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Biomedical subjects

M Richard

Publications and source records attributed to M Richard.

At least 37 records · Page 2Linked to original sources
PubMed2000

Glucosamine sulfate modulates dysregulated activities of human osteoarthritic chondrocytes in vitro.

OBJECTIVE: The efficacy of glucosamine sulfate (GS) in the symptomatic treatment of patients with osteoarthritis (OA) is suggested to be mediated by still unknown effects on the altered OA cartilage. DESIGN: Using human OA chondrocytes in culture, the effects of GS on protein synthesis, caseinase, collagenase, phospholipase A2 (PLA2) and protein kinase C (PKC) activities as well as production of nitric oxide and cyclic AMP were studied in both cells and culture medium. RESULTS: GS significantly reduced PLA2 activity, and more modestly collagenase activity, in the OA chondrocytes in a dose-dependent manner. By contrast, PLA2 and collagenase activity of the culture medium was not modified. No effects on caseinase activity was seen. GS significantly and dose-dependently increased protein synthesis. GS did not modify nitric oxide and cAMP production but significantly increased PKC production. CONCLUSION: GS modified cultured OA chondrocyte metabolism by acting on PKC, cellular PLA2, protein synthesis and possibly collagenase activation. Extrapolation of the effect to the in-vivo situation remains hypothetical but they might represent some possible mechanisms of action of the drug in human.

Caseins↗
PubMed2000

Pseudomonas aeruginosa cystic fibrosis isolates induce rapid, type III secretion-dependent, but ExoU-independent, oncosis of macrophages and polymorphonuclear neutrophils.

Pseudomonas aeruginosa, an opportunistic pathogen responsible most notably for severe infections in cystic fibrosis (CF) patients, utilizes the type III secretion system for eukaryotic cell intoxication. The CF clinical isolate CHA shows toxicity towards human polymorphonuclear neutrophils (PMNs) which is dependent on the type III secretion system but independent of the cytotoxin ExoU. In the present study, the cytotoxicity of this strain toward human and murine macrophages was demonstrated. In low-multiplicity infections (multiplicity of infection, 10), approximately 40% of the cells die within 60 min. Analysis of CHA-infected cells by transmission electron microscopy, DNA fragmentation assay, and Hoechst staining revealed the hallmarks of oncosis: cellular and nuclear swelling, disintegration of the plasma membrane, and absence of DNA fragmentation. A panel of 29 P. aeruginosa CF isolates was screened for type III system genotype, protein secretion profile, and cytotoxicity toward PMNs and macrophages. This study showed that six CF isolates were able to induce rapid ExoU-independent oncosis on phagocyte cells.

ADP Ribose Transferases↗
PubMed2000

[Congenital hypotrichosis and milia with spontaneous regression during adolescence or Oley syndrome: a variant of Bazex-Dupré-Christol syndrome].

BACKGROUND: We report a family presenting the syndrome initially described by Oley characterized by congenital profus milia and hypotrichosis that regress during adolescence. CASE REPORT: A female infant with severe congenital hypotrichosis had profus milia involving the entire face. The remainder of the physical examination was normal. The mother had normal skin and hair but indicated she had had the same signs as a child. The patient's condition regressed from the age of 10 to 15 years but she has undergone several surgical resections for basocellular carcinoma since the age of 20. The maternal grandfather had spontaneously regressive typical follicular atrophodermia involving the back and the hands and also had several milium grains and several basocellular carcinomas. He had never presented hypotrichosis. DISCUSSION: Oley syndrome is defined as an association of congenital hypotrichosis and milia spontaneously regressive during adolescence. The symptoms presented by our patient and her mother are similar to this genodermatosis. Concomitant hypotrichosis, milia, basocellular carcinomas and follicular atrophodermia define the Bazex-Dupré-Christol syndrome. The grandfather's condition would be closer to this syndrome than Oley syndrome despite the spontaneous regression of certain anomalies during adolescence. This family study would suggest that the Bazex-Dupré-Christol syndrome and the Oley syndrome are two variants of the same condition.

Adolescent↗
PubMed1999

Inactivation of brassinosteroid biological activity by a salicylate-inducible steroid sulfotransferase from Brassica napus.

