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B Arnoux

Publications and source records attributed to B Arnoux.

At least 55 records · Page 3Linked to original sources
PubMed1990

Towards the understanding of the function of Rb sphaeroides Y wild type reaction center: gene cloning, protein and detergent structures in the three-dimensional crystals.

We report various experiments aimed at the resolution of the 3-dimensional structure of the photosynthetic reaction center from wild type Y Rhodobacter sphaeroides. The genes encoding the L and M polypeptides have been cloned and sequenced. They bear 2 mutations each when compared to those already sequenced in another Rb sphaeroides strain (2.4.1). In the L gene, these codon changes are silent. In the M gene, one is silent and the other one leads to a Leu-Met substitution at position 140. At the present stage of the refinement of the X-ray data (0.3 nm resolution) the structure of the Y reaction center is shown to be highly similar to that of the Rhodopseudomonas viridis reaction center. The binding of spheroidene on the M side of the Y reaction center is shown to be determined by hydrophobic interactions with neighboring amino acids and by steric factors. Preliminary results concerning the localization of the detergent (beta-octylglucoside) in the unit cell are presented. This method combines low angle neutron scattering at different contrasts in H2O/D2O with X-ray crystallographic data.

Carotenoids↗
PubMed1990

Inhibition of human and rabbit platelet activation by Ketotifen.

The effects of Ketotifen and disodium cromoglycate were investigated on human and rabbit platelet activation. Ketotifen inhibited dose-dependently human and rabbit platelet aggregation. The paf-acether pathway was the most markedly influenced by Ketotifen in human and rabbit platelets (IC50 = 38.8 +/- 7.7 microM and 7.2 +/- 4.5 microM respectively) as compared to adenosine diphosphate (IC50 greater than 100 microM and 79 +/- 19 microM) and to arachidonic acid (IC50 greater than 100 microM and 98 +/- 28 microM). Similar concentrations of Ketotifen inhibited the ATP release from human platelets induced by paf-acether. Disodium cromoglycate up to 5 x 10(-4) M did not inhibit platelet aggregation induced by paf-acether, adenosine diphosphate and arachidonic acid.

Adenosine Triphosphate↗
PubMed1990

[Model of protease I from the crab Uca pugilator].

Collagenolytic protease I from the fiddler crab Uca pugilator is one of the serine proteases of the trypsin family. A graphic molecular model was built on the basis of the sequences and crystalline structures of four homologous proteins which were superimposed in order to identify structurally conserved regions. The sequence of protease I was matched to sequences of the reference proteins, without allowing any deletions or insertions in these regions. For structurally variable regions, the most similar sequences of the four reference proteins were selected. Intramolecular steric clumping due to replacement of reference side-chains by protease I side-chains were corrected by adjusting side-chain conformations. The model was optimized by energy minimization. The conformation of the primary specificity pocket for protease I predicted by the model indicated a preference for P1 hydrophobic or positively charged substrates. This prediction is consistent with biochemical findings. Because soya bean trypsin inhibitor (STI) has been shown to inhibit protease I, a tentative model of the complex was constructed and possible protease I-STI interactions were analyzed.

Animals↗
PubMed1989

Structure of spheroidene in the photosynthetic reaction center from Y Rhodobacter sphaeroides.

The structure of the reaction center of Y Rhodobacter sphaeroides has been solved at 3 A resolution, using the atomic coordinates of the reaction center from the carotenoidless mutant R26 Rhodobacter sphaeroides. The structure has been refined by a stimulated annealing with the computer program X-PLOR, leading to a crystallographic R factor of 0.22 using reflections between 8 and 3 A. The spheroidene molecule which is bound to the Y reaction center has been fitted in the electron density map as a 15-cis isomer with a highly asymmetric structure. The cis-bond is located at proximity from ring 1 of the accessory bacteriochlorophyll on the inactive M side. The nature of the cis-bond was confirmed by resonance Raman spectra obtained from Y reaction center crystals. The structure of spheroidene in Y reaction center is compared to that proposed for 1,2-dihydroneurosporene in Rhodopseudomonas viridis reaction center crystals.

