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Y Roche

Publications and source records attributed to Y Roche.

At least 19 recordsLinked to original sources
PubMed1991

Synovial chondromatosis of the temporomandibular joint possibly secondary to trauma. A case report.

A histologically confirmed case of synovial chondromatosis of the temporomandibular joint associated with a glenoid fossa callus is described. The lesion appeared 6 years after trauma to the chin. Conservative surgical treatment without excision of the synovial membrane or meniscus but including arthroplasty of both the eminence and the lateral side of the glenoid fossa was successful. The possible role of trauma in the etiology of synovial chondromatosis is discussed.

Adult↗
PubMed1991

[Hairy leukoplakia: current concepts].

Current data about oral hairy leukoplakia are reported. Clinical manifestations, histological and ultrastructural features and pathogenic mechanisms are firstly described. Then diagnosis are exposed. Finally, management is discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Effects of quinolones on tumor necrosis factor production by human monocytes.

Previous studies have shown that in lipopolysaccharide (LPS)-stimulated human monocytes, interleukin 1 (IL-1) production is altered by quinoline derivative antibiotics (quinolones), in a way which depends both on the dose and on the agents used. Given that IL-1 and tumor necrosis factor alpha (TNF) are produced in response to LPS and have some overlapping and synergistic activities, we sought to determine if TNF production was altered under the above-mentioned conditions. We investigated the effects of three quinolones: ciprofloxacin (Cip), pefloxacin (Pef) and ofloxacin (Ofl). These quinolones were found to decrease extracellular TNF production in a dose-dependent manner at concentrations higher than 25 micrograms/ml as previously described by our laboratory with regard to IL-1 production. Moreover, the order of the extracellular decrease in TNF and IL-1 induced by each drug was similar. However, in contrast to IL-1 activity, the quinolones studied also reduced cell-associated TNF. The kinetics of TNF production suggested that the quinolones affected TNF production at a very early step, probably during TNF synthesis rather than during its secretion into the extracellular medium. Furthermore, the quinolone-induced accumulation of intracellular cAMP could explain the extracellular decrease in both IL-1 and TNF production.

1-Methyl-3-isobutylxanthine↗
PubMed1990

[Etiopathology of dry socket: current data].

This review of the literature presents the current data and controversies regarding the etiology and pathogenesis of dry socket. After presenting arguments which support the theory of clot non-formation and those supporting its malformation, the thesis of fibrinolysis is discussed along with its mechanisms and origins. Finally, the various factors which could encourage this pathology are reviewed and the therapeutic and preventive management are presented.

Adult↗
PubMed1989

Oxidative injury amplifies interleukin-1-like activity produced by human monocytes.

Exposure of human monocytes to 95% normobaric oxygen (O2) was used as an in vitro oxidative injury model to study the effects of the O2-derived species produced by phagocytes at inflammatory sites on monocyte IL-1 production. Exposure to O2 enhanced production by monocytes of IL-1-like activity whether the adherent cells were cultured in the presence of opsonized zymosan, LPS or medium alone. This O2-induced increase in production of IL-1 activity was inhibited by cycloheximide and thus resulted from de novo protein synthesis. Furthermore, the increase was prevented by the addition of the protein kinase inhibitor N-2-methylaminoethyl-5-isoquinoline sulfonamide dihydrochloride (H8). Following exposure to O2, Ca2+/phospholipid-independent protein kinase activity increased in comparison to air-exposed monocytes, whereas the dependent form decreased. Since the Ca2+/phospholipid-independent form is known to derive from the dependent form (protein kinase C) by proteolysis in the presence of a thiol proteinase, our results suggest that oxidative injury stimulates thiol proteinase activity and enhances production of IL-1 activity by human monocytes partly by interfering with protein kinase C metabolism. Among the consequences of the generation of O2-derived species by phagocytes in inflammatory sites, the augmentation of the production of IL-1-like activity could amplify the inflammatory response.

Adult↗
PubMed1989

[Alveolar anesthesia].

