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Biomedical subjects

G Loyau

Publications and source records attributed to G Loyau.

At least 55 records · Page 3Linked to original sources
PubMed1989

Percutaneous automated lumbar nucleotomy.

The results of percutaneous automated lumbar nucleotomy in the treatment of lumbar disc herniation were assessed in a series of 39 patients. The technique consists of mechanical decompression of the herniated intervertebral disc without total excision. Only one-space discs were treated by this method. Sciatica was the predominant clinical symptom in 30 cases, and lumbar pain in 9 cases. Good to very good results were obtained in 70% of patients with sciatica and in 55% of patients with lumbar pain. After 4 cases of nucleotomy performed after failure of nucleolysis were excluded, the proportion of very good results rose to 77% in sciatica. Conversely, it seems that a number of failed nucleotomies can be treated by nucleolysis. Nucleotomy is very well tolerated and deserves to be used as first-line treatment of single and radiologically well documented lumbar disc herniations.

Adult↗
PubMed1988

Interleukin-1 alpha and beta induce interleukin-1 beta gene expression in human dermal fibroblasts.

The ability of the two forms of interleukin-1, IL-1 alpha and IL-1 beta, to induce IL-1 beta gene expression in human skin fibroblasts was studied in vitro, using Northern blot hybridization. Both recombinant IL-1 alpha and IL-1 beta caused a dramatic increase in IL-1 beta mRNA levels, IL-1 alpha being more efficient than IL-1 beta. Blockage of the prostaglandin synthesis by indomethacin reduced the basal level of IL-1 beta mRNA in control cultures and decreased also the stimulatory effect exerted by both IL-1s on IL-1 beta gene expression. These data suggest that IL-1 and prostaglandin (mainly PGE2) may act synergistically to stimulate IL-1 gene expression in dermal fibroblasts, contributing as a local amplifier system to the alterations of connective tissue in inflammatory processes.

Cells, Cultured↗
PubMed1988

Tumor necrosis factor inhibits collagen and fibronectin synthesis in human dermal fibroblasts.

Tumor necrosis factor (TNF) caused inhibition of collagen production by confluent cultures of human dermal fibroblasts in a dose-dependent manner. Concomitant increase of prostaglandin E2 release was observed as a result of TNF-induced cell activation. However, a blockade of the cyclooxygenase pathway of arachidonate metabolism by indomethacin did not abrogate the inhibitory effect of TNF on collagen synthesis, suggesting that this effect could be independent of prostaglandin metabolism. Gel electrophoresis of the newly synthesized macromolecules from the culture media showed that both type I and type III collagens as well as fibronectin were affected by the inhibition. Electrophoresis of cell layer-associated proteins demonstrated that the reduction in amounts of collagen and fibronectin in the medium did not result from an intracellular accumulation of these macromolecules. Production of procollagens was reduced in parallel to that of collagens, suggesting that the effect of TNF is exerted before the processing steps of procollagens. These results clearly show that TNF could play a role in modulation of matrix deposition by fibroblasts during inflammatory processes.

Cell Division↗
PubMed1988

Transforming growth factor beta stimulates collagen and glycosaminoglycan biosynthesis in cultured rabbit articular chondrocytes.

The effect of transforming growth factor beta (TGF-beta) on the production of matrix macromolecules was studied in cultures of rabbit articular chondrocytes. A 24 h exposure to TGF-beta at concentrations of 0.1, 1 and 10 ng/ml markedly stimulated the synthesis of collagen and non-collagen protein. Similar increases of glycosaminoglycan production was observed in the same experimental conditions. The distribution of these newly synthesized macromolecules between cell layer and medium was not altered by treatment with TGF-beta. The factor slightly enhanced the proliferation of chondrocytes in these experiments but its potent effect on matrix synthesis was independent of this growth stimulation. These results indicate that articular chondrocytes are target cells for TGF-beta and suggest that this growth factor could play a role in the repair process of cartilage during osteoarticular diseases.

