genes were ERBB4 and NRG1, providing further support for a role of these genes in schizophrenia susceptibility. The observation of extensive pleiotropy for some genes and singular associations for others in our data may suggest both converging and independent genetic (and neural) pathways mediating schizophrenia risk and pathogenesis
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