Tuberosity anesthesia is a loco-regional anesthesia aiming at anesthetizing with a single injection the superoposterior alveolar nerves, by approaching the maxillary tuberosity through a direct anteroexternal pathway. This anesthesia involves an area located behind the pyramidal process of the maxillary bone which includes the molars, gingival buccal mucosa, sinus bone and mucosa. Well-tolerated by the patient, since it is practically a painless procedure, tuberosity anesthesia is the preferred method to perform surgery in the posterior maxillary area. Its administration may be extended without condition to treatment of the upper molars: custy + crown + bridge preparations on vital teeth, pulpectomies, thanks to the rapid onset and efficacy of the anesthesia obtained. The only contraindication involves patients with vascular or hematologic disorders, ruling out procedures where a blood vessel might be injured with a needle. In that case, intraligamentary or transcortical instillation is indicated since para-apical anesthesia is not a valid alternative due to the proximity of the external alveolar artery.

Alveolar Process↗
PubMed1988

[Tooth grafts].

Explore the source record for details and available documents.

Humans↗
PubMed1988

Enhancement of interleukin 2 production by quinolone-treated human mononuclear leukocytes.

Previous studies have shown that lectin-induced human mononuclear leukocyte (MNL) proliferation was influenced by quinoline derivative antibiotics (quinolones), depending on both the dose and the antimicrobial agent used. Since the production of interleukin-2 (IL-2) is known to be involved in the proliferation of immune cells, we investigated the effects of three quinolones: ciprofloxacin (Cip), ofloxacin (Ofl) and pefloxacin (Pef) on IL-2 production in vitro by phytohemagglutinin (PHA)-stimulated human MNL. IL-2 activity in the supernatants of PHA-stimulated MNL was found to be enhanced by quinolones in a dose- and time-dependent manner. Increased IL-2 activity was observed using Cip, Ofl or Pef at therapeutically achievable blood concentrations (5-10 micrograms/ml). Since at these concentrations the PHA-induced proliferative response of MNL was not impaired by quinolones, the increased recovered IL-2 activity was not related to a decreased absorption of IL-2 by activated MNL. At high antibiotic concentrations (25 micrograms/ml), the enhanced IL-2 activity might be related (i) to increased accumulation resulting from the decreased proliferation induced by the quinolones at these concentrations, and (ii) to a true increased IL-2 production by the cells. In fact, an increased IL-2 recovery in presence of quinolones was always observed after blocking the cell cycle by mitomycin C, and was therefore independent of DNA-synthesis. Furthermore, the expression of IL-2 receptors was not modified by Cip, Ofl or Pef. These data show that quinolones increased IL-2 synthesis by MNL and suggest the potential usefulness of these antibiotics, not only as antimicrobial agents, but also as modulators of immune responses.

Anti-Infective Agents↗
PubMed1988

Interleukin-1 production by antibiotic-treated human monocytes.

The effects of penicillin, macrolides (spiramycin and erythromycin), cephalosporins (cefaclor and cefadroxil), tetracycline (doxycycline) and quinolones (pefloxacin, ciprofloxacin and ofloxacin) on extracellular and cell-associated interleukin 1 (IL-1) activity from human adherent mononuclear leucocyte cells were investigated in vitro. When cells were treated with an antibiotic concentration of 10 mg/l, no apparent effect could be detected for penicillin, erythromycin, cephalosporins or quinolones, while a slight increase of extracellular IL-1 activity associated with a decrease of intracellular IL-1 activity was observed with spiramycin and doxycycline. When high antibiotic concentration were used, extracellular IL-1 activity was increased by macrolides and tetracycline, while both cell-associated and class II human monocyte antigen expression were decreased. A toxic effect may have been exerted by these antimicrobial agents, since cell viability was altered when they were used at high concentrations. In contrast, extracellular IL-1 activity was found to be decreased by quinolones and cephalosporins. Intracellular IL-1 activity was also decreased by cephalosporins, while quinolones did not modify either cell-associated IL-1 activity or class II human monocyte antigen expression. The effect induced by quinolones and cephalosporins occurred without modification of cell viability. IL-1 activity was shown to be affected by antibiotics over the same range of concentrations which are known to inhibit mononuclear leucocyte proliferation. Our data may help in defining the mechanism by which the mitogen-induced mononuclear proliferative response is suppressed by antimicrobial agents since this appears to involve the inhibition of IL-1 production or of its release.

Anti-Bacterial Agents↗
PubMed1988

Mechanisms by which oxidative injury inhibits the proliferative response of human lymphocytes to PHA. Effect of the thiol compound 2-mercaptoethanol.

