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Biomedical subjects

S Jenner

Publications and source records attributed to S Jenner.

At least 19 recordsLinked to original sources
PubMed2005

Identification of methicillin-resistant Staphylococcus aureus (MRSA): Comparison of a new molecular genetic test kit (GenoType MRSA) with standard diagnostic methods.

Results obtained from 188 isolates of staphylococci using standard diagnostic methods for identifying MRSA were compared with those achieved with a newly available molecular genetic test kit, the GenoType, Version 1, MRSA (Hain Lifescience GmbH, Nehren, Germany). The GenoType MRSA detects the mecA gene and, in addition, a highly specific sequence for Staphylococcus aureus (S. aureus) by polymerase chain reaction (PCR) and reverse hybridization. There was a 100% overall correlation between the results of conventional and molecular genetic testing. 143 isolates were tested positive for MRSA, 10 isolates were identified as oxacillin-sensitive Staphylococcus aureus strains (MSSA), and 35 isolates were coagulase-negative staphylococci of various species. However, five of the 143 MRSA strains yielded ambiguous results with the first line standard tests and therefore required additional testing leading to delay of definitive diagnosis. As expected, mecA could not only be detected in MRSA strains, but also in coagulase-negative staphylococci. The reliable identification as S. aureus from the same isolate is therefore an essential prerequisite for MRSA diagnosis. The GenoType MRSA fulfills this requirement by parallel detection of a S. aureus-specific sequence and the mecA gene. Molecular genetic testing with the GenoType MRSA kit needs much less time than conventional microbiological methods. Therefore genetic testing provides not only a considerable advantage with respect to reliability but also to speed.

Bacterial Proteins↗
PubMed2000

A role for the actin cytoskeleton in the initiation and maintenance of store-mediated calcium entry in human platelets. Evidence for conformational coupling.

The nature of the mechanism underlying store-mediated Ca(2+) entry has been investigated in human platelets through a combination of cytoskeletal modifications. Inhibition of actin polymerization by cytochalasin D or latrunculin A had a biphasic time-dependent effect on Ca(2+) entry, showing an initial potentiation followed by inhibition of Ca(2+) entry. Moreover, addition of these agents after induction of store-mediated Ca(2+) entry inhibited the Ca(2+) influx mechanism. Jasplakinolide, which reorganizes actin filaments into a tight cortical layer adjacent to the plasma membrane, prevented activation of store-mediated Ca(2+) entry but did not modify this process after its activation. In addition, jasplakinolide prevented cytochalasin D-induced inhibition of store-mediated Ca(2+) entry. Calyculin A, an inhibitor of protein serine/threonine phosphatases 1 and 2 which activates translocation of existing F-actin to the cell periphery without inducing actin polymerization, also prevented activation of store-mediated Ca(2+) entry. Finally, inhibition of vesicular transport with brefeldin A inhibited activation of store-mediated Ca(2+) entry but did not alter this mechanism once initiated. These data suggest that store-mediated Ca(2+) entry in platelets may be mediated by a reversible trafficking and coupling of the endoplasmic reticulum with the plasma membrane, which shows close parallels to the events mediating secretion.

Actins↗
PubMed2000

Maternal behaviors associated with smothering: a preliminary descriptive study.

OBJECTIVES: To describe maternal behavior in 15 women identified as having smothered their children. DESIGN: A descriptive study of maternal behavior and interaction with her child, using videotapes of mother and child together. These were obtained by covert video surveillance in a hospital setting. Maternal behavior was rated using an assessment schedule designed to be used with video. RESULTS: The mothers showed a range of behaviors. Three groups emerged; one whose interaction with the child resembled normal maternal behavior, a second who interacted in a hostile way, and a third who showed a paucity of interaction. CONCLUSION: These preliminary data suggest that smothering may reflect more than one type of abnormal maternal relationship or attitude towards children. This may have implications for treatment and prognosis.

Adult↗
PubMed2000

Two pathways for store-mediated calcium entry in human platelets.

