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J Lecomte

Publications and source records attributed to J Lecomte.

At least 19 recordsLinked to original sources
PubMed1992

Evidence of genomic variations between infectious pancreatic necrosis virus strains determined by restriction fragment profiles.

Infectious pancreatic necrosis virus (IPNV) is the aetiological agent of an important disease in hatchery-reared salmonid fish in North America, Europe and Japan. It belongs to the family Birnaviridae and shows a high degree of antigenic heterogeneity. However, genomic variations between the 10 identified serotypes have not yet been studied. In order to correlate genomic heterogeneity with the different serotypes, oligonucleotides were synthesized according to the published sequence of the Jasper strain (serotype A9). They were used as primers for the amplification of a 359 bp cDNA fragment of the viral genome using the polymerase chain reaction. Fragments amplified from 37 strains were digested with five different restriction enzymes. Restriction fragment profiles obtained an agarose gels showed heterogeneity not only between strains of different serotypes, but also among those belonging to serotype A1. A cluster analysis of the restriction patterns showed that IPNV strains can be divided into three major groups, corresponding approximately to serotypes A1, A2 and A3, and 10 subgroups which do not correlate with the serotyping of the strains.

Animals↗
PubMed1992

Antigenic and genomic differences of two Jasper strains of infectious pancreatic necrosis virus.

Strains of infectious pancreatic necrosis virus (IPNV-Jasper) obtained from two different laboratories were compared serologically with polyclonal and monoclonal antibodies. Nucleotide sequence and restriction endonuclease patterns of 359-bp fragment of genome segment A cDNA were also compared. Substantial differences were found in both analyses that will support the fact that the two Jasper strains are not identical.

Animals↗
PubMed1991

Antiidiotypic vaccination against murine coronavirus infection.

Rabbit polyclonal antiidiotypic antibodies were generated against a neutralizing mAb specific for a conformational epitope on the S glycoprotein of murine hepatitis virus, strain A59 (MHV-A59). These anti-Id were directed predominantly against an Id that was undetectable in rabbit and rat anti-MHV-A59 sera and weakly represented in syngeneic and allogeneic antiviral sera. However, some partial idiotypic sharing was observed between the Id-bearing antibody and a mAb with a similar antigenic site specificity. The anti-Id inhibited the virus-binding and neutralizing activities of the immunizing antibody, demonstrating that they recognize paratope-associated idiotopes. Mice immunized with affinity-purified anti-Id developed MHV-A59-specific antibodies that neutralized viral infectivity to high titers. Moreover, these animals survived an otherwise lethal challenge with viral murine hepatitis virus, unlike control mice immunized with normal rabbit Ig. These results indicate that at least a subpopulation of the polyclonal anti-Id could induce a protective immune response directed toward a biologically important MHV-A59 epitope, and demonstrate the feasibility of antiidiotypic vaccination against a coronavirus infection.

Animals↗
PubMed1991

Identification of murine natural killer cell subsets with monoclonal antibodies derived from 129 anti-C57BL/6 immune spleen cells.

Two hybridomas producing monoclonal antibodies reactive with natural killer cells were selected after fusion of 129 anti-C57BL/6 immune spleen cells with P3X63-Ag8.653 myeloma cells. Treatment of normal or stimulated cells with the 4LO3311 or the 4LO439 mAb and rabbit complement inhibited natural killer and antibody-dependent cellular cytotoxicities, whereas cell lysis mediated by natural cytotoxic cells, cytotoxic T lymphocytes, or activated macrophages was unaffected. Lymphokine-activated killer activity was reduced after complement-mediated treatment of interleukin-2-stimulated spleen cells with the 4LO3311 mAb but not after treatment with the 4LO439 mAb. Similar treatment of spleen cells with either mAb had no effect on the mitogen-induced proliferation of T and B lymphocytes and did not alter the frequency of antibody plaque-forming cells in immune spleen cell suspensions. The 4LO3311 and 4LO439 mAbs thus appear to be specific for NK cells and their progeny. Flow cytometry analysis confirmed that 4LO3311+ and 4LO439+ cells are phenotypically identical to NK-1.1+ cells. The epitope recognized by the 4LO3311 mAb has the same strain distribution as the NK-2.1 alloantigen previously detected with NZB anti-BALB/c antiserum, whereas the 4LO439 mAb appears to identify a new NK cell marker exclusively expressed in mice of C57BL lineage. The relationship of the molecules detected with either the 4LO3311 or the 4LO439 mAb to polymorphic antigens of the Ly series is discussed.

