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Background Acute appendicitis is one of the most common emergency requiring operation. As the first discovered coagulation factor, plasma fibrinogen frequently increases with inflammation due to the activation of coagulation. The aim of this retrospective study was to investigate the diagnostic value of hyperfibrinogenemia as a preoperative laboratory marker for appendiceal perforation in patients with acute appendicitis. Materials and methods We identified 455 patients (202 females, 253 males; mean age, 31.7 years) with histologically confirmed acute appendicitis who underwent laparoscopic or open appendectomy. Results of preoperative laboratory values and post-operative histologic results were analysed retrospectively. A multivariate logistic regression model was performed to determine patient's age and laboratory tests associated with perforated appendicitis. Result Mean plasma fibrinogen level of all patients was 3.99 g/L (1.41 SD; range, 1.73–10.6 g/L; median, 3.69 g/L). Patients with appendiceal perforation had a mean fibrinogen level of 5.72 g/L (1.52 SD; range, 3.38–10.04 g/L; median, 5.28 g/L), which was significantly higher than those with nonperforated groups (P = 0.001). Multivariate analysis showed fibrinogen and D-dimer were associated with perforation (P = 0.001, P = 0.014, respectively). Areas under the receiver operating characteristic curve of fibrinogen for discriminating acute perforated appendicitis from non-perforated groups were larger than white blood cell and D-dimer. Conclusions Hyperfibrinogenemia was common in patients with acute appendicitis and fibrinogen may be useful as a predictive factor for appendiceal perforation.

Escherichia coli K-12 carries a gene for a protein denoted ClyA or SheA that can mediate a cytolytic phenotype. The ClyA protein is not expressed at detectable levels in most strains of E. coli, but overproduction suitable for purification was accomplished by cloning the structural gene in an hns mutant strain. Highly purified ClyA protein was cytotoxic to macrophage cells in culture and caused detachment and lysis of the mammalian cells. Results from osmotic protection assays were consistent with the suggestion that the protein formed pores with a diameter of up to 3 nm. Using Acholeplasma laidlawii cells and multilamellar liposomes, we studied the effect of ClyA on membranes with varying compositions and in the presence of different ions. ClyA induced cytolytic release of the fluorescent tracer from carboxyfluorescein-loaded liposomes, and the release was stimulated if cholesterol was present in the membranes whereas addition of calcium had no effect. Pretreatment of the ClyA protein with cholesterol inhibited the pore formation, suggesting that ClyA could bind to cholesterol. Efficient coprecipitation of ClyA with either cholesterol or 1,2,3-trioctadecanoylglycerol in aqueous solutions showed that ClyA directly interacted with the hydrophobic molecular aggregates. We tested the possible functional importance of selected ClyA protein regions by site-directed mutagenesis. Defined mutants of ClyA were obtained with alterations in postulated transmembrane structures in the central part and in a postulated membrane-targeting domain in the C-terminal part. Our results were consistent with the suggestion that particular amphiphilic segments are required for ClyA activity. We propose that these domains are necessary for ClyA to form pores.

One hundred and seventy-two strains of Escherichia coli isolated from diarrheal patients in Beijing, P. R. China, were analyzed for plasmid DNA profile, HEp-2 cell adherence ability and reactivity to 10 previously described DNA probes. They had not been recognized as pathogenic E. coli in China. Of the 110 strains tested, 76 (69%) contained one or multiple large plasmids. Of the 71 strains with the large plasmids 64 could adhere to HEp-2 cells. Of the 172 strains, 102 (59.3%) were hybridized with at least one of the 10 probes. Of those, seven strains hybridized with enteroaggregative E. coli (EAggEC) probe. Their serotypes were O128 (two strains), O6 (one strain), and O111 (one strain). Three strains were untypable. Six and three strains were hybridized with enteropathogenic E. coli (EPEC) attaching and effacing genes (eae) or EPEC adherence factor (EAF) probe, respectively. Two non-O157: H7 strains hybridized with enterohemorrhagic E. coli (EHEC) probe. Seventy-two strains (41.9%) hybridized with shiga-like toxin 2 or 1 (SLT2 or SLT1) probes. Among the SLT1 or SLT2 probe-positive strains, 54 hybridized with invasive (INV) plasmid probe developed for identification of enteroinvasive E. coli (EIEC) and Shigella species. The INV and SLT probe-positive strains might represent a new variety of verotoxin-producing E. coli (VTEC).