Charcot neuroarthropathy (CNA) is a disabling and devastating condition affecting patients with severe diabetic neuropathy. It can lead to foot deformity, recurrent foot ulceration and ultimately to amputation. The incidence is about 0.1±5 % in diabetic patients with peripheral neuropathy [1].The pathogenesis of CNA is not clear, one possible predisposing factor is reduced bone density [2,3], probably as a result of increases in bone turnover. Investigators measured carboxy-terminal telopeptide domain of type 1 collagen (1TCP) and carboxy-terminal propeptide of type 1 collagen (P1CP) as possible Diabetologia (2001) AbstractAims/hypothesis. The management of charcot neuroarthropathy, a severe disabling condition in diabetic patients with peripheral neuropathy, is currently inadequate with no specific pharmacological treatment available. We undertook a double-blind randomised controlled trial to study the effect of pamidronate, a bisphosphonate, in the management of acute diabetic Charcot neuroarthropathy. Methods. Altogether 39 diabetic patients with active Charcot neuroarthropathy from four centres in England were randomised in a double-blind placebo-controlled trial. Patients received a single infusion of 90 mg of pamidronate or placebo (saline). Foot temperatures, symptoms and markers of bone turnover (bone specific alkaline phosphatase and deoxypyridinoline crosslinks) were measured over the 12 months, in 10 visits. All patients also had standard treatment of the Charcot foot. Results. Mean age of the study group (59 % Type II (non-insulin-dependent) diabetes mellitus) was 56.3 10.2 years. The mean temperature difference between active and control groups was 3.6 1.7 C and 3.3 1.4 C, respectively. There was a fall in tem-

There may be receptor-specific endothelial dysfunction in subjects with uncomplicated Type 2 DM. This is not improved by treatment with alpha-tocopherol.

In this study, structured initial assessment by a specialist nurse was shown to be an accurate method of determining a diagnosis of cognitive impairment, when compared with formal MDT judgement. The principal benefit of this approach was that signposting to subsequent care pathways was expedited. Arguably, such distributed responsibility affords a viable option for the future detection of early dementia.

The generation of an autoimmune response against islet beta‐cells is central to the pathogenesis of type 1 diabetes mellitus, and this response is driven by the stimulation of autoreactive lymphocytes by components of the beta‐cells themselves. Reactive oxygen species (ROS) have been implicated in the beta‐cell destruction which leads to type 1 diabetes and may modify beta‐cell components so as to enhance their immunogenicity. We investigated the effects of oxidation reactions catalysed by copper or iron on the major beta‐cell autoantigen glutamic acid decarboxylase (GAD). Lysates of purified rat islets were exposed to copper or iron sulphate with or without hydrogen peroxide or ascorbic acid. Immunostaining showed that these treatments generated high molecular weight covalently linked aggregates containing GAD. These are not formed by intermolecular disulphide bonds between cysteine residues since they cannot be resolved into monomeric form when electrophoresed under extreme reducing conditions. There was no modification of insulin or pro‐insulin by ROS. The same oxidative changes to GAD could be induced in viable islet cells treated with copper sulphate and hydrogen peroxide, and thus the modifications are not an artefact of the catalysed oxidation of cell‐free lysates. Sera from patients with type 1 diabetes and stiffman syndrome containing GAD antibodies reacted predominantly with the highest molecular weight modified protein band of GAD: normal human sera did not precipitate GAD. Thus, oxidatively modified aggregates of GAD react with serum antibodies of type 1 diabetes patients and some SMS patients: this is consistent with oxidative modifications of autoantigens being relevant to the pathogenesis of type 1 diabetes.

It is expedient to consider new ways in which dementia care services may be configured to meet increasing demographic, societal and regulatory demands. Greater equity in the distribution of clinical responsibility across multidisciplinary teams has been suggested as one method that may offer a range of benefits to both the service user and the service itself. However, within the dementia workforce there are concerns about inconsistency and variability in both knowledge of dementia and competency in meeting the needs of those affected. Taking this into account it was felt important to explore perceived knowledge and competency of specialist dementia care nurses who would not only be expected to possess higher levels of knowledge and skill but are positioned as the obvious clinical group to engage with new ways of working. Consequently, this paper offers the results and subsequent discussion of a survey of senior nurses working in dementia care across the UK.

The responses of the adenohypophyseal hormones adrenocorticotrophin (ACTH), growth hormone (GH), thyroid stimulating hormone (TSH), prolactin, luteinizing hormone (LH) and follicle stimulating hormone (FSH) to sub-maximal doses of hypothalamic releasing factors were studied in six lean male volunteers (age 23-35 years) with and without infusions of oxytocin (OXT). OXT infusion (mean plasma concentration 133.6 +/- 2.6 pmol/l) completely inhibited the plasma ACTH responses to corticotrophin releasing hormone (CRH) (saline, peak increment ACTH 1.61 +/- 0.75 pmol/l; OXT, peak increment ACTH - 0.04 +/- 0.28 pmol/l; P less than 0.05). OXT infusion had no significant effect on the GH response to growth hormone releasing hormone (GHRH), the TSH and prolactin responses to thyrotrophin releasing hormone (thyroliberin, TRH) or the LH and FSH responses to gonadotrophin releasing hormone (luteoliberin, GnRH). The data support a role for OXT in the modulation of ACTH secretion in man.

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People with dementia are finding increasingly creative and diverse ways of making their voice heard in society and one such method is through the publication of autobiographical accounts. Following set inclusion criteria, this meta-ethnographic analysis compares and contrasts the contents of 12 books written by people with dementia and published between 1989 (the year of publication of the first text) and the end of 2007 (the selected cut-off point for inclusion). Of the 12 books, three authors were published twice, five were male, eight were from the United States of America, one was Australian and all nine had a professional background. Eight of the authors had Alzheimer's disease and one had fronto-temporal dementia. The average age of the narrator was 51.5 years (age range 38–61 years). Meta-ethnographic analysis of the 12 books inductively generated five themes that linked each story and these were: (a) awareness of change; (b) experiencing loss; (c) standing up and bearing witness; (d) sustaining continuity; and (e) liberation and death. The importance of reconstructing identity appeared a pivotal process in living with the onset and progression of dementia together with maintaining key social relationships and networks.