Recent discoveries from brassinosteroid-deficient mutants led to the recognition that plants, like animals, use steroids to regulate their growth and development. We describe the characterization of one member of a Brassica napus sulfotransferase gene family coding for an enzyme that catalyzes the O-sulfonation of brassinosteroids and of mammalian estrogenic steroids. The enzyme is specific for the hydroxyl group at position 22 of brassinosteroids with a preference for 24-epicathasterone, an intermediate in the biosynthesis of 24-epibrassinolide. Enzymatic sulfonation of 24-epibrassinolide abolishes its biological activity in the bean second internode bioassay. This mechanism of hormone inactivation by sulfonation is similar to the modulation of estrogen biological activity observed in mammals. Furthermore, the expression of the B. napus steroid sulfotransferase genes was found to be induced by salicylic acid, a signal molecule in the plant defense response. This pattern of expression suggests that, in addition to an increased synthesis of proteins having antimicrobial properties, plants respond to pathogen infection by modulating steroid-dependent growth and developmental processes.

Amino Acid Sequence↗
PubMed1999

Interleukin-9 regulates NF-kappaB activity through BCL3 gene induction.

BCL3 encodes a protein with close homology to IkappaB proteins and interacts with p50 NF-kappaB homodimers. However, the regulation and transcriptional activity of BCL3 remain ill-defined. We observed here that interleukin-9 (IL-9) and IL-4, but not IL-2 or IL-3, transcriptionally upregulated BCL3 expression in T cells and mast cells. BCL3 induction by IL-9 was detected as soon as 4 hours after stimulation and appeared to be dependent on the Jak/STAT pathway. IL-9 stimulation was associated with an increase in p50 homodimers DNA binding activity, which was mimicked by stable BCL3 expression. This contrasts with tumor necrosis factor (TNF)-dependent NF-kappaB activation, which occurs earlier, involves p65/p50 dimers, and is dependent on IkappaB degradation. Moreover, IL-9 stimulation or BCL3 transient transfection similarly inhibited NF-kappaB-mediated transcription in response to TNF. Taken together, our observations show a new regulatory pathway for the NF-kappaB transcription factors through STAT-dependent upregulation of BCL3 gene expression.

Animals↗
PubMed1999

Occurrence of monosialosyl pentahexaosylceramide GalNAc-GM1 as specific tumor-associated ganglioside of human head and neck squamous cell carcinomas.

In a recent study of the ganglioside profiles of human head and neck squamous cell carcinomas versus normal tissue, one unidentified GX ganglioside was found exclusively in tumor extracts, migrating between GM1 and GD3 by thin-layer chromatography. To determine the chemical structure of this ganglioside which accounted for 3-8% of the total gangliosides, the lipid samples were pooled and separated by high-pressure liquid chromatography to obtain individual ganglioside species purified to homogeneity. The tumor-associated GX ganglioside was analyzed by gas-liquid chromatography, mass spectrometry and immunostaining on thin-layer plates with mouse monoclonal antibodies after enzymatic cleavage. The data allowed the identification of GX ganglioside as GalNAc-GM1 that has been reported as a very minor brain ganglioside in humans. Thus, GalNAc-GM1 is a specific tumor-associated ganglioside in human head and neck squamous cell carcinomas that could be potentially valuable for clinicians.

Carcinoma, Squamous Cell↗
PubMed1999

Influence of a cellulosic ether carrier on the structure of biphasic calcium phosphate ceramic particles in an injectable composite material.

An injectable composite material based on biphasic calcium phosphate (BCP) and a nonionic cellulose ether has been elaborated for use in percutaneous surgery for spine fusion. This paper reports the characterization results of this material by spectroscopic techniques including X-ray diffraction (XRD), infrared spectroscopy (FTIR), X-ray photoelectron spectroscopy (XPS), scanning electron microscopy (SEM) fitted with an energy dispersive X-Ray analysis system and high-resolution transmission electron microscopy (HR-TEM). From FTIR and XPS results, it was observed that the adhesion between the polymer and the ceramic might be insured by oxygen bridging developed through an ionic bonding between calcium ions and (C-O) groups of the polymer. Moreover, XPS showed attraction of Ca2+ ions in the polymer matrix, while the ceramic surface was modified in a HPO4(2-) -rich layer. These results suggest a possible dissolution/precipitation process at the interface ceramic/polymer. HR-TEM observations supported this hypothesis, showing a light contrasted fringe at the surface of the ceramic grains in the composite paste. As well, changes in the XRD spectra could indicate a small decrease in the crystal size of the BCP powder through the contact to polymer solution. In addition, SEM observation showed a decrease of the initial BCP granulometry. Aggregates of 80-200 microm seemed to be mostly dissociated in micrograins. The ceramic grains were coated with and bonded between each other by the polymer matrix, which acted as spacer in between the ceramic grains, creating a macroporous-like material structure.