Animals↗
PubMed1988

Calcium ionophore and phorbol myristate acetate synergistically inhibited proteoglycan biosynthesis in articular chondrocytes by prostaglandin independent mechanism.

In rabbit articular chondrocytes, phorbol myristate acetate (PMA), 1,2-dioctanoyl-sn-glycerol (DG) and calcium ionophore (A23187), reduced the proteoglycan synthesis, in a dose-dependent manner. The combined treatment by PMA and A23187 resulted in an enhanced inhibition of proteoglycan production, indicating a synergistic effect. In presence of PMA or A23187, the release of prostaglandin E2 (PGE2) was dramatically increased. The addition of indomethacin and BW755c to chondrocytes stimulated by PMA or A23187, suppressed the liberation of PGE2, but did not stop the decrease of proteoglycan synthesis.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1988

Interleukin-1 alpha modulates collagen gene expression in cultured synovial cells.

The effects of porcine interleukin-1 (IL-1) alpha on collagen production were studied in cultured human rheumatoid synovial cells. Addition of 0.05-5 ng of IL-1/ml into the cultures resulted in a dose-dependent decreased rate of collagen released into the medium over 24 h. To determine whether this inhibition was due to secondary action of prostaglandin E2 (PGE2) secreted in response to IL-1, cultures were incubated in presence of various inhibitors of arachidonate metabolism. Depending on the cell strains, these inhibitors were able to suppress or diminish the effect of IL-1, suggesting that PGE2 is involved in the mechanism. Depression of collagen production caused by IL-1 mainly affected type I collagen and therefore led to a change in the type I/type III collagen ratio in the extracellular medium. Steady-state levels of mRNA for types I and III procollagens were estimated by dot-blot hybridization and compared with the amounts of respective collagens produced in the same cultures. IL-1 generally increased procollagen type I mRNA, but to a variable extent, as did indomethacin (Indo). Depending on the cell strain, the combination of indo and IL-1 could elevate the mRNA level of type I procollagen compared with Indo alone. These results did not correlate with the production rate of collagen in the medium, which was diminished by exposure to IL-1. The level of mRNA for collagen type III was not greatly changed by incubation with IL-1, and a better correlation was generally observed with the amount of type III collagen found in the medium. These data suggest that an additional control mechanism at translational or post-translational level must exist, counterbalancing the stimulatory effect of IL-1 on collagen mRNA transcription. It is likely that IL-1 could modulate the production of collagen in synovial cells by an interplay of different mechanisms, some of them limiting the effect of primary elevation of the steady-state mRNA level.

Bucladesine↗
PubMed1988

[A congestive bout of arthrosis: is it an inflammatory outbreak?].

The arthrotic disease is frequently dotted with "bouts" characterized by a new outbreak of pain which may lead to inflammation and sometimes, for superficial joints, characterized by increased local heat and, mostly, hydarthrosis. But, the inflammatory component usually remains moderate and many clinicians prefer the term of congestive bout which, in addition, respects the classical opposition arthrosis-arthritis. Actually, this opposition is not so clear-cut, and it appears more and more clearly that arthrosis is a multi-factorial disease where, in addition to mechanical, genetic or metabolic factors, the synovial inflammation plays a major role in the degeneration of the cartilage. The findings of arthroscopy and pathology let to believe that congestive bouts are actually inflammatory bouts.

Arthroscopy↗
PubMed1988

Gene expression of fibroblast matrix proteins is altered by indomethacin.

The role of indomethacin in the regulation of extracellular matrix synthesis was studied in dermal fibroblast cultures. Indomethacin (10 microM) blocked totally the prostaglandin secretion and markedly increased the synthesis of collagen. In parallel, measurement of fibronectin, type I and type III procollagen mRNA levels showed a substantial increase under the action of indomethacin. On the other hand, indomethacin did not modify the mRNA levels of dermatan sulfate proteoglycan core protein. Measurement of collagen production estimated as the amount of collagenase digestible protein and by specific radioimmunoassay indicated a good correlation with the corresponding mRNA levels. These results suggest that indomethacin can regulate the extracellular matrix deposition at a transcriptional level.

