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OBJECTIVE: Acute and hard-to-heal wounds are a significant burden to both a patient's quality of life and resources in healthcare systems. Here, we evaluate the outcomes of a non-comparative case series study in which Ringer's solution-preactivated polyacrylate dressings were used to treat acute and hard-to-heal wounds (the presence of Ringer's solution provides a wound dressing that allows, upon application, the immediate hydration of the underlying wound tissue). METHOD: Patients with acute and hard-to-heal wounds were enrolled into an open-labelled, non-comparative observational study. Patients were treated with Ringer's solution-preactivated polyacrylate dressings to enable wound debridement and wound cleansing for up to 12 weeks. RESULTS: A total of 303 patients were enrolled in the study and 278 were included in the analysis. Wound size decreased, from a median of 3.6cm2 (interquartile range (IQR): 1.2-9.3] at baseline to a median of 2.6cm2 (IQR: 1.1-7.8] at 84 days. Relative wound area reduction (WAR) was 43.1% at 84 days and estimated probability of achievement of a WAR of ≥40% and ≥60% was 68.7% and 53.4%, respectively. Median time to achieve a WAR of ≥40% and ≥60% was 54 days and 75 days, respectively. The median percentage of wound area covered by fibrin had decreased from 50.0% to 10% and granulation tissue had increased from 25% to 50% after 84 days. In addition, periwound skin condition, local signs of infection and pain all showed improvement. The majority of the wounds were assessed as 'healed' or 'better' at the conclusion of the evaluation period. CONCLUSION: Based on the findings of this study, the use of Ringer's solution-preactivated polyacrylate dressings in daily practice has the potential to improve clinical outcomes, including healing, in patients with acute and hard-to-heal wounds.

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A 42-year-old morbidly obese patient (BMI 44.1 kg/m(2)) was admitted to our emergency room with upper abdominal pain, nausea, and cholestasis. Nine years ago, a vertical banded gastroplasty had been performed (former BMI 53.5 kg/m(2)) with a subsequent weight loss to BMI 33.0 kg/m(2). After regaining weight up to a BMI of 47.6 kg/m(2), 5 years ago a conversion to a gastric bypass was realized. A computed tomography of the abdomen showed an invagination of the remaining stomach into the duodenum causing obstruction of the orifice of common bile duct. The patient underwent an open desinvagination of the intussusception and resection of the remaining stomach. Gastroduodenal intussusception is rare and mostly secondary to gastric lipoma. To prevent this rare but serious complication, the remaining stomach could be fixed at the crura of the diaphragm, tagged to the anterior abdominal wall by temporary gastrostomy tube, or resected.

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INTRODUCTION: Choledochal cysts are rare congenital anomalies. Their diagnosis is difficult, particulary in adults. CASE PRESENTATION: This case report demonstrates the diagnostic and therapeutic pitfalls. CONCLUSION: To prevent cost-intensive and potentially life-threating complications, a choledochal cyst must be considered in the differential diagnosis whenever the rather common diagnosis of a hepatic cyst is considered.

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A complication observed with revisional surgery involving a fistula between the former pouch after gastric banding and the fundus is described. A 59-year-old man with BMI 41 kg/m(2) presented for Roux-en-Y gastric bypass (RYGBP). He had previously undergone an open gastric banding operation, with the band removed for obstruction 1 year later. He presented to our hospital with a third incisional hernia which was so large that he suffered from abdominal angina following meals. A RYGBP and a hernia repair with mesh were performed. The postoperative contrast x-ray study disclosed a fistula between the pouch and fundus. A procedure to close the fistula became necessary. The reason for the fistula may have been an erosion at the former connection between the pouch and the fundus after gastric banding, although a preoperative gastroscopy had not revealed this fistula.

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The function of the pfr gene encoding the ferritin from Helicobacter pylori was investigated using the Fur titration assay (FURTA) in Escherichia coli, and by characterization of a pfr-deficient mutant strain of H. pylori. Nucleotide sequence analysis revealed that the pfr region is conserved among strains (> 95% nucleotide identity). Two transcriptional start sites, at least one of them preceded by a sigma 70-dependent promoter, were identified. Provision of the H. pylori pfr gene on a multicopy plasmid resulted in reversal of the Fur-mediated repression of the fhuF gene in E. coli, thus enabling the use of the FURTA for cloning of the ferritin gene. Inactivation of the pfr gene, either by insertion of a resistance cassette or by deletion of the up- and downstream segments, abolished this function. Immunoblot analysis with a Pfr-specific antiserum detected the Pfr protein in H. pylori and in E. coli carrying the pfr gene on a plasmid. Pfr-deficient mutants of H. pylori were generated by marker-exchange mutagenesis. These were more susceptible than the parental strain to killing by various metal ions including irons, copper and manganese, whereas conditions of oxidative stress or iron deprivation were not discriminative. Analysis by element-specific electron microscopy revealed that growth of H. pylori in the presence of iron induces the formation of two kinds of cytoplasmic aggregates: large vacuole-like bodies and smaller granules containing iron in association with oxygen or phosphorus. Neither of these structures was detected in the pfr-deficient mutant strain. Furthermore, the ferritin accumulated under iron overload and the pfr-deficient mutant strains lacked expression of a 12 kDa protein which was negatively regulated by iron in the parental strain. The results indicate that the nonhaem-iron ferritin is involved in the formation of iron-containing subcellular structures and contributes to metal resistance of H. pylori. Further evidence for an interaction of ferritin with iron-dependent regulation mechanisms is provided.

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