8 resultados para May family.

em Aston University Research Archive


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This article considers why the family nurse partnership (FNP) has been promoted as a means of tackling social exclusion in the UK. The FNP consists in a programme of visits by nurses to low-income first-time mothers, both while the mothers are pregnant and for the first two years following birth. The FNP is focused on both teaching parenthood and encouraging mothers back into education and/or into employment. Although the FNP marks a considerable discontinuity with previous approaches to family health, it is congruent with an emerging new approach to social exclusion. This new approach maintains that the most important task of social policy is to identify quickly the most 'at-risk' households, individuals and children so that interventions can be targeted more effectively at those 'at risk', either to themselves or to others. The article illustrates this new approach by analysing a succession of reports by the Social Exclusion Unit. It indicates that there is a considerable amount of ambiguity about the relationship between specific risk-factors and being 'at risk of social exclusion'. Nonetheless, this new approach helps to explain why British policy-makers may have chosen to promote the new FNP now. © 2009 Cambridge University Press.

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The CGRP (calcitonin gene-related peptide) receptor is a family B GPCR (G-protein-coupled receptor). It consists of a GPCR, CLR (calcitonin receptor-like receptor) and an accessory protein, RAMP1 (receptor activity-modifying protein 1). RAMP1 is needed for CGRP binding and also cell-surface expression of CLR. There have been few systematic studies of the ECLs (extracellular loops) of family B GPCRs. However, they are likely to be especially important for the interaction of the N-termini of the peptide agonists that are the natural agonists for these receptors. We have carried out alanine scans on all three ECLs of CLR, as well as their associated juxtamembrane regions. Residues within all three loops influence CGRP binding and receptor activation. Mutation of Ala203 and Ala206 on ECL1 to leucine increased the affinity of CGRP. Residues at the top of TM (transmembrane) helices 2 and 3 influenced CGRP binding and receptor activation. L351A and E357A in TM6/ECL3 reduced receptor expression and may be needed for CLR association with RAMP1. ECL2 seems especially important for CLR function; of the 16 residues so far examined in this loop, eight residues reduce the potency of CGRP at stimulating cAMP production when mutated to alanine.

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The calcitonin receptor (CTR) and calcitonin receptor-like receptor (CLR) are two of the 15 human family B (or Secretin-like) GPCRs. CTR and CLR are of considerable biological interest as their pharmacology is moulded by interactions with receptor activity-modifying proteins. They also have therapeutic relevance for many conditions, such as osteoporosis, diabetes, obesity, lymphatic insufficiency, migraine and cardiovascular disease. In light of recent advances in understanding ligand docking and receptor activation in both the family as a whole and in CLR and CTR specifically, this review reflects how applicable general family B GPCR themes are to these two idiosyncratic receptors. We review the main functional domains of the receptors; the N-terminal extracellular domain, the juxtamembrane domain and ligand interface, the transmembrane domain and the intracellular C-terminal domain. Structural and functional findings from the CLR and CTR along with other family B GPCRs are critically appraised to gain insight into how these domains may function. The ability for CTR and CLR to interact with receptor activity-modifying proteins adds another level of sophistication to these receptor systems but means careful consideration is needed when trying to apply generic GPCR principles. This review encapsulates current thinking in the realm of family B GPCR research by highlighting both conflicting and recurring themes and how such findings relate to two unusual but important receptors, CTR and CLR.

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As the existing team literature mostly excludes context and culture, little is known about how these elements affect real-life team working (Engestrom, 2008; Salas & Wildman, 2009), and how teams work in non-Western settings, such as in Chinese firms (Phan, Zhou, & Abrahamson, 2010).This research addresses this issue by investigating how new product design (NPD) teams use team working to carry out product innovation in the context of Chinese family businesses (CFBs) via an indigenous psychology perspective. Unlike mainstream teamwork literature which mostly employs an etic design, an indigenous psychology perspective adopts an emic approach which places emphasis on understanding real-life phenomena in context through a cultural-insider perspective (Kim, 2000). Compatible with this theoretical position, a multiple qualitative case study approach was used as the research methodology. Three qualitative case studies were carried out in three longstanding family-run manufacturing firms in Taiwan, where family firms have been the pillars of high economic growth in the past five decades (W.-w. Chu, 2009). Two salient findings were established across the three case studies. First, the team processes identified across the three family firms are very similar with the exception of owners’ involvement and on-the-job training. All three family firms’ NPD teams are managed in a highly hierarchical manner, with considerable emphasis placed on hierarchical ranking, cost-effectiveness, efficiency, practicability, and interpersonal harmony. Second, new products developed by CFBNPD teams are mostly incremental innovation or copycat innovation, while radical or original products are rare. In many ways, CFBNPD teams may not be the ideal incubators for innovation. This is because several aspects of their unique context can cast constraints on how they work and innovate, and thus limit the ratio of radical innovation. A multi-level review into the facilitators and inhibitors of creativity or innovation in CFBNPD teams is provided. The theoretical and practical implications of the findings and the limitations of the study are also addressed.