The use of normobaric exposure to O2 as a model for in vitro oxidative injury prevented phytohaemagglutinin (PHA)-stimulated human peripheral blood mononuclear cells (PBMC) from undergoing the G0 to G1 transition, but 5 x 10(-6) M 2-mercaptoethanol (2-ME) almost protected the cells from this blockade. The percentage of cells with IL-2 and transferrin-receptors was reduced by the O2 exposure and, like the cell cycle transition, was protected by 2-ME against oxidative injury. By contrast, IL-2 recovery in the supernatants of O2-exposed PHA-stimulated PBMC was enhanced. This enhancement may be due partly to the reduced IL-2 consumption caused by the decreases in IL-2 receptor expression and in proliferation. On the other hand, IL-2 recovery in the supernatants of O2-treated PBMC was always enhanced compared to the IL-2 control recovery after DNA synthesis was blocked in G1/S by mitomycin c, and the G0/G1 transition was protected by 2-ME. Furthermore, PHA-stimulated monocytes exposed to O2 produced more IL-1 than control cells. This enhanced IL-1 production was not modified by 2-ME. These results suggest that oxidative injury reduces the proliferation of PBMC by interfering with the cellular events that lead to the transition from the G0 to the G1 phase of the cell cycle. The protective effects of 2-ME suggest that thiol compounds have a critical role in the early events of the cell cycle. By contrast, exposure to O2 induced increases in the production of both IL-1 and IL-2 that may not be related to alterations in the thiol status of the cell.

Cell Cycle↗
PubMed1987

Effects of quinolones on interleukin 1 production in vitro by human monocytes.

The new quinoline derivative antibiotics (quinolones), pefloxacin and ciprofloxacin at concentrations higher than 50 micrograms/ml inhibit the PHA response of the human mononuclear leukocytes in vitro. Since monocytes have been shown to be accessory cells for the activation of lymphocytes by mitogens, we investigated the effects of pefloxacin and ciprofloxacin on extracellular interleukin 1 (IL-1) and cell-associated IL-1 from lipopolysaccharide-stimulated human monocytes. Pefloxacin and ciprofloxacin decreased the extracellular IL-1 in a dose-dependent manner, while cell-associated IL-1 was not altered. These effects were observed even after a short period of incubation (1 or 2 h). No inhibitory activity against purified IL-1 or IL-2 could be demonstrated in the dialyzed supernatants from pefloxacin- or ciprofloxacin-treated monocytes. Neither pefloxacin nor ciprofloxacin modified the biological activity of preformed IL-1. The decrease of extracellular IL-1 induced by pefloxacin and ciprofloxacin could, in part, account for the observed decrease in the proliferative response of human mononuclear leukocytes to phytohemagglutinin, as extracellular IL-1 and proliferative response were positively correlated (at various concentrations of pefloxacin and ciprofloxacin). The decrease in extracellular IL-1 was not associated with any alteration in the expression of the HLA-DR antigen on the monocytes membrane. These data suggested that pefloxacin and ciprofloxacin could antagonize IL-1 production and release by lipopolysaccharide-stimulated monocytes. These quinolones could be interesting tools to study the production, processing, transport and release from the monocytes of IL-1.

Adult↗
PubMed1987

Comparative effects of quinolones on human mononuclear leucocyte functions.

The effects of three quinoline derivatives--pefloxacin, ciprofloxacin and ofloxacin--were investigated in mitogen-stimulated human peripheral blood mononuclear leucocytes (MNL). At concentrations of 50 mg/l or more, pefloxacin, ciprofloxacin or ofloxacin significantly inhibited MNL proliferation in response to phytohaemagglutinin. This inhibition was more marked with ciprofloxacin than pefloxacin or ofloxacin. To determine the possible mechanism(s) involved in the inhibition of MNL proliferation following exposure to pefloxacin, ciprofloxacin or ofloxacin, we assessed (1) interleukin-1 (IL-1) activity in supernatants from monocytes treated with the quinolones and (2) the effects of 2-mercaptoethanol (2-ME) a thiol compound which acts as an antioxidant agent and the effect of indomethacin (INDO) an inhibitor of prostaglandin E2 synthesis. 2-ME and INDO did not prevent the decrease in the proliferation. IL-1 activity was shown to be decreased for the same range of antibiotic concentrations as observed for the inhibition of MNL proliferation. Cellular viability of the MNL or monocytes was not modified by any of the quinolones at the concentrations tested. Taken together, these results suggest that pefloxacin, ciprofloxacin and ofloxacin act as immunomodulators. The mechanism involved with the cascade of events that leads to the lymphocyte proliferation and the clinical relevance need further investigation.

Cell Survival↗