Rare presentation of atrial myxoma: chest pain, dysphagia and left upper extremity weakness.

Atrial myxoma is a benign primary heart tumour, which can be found incidentally on imaging studies. It is usually located in the left atrium and may manifest as dyspnoea, chest pain, heart failure, cough, shortness of breath when rising from a recumbent position, haemoptysis, hoarseness and as a source of cardiac embolism. However, dysphagia caused by an atrial myxoma has been reported only twice in the literature. We present a 53-year-old Caucasian man with a chronic history of dysphagia caused by an atrial myxoma, in which surgical resection resulted in complete resolution of his dysphagia.

Superior mesenteric venous thrombosis complicating acute appendicitis: A case report.

RATIONALE: Superior mesenteric venous thrombosis (SMVT) is a rare condition that carries high mortality. Very few cases have been reported of SMVT, complicating acute appendicitis. Early recognition requires a high index of suspicion and is crucial in successful treatment of such a life-threatening condition. PATIENT CONCERNS: A 33-year-old male presents with a 4-day history of right lower abdominal pain, nausea and subjective fever. CT scan showed acute appendicitis and a central filling defect in the superior mesenteric vein. DIAGNOSES: Acute appendicitis complicated by SMVT. INTERVENTIONS: Intravenous antibiotics, appendectomy, and anticoagulation. OUTCOMES: Repeat CT scan showed successful resolution of the SMVT at a 3-month follow up. LESSONS: Clinical awareness and high index of suspicion are essential to diagnose and manage SMVT, a serious complication of acute appendicitis.

Bulk and rhizosphere soil bacterial communities studied by denaturing gradient gel electrophoresis: plant-dependent enrichment and seasonal shifts revealed.

The bacterial rhizosphere communities of three host plants of the pathogenic fungus Verticillium dahliae, field-grown strawberry (Fragaria ananassa Duch.), oilseed rape (Brassica napus L.), and potato (Solanum tuberosum L.), were analyzed. We aimed to determine the degree to which the rhizosphere effect is plant dependent and whether this effect would be increased by growing the same crops in two consecutive years. Rhizosphere or soil samples were taken five times over the vegetation periods. To allow a cultivation-independent analysis, total community DNA was extracted from the microbial pellet recovered from root or soil samples. 16S rDNA fragments amplified by PCR from soil or rhizosphere bacterium DNA were analyzed by denaturing gradient gel electrophoresis (DGGE). The DGGE fingerprints showed plant-dependent shifts in the relative abundance of bacterial populations in the rhizosphere which became more pronounced in the second year. DGGE patterns of oilseed rape and potato rhizosphere communities were more similar to each other than to the strawberry patterns. In both years seasonal shifts in the abundance and composition of the bacterial rhizosphere populations were observed. Independent of the plant species, the patterns of the first sampling times for both years were characterized by the absence of some of the bands which became dominant at the following sampling times. Bacillus megaterium and Arthrobacter sp. were found as predominant populations in bulk soils. Sequencing of dominant bands excised from the rhizosphere patterns revealed that 6 out of 10 bands resembled gram-positive bacteria. Nocardia populations were identified as strawberry-specific bands.

Co-operative binding of human fibronectin to Sfbl protein triggers streptococcal invasion into respiratory epithelial cells.

Streptococcal fibronectin binding protein I (SfbI) mediates adherence to and invasion of Streptococcus pyogenes into human epithelial cells. In this study, we analysed the binding activity of distinct domains of SfbI protein towards its ligand, the extracellular matrix component fibronectin, as well as the biological implication of the binding events during the infection process. By using purified recombinant SfbI derivatives as well as in vivo expressed SfbI domains on the surface of heterologous organism Streptococcus gordonii, we were able to dissociate the two major streptococcal target domains on the human fibronectin molecule. The SfbI repeat region exclusively bound to the 30 kDa N-terminal fragment of fibronectin, whereas the SfbI spacer region exclusively bound to the 45 kDa collagen-binding fragment of fibronectin. In the case of native surface-expressed SfbI protein, an induced fit mode of bacteria-fibronectin interaction was identified. We demonstrate that binding of the 30 kDa fibronectin fragment to the repeat region of SfbI protein co-operatively activates the adjacent SfbI spacer domain to bind the 45 kDa fibronectin fragment. The biological consequence arising from this novel mode of fibronectin targeting was analysed in eukaryotic cell invasion assays. The repeat region of SfbI protein is mediating adherence and constitutes a prerequisite for subsequent invasion, whereas the SfbI spacer domain efficiently triggers the invasion process of streptococci into the eukaryotic cell. Thus, we were able to dissect bacterial adhesion from invasion by manipulating one protein. SfbI protein therefore represents a highly evolved prokaryotic molecule that exploits the host factor fibronectin not only for extracellular targeting but also for its subsequent activation that leads to efficient cellular invasion.

Characterization of group B streptococcal invasion in HEp-2 epithelial cells.

The invasion of group B streptococci (GBS) in HEp-2 epithelial cells was analyzed by electron microscopy and a quantitative antibiotic survival assay. Invasion of GBS involved intimate attachment of streptococcal chains, engulfment of the adherent bacteria by cellular protrusions, entry of the bacteria in a 'polar' fashion and formation of membrane-bound vacuoles in which most of the intracellular streptococci resided. At later stages of infection bacteria were also found free in the cytoplasm. Efficient uptake of streptococci by HEp-2 cells occurred within 20 min and live intracellular bacteria were detectable up to 48 h post-infection. Invasion of GBS required activation of the eukaryotic actin microfilament system involving, at least partially, protein kinase signal transduction pathways. Invasion was inhibited in a dose-dependent manner by decreasing extracellular Ca2+ levels as well as by substances known to interfere with eukaryotic calcium regulatory systems. These results suggest that GBS invade HEp-2 cells by triggering calcium-dependent phagocytosis-like internalization mechanisms and persist intracellularly both in vacuoles and free in the cytoplasm.