Biocompatible Materials↗
PubMed1999

Protection of personnel and environment against Creutzfeldt-Jakob disease in pathology laboratories.

Most neuropathology laboratories have been faced with the question of dealing with cases of Creutzfeldt-Jakob disease (CJD) which is a rare neurodegenerative disorder. Neuropathologists have been long aware of the transmissibility and unique properties of the agent which make it resistant to conventional inactivating reagents. The emergence of iatrogenic cases and of the bovine spongiform encephalopathy (BSE) crisis has induced anxiety among laboratory staff and raised questions about the efficiency of safety measures and procedures hitherto applied in pathology laboratories. This article aims at presenting an overview of the risk involved in handling CJD material. It gives practical advice and a key to more detailed procedures, guidelines and recommendations available in scientific literature and through government agencies. Neuropathologists and biochemists are at a higher potential risk than others since the diagnosing of CJD involves the handling of nervous tissue which contains the highest levels of infectivity.

Animals↗
PubMed1998

ABC50, a novel human ATP-binding cassette protein found in tumor necrosis factor-alpha-stimulated synoviocytes.

We have used the recently developed technique of differential display polymerase chain reaction to seek for new genes modulated by tumor necrosis factor-alpha (TNF-alpha) in cultured synoviocytes. One PCR fragment was shown to correspond to a new gene that was mapped by high-resolution fluorescence in situ hybridization to band 6p21.33. The cDNA of this gene was cloned, and the deduced amino acid sequence revealed consensus motifs for the nucleotide binding folds of the ATP-binding cassette (ABC) family of proteins. However, a hydropathy curve showed that the polypeptide does not contain the transmembrane domains that are typical of the subfamily of ABC transporters and are associated with transporter/channel functions. The new gene, called ABC50, is the first human and mammalian ABC protein found to lack transmembrane domains. Homology with some yeast ABC proteins suggests that ABC50 codes for a new human ribosomal protein involved in translation of mRNA. It could therefore play a role in the enhancement of protein synthesis that follows TNF-alpha treatment of synoviocytes and thus participate in the inflammatory processes mediated by this cytokine. Furthermore, since TNF-alpha also modulates the expression of MHC class I genes, and these genes are known to map to 6p21.33, it is hypothesized that ABC50 and MHC class I are part of the same chromatin expression domain.

ATP-Binding Cassette Transporters↗
PubMed1998

Ultrastructural and electron diffraction of the bone-ceramic interfacial zone in coral and biphasic CaP implants.

We investigated the influence of natural coral implants used as a bone substitute on the quality of bone ingrowth in rabbits 2, 3, and 6 weeks after implantation. Explants were characterized by transmission electron microscopy and electron diffraction. Bone ingrowth has been previously demonstrated by light microscopy, however, few have been performed in electron microscopy to compare mineralized tissue ingrowth in coral implants which occurs at the expense of calcium carbonate to that of calcium phosphate (CaP) implants. The interface between coral aragonite and mineralized tissue or bone was abrupt, with no invasion of the aragonite structure by newly formed crystals, as occurs in micropores when biphasic CaP (BCP) ceramics were used. The restoring process appears to be different from that induced by BCP implants. Precipitation of needle-like apatite crystals on the CaCO3 implant surface was not observed. Instead, apatitic smooth-shaped crystals formed in aggregates. The coral dissolution process does not release phosphate and so precipitation of apatite does not occur in the micropores of the coral implant, thereby limiting the formation of an apatite layer and hence bone bonding to the outer surface of the implant. In addition, on the outer surface of the implant, close to bone and a phosphorus source, the CaP crystals that do form are in aggregates presumably due to the carbonate and mismatch between the aragonite and the apatite. This seems to result in a delayed bone attachment or weaker bone bonding than CaP implants which encourage an epitaxial biological crystal deposition.

Animals↗
PubMed1998

Osteoarthritic cartilage fibrillation is associated with a decrease in chondrocyte adhesion to fibronectin.

