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C Bertrand

Publications and source records attributed to C Bertrand.

At least 91 records · Page 5Linked to original sources
PubMed1995

A simple quantitative culture of Malassezia spp. in HIV-positive persons.

BACKGROUND: Etiological role of Malassezia spp. remains controversial in certain skin diseases. OBJECTIVE: To adapt a 'tape method' for quantitative culture of Malassezia spp. METHOD: Samples for culture were taken from clinically normal forehead skin of HIV-positive and negative persons by stripping with a tape that was then placed on Leeming & Notman medium. The number of colonies was counted after 14 days. RESULTS: 74/78 (94.8%) cultures were positive, for a median count of 9 CFU/tape (range 0 to > 200). High skin density of Malassezia spp., defined as more than 100 CFU/tape, was found in 7/38 (18.4%) HIV-positive persons and was absent (0/40) in the HIV-negative group (p < 0.01). CONCLUSION: The method used is simple, unexpensive and reliable. High Malassezia spp. density was only found in HIV-positive patients.

Colony Count, Microbial↗
PubMed1995

Interleukin-4 is required for the induction of lung Th2 mucosal immunity.

Aerosol antigen challenge of ovalbumin-sensitized mice induced an eosinophilic airway inflammation that was dependent on interleukin (IL)-5 and CD4+, but not CD8+, T lymphocytes. The involvement of the Th2 phenotype of CD4+ T cells was supported by demonstrating that FACS-sorted purified lung T cells from sensitized, but not control, mice produced IL-4, IL-5, and IL-10 after activation of the CD3/TCR complex. To determine the role of IL-4 in this process, we used mice in which the gene for IL-4 was deleted by homologous recombination. Antigen challenge of IL-4 gene-targeted mice resulted in a marked attenuation of eosinophilic inflammation and IL-5 secretion. To more fully understand the time when IL-4 was involved, we administered a neutralizing anti-IL-4 antibody (11B11) either immediately before antigen challenge or during immunization. Inhibition of IL-4 before antigen challenge had little effect on antigen-induced eosinophil infiltration. However, when 11B11 was administered during immunization, there was a marked reduction in eosinophil infiltration. Cross-linking of the CD3/TCR complex of FACS-sorted lung T cells revealed that only when anti-IL-4 was administered during immunization was there an inhibition of T cell-derived IL-5 and IgE production. These results suggest that IL-4 is central both to the induction of a local Th2 response and to the development of eosinophilic inflammation of the lung. Moreover, we suggest a sequential involvement of IL-4 and IL-5, with IL-4 committing naive T cells to a Th2 phenotype which upon activation by aerosol provocation secrete IL-5, resulting in eosinophil accumulation.

Animals↗
PubMed1995

Activation of the Fas receptor on lung eosinophils leads to apoptosis and the resolution of eosinophilic inflammation of the airways.

While considerable progress has been made in understanding the events by which eosinophils accumulate in various pathophysiological conditions, the mechanisms controlling the resolution of eosinophilic inflammation are poorly understood. In the present study, we demonstrate that lung eosinophils obtained by bronchoalveolar lavage (BAL) after aerosol allergen provocation of immunized mice expressed the Fas receptor. Stimulation of purified eosinophils in vitro with a monoclonal anti-Fas mAb (1 ng-1 microg/ml) induced a dose/time dependent loss of cell viability from 24-72 h. Measurement of DNA fragmentation with propidium iodide confirmed that anti-Fas induced eosinophil death by apoptosis. While incubation with IL-3, IL-5, or GM-CSF prevented spontaneous apoptosis, these factors failed to prevent anti-Fas induced apoptosis. Administration of anti-Fas mAb to the lungs after the induction of a lung eosinophilia increased the number of peroxidase positive macrophages in BAL fluid 4-12 h later which was followed by a marked reduction in the number of eosinophils in the airways. Importantly, Fas-mediated resolution of eosinophilic inflammation occurred in the absence of any overt secondary inflammatory changes in the lungs. We speculate that defects in this pathway may at least in part explain the chronic eosinophilic inflammation often observed in the lungs of asthmatic individuals.