Cells, Cultured↗
PubMed1988

Proteoglycan biosynthesis by rabbit articular chondrocytes treated with D-penicillamine.

Rabbit articular chondrocytes in confluent monolayer cultures were treated with D-Penicillamine (D-Pen) during 3 or 5 days. The [35S]-sulfate incorporation in neosynthesized proteoglycans was not modified by D-Pen doses ranging from 50 to 800 micrograms/ml. After treatment during 5 days with D-Pen concentrations of 50 or 400 micrograms/ml, the chemical characteristics of proteoglycans from medium and cell-layer were determined. The aggregation capacity of proteoglycans from medium, the monomer molecular size, the glycosaminoglycan chain length and the relative rates of the different glycosaminoglycans (chondroitins, chondroitin 6-sulfate, chondroitin 4-sulfate, hyaluronic acid) remained unchanged. These results suggest that D-Pen does not alter some of the cartilage mechanical properties due to the presence of proteoglycans.

Animals↗
PubMed1988

Effects of an in vivo D-penicillamine treatment on glycosaminoglycan biosynthesis by synovial fibroblasts from arthritic-rendered rabbits.

Arthritic-rendered rabbits were treated in vivo with 50 mg/kg D-penicillamine (D-Pen) daily during 4 months. Glycosaminoglycan (GAG) synthesis by synovial fibroblast cultures from D-Pen treated and untreated normal or arthritic animals was studied. Cells from arthritic-rendered animals synthesized hyaluronic acid (HA) at the same rate as cells isolated from control rabbits. When D-Pen was administered to arthritic-rendered rabbits, it significantly inhibited GAG production by fibroblasts. The hyaluronate synthetase activity determined on synovial fibroblast homogenates, however, was not modified whatever the treatment undergone by the rabbits. Moreover, synovial fibroblasts from arthritic rabbits treated or not with D-Pen generally synthesized HA with a high molecular weight similar to that produced by D-Pen treated or untreated control animals.

Animals↗
PubMed1987

Interleukin-1 and osteoarthritis.

Il-1, a multifunctional monokine, can stimulate both synoviocytes and articular chondrocytes to release neutral proteases and prostaglandin E2. It is also capable of promoting bone resorption. Therefore, this molecule (or family of molecules) is likely to play an important role in the mechanism of articular cartilage destruction that occurs in degenerative arthropathies. The synovial tissue itself can produce Il-1 (Catabolin) in some conditions, such as a slight traumatism, so that the presence of local inflammation is not necessary for "Il-1-cartilage" interaction to occur. Fundamental macromolecules of cartilage (collagens, proteoglycans) exert a stimulatory effect on Il-1 production, either as such or in the form of immune complexes. Some activated complement fractions (C3a and C5a) may also be actively involved. Studies on the mechanisms which regulate Il-1 synthesis and release, as well as investigations on the response of target cells to Il-1, are presently fascinating goals that could lead to new strategies in therapeutic research.

Animals↗
PubMed1987

HLA DR, DQ, and DP antigen expression in rheumatoid synovial cells: a biochemical and quantitative study.