In human platelets and other non-excitable cell types depletion of the intracellular calcium stores promotes calcium entry across the plasma membrane. Although the mechanism of this store-mediated calcium entry remains uncertain, it has been suggested that a tyrosine phosphorylation step could be involved. In support of this hypothesis various tyrosine kinase inhibitors have been shown to reduce store-mediated calcium entry in platelets, although this inhibition is never complete. Here we investigate the properties of store-mediated calcium entry in human platelets during the time course of its activation. Our data suggest that at least two pathways may contribute to store-mediated calcium entry in these cells. An early component, activated soon after the initiation of Ca2+ store depletion, is insensitive to trivalent cations, SKF 96365 and tyrosine kinase inhibitors. This is followed by a second component which is inhibited by La3+, SKF 96365 and by tyrosine kinase inhibitors. These results suggest a role for tyrosine kinases in generating only the later stages of store-mediated calcium entry in platelets and may explain the incomplete inhibition of this pathway by inhibitors of tyrosine kinases.

Androstadienes↗
PubMed1997

Purinoceptor-evoked calcium signalling in human platelets.

ADP evokes a rise in platelet cytosolic Ca2+ concentration by stimulating Ca2+ entry and releasing Ca2+ from intracellular stores. Single cell studies indicate that the response consists of a series of spikes in cytosolic Ca2+. The release of stored Ca2+ is mediated by the generation of inositol 1,4,5-trisphosphate. Store depletion in turn leads to activation of a store-regulated Ca2+ entry pathway via a mechanism which appears to involve a protein tyrosine phosphorylation step. Preceding these events, ADP activates a receptor-operated non-selective cation channel, which mediates the entry of Ca2+ and Na+ with a latency of just a few milliseconds. Recent studies indicate that this channel is activated via a P2X1 purinoceptor at which ATP and diadenosine tetraphosphate are agonists. This receptor is distinct from that leading to the release of stored Ca2+ and to store-regulated Ca2+ entry.

Adenosine Diphosphate↗
PubMed1996

Wortmannin inhibits store-mediated calcium entry and protein tyrosine phosphorylation in human platelets.

The effects of the WT on store-mediated Ca2+ entry and protein tyrosine phosphorylation were investigated in fura-2-loaded human platelets. Wortmannin (2 microM) attenuated the rise in [Ca2+]i caused by Ca2+ entry while having no effect on the mobilisation of Ca2+ from internal stores. It also reduced store-depletion-evoked protein tyrosine phosphorylation. These findings demonstrate that WT is an inhibitor of tyrosine phosphorylation and store-mediated calcium entry and provide further evidence for the involvement of a tyrosine phosphorylation step in the link between Ca2+ store depletion and Ca2+ influx in human platelets.

Androstadienes↗
PubMed1996

Ionomycin-stimulated arachidonic acid release in human platelets: a role for protein kinase C and tyrosine phosphorylation.

Collagen (10-90 micrograms/ml) and ionomycin (1 microM; a calcium ionophore) each evoked rises in intracellular free calcium, protein kinase C activity and arachidonic acid release in human platelets, and as previously demonstrated for collagen, ionomycin (1 microM) stimulated protein tyrosine phosphorylation. However, at lower concentrations (60 and 250 nM) ionomycin selectively mobilised calcium. Ro31-8220 (a selective inhibitor of protein kinase C) inhibited (by 50%) ionomycin-stimulated arachidonic acid release. Genistein (an inhibitor of protein tyrosine kinases) also reduced by 50% ionomycin-stimulated arachidonic acid release. In combination, genistein and Ro31-8220 abolished ionomycin-stimulated arachidonic acid release. These findings show 1) that a rise in calcium is not sufficient, and 2) the activation of both protein kinase C and protein tyrosine phosphorylation is necessary, for full ionomycin-stimulated arachidonic acid release in human platelets.

Arachidonic Acid↗
PubMed1994

The effect of calcium-store depletion and refilling with various bivalent cations on tyrosine phosphorylation and Mn2+ entry in fura-2-loaded human platelets.

To investigate the possible involvement of tyrosine phosphorylation in the process of store-regulated Ca2+ entry, ionomycin (in the presence of EGTA) was used to deplete the intracellular Ca2+ stores of fura-2-loaded human platelets, and the effect of refilling with Ca2+, Ba2+ or Sr2+ evaluated. Depletion of the intracellular Ca2+ stores resulted in an increase in protein tyrosine phosporylation. This increase is reversed when the stores were refilled in Ca2+ or Sr2+, but not Ba2+. Refilling of the stores with Ca2+ or Sr2+, but not Ba2+, suppressed Mn2+ entry. These findings support the hypothesis that tyrosine phosphorylation plays a role in mediating store-regulated Ca2+ entry in human platelets and provides evidence for tyrosine phosphatase activity regulated by the Ca2+ content of the intracellular stores.

Barium↗
PubMed1981

Serotonin neurotoxins: recent advances in the mode of administration and molecular mechanism of action.

