Biomedical subjects

C Bertrand

Publications and source records attributed to C Bertrand.

At least 55 records · Page 3Linked to original sources

PubMed1999

Modulation of ET-1-induced contraction of human bronchi by airway epithelium-dependent nitric oxide release via ET(A) receptor activation.

1. The purpose of this work was to investigate whether endothelin-1 (ET-1) was able to induce the release of an inhibitory factor from the airway epithelium in isolated human bronchi and to identify this mediator as well as the endothelin receptor involved in this phenomenon. 2. In intact bronchi, ET-1 induced a concentration-dependent contraction (-logEC50 = 7.92+/-0.09, n = 18) which was potentiated by epithelium removal (-logEC50 = 8.65+/-0.11, n = 17). BQ-123 , an ET(A) receptor antagonist, induced a significant leftward shift of the ET-1 concentration-response curve (CRC). This leftward shift was abolished after epithelium removal. 3. L-NAME (3 x 10(-3) M), an inhibitor of nitric oxide (NO) synthase, induced a significant leftward shift of the ET-1 CRC, and abolished the potentiation by BQ-123 (10(-8) M) of ET-1-induced contraction. 4. In intact preparations, the ET(B) receptor antagonist BQ-788 induced only at 10(-5) M a slight rightward shift of the ET-1 CRC. In contrast, in epithelium-denuded bronchi or in intact preparations in the presence of L-NAME, BQ-788 displayed a non-competitive antagonism toward ET-1-induced contraction. 5. IRL 1620, a selective ET(B) receptor agonist, induced a contraction of the isolated bronchus (-logEC50=7.94+/-0.11, n= 19). This effect was not modified by epithelium removal or by BQ-123. BQ-788 exerted a competitive antagonism against IRL 1620 which was similar in the presence or absence of epithelium. 6. These results show that ET-1 exerts two opposite effects on the human airway smooth muscle. One is contractile via ETB-receptor activation, the other is inhibitory and responsible of NO release which counteracts via ETA-receptor activation the contraction.

Antihypertensive Agents↗

PubMed1999

Regulation of Escherichia coli cell division genes ftsA and ftsZ by the two-component system rcsC-rcsB.

Genes rcsC and rcsB form a two-component system in which rcsC encodes the sensor element and rcsB the regulator. In Escherichia coli, the system positively regulates the expression of the capsule operon, cps, and of the cell division gene ftsZ. We report the identification of the promoter and of the sequences required for rcsB-dependent stimulation of ftsZ expression. The promoter, ftsA1p, located in the ftsQ coding sequence, co-regulates ftsA and ftsZ. The sequences required for rcsB activity are immediately adjacent to this promoter.

Bacterial Proteins↗

PubMed1999

Malassezia spp carriage in patients with seborrheic dermatitis.

The role of Malassezia spp in seborrheic dermatitis (SD) is controversial. To compare the cutaneous density and the cultural characteristics of Malassezia in persons with or without SD, quantitative cultures were obtained by stripping the forehead with a tape placed on Leeming and Notman medium. Plates were incubated at 37 degrees C in a plastic bag, and colonies were counted after 14 days. High yeast density was defined as > 100 colony forming units (CFU)/tape. Volunteers were divided into four groups depending on their HIV serology [HIV (+) versus HIV (-) or unknown] and their clinical status (with or without SD). 126/129 cultures were positive (97.7%). Malassezia spp density was low on clinically normal skin in all HIV (-) persons (40/40) but was high in 8/34 (24%) HIV (+) persons without SD (p < 0.001). In SD patients, high densities were found in 10/22 (45%) HIV (+) and in 17/33 (52%) HIV (-) persons. The strains could be divided into three basic groups on the basis of their cultural characteristics. Colony morphology type A predominated on normal skin (72%), and morphology type C predominated on persons with SD (78%). High yeast density can be present without skin symptoms. The pathogenicity of Malassezia seems more likely to be determined by the subtype present on the skin rather than by its density.