Animals↗
PubMed1994

Tachykinins and kinins in antigen-evoked plasma extravasation in guinea-pig nasal mucosa.

The plasma extravasation evoked by instillation of 5% ovalbumin in the nasal mucosa of sensitized guinea-pigs was potentiated by the neutral endopeptidase inhibitor, phosphoramidon, and was reduced by the tachykinin NK1 receptor antagonist, CP-96,345. The bradykinin B2 receptor antagonist, HOE 140, also reduced the plasma extravasation evoked by the antigen. The combination of HOE 140 and CP-96,345 did not increase further the inhibition caused by HOE 140 alone. Plasma extravasation evoked by instillation of capsaicin was abolished by CP-96,345. HOE 140 blocked and CP-96,345 markedly reduced plasma extravasation caused by instillation of bradykinin. Plasma extravasation evoked by instillation of substance P was not affected by HOE 140. We conclude that antigen challenge causes plasma extravasation in the nasal mucosa of sensitized guinea-pigs, an effect that is due in part to the release of tachykinins from sensory nerve endings. Our evidence suggests that tachykinin release in response to antigen is provoked mainly by the release of kinins.

Animals↗
PubMed1994

Pharmacological characterization of tachykinin-induced intracellular calcium rise in a human NK2 receptor transfected cell line.

We have examined the effect of various natural and synthetic tachykinins on the steady state Ca(++)-rise ([Ca++]i) in transfected chinese hamster ovary cells expressing recombinant human Neurokinin 2 (NK2) receptors. The rank order of potency with natural tachykinins was NeurokininA > Neurokinin B > Eledoisin > Physaelamin > substance P. The selective NK2 agonist, [beta-Ala8]NKA(4-10) was very potent, with an EC50 value of 4.83 x 10(-9) M whereas Senktide, MePhe7NKB and Sar9, (MetO2)11 substance P, selective NK3 and NK1 agonists, respectively, did not have any effect on [Ca++]i in hrNK2CHO cells, suggesting a selective and preferential recognition and activation of NK2 receptors in these cells. (+/-) SR 48968, a selective NK2 antagonist, abolished the beta-AlaNKA-induced [Ca++]i with an IC50 value of 0.7 nM. Two other peptidic NK2 antagonists, MEN 10376 and L-658977, were less active with IC50 values of 49 nM and 5.29 microM, respectively. In contrast, (+/-) CP-96,345 and (+/-)CP-99,994 and RP 67580, all selective NK1 antagonists, did not have any effect on the beta-AlaNKA-induced [Ca++]i in hrNK2CHO cells (+/-) SR 140333, a potent and selective NK1 antagonist, had a 35% inhibition under similar conditions. These data demonstrate a high selectivity and sensitivity to NK2 receptor mediated [Ca++]i in rhNK2R-CHO cells and may be of value as a rapid, selective test of drug action at the human NK2 receptors in vitro.

Animals↗
PubMed1994

Effect of epinephrine on end-tidal carbon dioxide pressure during prehospital cardiopulmonary resuscitation.

This prospective study was designed to quantify the effect of epinephrine on end-tidal PCO2 (PetCO2) during prehospital cardiopulmonary resuscitation (CPR) in humans. It included 20 patients (age range, 26 to 90 years) who presented in ventricular asystole on arrival of the prehospital medical team. Protocol began 5 minutes after tracheal intubation and during chest compressions. Mechanical ventilation was applied at constant rate and tidal volume. PetCO2 was measured before and 3 minutes after peripheral intravenous (IV) injection of 2 mg epinephrine. No other resuscitative drugs were administered during the study period. Mean PetCO2 decreased from 16.7 +/- 9.3 mm Hg before epinephrine to 12.6 +/- 7.1 mm Hg after epinephrine. The mean change in PetCO2 was 4.15 +/- 3.5 mm Hg (P < .0001). Four patients exhibited return of spontaneous circulation (ROSC). The decrease in PetCO2 was similar between the patients who exhibited ROSC and those who did not. There was a significant relationship between the epinephrine-induced change in PetCO2 and the PetCO2 value before epinephrine injection (r = .760; P < .0001). This study demonstrates a variable decrease in PetCO2 after IV epinephrine injection during CPR. Isolated PetCO2 readings may be misleading in assessing CPR efficacy or predicting outcome, and continuous measurement is recommended.