Bacterial Proteins↗
PubMed1989

Evidence of PAF-acether metabolic pathway activation in antigen challenge of upper respiratory airways.

Lyso-PAF-acether and PAF-acether (formerly platelet-activating factor) were detected in nasal secretions from patients with hay fever who underwent local antigen challenge. Lyso-PAF release was observed in 12 of 13 patients, with a maximum (p less than 0.001) 5 min after stimulation and a progressive decrease during the first hour. PAF was detected in the 5-min postchallenge nasal washings from two of 13 subjects. After HPLC, this mediator was found in four of seven postchallenge nasal washings submitted to this procedure, with a peak 5 min and 10 min after provocation. Histamine analysis revealed a significant (p less than 0.001) but time-limited (5 min) release in nasal secretion. The pattern of immunoreactive leukotriene C4 showed a maximal peak (p less than 0.01) 5 min after allergen provocation, with raised levels for 20 min. Nasal stimulation with nebulized saline solution or grass pollens in healthy subjects and in patients suffering from allergic rhinitis caused by Dermatophagoides pteronyssinus was followed by no local mediator release. These data indicate that, in addition to histamine and peptide-leukotrienes, lyso-PAF and PAF are released in nasal secretions after local antigen stimulation in patients with hay fever, with a preponderance of lyso-PAF response. On the basis of these results, it is conceivable that these ether-phospholipids may be involved in allergic inflammation of human nasal airways.

Adult↗
PubMed1988

Accumulation of platelets and eosinophils in baboon lung after paf-acether challenge. Inhibition by ketotifen.

Intratracheal administration of platelet-activating factor (paf-acether) induced transient bronchoconstriction in baboons. Using an automated isotopic monitoring system, we found that intratracheal administration of paf-acether also elicited transient accumulation of platelets labeled with 111In oxine within the pulmonary vasculature after the increase in maximal peak inspiratory pressure. Bronchoalveolar eosinophilia were inhibited by prophylactic administration of the antiasthma drug ketotifen but not by pyribenzamine, suggesting that the effects of ketotifen are unrelated to H-1 receptor antagonism. Platelet accumulation was not affected by ketotifen or pyribenzamine. This study suggests that paf-acether may be a mediator of the eosinophil recruitment in bronchial asthma and that inhibition of this phenomenon by ketotifen may contribute to the therapeutic efficacy of this drug.

Animals↗
PubMed1987

[Our experience in reconstructive surgery in glottic cancers].

A retrospective study was carried out in 58 patients operated between 1978 and 1983 for cancer of larynx of glottic origin and mainly T1 and T2. Functional results were always of good quality, and the recurrence rate significantly lowered by the use of the Majer-Piquet or C.H.E.P. procedure when compared with results after thyroidectomy. A simplified technique is proposed.

Adult↗
PubMed1983

Acute effects of intratracheal administration of platelet-activating factor in baboons.

The bronchomotor effect of intratracheal administration of PAF-acether (60 micrograms X kg -1) was investigated in 37 curarized baboons mechanically ventilated with constant volume and frequency. PAF-acether caused an immediate bronchoconstriction as assessed by a marked increase in peak inspiratory pressure with no change in static pulmonary compliance and chest X-rays. There was a concomitant fall in arterial PO2 and a significant increase in ventilated unperfused lung zones. A decrease of circulating platelets and leucocytes was also observed. Local anesthesia with lidocaine and atropine did not prevent PAF-acether-induced bronchoconstriction although both markedly reduced the bronchial response to histamine. Albuterol significantly reduced the bronchial response to PAF-acether. Pretreatment with aspirin (80 mg X kg -1 iv) did not prevent the bronchoconstriction caused by PAF-acether, and intravenous or intratracheal arachidonic acid caused no bronchial response. Thus the role of cyclooxygenase metabolites of arachidonic acid in PAF-acether-induced bronchoconstriction is unlikely. In conclusion, an acute bronchoconstriction probably not triggered by stimulation of irritant receptors of the airways and associated with aggregation of platelet takes place subsequent to intratracheal administration of PAF-acether. These data suggest that PAF-acether might play a role in the pathogenesis of human asthma.