Adult↗

PubMed1999

Fas-induced death of a murine pulmonary epithelial cell line: modulation by inflammatory cytokines.

Here we report that a murine pulmonary epithelial cell line (LA-4) expresses Fas (CD95) under resting conditions. Exposure of untreated cells to an anti-Fas monoclonal antibody induces apoptosis in a time- and dose-dependent fashion as revealed by cell viability and by propidium iodide staining followed by FACS analysis. Fas surface expression was increased, in a time-dependent fashion, by the inflammatory cytokines IL-1beta and TNF-alpha. Other inflammatory mediators such as IFN-gamma or endothelin-1 were without any effect. This increase in Fas expression was associated with an increase in sensitivity to anti-Fas-induced apoptosis of LA-4 cells. IL-4, which is known to induce CD95 resistance in other cell types, did not protect LA-4 cells against anti-CD95-induced cell death. These results suggest that Fas-induced apoptosis of epithelial cells may contribute to the epithelial shedding observed in asthmatic airways.

Animals↗

PubMed1999

Tachykinins and kinins in airway allergy.

Using models of airway diseases, our understanding of the role of tachykinins and kinins in airway pathophysiology has been greatly enhanced by the recent development of a large series of peptide, peptoid and non-peptide antagonists for tachykinin and kinin receptors. This article reviews the experimental findings of the contribution of kinins and tachykinins and their respective receptors, in models of airway inflammation in response to agents known to trigger or worsen asthma attacks, such as antigen and cold air. Some new antagonists, mostly of a non-peptide nature, exhibit excellent pharmacodynamic and pharmacokinetic profiles; a brief account of early clinical studies in which they have been used is also given.

Journal Article↗

PubMed1999

Systematic use of total vascular exclusion in 14 elective hepatic resections.

Between March 1992 and May 1995, 14 hepatic resections under total vascular exclusion were performed (10 major resections and 4 minor resections involving central segments). Mean age was 64 years (SD +/- 12). During hepatic resection, 4 patients required blood transfusion. The reason was a too low level of haemoglobin (< 10 gr/100 ml) to undergo Hepatic Vascular Exclusion (HVE) (1 patient), an unacceptable decrease in blood pressure following HVE leading to insertion of venovenous bypass (1 patient), or an extensive bleeding following removal of the clamps (2 patients). The 10 remaining patients did not need peroperative blood transfusion. Two patients were transfused after the 6th postoperative day. Complications usually described during HVE were not encountered except for one pleural effusion needing thoracocentesis.

Adult↗

PubMed1998

An immunohistochemical study of putative neuromodulators and transmitters in the centrifugal visual system of the quail (Coturnix japonica).

The aim of the present study was to analyze the neurochemical properties of the centrifugal visual system (CVS) of the quail using an immunohistochemical approach by testing 16 neuropeptides (angiotensin: ANG, bradykinin: BK, cholecystokinin, dynorphin, L and M-enkephalin, beta-endorphin: beta-END, galanin, alpha-neoendorphin, neurokinin A, neuropeptide Y (NPY), ocytocin, somatostatin, substance P, vasopressin, vasoactive intestinal polypeptide) and three neurotransmitters or their synthetic enzymes (choline acetyltransferase: ChAT, tyrosine hydroxylase: TH, serotonin: 5-HT and nitric oxide synthase: NOS, including the histochemical nicotinamide adenine dinucleotide phosphate diaphorase technique). For each substance, the somatic and afferent fiber and terminal labeling was analyzed within the nucleus isthmo-opticus (NIO) and the ectopic area (EA) and compared with that of retinopetal cell bodies labeled retrogradely with RITC following its intraocular injection (double-labeling procedure). The results showed that none of the centrifugal neurons were reactive to any of the substances tested. In contrast, all with the exception of ANG, BK and beta-END, labeled fibers and terminals within the EA and only four (ChAT, 5-HT, NPY and NOS) within the NIO. Possible sources of these immunoreactive fibers terminating in the NIO and EA were investigated by mapping the somatic immunolabeling of the different substances within brainstem regions previously shown by Miceli and other authors to project upon the centrifugal neurons. The data suggests that, besides the rapid retino-tecto-NIO-retinal loop, which facilitates the transfer of meaningful or more relevant information within particular portions of the visual field, the multiple afferent input which stems from various brainstem regions utilizes a wide range of neuroactive substances. Some of these afferent projections upon the centrifugal neurons appear to belong to nonspecific systems which might play a role in modulating the excitability of centrifugal neurons as a function of arousal.