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Background: Peanut allergy (PA) is known to impact on quality of life (QoL) of the sufferer, but little research has focused on all family members. We therefore sought to establish the impact of PA on QoL and reported anxiety of children with clinically confirmed PA, their parents and older siblings. Methods: Forty-six families, who had a child with PA, completed QoL (PedsQLTM or WHOQOL-BREF), anxiety (SCAS or STAI) and perceived stress (PSS) scales. PA children completed a PA specific QoL questionnaire (Pediatr Allergy Immunol 2003;14:378). Parents and sibling also completed QoL proxy questionnaires for the PA child (PedsQLTM, Pediatr Allergy Immunol 2003;14:378). Results: Mothers rated their own psychological (P < 0.01) and physical (P < 0.05) QoL significantly worse than fathers rated theirs, and had higher scores than fathers for anxiety (P < 0.05) and stress (P < 0.001). Children with PA had significantly poorer physical health-related QoL (P < 0.05), QoL within school (P < 0.01) and general QoL (P < 0.05) than their siblings did, and greater separation anxiety (P < 0.05). The majority of differences were between girls with PA and female siblings. Mothers felt that there was a greater impact on QoL for their PA child, compared with that reported by siblings, fathers or the PA children themselves (P < 0.01). Conclusions: Mothers report that they have significantly poorer QoL and suffer more anxiety and stress than fathers do; this inter-parental difference may be an important feature of family stress caused by PA. Siblings have a similar view of how QoL affects the PA child as the PA child does, while mothers may possibly overestimate this impact.

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In an ever-changing higher education (HE) environment, institutions are seeing the involvement of parents in students' education increasing. This may partly be due to tuition fees and the introduction of deferred variable tuition fees ("top-up fees") from 2006, and also because of the increased number of students choosing to remain in the family home for the duration of their studies. Many students see their families as the most important source of motivation and advice right through from school age to when they make decisions about HE. In the light of this increase in involvement, institutions need to provide information about, and access to, university to ensure that families are fully prepared and able to support their children throughout the university experience. In recognition of the vital role parents play, the Involving the Family project focuses on parents or key family members from groups currently under-represented in HE in order to increase their awareness and understanding of HE. This article evaluates research undertaken to investigate the views, perceptions and key concerns held by minority ethnic parents with regards to their children and participation in HE. The article then details how these results were utilised in the development of the Involving the Family project.

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Becoming the parent of a child diagnosed with learning disabilities can have a dramatic impact. Chrissie Rogers, the author of this article, is both a lecturer in education studies at Keele University and the mother of a daughter who has learning disabilities. She argues here that the pressures on mothers to produce ‘perfect’ babies and to meet all their needs are immense. These pressures arise from both internalised norms and societal expectations and, in the face of these pressures, parents may feel shock, loss and disappointment. These feelings may lead, in turn, to denial, anxiety and conflict affecting both the parents and the professionals involved with the family. Drawing on a series of in-depth interviews and personal narratives, Chrissie Rogers makes a powerful case for the importance of support, whether that support is formal or informal. She suggests that, without the right levels of support and understanding, having a child with a diagnosis of learning disability can disable the whole family.

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Background: Vascular endothelial growth factor (VEGF) mediates endothelial cell mitogenesis and enhances vascular permeability. The existence of single or multiple VEGF isoforms and receptors suggests that these proteins may have overlapping but distinct functions, which may be reflected in their cell expression and distribution. Methods: The localisation of VEGFs A–C and their receptors (VEGFRs 1–3, respectively) in 30 fresh human atherosclerotic arteries, 15 normal uterine arteries, and 15 saphenous veins using immunohistochemistry and western blotting. Results: Saphenous veins showed no staining for VEGF-B or VEGFR-2. Smooth muscle cells (SMCs) showed the strongest staining for VEGF-A, VEGF-B, VEGFR-1, and VEGFR-2 in all specimens. Conversely, VEGFR-3 and VEGF-C were predominately localised to the endothelial vasa vasorum in normal arteries, whereas medial SMCs showed the strongest staining in atherosclerotic arteries. Western blotting showed variations in VEGF protein localisation, with lower amounts of VEGF-B and VEGF-C in saphenous veins, compared with arterial tissue. Amounts of VEGF-C were lower than those of VEGF-A and VEGF-B in all specimens. Conclusion: This study provides direct evidence of the presence of VEGF proteins and receptors in human physiology and pathology, with variations in both the amounts of VEGF proteins expressed and their cellular distribution in normal arteries compared with atherosclerotic arteries. The presence of VEGFs A–C and their receptors in normal arterial tissue implies that VEGF functions may extend beyond endothelial cell proliferation. Reduced VEGFR-2 staining in atherosclerotic arteries may have implications for the atherosclerosis process and the development of vascular disease and its complications.