Animals↗
PubMed1991

Antipyretic effects of nimesulide in paediatric practice: a double-blind study.

A double-blind, multi-centre study was carried out in 42 hospitalized children, aged 6 months to 8 years, suffering from acute respiratory tract infections with fever, to investigate the antipyretic activity of nimesulide. On entry, patients were allocated at random to receive either nimesulide oral suspension, 5 mg/kg/day divided into 3 daily doses, for 5 days or placebo. Both groups were treated simultaneously with antibiotics: children under 5 years of age received 100 mg amoxycillin/kg/day, those over 5 years received 40 to 50 mg erythromycin/kg/day. Measurements of rectal temperature before and during the 6 hours after the first dose of nimesulide showed a significant mean decrease from a baseline value of 38.89 +/- 0.74 degrees C to 37.28 +/- 0.76 degrees C at 6 hours. In the placebo group, no significant changes were observed between baseline (38.82 +/- 0.67 degrees C) and the 6-hour value (38.28 +/- 1 degree C). Morning temperatures remained within the normal range on the following days. Nimesulide was well tolerated. The results indicate that nimesulide has a prompt antipyretic effect which may well be clinically helpful before the correct antibiotic therapy is effectively established.

Acute Disease↗
PubMed1991

[Chemostimulation and catecholamine content of the rat adrenal medulla].

Unanaesthetized rats whose arterial chemoreceptors were stimulated by an one hour acute exposition to hypoxic gaseous mixtures with various carbon dioxide concentrations, presented depletion of the catecholamines content of their adrenal glands only when hypocapnia or increased pH was present (non compensated hypoxia). Moreover, exposition to simultaneous hypoxia and hypercapnia increased the epinephrine stock of the adrenal glands. No changes were found in the myocardium amine content in the same conditions. When anaesthetized rats were treated by iv injection of almitrine bismesylate, a peripheral chemoreceptors stimulating drug, adrenal catecholamines content was insignificantly reduced. In the myocardium, the amines remained at control levels. The most powerful factor related to catecholamines depletion in the adrenals seems to be the hypocapnia or the alkalosis induced by the hyperventilation provoked by glomic stimulation. No indication has been found in favor of an effective adrenergic stimulation caused directly by chemoreceptors stimulation.

Adrenal Medulla↗
PubMed1991

[Pathogenic mechanisms of acute pulmonary edema of hemodynamic origin in rats].

In normal anaesthetized rats (pentobarbital, 40 mg/kg i.p.), intravenous injection of a bolus of vasopressin (0.3 micrograms/kg) provoked a large increase in pulmonary and in systemic blood pressures. About three minutes later, some rats (60%) developed an acute pulmonary edema (OPA), froth appearing at the trachea. Other animals presented no OPA at the 4th minute following the injection, but OPA appeared immediately when bilateral vagotomy was performed at that time. Factors explaining the appearance of OPA are mechanical ones, circulatory or respiratory, without interferences with autonomous nervous processes.

Acute Disease↗
PubMed1990

A randomized study comparing etoposide and vindesine with or without cisplatin as induction therapy for small cell lung cancer. EORTC Lung Cancer Working Party.