Animals↗

PubMed1998

Characterization of the endothelin receptor subtype mediating epithelium-derived relaxant nitric oxide release from guinea-pig trachea.

1. The endothelin (ET) receptor subtype that mediates niric oxide (NO)-dependent airway relaxation in tracheal tube preparations precontracted with carbachol and pretreated with indomethacin was investigated. The release of NO induced by ET from guinea-pig trachea using a recently developed porphyrinic microsensor was also measured. 2. ET-1 (1 pM-100 nM) contracted tracheal tube preparations pretreated with the NO-synthase inhibitor, L-NMMA, and relaxed, in an epithelium-dependent manner, preparations pretreated with the inactive enantiomer D-NMMA. The effect of L-NMMA was reversed by L-Arg, but not by D-Arg. 3. The selective ET(B) receptor agonists, IRL 1620 or sarafotoxin S6c, both (1 pM-100 nM) contracted tracheal tube preparations in a similar manner either after treatment with D-NMMA or with L-NMMA. In the presence of the ET(A) receptor antagonist, FR139317 (10 microM), ET-1 administration resulted in a contraction that was similar after either L-NMMA or D-NMMA. In the presence of the ET(B) receptor antagonist, BQ788 (1 microM), ET-1 relaxed and contracted tracheas pretreated with D-NMMA and L-NMMA, respectively. 4. Exposure of tracheal segments to ET-1 (1-1000 nM) caused a concentration-dependent increase in NO release that was reduced by L-NMMA. IRL1620 (1 microM) did not cause any significant NO release. FR139317 (10 microM), but not, BQ788 (1 microM), inhibited the NO release induced by ET-1. 5. These results demonstrate that in the isolated guinea-pig trachea activation of ET(B) receptors results in a contractile response, whereas activation of ET(A) receptors cause both a contraction, and an epithelium-dependent relaxation that is mediated by NO release.

Animals↗

PubMed1998

An outbreak of Serratia marcescens infections related to contaminated chlorhexidine.

An outbreak of Serratia marcescens infections occurred in a university tertiary-care hospital. Alcohol-free chlorhexidine solutions were contaminated with S marcescens. The majority of patient and chlorhexidine strains had similar pulsed field-gel electrophoresis banding patterns. Chlorhexidine was recalled, and the rate of S marcescens isolation returned to baseline. Chlorhexidine without alcohol should not be used as an antiseptic.

Anti-Infective Agents, Local↗

PubMed1998

Penetration of ceftazidime into middle ear fluid in children with otitis media with effusion.

Twenty-five children with otitis media with effusion received ceftazidime 50 mg/kg intravenously before bilateral myringotomy with insertion of tympanostomy tubes. Concentrations of ceftazidime measured in serum and middle ear fluid exceeded 4 mg/L (i.e., largely above the minimal inhibitory concentrations for the gram-negative pathogens commonly recovered from children with otitis media) for at least 4 hours. Mean peak concentrations occurred 30 to 90 minutes after the injection and reached 11 to 14 mg/L. These results are in keeping with the clinical efficacy of ceftazidime in the treatment of chronic middle ear infections in children.

Ceftazidime↗

PubMed1998

Interleukin-1beta induces bradykinin B2 receptor gene expression through a prostanoid cyclic AMP-dependent pathway in human bronchial smooth muscle cells.