OBJECTIVE: Cartilage destruction in osteoarthritis (OA) is generally accepted as a failed repair process. Cell adhesion is implicated in tissue repair. Therefore, adhesion of OA chondrocytes to extracellular matrix proteins was investigated. DESIGN: Using chondrocytes from human OA femoral head cartilage, adhesion to fibronectin and type II collagen of cells from distinct areas showing an intact cartilage surface or a fibrillated cartilage surface was studied. Modulation of chondrocyte adhesion by both protein kinase C (PKC) inhibitors and glucosamine sulfate (GS) was also investigated. RESULTS: A significant (P < 0.05) decrease in adhesion to fibronectin of chondrocytes from fibrillated cartilage, relative to those from grossly normal OA cartilage, was demonstrated. Adhesion to type II collagen was not modified by the chondrocyte origins (either from normal or fibrillated OA cartilage). Adhesion to fibronectin of cells from grossly intact cartilage was decreased by the addition of PKC and calmodulin-dependent kinase inhibitors, W7 and sphingosine, to the cell culture. Adhesion to fibronectin of chondrocytes from fibrillated cartilage was significantly (P < 0.05) increased after glucosamine sulfate treatment. CONCLUSION: Fibrillation of cartilage from OA femoral head is associated with a defective adhesion of chondrocytes to fibronectin. The process is suggested to be dependent of PKC and/or calmodulin-dependent kinases and potentially reversible. Conceivably, it could play a role in OA cartilage destruction.

Aged↗
PubMed1998

Analysis of glycosphingolipids of human head and neck carcinomas with comparison to normal tissue.

Glycosphingolipids of head and neck carcinomas from six tumor-bearing patients were analyzed and compared to those of normal tissue from similar areas. The total glycosphingolipid content and the lipid-bound sialic acid were much higher in carcinomas than in normal tissue. Major neutral glycolipids were glucosylceramide, lactosylceramide, trihexosylceramide and paragloboside. Sulfatides were seen only in extracts from normal tissue which also showed a rather simple ganglioside pattern with #GM3 and GD3 as major species, whereas tumors showed additional species such as GM2 and GD2, along with a strong increase in LM1, GM1, GD1a and GT1b.

Biomarkers, Tumor↗
PubMed1998

Changes in specific markers of haemostasis during reduction mammoplasty.

We have investigated the time course of the coagulation and fibrinolytic changes during moderate surgical trauma (elective reduction mammoplasty) in the absence of other confounding factors that could affect haemostasis. Specific markers for coagulation (prothrombin fragment 1.2 (F1.2), thrombin-antithrombin III complex (TAT)) and fibrinolysis (plasmin-antiplasmin complex (PAP) and D-dimer) were examined. Blood samples were obtained in 20 ASA I anaesthetized female patients at T0 (before operation), T75 (during operation) and T150 (before the end of operation). There was a progressive increase in blood loss during operation:mean 110 (SD 80) ml at T75 and 470 (180) ml at T150. This was associated with a significant increase in plasma concentrations of F1.2, PAP and D-dimer at T150 only (P < 0.05 vs T0). We conclude that moderate surgical trauma with blood losses greater than 300 ml can activate thrombin generation and fibrinolysis during operation.

Adult↗
PubMed1998

Abnormal uptake of Tc-99m MIBI, a novel myocardial imaging agent, in the lungs of patients with systemic sclerosis.

OBJECTIVE: Fibrosing alveolitis is a prominent feature of systemic sclerosis (SSc), and accounts for much of the morbidity and mortality of this disease. Sensitive techniques for the detection and monitoring of fibrosing alveolitis could target patients for early therapeutic intervention. The objective of this small pilot study was to assess the frequency and clinical significance of abnormal lung uptake of Tc-99m MIBI, a novel radionuclide imaging agent that selectively accumulates in cells rich in mitochondria. METHODS: Sixteen patients with SSc and evidence of pulmonary involvement were studied. The uptake of radionuclide in the lungs, and the ratio of pulmonary to cardiac uptake were evaluated after intravenous injection of Tc-99m MIBI. Results were correlated with clinical and laboratory parameters. RESULTS: Lung uptake of Tc-99m MIBI was increased in all 16 SSc patients compared to control patients with coronary heart disease but no evidence of pulmonary abnormality. The degree of isotope uptake in the lungs was correlated with the extent of maximal skin induration and with radiologic evidence of interstitial lung disease, but not with other clinical or laboratory parameters of disease activity or extent of pulmonary involvement. The ratio of pulmonary to cardiac uptake of isotope was also increased in patients with SSc compared to controls. CONCLUSION: Accumulation of Tc-99m MIBI is abnormally elevated in the lungs of SSc patients with pulmonary involvement. Isotope accumulation in the lungs may be related to activation of fibroblasts or endothelial cells. The specificity and sensitivity of Tc-99m MIBI scanning in the detection and monitoring of pulmonary involvement, and its potential role in the management of SSc, deserve further investigation.