Adult↗
PubMed1994

Epithelium modulates the kinetics of the response to substance P and its intrinsic activity in the guinea-pig trachea.

The contractile response of guinea-pig tracheal preparations with or without epithelium to substance P has been studied in the presence or absence of thiorphan, an endopeptidase 24.11 inhibitor, paying special attention to the kinetics of the response. Without thiorphan, the response to substance P was greater in tracheal preparations without epithelium than in tracheal preparations with epithelium. The concentration-response curve was shifted to the left in the absence of the epithelium. In the presence of 10 microM thiorphan, the maximal contractile response induced by single doses of substance P (0.1 to 10 microM) was lower in tracheal preparations without epithelium. The maximal responses required 10 min in tracheal preparations with epithelium and 2 min in tracheal preparations without epithelium. These epithelium-dependent differences of reactivity remained in the presence of lipoxygenase or cyclooxygenase inhibitors and of selective antagonists of muscarinic, serotoninergic and histaminergic receptors, after the pre-treatment of tissues with capsaicin or compound 48/80 and in the presence of tetrodotoxin. The profile of the cumulative concentration-response curves for substance P was largely dependent on the time between two successive doses. When this time was short (2-4 min), curves established with or without the epithelium were parallel and both reached similar maximal values (2696 +/- 214 mg and 2780 +/- 62 mg, respectively). The curve in tracheal preparations without epithelium was slightly shifted to the left (EC50s: 24 +/- 10 nM and 78 +/- 19 nM). When this time was longer (10 min, ie corresponding to the time required for a full response to a single dose in intact trachea) the potency of substance P was not modified (EC50s: 13 +/- 3 nM and 52 +/- 11 nM), but a lower maximal response was observed with tracheal preparations without epithelium (1440 +/- 182 mg and 2832 +/- 209 mg). Similar results were observed with neurokinin A and neurokinin B. Thus, the removal of the epithelium led to a more rapid contraction and to a decrease of the maximal response to neurokinins, ie a decreased intrinsic activity, a property known to be drug- and tissue-dependent. These data suggest that the intrinsic activity of drugs depends on the cellular environment of the target cells in a tissue and is partly related to the diffusion and metabolism of drugs and to drug-induced hyporeactivity of the target cells.

Animals↗
PubMed1994

Role of kinins in anaphylactic-induced bronchoconstriction mediated by tachykinins in guinea-pigs.

1. In the present study, we have investigated the role of kinins in allergen-induced bronchoconstriction. 2. Anaesthetized guinea-pigs were sensitized to ovalbumin, ventilated artificially, pretreated with atropine (1.4 mumol kg-1, i.v.) and total pulmonary resistance (RL) measured. In preliminary studies in the presence of the neutral endopeptidase inhibitor, phosphoramidon (4.5 mumol kg-1, i.v.), the bradykinin B2 receptor antagonist Hoe 140 (0.1 mumol kg-1, i.v.) completely abolished the increase in RL following aerosolized bradykinin (1 mM, 40 breaths), but had no effect on the increase in RL following aerosolized neurokinin A (NKA, 10 microM, 40 breaths). On the other hand, a combination of the NK1 (CP-96,345, 2 mumol kg-1, i.v.) and NK2 (SR 48968, 0.3 mumol kg-1, i.v.) tachykinin receptor antagonists abolished completely the increase in RL produced by NKA and partially inhibited the increase in RL produced by bradykinin. These results confirm previous studies that suggest that bradykinin induces the release of tachykinins from sensory nerves in guinea-pig airways. 3. Aerosolized ovalbumin (0.5%, 5 breaths) increased RL in sensitized guinea-pigs pretreated with atropine (1.4 mmol kg-1, i.v.), an effect that began within 2 min and reached a maximum within 5 min; RL remained above baseline at 20 min. Pretreatment with the bradykinin B2 receptor antagonist, Hoe 140, decreased the bronchoconstrictor effect of ovalbumin markedly at 10 to 20 min. In the presence of phosphoramidon (4.5 mumol kg-1, i.v.) the inhibition induced by Hoe 140 was apparent earlier and remained over the 20 min period of study. 4. Pretreatment with a combination of NK1 (CP-96,345) and NK2 (SR 48968) tachykinin receptor antagonists also markedly inhibited ovalbumin-induced bronchoconstriction; addition of the bradykinin B2 receptor antagonist to the NK1 and NK2 tachykinin receptor antagonists had no additional inhibitory effect on antigen-induced bronchoconstriction.5. These findings confirm that activation of sensory nerves to release tachykinins in guinea-pig airways contribute to antigen-induced bronchoconstriction, and provide evidence that tachykinin release is due to kinins generated during the allergic response.

