Pathways of care for patients with suspected cancer of the pancreas: a tiered questionnaire-based survey of medical personnel across a single United kingdom Calman-Hine cancer network.

Objective: This study examines clinical management pathways for patients with suspected pancreatic cancer within a single United Kingdom Calman-Hine NHS cancer network with particular focus on referral patterns and the primary care-hospital specialist interface.

Methods: A questionnaire-based study appraising responses from three key groups (general practitioners, gastrointestinal physicians and gastrointestinal surgeons) practising within a cancer network. The questionnaire addressed caseload, referral pathways, multidisciplinary care teams and involvement of specialists.

Differential nitric oxide synthase expression during hepatic ischemia-reperfusion.

Background: In recent years the important role of nitric oxide in hepatic ischemia-reperfusion injury has been increasingly recognised. The prevailing consensus is that reperfusion injury may be partly the result of decreased production of nitric oxide from endothelial nitric oxide synthase and excessive production of nitric oxide from the inducible isoform. We therefore undertook this study to characterize the expression of different nitric oxide synthase isoforms during hepatic reperfusion.

Differential expression of pulmonary nitric oxide synthase isoforms after intestinal ischemia-reperfusion.

Background/aims: Nitric oxide has been implicated in both attenuating and aggravating ischemia-reperfusion injury in most organs. This study aimed to investigate the role of nitric oxide produced by the two principal isoforms of nitric oxide synthase in the lung during post-ischemic reperfusion of the intestine.

Methodology: Rats were randomized into four groups of 6 animals: Group A: laparotomy and superior mesenteric artery dissection without occlusion and maintenance for 2 h (control group at 2 h).

Adenosine preconditioning attenuates hepatic reperfusion injury in the rat by preventing the down-regulation of endothelial nitric oxide synthase.

Background: Previous work has suggested that in the liver, adenosine preconditioning is mediated by nitric oxide. Whether the endothelial isoform of nitric oxide synthase plays a part in this mechanism has however not yet been investigated.

Methods: Wistar rats were used (6 in each group)--Groups: (1) sham, (2) ischemia-reperfusion, (3) adenosine + ischemia-reperfusion, (4) endothelial isoform inhibitor + adenosine + ischemia-reperfusion.