We conducted a randomized trial testing etoposide (120 mg/m2 d1-3) + vindesine (3 mg/m2 d1) with or without cisplatin (60 mg/m2 d1) in patients with SCLC. A total of 8 courses were given at 3-week intervals. 221 patients were registered and 201, 95 in the CEV arm and 106 in the EV arm, were eligible for survival analysis. 183 patients were evaluable for response: 74% had an objective response (OR) with CEV versus 55% with EV (p = 0.01). Complete response rates were, respectively, 21% and 13% (NS). In patients with limited disease (LD), OR rates were 72% and 61% (NS), and 76% and 48% in extensive disease (ED) (p = 0.01). There was no statistically significant difference in survival between the two regimens (p = 0.745, log rank test). Median survival for EV and CEV were, respectively, 40 and 45 weeks, and two-year survivals were 11% and 9%; in patients with LD, the corresponding figures were 14% and 16% (NS) and in those with ED, 8% and 3% (NS). Disease extent (LD vs ED), Karnofsky performance status and loss of body weight were significant prognostic factors for survival; age, sex, type of treatment and type of lesion were not. The CEV regimen was not significantly more myelotoxic than EV but was associated with more severe nausea, vomiting and alopecia. In conclusion, the addition of cisplatin to the EV regimen, a combination reported to be easily manageable, was associated with a significantly higher OR rate but survival was not significantly improved.

Adult↗
PubMed1990

[Alpha 2 adrenergic control of ventilation in the rat].

In anaesthetized rats, ventilatory stimulation induced by phentolamine, an alpha sympatholytic agent, emphasizes the role of some adrenergic mechanisms in the control of the respiratory centres activity. Phentolamine (5 and 10 mg.kg-1, iv) stimulates ventilation after a 4 s latency, tidal volume and respiratory rate being both increased. A same response can also be provoked 10 min later, by a second identical iv administration, systemic blood pressure remaining then stable at its previous low level. Hyperventilation is also observed when phentolamine is injected in totally denervated rats, without any remaining baro- or chemosensitivity. Stimulation is thus due to a central activity in relation with the release of inhibitory influences. Phentolamine also causes hyperventilation after prazosin pretreatment indicating that the alpha 1 adrenergic blockade is not involved in the post-phentolamine stimulation. This is an alpha 2 adrenergic transmission dependent mechanism. Variation of the systemic blood pressure is not the main mechanism involved in the hyperventilation induced by phentolamine. Meanwhile, baroreceptor activity modulates the central response to the drug, as shown by the negative influence of the post-vasopressin arterial hypertension. Hyperoxia is also a modulating factor acting by two ways: an inhibition of the peripheral chemoreceptors activity is added to an arterial hypertension. On the other side, activation of these chemoreceptors by almitrine bismesilate increases the respiratory responses to phentolamine. As already shown by one of us (Lagneuax, 1986), phentolamine pretreated rats are more responsive to hypoxia and to almitrine. Moreover, these phentolamine pretreated rats are protected against cardiovascular collapses and against apnea, frequently observed during hypoxia without CO2 compensation.

Animals↗
PubMed1990

A randomized trial of two platinum combinations in patients with advanced non-small cell lung cancer: a preliminary report. European Organization for the Research and Treatment of Cancer--Lung Cancer Working Party.

A randomized study with cisplatin (120 mg/m2) or carboplatin (325 mg/m2) plus etoposide (100 mg/m2, days 1 to 3) in 162 evaluable patients with advanced non-small cell lung cancer (NSCLC) compared response and survival after treatment. No statistically significant difference in survival rates was detected; median survival was 25 weeks for patients receiving cisplatin and 24 weeks for those receiving carboplatin. The objective response rate was 25% for cisplatin plus etoposide and 20% for carboplatin plus etoposide. Granulocytopenia, diarrhea, and nephrotoxicity were significantly more frequent with cisplatin plus etoposide than with carboplatin plus etoposide. Severe nausea and/or vomiting occurred during 59 of 77 courses (77%) with cisplatin and 48 of 75 (64%) with carboplatin (P = .13). Unlike cisplatin plus etoposide, carboplatin plus etoposide was administered on an outpatient basis. At the dose used in the present study, carboplatin plus etoposide was as effective as but less toxic than cisplatin plus etoposide for NSCLC and could be given more easily.

Adenocarcinoma↗