801 research outputs found

    Children's Well-being in Contexts of Poverty: Approaches to Research, Monitoring and Participation

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    Monitoring, protecting and promoting 'well-being' are central to realisation of children's rights. Yet definitions of the concept are both variable and can appear conceptually confused. Competing research paradigms engage with the concept and its measurement, while applications of well-being in policy are equally contested. This paper outlines some of the major debates, as a starting point for reviewing three contrasting approaches to well-being: indicator-based, participatory and longitudinal research. In particular, it focuses on applications of the concept in contexts of child poverty worldwide. We suggest there are some promising signs of integration amongst these approaches, and argue that well-being does have potential as a bridging concept, at the same time highlighting inequalities, acknowledging diversities, and respecting children's agency

    Education and HIV and AIDS in Malawi : the role of open, distance and flexible learning

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    Analysis of inhibitor of apoptosis protein family expression during mammary gland development

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    <p>Abstract</p> <p>Background</p> <p>Inhibitors-of-Apoptosis-Proteins (IAPs) are an evolutionarily conserved family of proteins capable of regulating several facets of apoptosis. IAPs are frequently dysregulated in cancer, but their role in the regulation of apoptosis during developmental processes is not fully understood. Here we examined the expression of IAPs during the post-natal development of the mouse mammary gland, which is a tissue that exhibits a profound induction of apoptosis during involution.</p> <p>Results</p> <p>Six out of eight mammalian IAP family members are expressed in the mammary gland. Notably, quantitative PCR and immunoblotting revealed that XIAP, c-IAP1 and c-IAP2 are down-regulated in pregnancy and lactation, and prior to the onset of involution. In cultured mammary epithelial cells (MECs), XIAP levels decreased in response to inhibition of growth factor signalling. Maintaining XIAP levels in MECs by expressing exogenous XIAP protected them from all apoptotic stimuli tested.</p> <p>Conclusions</p> <p>These data suggest that the developmental regulation of IAP expression <it>in vivo </it>contributes to naturally occurring programmes of cell death.</p

    Compact Frontend-Electronics and Bidirectional 3.3 Gbps Optical Datalink for Fast Proportional Chamber Readout

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    The 9600 channels of the multi-wire proportional chamber of the H1 experiment at HERA have to be read out within 96 ns and made available to the trigger system. The tight spatial conditions at the rear end flange require a compact bidirectional readout electronics with minimal power consumption and dead material. A solution using 40 identical optical link modules, each transferring the trigger information with a physical rate of 4 x 832 Mbps via optical fibers, has been developed and commisioned. The analog pulses from the chamber can be monitored and the synchronization to the global HERA clock signal is ensured.Comment: 13 pages, 10 figure

    1,2-Bis{bis­[4-(trifluoro­meth­yl)phen­yl]phosphino}ethane

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    Crystals of the title compound, C30H20F12P2 or R 2PCH2CH2PR 2 (R = 4-C6H4CF3), were inadvertently prepared while attempting to recrystallize a crude sample of trans-Re(Cl)(N2)(R 2PCH2CH2PR 2)2 from diethyl ether. The molecule lies on a center of inversion. One of the rings lies approximately in the P—C—C—P plane; the dihedral angle is 174.53°.The other ring is not quite perpendicular; the dihedral angle is 71.1°. The compound is isostructural with the R = Ph, 4-C6H4CH3 and 4-C6H4CH2CH3 analogues. It is well known that the basicity of phosphines and diphosphines can be altered by changing the electron-donating ability of R; however, the structural parameters for the title compound do not significantly differ from those of the aforementioned substituted-phenyl compounds

    Familial Transmission of a Serious Disease—Producing Group A Streptococcus Clone: Case Reports and Review

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    Invasive group A streptococcus (GAS) infections are emerging diseases; however, person-to-person transmission of invasive GAS producing life-threatening infection has been observed rarely. We report a small intrafamilial cluster of life-threatening GAS infections. A previously healthy 47-year-old father developed necrotizing fasciitis of the neck. Two days later, his 16-year-old daughter developed streptococcal angina, pneumonia, and pleural empyema. Both patients had signs of streptococcal toxic shock syndrome. Pulsed field gel electrophoresis revealed that the M6 strains of GAS isolated from the father and daughter had identical patterns. Cases of person-to-person transmission of invasive GAS infection reported in the literature are also reviewe

    Elevated EDAR signalling promotes mammary gland tumourigenesis with squamous metaplasia

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    Ectodysplasin A receptor (EDAR) is a death receptor in the Tumour Necrosis Factor Receptor (TNFR) superfamily with roles in the development of hair follicles, teeth and cutaneous glands. Here we report that human Oestrogen Receptor (ER) negative breast carcinomas which display squamous differentiation express EDAR strongly. Using a mouse model with a high Edar copy number, we show that elevated EDAR signalling results in a high incidence of mammary tumours in breeding female mice. These tumours resemble the EDAR-high human tumours in that they are characterised by a lack of oestrogen receptor expression, contain extensive squamous metaplasia, and display strong β-catenin transcriptional activity. In the mouse model, all of the tumours carry somatic deletions of the third exon of the CTNNB1 gene that encodes β-catenin. Deletion of this exon yields unconstrained β-catenin signalling activity. We also demonstrate that β-catenin activity is required for transformed cell growth, showing that increased EDAR signalling creates an environment in which β-catenin activity can readily promote tumourigenesis. Together, this work identifies a novel death receptor oncogene in breast cancer, whose mechanism of transformation is based on the interaction between the WNT and Ectodysplasin A (EDA) pathways
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