Because an increased expression of HLA class II antigens appears to be a central feature in local lesions of rheumatoid arthritis (RA), we have developed specific tools to quantify Ia expression in RA at both the protein and mRNA levels. An original dot immunobinding assay and a quick blot hybridization with chain-specific HLA class II probes allowed quantification of HLA DR antigens and chain transcripts on small-size samples of adherent synovial lining cells (ASLC) from normal individuals or RA patients. These methods associated with Western blot techniques detecting class II and beta-chain expression showed that ASLC from RA patients freshly put in short-term culture expressed greater amounts of class II transcripts and proteins than ASLC from controls. Class II proteins and mRNA rapidly disappeared in culture. Recombinant interferon-gamma (rIFN-gamma) induced their re-expression. A study of the kinetics and levels of the HLA-D products showed similar patterns of activation in RA patients and controls. A qualitative analysis of HLA class II antigens synthesized in ASLC after rIFN-gamma induction was performed by two-dimensional gel electrophoresis. It revealed a normal pattern for alpha- and beta-chains in ASLC from normal and RA patients, thus eliminating the possibility that abnormal protein structure of Ia antigen expressed on ASLC is responsible for the activation of T cell immune responses in RA. Nevertheless, the invariant chain exhibited a particular pattern in ASLC with additional basic spots, and this might interfere with transport and glycosylation of HLA class II antigens in such cells.

Antibodies, Monoclonal↗
PubMed1987

Interleukin-1-like factor (mononuclear cell factor) modulates proteoglycan synthesis in cultured human synovial cells.

Cultured human synovial cells treated with an interleukin-1-like mononuclear cell factor incorporated more 35S in proteoglycans than control cultures, but the radioactivity distribution between medium and cell layer was not modified. Proteoglycans were synthesized essentially in monomeric form and the mononuclear cell factor increased the molecular weight of these monomers. The [3H]hexosamine/[14C]serine ratio in purified proteoglycans on the one hand, and the study of [35S]glycosaminoglycan molecular weight, on the other hand, indicated that this increase is not modulated through enhanced synthesis of core protein but by an increase in the glycosaminoglycan chain length. After enzyme hydrolysis, dermatan sulfate (62% of the total glycosaminoglycans) and chondroitin 4/6-sulfate (30%) were found to be the major glycosaminoglycans synthesized by cultured synovial cells, and the existence of 8% heparan sulfate was evidenced by nitrous acid treatment. In the presence of the mononuclear cell factor, the dermatan sulfate synthesis was decreased (47%), with a concomitant increase of chondroitin sulfate synthesis (45%).

Aged↗
PubMed1987

[Fasciitis and Shulman's syndrome. A nosologic discussion].

Eosinophilic fasciitis or Shulman's syndrome is linked to scleroderma, systemic sclerodermia as various types of localized sclerodermia, by a nosological relationship analyzed by the authors. But, excluding the one concerning eosinophilic fasciitis and deep morphea, the authors seem to believe that the current differences are still justified, since the clinical picture and the levels of the histological lesions vary from one entity to the other. The nosological debate concerning eosinophilic fasciitis demonstrates also that a histologically recognized fasciitis has no complete specificity. By far, it goes beyond sclerodermia. Inflammation of the fascia is possible in the course of disseminated lupus erythematosus and other connective tissue inflammations. It is also described beyond connective tissue inflammations during rhizomelic pseudo-polyarthritis, and mostly in the course of three diseases: Texier's disease, drepanocytosis, and the spanish toxic syndrome, where it may be associated to a hypereosinophilia.

Anemia, Sickle Cell↗
PubMed1986

Effect of a interleukin-1 like factor (mononuclear cell factor) on proteoglycan synthesis in cultured human articular chondrocytes.

A partially purified monocyte factor, with Interleukin-1 properties (MCF/IL-1), enhances the proteoglycan synthesis of human neonatal articular chondrocytes in culture, and changes the repartition of these macromolecules between medium and cell layer. The size of the proteoglycan monomers, the length of the glycosaminoglycan chains and the respective levels of chondroitin-6-sulfate, chondroitin-4-sulfate and non sulfated chondroitin remain unchanged under MCF/IL-1 exposures. The addition of indomethacin reduces the stimulation effect by 60-70% only, suggesting that the MCF/IL-1 action is partially dependent on prostaglandins but seems also related to mechanisms distinct from the cyclooxygenase pathway.

Cartilage, Articular↗