Improving acute care for adolescents and young adults on medical admission units: The interventions that matter.

It had become a familiar routine. My seventh admission with diabetic ketoacidosis (DKA) in a year. Each time I was admitted it was the same; a DKA protocol, a diabetes specialist nurse visit, and a few questions from the doctors checking if "everything is okay?" On each admission, I would be discharged home after a couple of days. We all knew I'd be back again within a month or two.

Typical bronchial carcinoid tumour presenting as pneumomediastinum.

The authors present a case of a 44-year-old man who presented with acute onset shortness of breath. He had severe subcutaneous emphysema and his chest x-ray and CT scan confirmed presence of air in mediastinum. Rigid bronchoscopy revealed a bronchial tumour which was proven to be a carcinoid on histology. Patient recovered following the surgical excision of the tumour.

Dialogue and interchange across the primary/secondary interface: piloting SpR secondment to a general practice diabetic clinic.

The growing volume of diabetic care taking place in UK general practice and pressure to unload hospital clinics are resulting in entirely separate patient caseloads, in which structured care and monitoring of large numbers of patients over many years can take place in one health care sector alone. In these circumstances, it is important to guard against the GP service becoming educationally and clinically isolated from hospital diabetic clinic care and vice versa. Greater interplay of staff between health sectors could serve as an antidote. Educational objectives for brief SpR secondment to general practice diabetic clinics were formulated and three month SpR secondment to a central London practice clinic was set up and judged a success for GP and SpR alike. This was followed by GP and consultant sitting in on each other's diabetic clinics, allowing each to appreciate similarities and differences in their clinic, case load and practice setting.

An uncoupling protein 2 gene variant is associated with a raised body mass index but not Type II diabetes.

AIMS/HYPOTHESIS: Linkage between markers close to the uncoupling protein 2 and 3 genes (11q13) and resting metabolic rate and a pre-diabetic phenotype have been found. The syntenic region in mouse has been found to be linked to quantitative traits associated with obesity and diabetes. UCP2 and UCP3 could therefore have an important role in body weight regulation and susceptibility to diabetes. We investigated a recently identified variant of the UCP2 gene in exon 8 as a marker for glucose and weight homeostasis. METHODS: Length variation of the UCP2 exon 8 variant was studied by the polymerase chain reaction and agarose gel electrophoresis. Sequence variants of the UCP3 gene were sought by semi-automated DNA sequencing. RESULTS: In 453 South Indian subjects, we found an association in women between the UCP2 exon variant and body mass index (p = 0.018). These findings were replicated in a separate group of South Indian subjects (n = 143, p < 0.001) irrespective of sex. Although no association was found between the UCP2 exon 8 variant and overt obesity in British subjects, the UCP2 genotype of obese women (n = 83) correlated with fasting serum leptin concentration (p = 0.006) in the presence of extreme obesity. These observations could not be explained by tight linkage disequilibrium with a coding region variant in the region of the UCP3 gene of biological significance. Lastly, no association was found between UCP2 and Type II (non-insulin-dependent) diabetes using either a family based design (85 families) or case control study (normal glucose tolerance n = 335, impaired glucose tolerance n = 42, Type II diabetes n = 76). CONCLUSION/INTERPRETATION: We have described a UCP2 gene exon 8 variant that may affect susceptibility to weight gain by influencing regulation of leptin.

Obesity, non-insulin-dependent diabetes mellitus and the metabolic syndrome.

Obesity is characterised by alterations in metabolic function which result from a combination of increasing total body fatness and the regional distribution of adipose tissue. Abdominal visceral obesity is particularly associated with hyperinsulinaemia, increased portal vein free fatty acid concentration, hepatic gluconeogenesis, altered adrenocortical activity and androgen secretion and reduced plasma sex hormone binding globulin levels. These alterations, which are accompanied by changes in visceral adipocyte sensitivity to plasma catecholamine stimulation, enhance further visceral fat deposition and the perpetuation of the metabolic derangements. The characteristic dyslipidaemia associated with upper body obesity and the frequent development of NIDDM are predictable consequences. In contrast to the considerable knowledge about the biochemical background to these alterations, relatively little is understood about the mechanisms through which an individual's ethnic background influences the changes. This chapter reviews these important issues.