We investigated the hypothesis that inflammatory mediators such as interleukin-1beta (IL-1beta) might be responsible for the hyperreactivity of asthmatic patients to bradykinin. In cultured human bronchial smooth muscle cells, IL-1beta elicited a rapid and transient increase in the density of bradykinin B2 receptors without affecting their affinity for ligands. The increase in B2 receptors was correlated to an enhancement of inositol phosphate formation elicited by bradykinin, indicating its relevance to the contractile response of smooth muscle cells to bradykinin. The increase in receptor density was related to an increase in B2 receptor mRNA level corresponding to a 5-fold enhancement of the transcriptional rate and to a lengthened half-life of mRNA. These effects of IL-1beta were largely inhibited by indomethacin, suggesting the involvement of a prostanoid pathway in IL-1beta transduction process. An increase in prostaglandin E2 levels preceded the mRNA increase, confirming this involvement. Moreover, IL-1beta and prostaglandin E2 led to cAMP formation. We propose this predominant transduction pathway of IL-1beta to stimulate the transcription of the bradykinin B2 gene in human bronchial smooth muscle cells as a major mechanism involved in the hyperresponsiveness of asthmatic patients to bradykinin.

Bronchi↗

PubMed1998

[Analysis of hematopoietic growth factor prescriptions in 19 french cancer centers].

Medical prescription of hematopoietic growth factors (HGF) was analysed in 19 anticancer french centers during 2 months. About 4% of anticancer chemotherapeutic cycles prescribed during this period were supported by HGF prescription. The mean duration of treatment was 8 days. Among the 755 collected prescriptions, two tumor localizations represented about 50% of the prescriptions: malignant non Hodgkin lymphomas and breast cancer. The other main localizations concerned adult or pediatric soft tissue sarcomas (18%), testicular cancer (7%) and gynecologic tumors (6%). The prescription for primary prophylaxis for febrile neutropenia remains the main use of HGF (44%). The respect of the guidelines established by the F|d|ration nationale des centres de lutte contre le cancer was analyzed. Overall, 66% of the prescriptions were in adequation with these guidelines. Whereas the consommation of HGF decreased in the 19 considered institutions, it did not reach a plateau and could decrease in institutions which are awaked to the international and national recommendations.

Adult↗

PubMed1997

[Tracheal intubation in prehospital resuscitation: importance of rapid-sequence induction anesthesia].

OBJECTIVE: To investigate complications of emergency endotracheal intubation (EEI), possibly facilitated by rapid-sequence induction, in the prehospital critical care setting: 1) the difficulty of intubation; 2) the cardiorespiratory consequences of intubation; 3) the relationship between the occurrence of complications and prognosis. STUDY DESIGN: Prospective non randomized, open study. PATIENTS: All patients treated over a 5-month period by a physician-manned ambulance service and requiring EEI. METHODS: Patients were allocated either in with cardiac arrest (CA) group or a group with maintained spontaneous circulation (SC). Difficulty of intubation was assessed by the number of attempts. RESULTS: Two hundred and twenty-four consecutive EEI were carried out by physicians (46%) and residents (38%) not trained in anaesthesia, anaesthetists (8%), or nurse anaesthetists (7%). Trachea was intubated after a maximum of three attempts in all patients. Success rate at the first attempt was 91%. It was 92% in CA patients (n = 76) and 90% in SC patients (P = 0.59). Anaesthetic induction, with (n = 112) or without (n = 12) succinylcholine, was used to facilitate 84% of intubations in SC patients. Complications occurred in 30 patients (20%). There was no relationship between the latter and hospital mortality, duration of ventilatory support, duration of stay in the intensive care unit. CONCLUSION: In this study, EEI in SC patients was frequently facilitated by rapid sequence induction and was associated with a high success rate at the first attempt, as in CA patients. Morbidity was low. All physicians involved in emergency airway management should be skilled in this technique.

Adolescent↗

PubMed1997

Differential activation of the epithelial and smooth muscle NK1 receptors by synthetic tachykinin agonists in guinea-pig trachea.

