ObjectiveThe authors evaluated the morbidity, mortality, and quality of life after pancreatic debridement for necrosis and compared these values to those for quality of life after elective medical and surgical management for chronic pancreatitis. Summary Background DataQuality of life after pancreatic debridement for necrosis has received little attention. Although quality of life after other pancreatic surgery has been evaluated and is thought to be good, management of patients with pancreatic necrosis can be labor intensive and require extraordinary resources. Therefore, further evaluation of the quality of life achieved after treatment is appropriate. MethodsForty patients (group 1) underwent operative debridement for necrosis between 1986 and 1994. Medical records of these patients were reviewed for morbidity, mortality, and in-hospital costs. Follow-up of quality of life was assessed by the Short Form-36 Health Survey. Patients in group 2 (n = 89) underwent medical management of chronic pancreatitis. Group 3 included 47 patients who underwent elective operations for ductal abnormalities. The Short Form-36 Health Surveys were administered to all three groups and compared statistically. ResultsMortality and morbidity from pancreatic debridement was 18% and 77%, respectively. Quality-oflife evaluations in groups 1 through 3 and age-matched controls were statistically similar. ConclusionsPancreatic debridement for necrosis requires intense application of resources and is associated with a high mortality and morbidity. Long-term follow-up shows good quality of life for patients who survive this morbid disease. This study supports the continued aggressive approach to the management of pancreatic necrosis, given that long-term outcome about quality of life is good. outcome is expected. In patients with infected necrosis and managed without surgery, the mortality approaches 100%.1-3 After surgical treatment, patient mortality has ranged from 9% to 40%, with the highest mortality associated with infected necrosis.4-6 Morbidity approaches 100% in these patients who require operative debridement.7 With improvement in intensive care medicine and supportive care over the past 2 to 3 decades, mortality has improved and the majority ofthese patients, even 665

SummaryTissue‐resident memory T (TRM) cells are CD8+ T lymphocytes that reside in the tissues, including tumours. This T cell subset possesses a magnitude of cytotoxicity, but its epigenetic regulation has not been studied. Here, we investigate the impact of perforin DNA methylation in TRM cells and correlate it with their functional potential. Fifty‐three urothelial urinary bladder cancer (UBC) patients were recruited prospectively. The DNA methylation status of the perforin gene (PRF1) locus in TRM cells was investigated by pyrosequencing. Flow cytometry with ViSNE analysis and in‐vitro stimulation were used to evaluate TRM cell phenotypes. We discovered that tumour TRM cells have low DNA methylation in the PRF1 locus (32·9% methylation), which corresponds to increased numbers of perforin‐expressing TRM cells. Surprisingly, programmed cell death 1 (PD‐1) expression is high in tumour TRM cells, suggesting exhaustion. Following interleukin‐15 and T cell receptor stimulation, perforin and T‐bet expressions are enhanced, indicating that TRM cells from tumours are not terminally exhausted. Moreover, a high number of TRM cells infiltrating the tumours corresponds to lower tumour stage in patients. In conclusion, TRM cells from UBC tumours are epigenetically cytotoxic with signs of exhaustion. This finding identifies TRM cells as potential new targets for cancer immunotherapy.

Gastrin activity was determined in sections, cut parallel to the surface, of the antral mucosa and submucosa of cats and dogs and in the aboral corpus mucosa of dogs and man. The maximal gastrin activity in the antrum was found in the basal 2/3 of the gland crypt region of the mucosa. The superficial 1/3 of the antral mucosa of the cat contained no gastrin activity, whereas in the dog traces of activity were found in this part of the mucosa. Extracts from the submucosa of the cat antrum contained no gastrin activity, but in the submucosa of 1 dog out of 3 low activity was found. The results suggest that the gastrin cells are localized predominantly in the region of the middle and basal parts of the gland crypts of the antral mucosa in the dog and cat. In the corpus mucosa immediately oral to the visualized antrum‐corpus boundary, no gastrin activity was found in 3 dogs and activity was present in only 4 of 14 doudenal ulcer patients. Thus the gastrin cells do not seem to be present in the corpus mucosa of dog or man, but the occasional finding of gastrin activity in the most aboral part of the acid secreting gastric mucosa of man speaks in favour of a dentate, or sometimes notchy, antrum‐corpus boundary.

_ BROOME, A., B. FVRO and L. OLBE. Localization of gastrin activity In the gastric antrum. Acta physiol. scand. 1968. 74. 331-339.