Adrenergic beta-Antagonists↗
PubMed1994

Airway vasodilation by bradykinin is mediated via B2 receptors and modulated by peptidase inhibitors.

We studied the effect of exogenous bradykinin on blood flow in the airway microcirculation of anesthetized F344 rats in vivo. We made three successive determinations of airway blood flow and cardiac output using a modification of the reference sample microsphere technique. Injection of bradykinin into the left ventricle increased airway blood flow in a dose-related manner. Pretreatment with the bradykinin B2 receptor antagonist, Hoe 140, completely abolished bradykinin-, but not histamine-induced vasodilation. A bradykinin B1 receptor agonist, [des-Arg9]bradykinin, did not affect airway blood flow. We also studied the effect of inhibitors of angiotensin-converting enzyme (captopril) and neutral endopeptidase (phosphoramidon) on bradykinin-induced vasodilation. Pretreatment with captopril, but not phosphoramidon, potentiated the bradykinin-induced vasodilation. However, the addition of phosphoramidon further potentiated the effect of captopril. We conclude that injection of bradykinin into the left ventricle produces a dose-related vasodilation in the airway microcirculation mediated via B2 receptors, an effect that is modulated primarily by angiotensin-converting enzyme and, to a lesser extent, by neutral endopeptidase.

Animals↗
PubMed1994

Dextromethorphan test for evaluation of congenital predisposition to lung cancer.

We report the results of an investigation conducted in 992 healthy control subjects (854 adults and 138 adolescents) and in 116 subjects with lung cancer (LC) for the purpose of detecting those individuals with a possible genetic predisposition to lung cancer. The test consists of the oral administration of 64 mumol of dextromethorphan (DMP) with collection of urine samples over the following 8-h period and urine assay of the drug (DMP) and its main metabolite, dextrorphan (DOP). The ratio of the urinary concentrations of DMP to those of DOP is called the metabolic ratio (DMP/DOP) and is inversely proportional to the DMP demethylation rate. The pattern of the metabolic ratio (Log10 DMP/DOP) allowed, using a maximum likelihood approach, the identification of three subpopulations in the 854 control subjects (adults): (1) probable homozygous extensive metabolizers with Log10 DMP/DOP < -1.74 (73.1 percent); (2) probable heterozygous intermediate metabolizers with Log10 DMP/DOP in the -1.74 to -0.40 range (22.3 percent); and (3) probable homozygous poor metabolizers with Log10 DMP/DOP > -0.4 (4.6 percent). Most of the patients with LC (89 percent) were probable homozygous extensive metabolizers. As the latter have a cancer risk that is 2.54-fold greater than that of intermediate metabolizers (95 percent confidence interval [CI]: 1.37 to 4.73) and 7.43-fold greater than that of poor metabolizers (95 percent CI: 1.01 to 54.5), their identification by means of the DMP test may be particularly useful for subjects exposed to environmental and occupational carcinogens. The phenotype test used is similar to that of the debrisoquin test, but presents the advantage that DMP is a widely used, harmless drug with a faster and simpler urinary assay procedure.

Adolescent↗
PubMed1994

[Microscopic diagnosis of onychomycoses].