1. The presence of tachykinin NK1 receptors have been shown in the epithelium and smooth muscle of guinea-pig airways. Previous data showed that substance P (SP), and the NK1 receptor agonist, [Sar9, Met (O2)11]-SP, relax guinea-pig tracheal tube preparations by stimulation of epithelial NK1 receptors and via nitric oxide (NO) release. However, the selective tachykinin NK1 receptor agonist, septide, was unable to produce this effect. The aim of the present study was to investigate the ability of a series of SP analogues to stimulate NK1 receptors of guinea-pig airway epithelium. 2. Isometric tension was recorded in isolated tracheal tube preparations in which compounds were administered intraluminally in the presence of phosphoramidon, indomethacin (both 1 microM) and the tachykinin NK2 receptor antagonist, SR 48,968 ((S)-N-methyl N-(4-acetyl-amino-4-phenylpiperidino)-2-(3,4-dichlorophenyl)butyl)benzam ide) (0.1 microM). Cumulative concentration-response curves were obtained in preparations under resting tone or in preparations precontracted with acetylcholine (ACh, 10 microM). 3. Contractile responses to low concentrations (0.1-10 nM) of substance P (SP) and the selective agonist of NK1 receptors, [Pro9]-SP. in non precontracted tracheae were higher in preparations pretreated with the NO-synthase inhibitor, NG-monomethyl L-arginine (L-NMMA, 100 microM) than in preparations pretreated with its inactive enantiomer D-NMMA (100 microM). Tracheal tube preparations precontracted with ACh and pretreated with D-NMMA were relaxed by low concentrations of SP and [Pro9]-SP (0.1-10 nM). In contrast, after pretreatment with L-NMMA, SP and [Pro9]-SP contracted tracheae at all the concentrations tested. 4. Concentration-response curves to the NK1 receptor agonists, SP methyl ester, [Apa9-10]-SP and [pGlu6] SP (6-11) obtained in non-precontracted tracheae were similar in the presence of either D-NMMA or L-NMMA. SP methyl ester, [Apa9-10]-SP and [pGlu6] SP (6-11) did not produce any relaxation, but instead, cause contractions in tracheal tube preparations precontracted with ACh and pretreated with D-NMMA. Concentration-response curves produced by all these agonists were similar in preparations precontracted with ACh and pretreated with L-NMMA or D-NMMA. 5. In guinea-pig tracheal tube preparations two groups of NK1 receptor agonists can be distinguished: one group, including [Pro9]-SP, stimulator epithelial NK1 receptors, the other group, including SP methyl ester, [Apa9-10]-SP and [pGlu6] SP (6-11), does not. One possible explanation for these findings and for the existence of compounds with a peculiar 'septide-like' pharmacological profile in the guinea-pig trachea could be the recently proposed phenomenon referred to as 'agonist-directed receptor trafficking'.

Animals↗

PubMed1997

ET-1 cooperates with EGF to induce mitogenesis via a PTX-sensitive pathway in airway smooth muscle cells.

We have examined the mitogenic effect of endothelin-1 (ET-1) alone or in combination with epidermal growth factor (EGF) in cultured airway smooth muscle cells (ASM) from guinea pig. ET-1 showed a weak mitogenic activity compared with the effect of EGF. However, when ET-1 and EGF were applied simultaneously, ET-1 synergistically enhanced the mitogenic activity of EGF. Neither inhibition of phospholipase C-beta nor depletion of protein kinase C affected this synergism. On the other hand, pertussis toxin (PTX), a Gi protein inhibitor, abolished the synergistic effect of ET-1 on EGF-induced mitogenesis. ET-1 induced a transient mitogen-activated protein (MAP) kinase activation peaking at 5 min. In contrast, EGF induced a stronger signal that was maintained for up to 20 min. However, concomitant stimulation of ASM with ET-1 and EGF caused an enhanced MAP kinase activation compared with EGF alone. Moreover, PTX abolished the enhanced MAP kinase activation observed in this condition. These results indicate that ET-1 can interact with an EGF-induced mitogenic axis through the Gi protein-dependent pathway, which is distinct from its direct mitogenic pathway.

