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Biomedical subjects

L M Brady

Publications and source records attributed to L M Brady.

10 recordsLinked to original sources
PubMed1998

Polyenylphosphatidylcholine inhibits PDGF-induced proliferation in rat hepatic stellate cells.

Polyenylphosphatidylcholine (PPC), a polyunsaturated phospholipid extract from soy beans, prevents the development of liver cirrhosis in animal models. Its mechanism of action is unknown. Based on the hypothesis that PPC might act by decreasing hepatic stellate cell proliferation, we studied the effect of PPC and its main components, dilinoleoylphosphatidylcholine (DLPC) and palmitoyl-linoleoylphosphatidylcholine (PLPC), on PDGF-induced stellate cell proliferation and intracellular signal transduction. Normal rat hepatic stellate cells in tissue culture were serumstarved, and incubated with 10ng/ml PDGF in the absence or presence of phospholipids. Cell proliferation was measured by 3H-thymidine incorporation. P44MAPK activation was determined by kinase assay, and AP-1 binding by electrophoretic mobility shift assay. PPC (200 ng/ml) significantly inhibited PDGF-induced proliferation (p < 0.05; ANOVA, n = 3) and antagonized PDGF-induced P44MAPK activation and AP-1 binding. This effect was mimicked by DLPC but not by PLPC. Neither DLPC nor PLPC prevented PDGF receptor activation. We conclude that PPC exerts a previously unrecognized effect on mitogen-induced stellate cell proliferation which may be mediated by DLPC. Inhibition of this cascade represents a potential mechanism for the inhibitory effect of PPC on hepatic fibrogenesis.

Animals↗
PubMed1996

Bile acid stimulation of early growth response gene and mitogen-activated protein kinase is protein kinase C-dependent.

Hepatic stellate cells are exposed to elevated bile acid levels during hepatic injury and fibrogenesis. Upon activation, the stellate cell becomes a major effector cell during the development of hepatic fibrosis and cirrhosis. Bile acids may function as costimulatory signalling molecules. This hypothesis was tested in vitro using rat-derived hepatic stellate cells. Bile acids were studied at concentrations that occur during cirrhosis in vivo. Conjugated and unconjugated bile acids rapidly induced egr and fos gene expression as well as cytoplasmic mitogen-activated protein kinase (MAPK) activation. Protein kinase C was required for both egr induction and MAPK activation. These studies imply that bile acids could contribute to the perpetuation of hepatic fibrosis by helping to keep the stellate cell in an activated state.

Animals↗
PubMed1995

Protein kinase C and mitogen-activated protein kinase are required for 1,25-dihydroxyvitamin D3-stimulated Egr induction.

Recent studies have demonstrated that 1,25-dihydroxyvitamin D3 (D3) can activate Raf kinase and induce Egr expression in cultured rat hepatic Ito cells (Lissoos, T. W., Beno, D. W. A., and Davis, B. H. (1993) J. Biol. Chem. 268, 25132-25138). Since Raf is an upstream activator of mitogen-activated protein kinase (MAPK), the current study evaluated the ability of D3 to activate MAPK. D3-activated MAPK and induced its cytoplasmic to perinuclear translocation in Ito cells. MAPK activation was found to be protein kinase C-dependent, which was analogous to previous studies of D3 and Raf activation. To further explore the D3 cascade, a series of transient transfections were performed using dominant negative raf and MAPK mutant plasmids which effectively block Ras-induced Raf and MAPK activity, respectively. D3 induced a marked increase in the expression of a chloramphenicol acetyltransferase reporter gene linked to the Egr promoter (egr-CAT). When the dominant negative Raf plasmid was co-transfected, there was no significant reduction in egr-CAT. In contrast, when the dominant negative MAPK plasmid was co-transfected, egr-CAT induction was completely abolished. These results suggest that 1) D3 stimulates MAPK via a protein kinase C-dependent pathway, 2) D3-induced Egr expression can occur via a pathway independent of Ras-induced Raf, and 3) D3 absolutely requires MAPK activity for Egr expression.

Animals↗
PubMed1990

Successful control of endemic MRSA in a cardiothoracic surgical unit.

After a substantial increase in the prevalence of methicillin-resistant Staphylococcus aureus (MRSA) in the Cardiothoracic Surgical Unit at St. Vincent's Hospital, Sydney, a prospective study was undertaken in early 1986 to ascertain the carrier status of all patients entering the Unit. Of 84 patients, 27.4% were found to carry MRSA and the perineum was the major site of carriage, with 69.6% of MRSA positive cases carrying the organism in this site. As a result of these findings, the period of perioperative antibiotic cover was shortened, whole-body washing of patients with a 1% triclosan preparation was instituted and routine postoperative perineal swabs were taken. During the 18 months after implementation of these policies, a highly significant reduction in the number of MRSA carriers and infections was observed. The monitoring of perineal colonization proved to be a useful marker for increases in MRSA in the Unit.

Carrier State↗
PubMed1985

MRSA revisited.

Explore the source record for details and available documents.

Humans↗
PubMed1984

Vibrio vulnificus septicaemia.

A patient, who had been receiving treatment for refractory anaemia with excess of myeloblasts for three years, developed septic shock due to Vibrio vulnificus septicaemia. The infection was believed to have been introduced with the ingestion of raw oysters. This organism is comparatively rare, but it can cause serious infection, and is known to be capable of very rapid tissue invasion.

Female↗
PubMed1983

Pasteurella ureae meningitis.

A 54-year-old man, with a history of alcohol abuse and previous skull fractures, developed a low-grade meningitis. The causative organism was Pasteurella ureae, an uncommon cause of bacterial infection, which has not been reported previously in Australia. The patient recovered after therapy with penicillin. A review of the cases of serious infection with this organism suggests that liver disease and skull trauma are common predisposing factors. Problems with the identification of P.ureae may be encountered unless its particular biochemical properties are recognized.

Humans↗
PubMed1981

Serratia cross-infection in an intensive therapy unit.

During a 10-week period, 11 patients were involved in an outbreak of cross-infection with a non-pigmented strain of Serratia marcescens resistant to sulphonamides, trimethoprim, ampicillin, tetracycline, chloramphenicol, cephalexin, gentamicin, tobramycin, colistin, ticarcillin and kanamycin. The problem was confined to the intensive therapy areas of the hospital. The organism was apparently spread by a nursing sister who harboured it in a paronychial lesion. Prolonged carriage of S. marcescens was demonstrated. Methods of investigation of the outbreak and the measures adopted to terminate it are described.

Aged↗