INTRODUCTION: The microbiological identification of onychomycosis may be uncertain as some fungi growing in culture from this material are not necessarily pathogen and invasive. Conversely, the negativity of a culture is not rare even when fungi are seen by microscopy. MATERIALS AND METHODS: We compared the information brought by standard histological examination, immunohistochemistry and in vivo confocal microscopy. RESULTS: The histological examination of nails is of importance in this pathology. We present a laboratory technique that proves to be easy and rapid. We report diagnostic criteria allowing the distinction between dermatophytes, yeasts and non-dermatophyte molds. The standard microscopic examination may further be improved by immunohistochemistry using some antibodies to fungi. In vivo confocal microscopy is a technique for the future. The dermatologist will be able to see fungi in the nail at the clinical examination, without any sampling or peculiar preparation. CONCLUSION: The histological examination is a routine technique useful for defining the nature and localization of fungi in the nail plate. Immunohistochemistry applied to onychomycosis is an experimental approach bringing prominent informations about the identification of fungi. In vivo confocal microscopy is a door opened to the future.

Arthrodermataceae↗
PubMed1994

Prognostic implications of transient left ventricular cavitary dilation during exercise and dipyridamole-thallium imaging.

OBJECTIVE: To determine the prognostic implication of exercise and dipyridamole-induced transient left ventricular cavitary dilation (TLVD). DESIGN: TLVD was observed and a follow-up obtained in 61 patients after exercise and in 62 patients following dipyridamole infusion. PATIENTS: There was no statistical difference between groups in terms of sex, history of hypertension, diabetes, renal failure, previous myocardial infarction, severity of angina syndrome, congestive heart failure, resting electrocardiographic (ECG) abnormalities, clinical or ECG signs of ischemia during stress, number of reversible perfusion defects on thallium images or duration of follow-up (21 months). RESULTS: Dipyridamole patients were slightly older (64 versus 57 years) and displayed more thallium redistribution (P = 0.002). After a mean follow-up of 21 months, both fatal and nonfatal (myocardial infarction or cardiac death) cardiac events were more frequent in the dipyridamole group (50% versus 9%, P = 0.0001). CONCLUSIONS: Patients with dipyridamole-induced TLVD are at greater risk than those with exercise-induced TLVD at the authors' institution.

Aged↗
PubMed1993

Budesonide inhibits plasma extravasation induced by capsaicin and by substance P in the rat nasal mucosa.

We studied the effect of the locally administered glucocorticoid budesonide on plasma extravasation induced by capsaicin and by substance P (SP) in the nasal mucosa of pathogen-free rats. Using Evans blue dye as a tracer, we measured plasma extravasation induced by capsaicin (150 micrograms kg-1 i.v.) or SP (0.5 and 2.5 micrograms kg-1 i.v.) in the rat naso- and maxilloturbinates after pretreatment with budesonide (0.1-50 micrograms twice/day for 2 days in the right nostril; 50 micrograms only for SP) or its vehicle. We found that budesonide inhibits plasma extravasation induced by capsaicin in a dose-dependent fashion in the nasal cavity. After the highest dose (50 micrograms) of budesonide, the values of Evans blue in the nasal mucosa were not different from the values observed after capsaicin vehicle alone. Budesonide also reduced plasma extravasation induced by capsaicin in the trachea and the urinary bladder of the rats in a dose-dependent fashion. Budesonide (50 micrograms) delivered to the nose inhibited the plasma extravasation caused by 0.5 but not by 2.5 micrograms SP kg-1 in the nasal mucosa. We conclude that the postjunctional part of the neurogenic pathway is a target for glucocorticoid antiinflammatory action in the nasal mucosa, at least of the rat. Budesonide's effect on organs other than the nose can be explained by systemic absorption.

Administration, Topical↗
PubMed1993

Role of kinins in the vascular extravasation evoked by antigen and mediated by tachykinins in guinea pig trachea.