Animals↗

PubMed1997

Endothelin receptor antagonists inhibit antigen-induced lung inflammation in mice.

In this study, we have examined the effect of endothelin (ET) receptor antagonists on lung granulocyte inflammation after antigen challenge in sensitized mice. The antagonists used were BQ-123, an ETA antagonist, BQ-788, an ETB antagonist, and SB209670, an ET(A&B) antagonist. Thirty minutes prior exposure to aerosolized ovalbumin, ET antagonists (50 pmol/mouse) were administered directly into the lungs of sensitized Balb/c mice via the intranasal route. BQ-123 and SB209670 significantly decreased eosinophil number in the bronchoalveolar lavage fluid by 47 and 68%, respectively. Both compounds also inhibited neutrophil infiltration into the lungs. In contrast, BQ-788 did not affect granulocyte infiltration. A similar inhibition of lung eosinophilia was also obtained with an anti-ET antibody applied via the intranasal route. BQ-123 and SB209670, but not BQ-788, significantly increased the production of interferon-gamma (Th1 cytokine) from purified lung Thy1.2+ cells without affecting interleukin-4 and interleukin-5 (Th2 cytokines) secretion. Furthermore, neutralizing antibody against interferon-gamma prevented the inhibitory effect of the ETA antagonist. Taken together, these results suggest an important pathophysiologic role for ET in the development of lung inflammation in asthma and highlight the potential of ET antagonists for the treatment of the disease.

Administration, Intranasal↗

PubMed1997

[Study of the toxicity and results of intraperitoneal hyperthermic chemotherapy in 28 patients with peritoneal carcinomatosis].

Based on a few previous studies, intra-peritoneal hyperthermic perfusion (IPHP) with Mitomycin C could become a beneficial treatment for peritoneal carcinomatosis. Twenty eight patients with peritoneal carcinomatosis arising from intra-abdominal cancers were treated by IPHP, Mitomycin C, diluted in 3 liters of saline solution warmed to a mean temperature of 45 degrees C, was injected into the abdominal cavity for one hour. Median survival for the whole series (postoperative mortality included) was 260 days. For patients with incomplete resection, median survival was 104 days. For patients with complete resection of carcinomatous nodules larger than 3 mm (19 patients), it was 450 days. In this group, actuarial survival was 56% at 1 year and 42% at 2 years. Only 5 (18%) of the 28 patients developed ascitic effusion during follow-up. These results confirm the efficacity of IPHP on ascitic effusion and on survival rate in patients with nearly complete resection of peritoneal carcinomatosis.

Abdominal Neoplasms↗

PubMed1996

IL-4 differentiates naive CD8+ T cells to a "Th2-like" phenotype: a link between viral infections and bronchial asthma.

Viral infections of the lung have been postulated to be a major factor in the etiology of bronchial asthma, a disease characterized by eosinophilic inflammation of the airways. In addition, upper respiratory tract infection in asthmatic individuals results in an exacerbation of the disease. Nevertheless, the mechanisms by which viral infection leads to disease exacerbation are poorly understood. CD8+ T cells play an important role in the host defense responses against viral infection, although to date, there are no reports to suggest that CD8+ T cells play any role in eosinophil recruitment. In the present study, we report that CD8+ T cells activated by either immobilized CD3 mAb or specific antigen can switch to a phenotype that produces Th2 cytokines and secretes less IFN-gamma. Moreover, in vivo, if a lung mucosal Th2 immune response exists, then antigen-specific activation of CD8 cells results in the development of lung eosinophilic inflammation mediated by the secretion of IL-5 from CD8+ T cells. These results may explain the link between viral infections and bronchial asthma, as this IL-4-dependent switch to CD8+ T cells to IL-5 secretion may not only exacerbate asthma by recruiting eosinophils into the lungs, but the impaired IFN-gamma production may also lead to delayed viral clearance.

Animals↗