Anesthesia, Local↗
PubMed1983

Involvement of immunoglobulin E in the secretory processes of alveolar macrophages from asthmatic patients.

Alveolar macrophages from nonatopic donors were passively sensitized with allergen-specific IgE antibody from the serum of asthmatic patients. A selective release of 4-8% of the lysosomal beta-glucuronidase of these cells occurred within 30 min of contact with the related allergen or with anti-human IgE antibody, in the absence of any mast or basophil cells. The cell reactivity was dependent on the interaction of macrophages with IgE, as shown by the disappearance of the allergen-induced enzyme release after heating or IgE-immune adsorption of the sensitizing serum, but not after IgG-adsorption. Alveolar macrophages from asthmatic patients behaved similarly to passively sensitized normal macrophages. Contact with the related allergen or with anti-IgE antibody induced the same percentage of enzyme release, demonstrating that these cells possess allergen-specific IgE bound on their surface. 18% of them formed rosettes with anti-IgE-coated sheep erythrocytes, and 15-22% with allergen-coated erythrocytes, but lost this property after preincubation with the specific allergen. The presence of IgE-specific receptors on the macrophage surface was demonstrated both at the ultrastructural level with immunoperoxidase labeling, and at low magnification by the formation of 15-18% rosettes with human IgE-coated erythrocytes. The formation of such rosettes was inhibited after incubation of alveolar phagocytes with aggregated myeloma IgE. On the basis of these observations, the participation of the alveolar macrophages in IgE-mediated pulmonary hypersensitivity must be considered. Its precise involvement requires, however, further investigations.

Adult↗
PubMed1982

Release of PAF-acether from human blood monocytes.

Stimulation of human blood monocytes with ionophore A 23187 induced the release of platelet-activating factor (PAF-acether). Phagocytosis of zymosan, coated or not with complement, bacteria or immune complexes, stimulated the release of PAF-acether whereas that of latex particles was without effect. Such release did not occur at 4 degrees C or in the presence of EDTA. PAF-acether derived from monocytes shared the same characteristics as hog leucocyte PAF-acether or synthetic 1-O-alkyl-2-acetyl-glyceryl-3-phosphorylcholine. In lung physiology, the release of PAF-acether from monocytes and alveolar macrophages could lead, via the platelets, to bronchoconstriction. It could represent a cause for asthma other than the classical IgE-mastocyte interaction.

Humans↗
PubMed1981

Release of platelet-activating factor (PAF-acether) and arachidonic acid metabolites from alveolar macrophages.

Human, monkey and rat alveolar macrophages (AM) release PAF-acether in a dose-dependent fashion in the presence of 1 to 5 microgram/ml ionophore A 23187 (2.5 pmol of PAF-acether from 2.5 x 10(5) cells) but not in the presence of zymosan. Arachidonic acid (AA) metabolites released from AM from these species were studied. Thromboxane A2 TxA2) - detected by its action on rabbit arteries - was released from human, monkey and rat AM upon addition of 0.5 mM AA. This release was inhibited by aspirin and indomethacin. Lipoxygenase and cyclooxygenase AA metabolites from rat AM were identified using high efficiency glass capillary column gas chromatography coupled to mass spectrometry. The cyclooxygenase metabolites PGF2 alpha, E2 and D2 and TxB2 were identified. The lipoxygenase-dependent AA metabolites were explored using aspirin-pretreated AM. Only 12 HETE was found. These data indicate that AM secrete several substances with bronchoconstrictive activity: PGF2 alpha, D2, TxA2 and PAF-acether. Therefore an active role of AM in human and experimental bronchoconstriction must be considered.

Animals↗