Tachykinins released from sensory nerves mediate, at least in part, the plasma extravasation induced by allergen challenge to the airways of sensitized guinea pigs. We investigated the role of kinins in this activation of sensory nerves. We found that the increase in Evans blue dye extravasation evoked by aerosol of bradykinin (100 microM, 2 min) in the presence of phosphoramidon (2.5 mg/kg, i.v.) was abolished completely by the selective B2 bradykinin antagonist, HOE 140 (0.1 mumol/kg, i.v.), and was inhibited (60%) by the selective NK1 tachykinin receptor antagonist, CP-96,345 (2 mumol/kg, i.v.). Plasma extravasation evoked by aerosolized substance P (10 microM/kg, 2 min) in presence of phosphoramidon was abolished by CP-96,345, but was not affected by HOE 140. The extravasation of the Evans blue dye evoked by OVA (5%, 2 min) in sensitized guinea pigs was reduced by HOE 140 (45%) when the animals were perfused after 5 min and by 39% when perfusion was performed at 10 min. In the presence of phosphoramidon, the response to OVA at 10 min was reduced by 57% by HOE 140 and by 72% by CP-96,345. The combination of CP-96,345 and HOE 140 did not further increase the inhibition obtained with CP-96,345 alone. The results provide evidence that the activation of sensory nerves that contribute to Ag-evoked plasma extravasation is due to kinin release. The contribution of this cascade of events may be exaggerated in pathophysiologic conditions in which neutral endopeptidase is down-regulated.

Animals↗
PubMed1993

Levodropropizine reduces capsaicin- and substance P-induced plasma extravasation in the rat trachea.

We investigated the effect of the non-opioid, peripherally acting antitussive agent levodropropizine to reduce neurogenic plasma extravasation in the rat trachea. Levodropropizine (10, 50 and 200 mg/kg) reduced in a dose-dependent manner the extravasation of Evans blue dye evoked by capsaicin. Levodropropizine inhibited also substance P-evoked extravasation, whereas it did not affect the extravasation evoked by platelet activating factor. Levodropropizine (10 and 100 microM) did not affect the contraction produced by [Sar9,Met(O2)11]substance P, a selective agonist for tachykinin NK1 receptors, in the rat urinary bladder in vitro. These data indicate that levodropropizine inhibits capsaicin-induced plasma extravasation: (a) acting at a postjunctional level; (b) exhibiting neuropeptide selectivity and; (c) via a mechanism independent of tachykinin NK1 receptor blockade. Irrespective of the mechanism, this novel antiinflammatory action of levodropropizine underlines its potential role in inflammatory airway diseases such as bronchial asthma.

Animals↗
PubMed1993

Tachykinins mediate contraction of the human lower esophageal sphincter in vitro via activation of NK2 receptors.

The contractile response to natural tachykinins and selective peptide agonists for tachykinin receptors was studied in strips of circular smooth muscle of human lower esophageal sphincter in vitro. The effects of phosphoramidon, which inhibits neutral endopeptidase (EC.3.4.24.11) and of the non-peptide compounds, SR 48968 and CP-96,345, which selectively block NK1 and NK2 receptors, respectively, were also investigated. Substance P, neurokinin A and neurokinin B produced a concentration-dependent contractile response. The rank order of potency was neurokinin A > neurokinin B > substance P. Phosphoramidon (1 microM) potentiated the response to substance P without changing the order of potency of natural tachykinins. The NK2-selective agonist, ([ beta Ala8]neurokinin A-(4-10)), produced a concentration-dependent contraction. The NK1 ([Sar9,Met(O2)11]substance P, 1 microM) and NK3 ([MePhe7]neurokinin B, 1 microM) selective agonists, however, did not exert any contractile effect. The selective NK2 antagonist, SR 48968, potently inhibited in a concentration-dependent (10 nM-1 microM) manner the response to neurokinin A, without affecting the response to carbachol. The selective NK1 antagonist, CP-96,345 (1 microM), did not affect the response to neurokinin A. These results indicate that tachykinins contract the circular muscle of human lower esophageal sphincter, and that this effect is mediated by NK2 receptor stimulation. Moreover, a phosphoramidon-sensitive mechanism plays a role in the regulation of the response to substance P.

Benzamides↗