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S Bodin

Publications and source records attributed to S Bodin.

14 recordsLinked to original sources
PubMed2004

[The Voice Handicap Index: impact of the translation in French on the validation].

The aim of this prospective investigation was to validate a French version of the Voice Handicap Index (VHI). A population of 52 normal subjects and 63 patients with voice disorders replied to the questionnaire at the day of their first consultation and ten to thirty days after the consultation (before any treatment). Reproducing the methodology of the American authors, the test-retest reliability and the internal consistency reliability were measured. The validity and the sensibility related to a non dysphonic population were also analysed. Regarding the normal subjects, the maximum scores for total score and subscale scores were 20 (total), 12 (physical), 7 (functional), 6 (Emotional). These scores are statistically different when compared with pathological subjects (p < 0.00001). Test-Retest stability of the pathological subjects was found to be satisfactory for both total score and subscale scores (r > 0.87). From this data set, the critical difference scores were derived for the VHI total score (15 points), for the physical subscale (9 points) and for the functional and emotional.subscales (6 points each). As for as the internal consistency reliability, Cronbach's alpha is correct (r > 7) for the pathological subjects. Yet, the analysis of the validity reply by reply, reveals some abnormalities. In conclusion, the validity of the French translation of the VHI is confirmed but the results prompt us to improve the quality of the translation.

Adult↗
PubMed2001

Production of phosphatidylinositol 3,4,5-trisphosphate and phosphatidic acid in platelet rafts: evidence for a critical role of cholesterol-enriched domains in human platelet activation.

Glycosphingolipid- and cholesterol-enriched membrane microdomains, called rafts, can be isolated from several mammalian cells, including platelets. These microdomains appear to play a critical role in signal transduction in several hematopoietic cells, but their function in blood platelets remains unknown. Herein, we first characterized the lipid composition, including the fatty acid composition of phospholipids, of human platelet rafts. Then their role in platelet activation process was investigated. Interestingly, thrombin stimulation led to morphological changes of rafts correlating with the production of lipid second messengers in these microdomains. Indeed, we could demonstrate for the first time that a large part of the stimulation-dependent production of phosphatidic acid and phosphoinositide 3-kinase products was concentrated in rafts. Moreover, cholesterol depletion with methyl-beta-cyclodextrin disrupted platelet rafts, dramatically decreased the agonist-dependent production of these lipid signaling molecules, and impaired platelet secretion and aggregation. Cholesterol repletion restored the physiological platelet responses. Altogether our data indicate that rafts are highly dynamic platelet membrane structures involved in critical signaling mechanisms linked to the production of lipid second messengers. The demonstration of phosphatidylinositol 3,4,5-trisphosphate production in rafts may have general implications for the understanding of the role of this key second messenger found ubiquitously in higher eucaryotic cells.

Blood Platelets↗
PubMed2001

Phosphoinositides: key players in cell signalling, in time and space.

Over the last few years, many reports have extended our knowledge of the inositol lipid metabolism and brought out some exciting information about the location, the variety and the role of phosphoinositides (PIs). Besides the so-called "canonical PI pathway" leading to the production of phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2), the precursor of the intracellular second messengers inositol 1,4,5-trisphosphate and diacylglycerol (DAG), many other metabolic pathways have been identified to produce seven different polyphosphoinositides. Several of these quantitatively minor lipid molecules appear to be specifically involved in the control of cellular events, such as the spatial and temporal organisation of key signalling pathways, the rearrangement of the actin cytoskeleton or the intracellular vesicle trafficking. This is consistent with the fact that many of the enzymes, such as kinases and phosphatases, involved in the tight control of the intracellular level of polyphosphoinositides, are regulated and/or relocated through cell surface receptors for extracellular ligands. The remarkable feature of PIs, which can be rapidly synthesised and degraded in discrete membrane domains or even subnuclear structures, places them as ideal regulators and integrators of very dynamic mechanisms of cell regulation. In this review, we will summarise recent studies on the potential location, the metabolic pathways and the role of the different PIs. Some aspects of the temporal synthesis of D3 PIs will also be discussed.

