Type I diabetes is marked by a deficiency of endocrine β cells in the pancreatic islets of Langerhans. Daily injection of insulin is the current treatment for the disease. Because insulin injection cannot match the precise timing and dosing of physiological secretion of insulin by islets in response to hyperglycemia, severe side effects develop over time. Transplantation of islets represents a potential cure; however, limitations on the availability of cadaveric organs restrict this procedure to only a small percentage of patients. Pancreatic endocrine stem cells exist in the developing embryonic pancreas. The isolation, expansion, and differentiation of pancreatic endocrine stem cells would provide an unlimited source of islet cells for transplantation and treatment for type I diabetes. A potential source for endocrine stem cells is embryonic stem (ES) cells. Because of their unlimited proliferation and differentiation potentials, ES cells are considered an important source for cell therapies targeted to several diseases, including diabetes.There are two nonallelic insulin genes (insulin I and II) expressed in multiple sites in mice during development [1][2][3][4][5][6][7] Abstract A panel of genetic markers was used to assess the in vitro commitment of murine embryonic stem (ES) cells toward the endoderm-derived pancreas and to distinguish insulin-expressing cells of this lineage from other lineagessuch as neuron, liver, and yolk sac. There are two nonallelic insulin genes in mice. Neuronal cells express only insulin II, whereas the pancreas expresses both insulin I and II. Yolk sac and fetal liver express predominately insulin II, small amounts of insulin I, and no glucagon. We found that ES-derived embryoid bodies cultured in the presence of stage-specific concentrations of monothioglycerol and 15% fetal calf serum, followed by serum-free conditions, give rise to a population that expresses insulin I, insulin II, pdx-1 (a pancreas marker), and Sox17 (an endoderm marker). Immunohistochemical staining shows intracellular insulin particles, and its de novo production was confirmed by staining for C-peptide. Most, but not all, of the insulin + or C-peptide + cells coexpress glucagon, demonstrating a differentiation pathway to pancreas rather than yolk sac or fetal liver. Addition of β-cell specification and differentiation factors activin βB, nicotinamide, and exendin-4 to later-stage culture increased insulin-positive cells to 2.73% of the total population, compared with the control culture, which gave rise to less than 1% insulin-staining cells. These findings suggest that stepwise culture manipulations can direct ES cells to become early endocrine pancreas.

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Although the therapeutic benefits of endoscopic retrograde cholangiopancreatography (ERCP) usually outweigh the risks, there can be rare complications, including stent migration leading to perforation, intestinal obstruction or penetration. An 87-year-old woman presented with symptomatic choledocholithiasis. Two previous endoscopic attempts at stone removal were unsuccessful. On repeat ERCP at our institution, multiple large stones were removed, but complete duct clearance could not be achieved. A plastic biliary stent was placed with plans to reattempt in 6 weeks. Postoperatively, she had mild back pain radiating into her right leg that gradually worsened to the point where she was unable to ambulate. An abdominal CT scan showed the distal aspect of the biliary stent extending through the wall of the duodenum with the tip positioned within the right psoas muscle. The stent was successfully removed via a rat-toothed forceps. Our case illustrates an extremely rare complication of biliary stent placement.

Summary:The report concerns a case of primary carcinoma of the gall bladder in a 53 year old man, who, 13 years previously underwent a pan-proctocolectomy for ulcerative colitis. Previous reports are reviewed, highlighting the difficulty of early diagnosis.

SUMMARY Twenty three cases of pseudomembranous colitis (PMC) occurred in three hospitals in 10 months. Retrospective analysis shows that they represented a single epidemic with a readily traceable chain of person-to-person contact within and between hospitals. Most patients had severe pre-existing illness and all had broad spectrum antibiotics, including either ampicillin/ amoxycillin, a broad spectrum cephalosporin (particularly cefotaxime), or both. All patients had severe diarrhoea and all responded to vancomycin, but relapse occurred in five. Ten patients eventually died, principally because of underlying disease rather than from PMC. Failure to find fibrin thrombi in blood vessels in biopsies and the scanty distribution of non-invasive bacteria supports the concept of mucosal damage by bacterial toxin, rather than by direct infection, or ischaemia. Although environmental colonisation cannot be excluded, the observed pattern of spread suggests a major role for direct person-to-person crossinfection in the spread of disease in this outbreak.Pseudomembranous colitis (PMC) is an inflammatory condition of the colon, usually occurring after broad spectrum antibiotic therapy, and associated with colonisation by toxigenic Clostridiium difficile.We report an epidemic of PMC in three hospitals of our hospital group, in which there was temporal and geographical clustering of cases suggestive of crossinfection. C cdifficile is generally considered an opportunistic pathogen which may cause PMC in patients who have received broad spectrum antibiotics. This outbreak, taken in conjunction with other recent reports of case clustering,"' emphasises the role of cross infection in the pathogenesis of PMC. Reccied for puhblication IS April 1987. had also been identified in hospital 2. A retrospective study was started. Clinicians in all seven hospitals of the group were questioned (in particular all endoscopists) about cases of PMC occurring in the previous year. Histopathological surgical and autopsy records for the previous year were reviewed for cases diagnosed as PMC and all microbiological isolates of C difficile were recorded. Hospital charts of all patients identified by these procedures were reviewed and those not having a clinical illness consistent with PMC were excluded. In addition to 15 cases initially known to the clinicians at hospitals I and 2 a further eight cases were identified by this screening procedure. Twenty patients in whose faeces C difficile was cultured showed no clinical evidence of PMC and these, regarded as asymptomatic colonisation, were eliminated from the study. We feel it unlikely that any diagnosed cases of PMC within our hospital group were not included in the study.After these investigations it was found that the cases of PMC were limited to three hospitals, all of which are members of a larger hospital group, served by a central laboratory. Each affected hospital has 1467 on 11 May 2018 by guest. Protected by copyright.