Clin. Otolaryngol. 2012, 37, 44–52 Background:  Although relatively uncommon, penetrating neck trauma has the potential for serious morbidity and an estimated mortality of up to 6%. The assessment and management of patients who have sustained a penetrating neck injury has historically been an issue surrounded by significant controversy. Objectivesof review:  To assess recent evidence relating to the assessment and management of penetrating neck trauma, highlighting areas of controversy with an overall aim of formulating clinical guidelines according to a care pathway format. Type of review:  Structured, non‐systematic review of recent medical literature. Search strategy:  An electronic literature search was performed in May 2011. The Medline database was searched using the Medical Subject Headings terms ‘neck injuries’ and ‘wounds, penetrating’ in conjunction with the terms ‘assessment’ or ‘management’. Embase was searched with the terms ‘penetrating trauma’ and ‘neck injury’, also in conjunction with the terms ‘assessment’ and ‘management’. Results were limited to articles published in English from 1990 to the present day. Evaluation method:  Abstracts were reviewed by the first three authors to select full‐text articles for further critical appraisal. The references and citation links of these articles were hand‐searched to identify further articles of relevance. Results:  147 relevant articles were identified by the electronic literature search, comprising case series, case reports and reviews. 33 were initially selected for further evaluation. Conclusions:  Although controversy continues to surround the management of penetrating neck trauma, the role of selective non‐operative management and the utility of CT angiography to investigate potential vascular injuries appears to be increasingly accepted.

Aims and method We aimed to evaluate the availability and nature of services for people affected by personality disorder in England by conducting a survey of English National Health Service (NHS) mental health trusts and independent organisations.Results In England, 84% of organisations reported having at least one dedicated personality disorder service. This represents a fivefold increase compared with a 2002 survey. However, only 55% of organisations reported that patients had equal access across localities to these dedicated services. Dedicated services commonly had good levels of service use and carer involvement, and engagement in education, research and training. However, a wider multidisciplinary team and a greater number of biopsychosocial interventions were available through generic services.Clinical implications There has been a substantial increase in service provision for people affected by personality disorder, but continued variability in the availability of services is apparent and it remains unclear whether quality of care has improved.

Somatostatin potently inhibits insulin secretion from pancreatic beta-cells. It does so via activation of ATP-sensitive K+-channels (KATP) and G protein-regulated inwardly rectifying K+-channels, which act to decrease voltage-gated Ca2+-influx, a process central to exocytosis. Because KATP channels, and indeed insulin secretion, is controlled by glucose oxidation, we investigated whether somatostatin inhibits insulin secretion by direct effects on glucose metabolism. Oxidative metabolism in beta-cells was monitored by measuring changes in the O2 consumption (DeltaO2) of isolated mouse islets and MIN6 cells, a murine-derived beta-cell line. In both models, glucose-stimulated DeltaO2, an effect closely associated with inhibition of KATP channel activity and induction of electrical activity (r > 0.98). At 100 nm, somatostatin abolished glucose-stimulated DeltaO2 in mouse islets (n = 5, P < 0.05) and inhibited it by 80 +/- 28% (n = 17, P < 0.01) in MIN6 cells. Removal of extracellular Ca2+, 5 mm Co2+, or 20 microm nifedipine, conditions that inhibit voltage-gated Ca2+ influx, did not mimic but either blocked or reduced the effect of the peptide on DeltaO2. The nutrient secretagogues, methylpyruvate (10 mm) and alpha-ketoisocaproate (20 mm), also stimulated DeltaO2, but this was unaffected by somatostatin. Somatostatin also reversed glucose-induced hyperpolarization of the mitochondrial membrane potential monitored using rhodamine-123. Application of somatostatin receptor selective agonists demonstrated that the peptide worked through activation of the type 5 somatostatin receptor. In conclusion, somatostatin inhibits glucose metabolism in murine beta-cells by an unidentified Ca2+-dependent mechanism. This represents a new signaling pathway by which somatostatin can inhibit cellular functions regulated by glucose metabolism.

The results suggest that treating people with borderline personality disorder with lamotrigine is not a clinically effective or cost-effective use of resources.