Animals↗
PubMed2000

The integrin alpha IIb/beta 3 in human platelet signal transduction.

Platelets are critical for the maintenance of the integrity of the vascular system and are the first line of defence against haemorrhage. When they encounter a subendothelial matrix exposed by injury to a vessel, platelets adhere, are activated, and become adhesive for other platelets so that they aggregate. alpha IIb/beta 3, a platelet-specific integrin, is largely prominent amongst the adhesion receptors and is essential for platelet aggregation. The ligands for alpha IIb/beta 3 are the multivalent adhesive proteins fibrinogen and von Willebrand factor. In resting platelets, alpha IIb/beta 3 is normally in a low activation state, unable to interact with soluble fibrinogen. Stimulation of platelets with various agonists will induce a conformational change in alpha IIb/beta 3 (inside-out signalling), which is then able to bind soluble fibrinogen resulting in the onset of platelet aggregation. However, fibrinogen binding to its membrane receptor is not simply a passive event allowing the formation of intercellular bridges between platelets. Indeed, a complex signalling pathway triggered by integrin ligation and clustering (outside-in signalling) will regulate the extent of irreversible platelet aggregation and clot retraction. Amongst the signalling enzymes activated downstream of alpha IIb/beta 3 engagement, phosphoinositide 3-kinase plays an important role in the control of the irreversible phase of aggregation.

Animals↗
PubMed2000

Myotubularin, a phosphatase deficient in myotubular myopathy, acts on phosphatidylinositol 3-kinase and phosphatidylinositol 3-phosphate pathway.

Myotubular myopathy (MTM1) is an X-linked disease, characterized by severe neonatal hypotonia and generalized muscle weakness, with pathological features suggesting an impairment in maturation of muscle fibres. The MTM1 gene encodes a protein (myotubularin) with a phosphotyrosine phosphatase consensus. It defines a family of at least nine genes in man, including the antiphosphatase hMTMR5/Sbf1 and hMTMR2, recently found mutated in a recessive form of Charcot-Marie-Tooth disease. Myotubularin shows a dual specificity protein phosphatase activity in vitro. We have performed an in vivo test of tyrosine phosphatase activity in Schizosaccharomyces pombe, indicating that myotubularin does not have a broad specificity tyrosine phosphatase activity. Expression of active human myotubularin inhibited growth of S.pombe and induced a vacuolar phenotype similar to that of mutants of the vacuolar protein sorting (VPS) pathway and notably of mutants of VPS34, a phosphatidylinositol 3-kinase (PI3K). In S.pombe cells deleted for the endogenous MTM homologous gene, expression of human myotubularin decreased the level of phosphatidylinositol 3-phosphate (PI3P). We have created a substrate trap mutant which shows relocalization to plasma membrane projections (spikes) in HeLa cells and was inactive in the S.pombe assay. This mutant, but not the wild-type or a phosphatase site mutant, was able to immunoprecipitate a VPS34 kinase activity. Wild-type myotubularin was also able to directly dephosphorylate PI3P and PI4P in vitro. Myotubularin may thus decrease PI3P levels by down-regulating PI3K activity and by directly degrading PI3P.

Animals↗
PubMed2000

pp60c-src associates with the SH2-containing inositol-5-phosphatase SHIP1 and is involved in its tyrosine phosphorylation downstream of alphaIIbbeta3 integrin in human platelets.