1. Slow infusion of 5,7-DHT into the left lateral ventricle of nomifensine pretreated, pentobarbitone anaesthetized rats produces moderate, asymmetric regional forebrain 5-HT depletions 24 h after the injection; rapid pulse injection of 5,7-DHT results in more extensive and almost symmetric 5-HT reductions. By the eighth day, both injection procedures cause a comparable pattern of 5-HT depletion throughout the CNS. RAdioactivity distribution patterns (following 14C-5,7-DHT) correlate with the characteristics of 5-HT depletions. The type of anaesthetic used (pentobarbitone; pentobarbitone plus ketamine; ether) has little, if any, influence on the long-term 5-HT reductions in the rat CNS. 2. In forebrain regions, near the ventricle, nomifensine does not totally protect catecholamine fibre systems when pentobarbitone is used as the anaesthetic. However, optimum selectivity is provided by a combination of DMI and nomifensine in animals anaesthetized with a combination of pentobarbitone and ketamine. 3. Reaction of 5,6- and 5,7-DHT with oxygen is essential for these drugs to act as neurotoxins. Both drugs interact with the electron transfer chain of mitochondria (at the site of complex III) resulting in accelerated formation of reactive quinoidal intermediates. Metabolism of 5,7-DHT by MAO contributes to the overall in vivo neurotoxicity of this m-substituted dihydroxytryptamine.

5,7-Dihydroxytryptamine↗
PubMed1980

Structural and biochemical changes in rat cerebral cortex after neonatal 6-hydroxydopamine administration.

Newborn rats received an intracisternal injection of 6-hydroxydopamine (100 micrograms) within 16 h after birth. Treatment effects upon noradrenaline uptake (with or without desmethylimipramine pre-incubation), endogenous noradrenaline, dopamine, and serotonin were biochemically assayed. Noradrenaline uptake and endogenous noradrenaline content were permanently reduced to less than 5% of control values. Reduction of endogenous dopamine content was less marked: at day 60, values were about 40% of controls. Serotonin content remained unaffected. Cell density countings in postnatal day 15 temporal cortex revealed an about 16% reduction in layers II and III of treated animals. These modifications of cortical geometry were discussed with reference to measurements of cortical thickness and ultrastructural observations on postnatal days 2, 5 and 15. Both supranormal involution and growth processes might result from the neurotoxin treatment. Whereas some of the degeneration processes might be due o general cytotoxic effects, this is less likely for the supranormal growth processes.

Animals↗
PubMed1980

In vivo labelling of alpha-adrenoceptor-binding sites and membrane-bound extraneuronal transport sites in the urinary bladder of the rat by 3H-ST-1059 and 3H-phentolamine. An autoradiography study.

An attempt was made to trace alpha-adrenoceptor-binding sites in the lower urinary tract tissue of the rat by means of analyzing the distribution of radioactivity in autoradiograms of freeze-dried or glutaraldehyde-fixed tissue following intravenous injection of an alpha-agonist, 3H-ST-1059, or an alpha-antagonist, 3H-phentolamine. Both drugs were rapidly excreted into the urine and reabsorbed by the bladder mucosa. This is evidenced by the presence of high amounts of silver grains superimposed onto the epithelium and bordering the lamina propria structures 10-30 min after intravenous injection of 3H-ST-1059 or 3H-phentolamine in rats not subjected to ligation of their ureters. In rats that underwent ligation of their abdominal ureters prior to intravenous injection of 3H-ST-1059 or 3H-phentolamine, silver grains were preferentially localized over the plasmalemmata of smooth muscle cells and fibroblasts of the detrusor and trigonum of the urinary bladder. Phentolamine and phenoxybenzamine but not propranolol counteracted the labelling of the plasma membranes of smooth muscle cells, fibroblasts and striated muscle fibres of the pelvic floor by low doses of 3H-ST-1059 and 3H-phentolamine, suggesting that both drugs have affinity to alpha-adrenoceptor-agonist and alpha-adrenoceptor-antagonist binding sites. Since phentolamine and phenoxybenzamine as well as hydrocortisone pretreatment also attenuated the accumulation of radiolabel in the perikarya of the three types of cells mentioned, both drugs--at the concentration used--are also substrates for membrane-bound carriers, such as uptake two according to Iversen. A more selective in vivo demonstrationof alpha-agonist-binding and alpha-antagonist-binding sites requires drugs of higher specific activity than available at present.

Adrenergic alpha-Agonists↗