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J Nephrol. 2002 Mar-Apr;15(2):183-5.
Compartment syndrome, rhabdomyolysis and risk of acute renal failure as complications of the lithotomy position.

Bocca G, van Moorselaar JA, Feitz WF, van der Staak FH, Monnens LA.

Department of Pediatrics, University Medical Centre St Radboud, Nijmegen, The Netherlands.

Compartment syndrome, rhabdomyolysis and the risk of acute renal failure are potential complications of the lithotomy position. A six-year-old girl is described who developed a compartment syndrome with rhabdomyolysis after prolonged surgery in the lithotomy position. This complication occurred three times over ten years in our hospital. Rhabdomyolysis may induce acute renal failure. The pathogenesis of rhabdomyolysis--induced renal failure has not yet been elucidated. However, forced diuresis by intravenous administration of mannitol and furosemide can prevent acute renal failure.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12018636&dopt=Abstract

J Med Microbiol. 2002 Jun;51(6):468-78.
Identification of medically important pathogenic fungi by reference strand-mediated conformational analysis (RSCA).

McIlhatton BP, Keating C, Curran MD, McMullin MF, Barr JG, Madrigal JA, Middleton D.

Northern Ireland Regional Histocompatibility and Immunogenetics Laboratory, City Hospital, Belfast, Northern Ireland. Brian.McIlhattoll.n-i.nhs.uk

This report describes the application of reference strand-mediated conformational analysis (RSCA), a novel DNA typing technique, for the identification of clinically significant fungal pathogens. RSCA is a heteroduplex-based conformational method which relies on detecting differences in the DNA conformation of heteroduplexes generated in this study by the annealing of different fungal 18S rRNA amplicons to a common fluorescent-labelled reference (FLR). These heteroduplexes are then observed with laser-based instrumentation and computer software to detect differences in the DNA conformation reproducibly. This technique was shown to generate unique and reproducible profiles for the 18S rRNA gene sequences of a number of medically important fungi, distinguishing different Candida species (C. albicans, C. kefyr, C. dubliniensis, C. lusitaniae, C. guilliermondii, C. tropicalis, C. krusei, C. glabrata, C. sake and C. parapsilosis), and in some cases detecting single nucleotide differences between 18S rRNA sequences. The RSCA technique was further evaluated with 50 human clinical isolates of Candida spp., previously identified by culture techniques, and was shown to identify the isolates correctly. This technique displays enormous potential as an alternative to DNA sequence determination and has the potential to become an automated technique that can be implemented in the routine setting.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12018653&dopt=Abstract

J Med Microbiol. 2002 Jun;51(6):484-90.
Role of the respiratory burst in co-operative reduction in neutrophil survival by influenza A virus and Escherichia coli.

Engelich G, White M, Hartshorn KL.

Department of Medicine and Pathology, Boston University School of Medicine, MA 02218, USA.

Influenza A virus (IAV)-induced impairment of neutrophil function or survival may be a cause of bacterial superinfection of IAV-infected subjects. This study was performed to determine the mechanism through which the combination of IAV and Escherichia coli co-operatively reduces neutrophil survival. Neutrophil binding of annexin-V and caspase-3 activation was significantly increased by either IAV or E. coli, supporting the concept that the micro-organisms accelerate neutrophil apoptosis. The anti-apoptotic agent granulocyte-macrophage colony stimulating factor (GM-CSF) did not improve, but further reduced, survival of neutrophils treated with IAV and E. coli. As addition of E. coli resulted in greater neutrophil uptake of IAV and greater neutrophil respiratory burst responses to IAV, this study tested whether respiratory burst activation by IAV and E. coli contributes to reducing neutrophil survival. The cell-permeant NADPH oxidase inhibitor, diphenylene iodonium, significantly increased survival of neutrophils treated with either E. coli alone or the combination of IAV and E. coli. In contrast, catalase, which is not cell permeant, did not alter survival of E. coli- and IAV-treated neutrophils. Azide enhanced neutrophil hydrogen peroxide responses to IAV and E. coli, and reduced survival of these cells. These results indicate that co-operative induction of intracellular respiratory burst responses by IAV and E.coli mediates the reduced neutrophil survival caused by these pathogens in vitro.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12018655&dopt=Abstract

J Med Microbiol. 2002 Jun;51(6):495-502.
Helicobacter pylori adherence to gastric epithelial cells: a role for non-adhesin virulence genes.

Zhang ZW, Dorrell N, Wren BW, Farthingt MJ.

Division of Surgery, Bristol Royal Infirmary, University of Bristol, UK. z.w.zhanristol.ac.uk

Helicobacter pylori is a major aetiological agent in gastroduodenal disorders and adherence of the bacteria to the gastric mucosa is one of the initial stages of infection. Although a number of specific adhesins has been identified, other H. pylori virulence factors may play a role in adherence to gastric epithelial cells directly or through interaction with other adhesins. This study assessed the effect of 16 H. pylori virulence factors on the adherence of the bacteria to gastric AGS cells and on gastric epithelial cell cycle distribution. Defined isogenic H. pylori SS1 mutants were used. After co-incubation of gastric AGS cells and bacteria, adherence of H. pylori to AGS cells was visualised by immunofluorescence microscopy and quantified by flow cytometry. Cell cycle phase distribution was analysed by flow cytometry with propidium iodide staining. Mutants were tested for their ability to adhere to AGS cells and compared with the wild-type SS1 strain. Mutations in genes in the cag pathogenicity island showed that cagP and cagE mutants adhered less than the wild-type strain to AGS cells, whereas a cagF mutant showed no reduction in adherence. Mutations in genes involved in flagellar biosynthesis showed that the adherence ability of fliQ, fliM and fliS mutants was reduced, but a flhB mutant possessed wild-type levels of adherence. Mutations in genes coding for the urease (ureB) and phospholipase (pldA) enzymes did not affect adherence, but mutation of the tlyA gene encoding an H. pylori haemolysin resulted in a reduced adherence. A fliQ mutant, with reduced adherence to AGS cells, was less able to induce AGS cell apoptosis than SS1. The ability to induce G0G1 cell cycle arrest was also abolished in the fliQ mutant. However, an increased cell number in S phase was observed when AGS cells were exposed to the fliQ mutant compared with SS1, suggesting that unattached bacteria may still be able to stimulate cell proliferation. In addition to known adhesins, other bacterial virulence factors such as CagE, CagP, FliQ, FliM, FliS and TlyA appear to play a role in H. pylori adherence to gastric epithelial cells. Mutations in these genes may affect H. pylori pathogenicity by reducing either the ability of the bacteria to attach to gastric epithelial cells or the intensity of bacteria-host cell interactions.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12018657&dopt=Abstract

Am J Med Sci. 2002 May;323(5):279-80.
Fatal acute myocardial infarction during severe thrombocytopenia in a patient with idiopathic thrombocytopenic purpura.

Fruchter O, Blich M, Jacob G.

Recanati Autonomic Dysfunction Center, Department of Internal Medicine C, Rambam Medical Center, Haifa, Israel.

Because platelets play a major role in most thrombotic events, it is not surprising that all cases of myocardial infarctions in patients with idiopathic thrombocytopenic purpura (ITP) have been reported to occur only when platelets counts begin to rise. We report on a 69-year-old man with ITP who had acute myocardial infarction while he was severely thrombocytopenic (2000/microL). We hypothesize that the pathogenesis of myocardial infarction in thrombocytopenic patients with ITP may result from endothelial damage induced by autoantibodies directed against antigens present on both platelets and coronary endothelial cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12018673&dopt=Abstract

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