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group meets at six 3-day meetings. These takes place at the different universities where the mentors are working. To the fi rst course, which started in August 1999, participants were recruited from the Nordic and Baltic countries, to the second and 3rd courses participants from several northern European countries, including Germany, Switzerland, UK, France, and the Czech republic, were invited. Along with pancreatological education and leadership training the participants also plan and carry through scientifi c projects in network-based groups of 5–6 persons, guided by two mentors. This implies brain-storming for research ideas (fi rst meeting), implement ideas to research protocols, apply for ethical approval and funding, realise the projects and write a manuscript suitable for submission. The scientifi c projects also runs between the meetings and the aim is to fi nish the different projects during the two and a half years. This has, however, not always been possible. Some of the groups have thus continued and fi nished their projects outside the timeframe of the six meetings but still within the Pancreas 2000 network. This far, 13 different projects have been initiated and of these 5 have been accepted or published [1–5] and 4 have been, or will soon be, submitted [6–9] . One study of risk factors, predictors and course in ERCP-induced acute pancreatitis is ongoing and three of the initiated projects will probably not be completed. During the last decades the number of active scientists within pancreatology has decreased in Europe and the age of the active scientists has increased. To guarantee the future of clinical pancreatology and pancreatic research, the educational program ‘Pancreas 2000’ started in August 1999. This is a new concept for continuous collaboration between the university (Karolinska Institutet) and the pharmacological industry (Solvay Pharmaceuticals) with the purpose of creating an international network of physicians/scientists interested in pancreatology and thus to contribute to a positive development of European pancreatology. This is a true collaboration, scientifi c as well as economic, as the program is sponsored partly by the respective departments of the participants and partly by the industry. The program is designed to stimulate development in especially three areas: pancreatology, scientifi c thinking and group leadership. The program, of which the 3rd course now is running, has recruited 22–25 young physicians/scientists to each course. They work together with 10 senior pancreatologists, the mentors. The mentors are actively contributing to the lectures and discussions and, furthermore, to every meeting special guests (world leading pancreatologists) are also invited to give lectures. Associated to the program is one leadership expert, who participates in every meeting, and a statistician. One program runs over two and a half years during which the Published online: August 18, 2005

Hemorrhage from the pancreatic duct, i.e. hemosuccus pancreaticus (HP), is a rare cause of gastrointestinal bleeding. This potentially life-threatening complication of chronic pancreatitis may pose a significant diagnostic and therapeutic dilemma, especially in patients with silent forms of the disease.We report a case of a 64-year-old man with no history or symptoms but positive findings of chronic calcifying pancreatitis at computed tomography (CT) scan.The patient presented with repeated episodes of gastrointestinal bleeding requiring transfusion and did not, until later in the disease, develop hyperamylasemia and epigastric pain. Repeated endoscopies could not reveal the source of bleeding. The radiological diagnosis and successful transcatheter embolization of a small splenic pseudoaneurysm were performed during an interval when the patient was asymptomatic and showed no signs of bleeding.We suggest that when HP is suspected, a contrast-enhanced CT angiography with reconstruction of the arteries should be performed regardless of whether the patient shows signs of active bleeding or not.

Islet amyloid polypeptide (IAPP) reduces food intake and body weight in laboratory animals. In addition, IAPP appears to regulate nutrient metabolism. In the present studies, we investigated the effect of chronic IAPP treatment on different aspects of energy homeostasis.IAPP was infused (25 pmol/kg/min) from subcutaneous osmotic pumps for 2-7 days. Rats in 2 saline-infused control groups were fed ad libitum (AF) or pair-fed (PF) against the IAPP-treated rats.As expected, the IAPP infusion reduced food intake and body weight gain. In addition, the IAPP treatment decreased the epididymal fat pad (vs. PF rats, p0.05) and lowered circulating levels of triglycerides (vs. PF rats, p0.05), free fatty acids (vs. PF rats, p0.05), leptin (vs. both AF and PF rats, p0.05) and insulin (vs. AF rats, p0.05). In contrast, glucose and protein metabolism in the IAPP-treated rats was largely unchanged, as shown in results regarding serum glucose, glucose transport in skeletal muscle, blood urea nitrogen, and glycogen and protein content in the liver and in skeletal muscle.In summary, chronic IAPP exposure led to a changed lipid metabolism, which was characterized by decreased adiposity, hypolipidemia and hypoleptinemia, and to unchanged glucose and protein homeostasis. These results were similar to those seen in rodents during chronic exposure to another satiety/adiposity regulator, leptin. In conclusion, chronically administered IAPP plays a role as a satiety and adiposity signal in rats, and helps regulate energy homeostasis.

Background: In malignant diseases, circulating amino acid profiles correlate with organ sites of malignancy. Direct effects of malignant cells on the extracellular amino acid profile are still uncertain. Methods: Free amino acids were measured in serum-free culture media (RPMI-1640) conditioned by two human pancreatic cancer cell lines (Panc-1 and HPAF), a hamster pancreatic cancer cell line (PC-1), a human epidermoid carcinoma cell line (A-431), and a human fibroblastic cell line (Ag-1523). Non-conditioned RPMI-1640 medium was used as control. Results: Amino acid profiles were changed in all the conditioned media, caused by a decrease or increase in the original amino acids and by the appearance of amino acids that were not present in non-conditioned medium. Media conditioned by two human pancreatic cancer cell lines showed similar amino acid profiles, which were characterized by a decrease in glutamine, cysteine and serine, increase in glycine, proline and glutamic acid and appearance of ornithine and alanine. Conclusion: Culture media show changed amino acid profiles following incubation with cell lines of pancreatic or non-pancreatic origins. Different human pancreatic cancer cell lines cause similar changes in amino acid profiles of media.