36 research outputs found

    Making sense of joint commissioning: three discourses of prevention, empowerment and efficiency

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    Background: In recent years joint commissioning has assumed an important place in the policy and practice of English health and social care. Yet, despite much being claimed for this way of working there is a lack of evidence to demonstrate the outcomes of joint commissioning. This paper examines the types of impacts that have been claimed for joint commissioning within the literature. Method: The paper reviews the extant literature concerning joint commissioning employing an interpretive schema to examine the different meanings afforded to this concept. The paper reviews over 100 documents that discuss joint commissioning, adopting an interpretive approach which sought to identify a series of discourses, each of which view the processes and outcomes of joint commissioning differently. Results: This paper finds that although much has been written about joint commissioning there is little evidence to link it to changes in outcomes. Much of the evidence base focuses on the processes of joint commissioning and few studies have systematically studied the outcomes of this way of working. Further, there does not appear to be one single definition of joint commissioning and it is used in a variety of different ways across health and social care. The paper identifies three dominant discourses of joint commissioning – prevention, empowerment and efficiency. Each of these offers a different way of seeing joint commissioning and suggests that it should achieve different aims. Conclusions: There is a lack of clarity not only in terms of what joint commissioning has been demonstrated to achieve but even in terms of what it should achieve. Joint commissioning is far from a clear concept with a number of different potential meanings. Although this ambiguity can be helpful in some ways in the sense that it can bring together disparate groups, for example, if joint commissioning is to be delivered at a local level then more specificity may be required in terms of what they are being asked to deliver

    Living on the edge - plants and global change in continental and maritime Antarctica

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    Clomiphene and Its Isomers Block Ebola Virus Particle Entry and Infection with Similar Potency: Potential Therapeutic Implications

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    The 2014 outbreak of Ebola virus (EBOV) in Western Africa highlighted the need for anti-EBOV therapeutics. Clomiphene is a U.S. Food and Drug Administration (FDA)-approved drug that blocks EBOV entry and infection in cells and significantly protects EBOV-challenged mice. As provided, clomiphene is, approximately, a 60:40 mixture of two stereoisomers, enclomiphene and zuclomiphene. The pharmacokinetic properties of the two isomers vary, but both accumulate in the eye and male reproductive tract, tissues in which EBOV can persist. Here we compared the ability of clomiphene and its isomers to inhibit EBOV using viral-like particle (VLP) entry and transcription/replication-competent VLP (trVLP) assays. Clomiphene and its isomers inhibited the entry and infection of VLPs and trVLPs with similar potencies. This was demonstrated with VLPs bearing the glycoproteins from three filoviruses (EBOV Mayinga, EBOV Makona, and Marburg virus) and in two cell lines (293T/17 and Vero E6). Visual problems have been noted in EBOV survivors, and viral RNA has been isolated from semen up to nine months post-infection. Since the clomiphene isomers accumulate in these affected tissues, clomiphene or one of its isomers warrants consideration as an anti-EBOV agent, for example, to potentially help ameliorate symptoms in EBOV survivors

    Towards understanding Sure Start local programmes: Summary of findings from the national evaluation

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    Sure Start is the Government\u27s programme to support children, families and communities through the integration of early education, childcare, health and family support. Sure Start local programmes are one element of this, based in areas of disadvantage, whose aim is to improve the health and well being of young children under 4 and their families, so that children have a greater opportunity to flourish when they start school. The National Evaluation of Sure Start local programmes has now been in place for 3 years, during which a large amount of information has been collected and reported. This summary draws together some of main published findings from the different strands of the evaluation and in particular highlights some of the newly published findings. These are only a very small selection of findings, intended to provide a flavour and whet the appetite to find out more. At this stage, findings from different parts of the evaluation are reported separately although these will be drawn together more substantially later in the year to assess the overall effect Sure Start local programmes have had on children, parents, families and communities and whether variations in implementation, local community context and costs can explain any differences in effects

    Modulation of cholinergic neural bronchoconstriction by endogenous nitric oxide and vasoactive intestinal peptide in human airways in vitro

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    Human airway smooth muscle possesses an inhibitory nonad-renergic noncholinergic neural bronchodilator response me-diated by nitric oxide (NO). In guinea pig trachea both endoge-nous NO and vasoactive intestinal peptide (VIP) modulate cholinergic neural contractile responses. To identify whether endogenous NO or VIP can modulate cholinergic contractile responses in human airways in vitro, we studied the effects of specific NO synthase inhibitors and the peptidase a-chymo-trypsin on contractile responses evoked by electrical field stimu-lation (EFS) at three airway levels. Endogenous NO, but not VIP, was shown to inhibit cholinergic contractile responses at all airway levels but this inhibition was predominantly in tra-chea and main bronchus and less marked in segmental and subsegmental bronchi. To elucidate the mechanism ofthis mod-ulation we then studied the effects ofendogenous NO on acetyl-choline (ACh) release evoked by EFS from tracheal smooth muscle strips. We confirmed that release was neural in origin, frequency dependent, and that endogenous NO did not affect ACh release. These findings show that endogenous NO, but not VIP, evoked by EFS can inhibit cholinergic neural responses via functional antagonism ofACh at the airway smooth muscle and that the contribution of this modulation is less marked in lower airways. (J. Clin. Invest. 1993.92:736-743.) Key words: acetylcholine release * functional antagonism * bronchodilation * parasympathetic innervation * inhibitory nonadrenergic non-cholinergic (i-NANC

    Modeling of variables in cellular infection reveals CXCL10 levels are regulated by human genetic variation and the Chlamydia-encoded CPAF protease

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    Susceptibility to infectious diseases is determined by a complex interaction between host and pathogen. For infections with the obligate intracellular bacterium Chlamydia trachomatis, variation in immune activation and disease presentation are regulated by both host genetic diversity and pathogen immune evasion. Previously, we discovered a single nucleotide polymorphism (rs2869462) associated with absolute abundance of CXCL10, a pro-inflammatory T-cell chemokine. Here, we report that levels of CXCL10 change during C. trachomatis infection of cultured cells in a manner dependent on both host and pathogen. Linear modeling of cellular traits associated with CXCL10 levels identified a strong, negative correlation with bacterial burden, suggesting that C. trachomatis actively suppresses CXCL10. We identified the pathogen-encoded factor responsible for this suppression as the chlamydial protease- or proteasome-like activity factor, CPAF. Further, we applied our modeling approach to other host cytokines in response to C. trachomatis and found evidence that RANTES, another T-cell chemoattractant, is actively suppressed by Chlamydia. However, this observed suppression of RANTES is not mediated by CPAF. Overall, our results demonstrate that CPAF suppresses CXCL10 to evade the host cytokine response and that modeling of cellular infection parameters can reveal previously unrecognized facets of host-pathogen interactions
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