Coronary Disease↗
PubMed1998

Interaction of per 3,6-anhydro-alpha cyclodextrins (alpha 36CD) and lead-alpha 36CD complex with biological systems.

The interactions of per (3,6 anhydro) alpha cyclodextrin (alpha 36CD) and of lead-alpha 36CD complex with biological systems were tested by NMR, ESR and electronic microscopy using erythrocytes and model membranes. It was found that the haemolytic activity of alpha 36CD alone was seven fold lower than that of natural alpha cyclodextrin (evaluated by the concentration inducing 50% haemolysis, DH50 = 35 mM). Conversely, the formation of the complex resulted in an increase of haemolytic properties, with DH50 of 1 mM. The mechanism proposed was an increased membrane diffusion by endocytosis of the complex, leading to higher amounts of intracellular lead.

Chelating Agents↗
PubMed1998

Increased serum C-reactive protein levels by immunonephelometry in patients with rapidly destructive hip osteoarthritis.

OBJECTIVE: To compare serum C-reactive protein levels measured using a highly sensitive immunonephelometry method in patients with rapidly destructive versus slowly progressive hip osteoarthritis. METHODS: Ten patients meeting criteria for rapidly destructive hip osteoarthritis were compared to 25 patients with slowly progressive hip osteoarthritis defined as less than 0.20 mm joint space loss over the last year. Serum C-reactive protein was assayed using an immunonephelometry method with a detection threshold of 0.17 mg/L and a coefficient of variation of less than 5%. RESULTS: One patient in each group was excluded because of a C-reactive protein level greater than 15 mg/L. The mean C-reactive protein level in the remaining 33 patients was 3.05 +/- 3.46 mg/L (range, 0.10-14.9 mg/L). Mean C-reactive protein was significantly higher in the rapidly destructive group than in the slowly progressive group (5.61 +/- 4.75 versus 1.94 +/- 1.98 mg/L, P = 0.01), even after adjustment for potential confounding factors. CONCLUSION: Our data suggest that rapidly destructive hip osteoarthritis may be associated with some degree of inflammation reflected by a small but significant increase in serum C-reactive protein levels.

Aged↗
PubMed1997

Phospholipase A2 activity in herniated lumbar discs. Clinical correlations and inhibition by piroxicam.

STUDY DESIGN: Prospective study of phospholipase A2 activity in the serum and intervertebral discs of patients undergoing surgery for sciatica due to disc herniation. OBJECTIVES: To determine correlations between herniated disc phospholipase A2 and clinical, radiographic, and anatomic signs of common sciatica; to evaluate serum phospholipase A2 activity as a marker of disc phospholipase A2; and to investigate the in vivo effect of piroxicam on disc phospholipase A2. SUMMARY OF BACKGROUND DATA: Several studies suggest disc inflammation as a mechanism of sciatica due to disc herniation, and phospholipase A2 emerges as a key enzyme of cartilage and disc tissues. METHODS: Phospholipase A2 activity was determined, using the degradation of a specific substrate, in the serum and discs of 31 patients (14 treated with acetaminophen and 17 treated with piroxicam) undergoing surgery for sciatica due to lumbar disc herniation. Visual analog scale for pain, Dallas Pain Questionnaire, Lasègue's sign, radiographic stage of degeneration of the herniated disc, volume of disc herniation shown by computed tomography, and surgical findings were recorded. RESULTS: Disc phospholipase A2 activity was independent of the patient's age or sex, the radiologic stage of disc degeneration, and the volume of the herniation, and showed no significant correlation with Lasègue's sign or pain measured on a visual analog scale. The correlation between disc phospholipase A2 and the Dallas category of items measuring the impact of pain on daily activities approached the level of significance (P = 0.07). Disc phospholipase A2 activity was significantly higher in cases of sequestrated discs than in other herniations. Disc phospholipase A2 was significantly correlated with serum phospholipase A2, and was significantly lower in patients treated with piroxicam than in those treated with acetaminophen. CONCLUSIONS: Disc phospholipase A2 is thought to participate in the physiopathology of sciatica and to bemodulated by nonsteroidal anti-inflammatory drug therapy. Serum phospholipase A2 is suggested as a biologic marker of disc inflammation in patients with sciatica.

Acetaminophen↗