SH2-containing inositol-5-phosphatase 1 (SHIP1) was originally identified as a 145 kDa protein that became tyrosine-phosphorylated in response to multiple cytokines. It is now well established that SHIP1 is specifically expressed in haemopoietic cells and is important as a negative regulator of signalling. We found recently that SHIP1 was present in human blood platelets as an Ins(1,3,4, 5)P(4)-phosphatase and a PtdIns(3,4,5)P(3)-5-phosphatase that became tyrosine-phosphorylated and was relocated to the cytoskeleton in an integrin-dependent manner. Here we report biochemical and pharmacological evidence that the tyrosine kinase pp60(c-src) is constitutively associated with SHIP1 and is involved in its tyrosine phosphorylation downstream of integrin engagement in thrombin-activated human platelets. The use of cytochalasin D allowed us to demonstrate that the actin cytoskeleton reorganization induced on thrombin stimulation was not required for its integrin-mediated phosphorylation. Moreover, the integrin-dependent relocation of SHIP1 to the cytoskeleton did not require its tyrosine phosphorylation. These results suggest that SHIP1 is first recruited to the integrin-linked signalling complexes and then becomes tyrosine-phosphorylated through a Src-kinase-dependent mechanism but independently of the actin cytoskeleton reorganization.

Actins↗
PubMed1999

Amino acid sequence and embryonic expression of msr/apj, the mouse homolog of Xenopus X-msr and human APJ.

We have recently identified a new G protein-coupled receptor, X-msr, whose expression is associated with the endothelial lineage in Xenopus laevis (Devic, E., Paquereau, L., Vernier, P., Knibiehler, B., Audigier, Y., 1996. Expression of a new G protein-coupled receptor X-msr is associated with an endothelial lineage in Xenopus laevis. Mech. Dev. 59, 129-140). Based on its structural analogy to the human orphan receptor APJ, we cloned the murine msr/apj receptor and analyzed its expression in developing tissues. As observed for X-msr, msr/apj transcripts are detected in the endothelium of the primary blood vessels and the forming heart. In addition, they are expressed in somites, limb bud and branchial arches. This expression pattern is distinct from that of the Flk1 gene and suggests that the msr/apj gene is expressed in a subpopulation of endothelial precursors and a mesenchymal population derived from paraaxial mesoderm.

Amino Acid Sequence↗
PubMed1999

[Expression of a new family of receptors similar to CXC chemokine receptors in endothelial cell precursors].

Characterization of a new family of G protein-coupled receptors is reported. Expression of these receptors is associated with endothelial lineage. Cloning of the Xenope X-msr receptor allowed to show that embryonic expression of this receptor occurred in the heart and developing primary blood vessels. Furthermore, within these cardiovascular structures, expression was restricted to the endothelial layer. Because structural similarities with the human orphan receptor h-APJ were found, the msr/apj receptor was cloned in mice. This showed that embryonic expression of this receptor was also confirmed to endothelial precursors. Thus, this receptor is the orthological equivalent in mice to the amphibian receptor X-msr. Molecular phylogenesis studies showed that the X-msr, msr/apj, and h-APJ receptors shared considerable homology with two CXC chemokine receptors, namely LCR1, whose name was recently changed to CXCR4, and RDC1, which is structurally similar to the CXCR2 receptor. The human h-APJ receptor is a co-receptor for entry of the HIV into T cells, a property associated only with CXC chemokine receptors in the lymphocyte population. These data suggest that this new signaling system may participate in endothelial precursor migration during developmental angiogenesis and in endothelial cell migration and proliferation during neoangiogenesis in adults.

Adult↗
PubMedDate not supplied

JCAHO educational strategies that work! Joint Commission on Accreditation of Healthcare Organizations.

Preparing a large hospital for a Joint Commission on Accreditation of Healthcare Organizations (JCAHO) survey is always a challenging endeavor. Because staff members have diverse learning needs it is important that staff be educated in the JCAHO standards. In this article, the author describes the educational strategies used to prepare a healthcare organization for an impending JCAHO survey. Learning styles, the domains of learning, and the accessibility to education by the satellite facilities were determining factors in the selection of the various educational strategies.

Academic Medical Centers↗
PubMedDate not supplied

Joint Commission preparation in a large academic medical center: a framework for success.

A large urban university medical center used a unique set of strategies in preparation for its triennial survey conducted by the Joint Commission on Accreditation of Healthcare Organizations. Although the medical center had experienced many Joint Commission surveys, this particular survey was the first to include associated physician offices in multiple diverse settings. To address these challenges, the hospital developed a structure and process that engaged all levels of staff and ensured a successful survey outcome.

Academic Medical Centers↗