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Biomedical subjects

M Fournier

Publications and source records attributed to M Fournier.

At least 253 records · Page 14Linked to original sources
PubMed1986

[Experimental allergic asthma].

This paper is concerned with the induction of experimental allergic asthma by active sensitization of the airways "vis-à-vis" heterologous protein. Thus in the rodent it is possible to sensitize the airways by direct intra-tracheal injection of the allergen without producing an allergic alveolitis; the concomitant injection of an adjuvant is however indispensable. Confirmation of the sensitized state can be made by in vitro measurements of isometric contraction of tracheal smooth muscle in the presence of the allergen. This active sensitization is accompanied by histocytological changes which are detected by immunomorphological techniques: the rise in the number of plasma cells sensitized to IgE in the mediastinal modes: the appearance (or increase in number) of intra-cytoplasmic IgE in the sub-epithelial tracheal mast cells and in certain non ciliated intra-epithelial cells, probably basophils, morphologically close to the mast cells.

Allergens↗
PubMed1985

Studies on the release of leukotrienes and histamine by human lung parenchymal and bronchial fragments upon immunologic and nonimmunologic stimulation. Effects of nordihydroguaiaretic acid, aspirin, and sodium cromoglycate.

Fragments of human lung parenchyma or bronchi were studied by high performance liquid chromatography, gas chromatography-mass spectrometry, and bioassay for the biosynthesis of 5-lipoxygenase metabolites of arachidonic acid, and by radioenzymatic assay for the release of histamine, upon immunologic and nonimmunologic stimulation. Human lung parenchyma were passively sensitized with serum from timothy-positive allergic patients (radioallergosorbent test, 30-40%) and challenged with 0.5 microgram/ml of timothy allergen. Analysis of the incubation media showed the presence of LTB4, LTC4, LTD4, LTE4, and histamine. Maximum release of LTB4 and LTD4 was observed after 15 min of challenge (92.8 +/- 21, and 67.8 +/- 14 pmol/g tissue wet weight, respectively; mean +/- SEM) whereas maximum release of LTC4 was observed after 5 min of challenge (25 +/- 7.1 pmol). In parallel to leukotriene formation, histamine was released rapidly and reached a maximum after approximately 15 min of challenge (2.85 +/- 0.76 nmol/g tissue). When fragments of human lung parenchyma were stimulated with ionophore A23187 (4 microM), we observed a profile of leukotriene and histamine release similar to that seen in response to the allergen. Ionophore A23187 stimulated the release of two- to fivefold greater amounts of leukotrienes and histamine than did the allergen. Release of LTC4 and histamine was maximal after 5 min of stimulation (83 +/- 22.2 and 5.2 +/- 0.95 nmol/g tissue, respectively), whereas LTB4 and LTD4 release reached a maximum after 15 min (438 +/- 66.6 and 205 +/- 68 nmol/g tissue, respectively). In addition, human lung parenchyma metabolized LTB4 into omega-OH-LTB4 and omega-COOH-LTB4. This tissue also released 5-hydroxy-eicosatetraenoic acid (5-Hete), 12-Hete, and 15-Hete. Fragments of human lung bronchi also released a similar profile of leukotrienes (except LTC4) and histamine when challenged with the allergen or ionophore A23187. Maximum release of LTB4 and LTD4 by allergen or ionophore stimulation was observed after approximately 15 min (40 +/- 7.5 and 21 +/- 8 pmol/g tissue, respectively, upon allergen challenge; 100 +/- 13 and 47 +/- 10.6 pmol/g tissue, respectively, upon ionophore stimulation). The maximum release of histamine by bronchi was observed after approximately 15 min of allergen challenge and 5 min of ionophore stimulation (2.25 +/- 0.65 and 3.15 +/- 0.9 nmol/g tissue, respectively). The release of leukotrienes but not of histamine by human lung parenchyma upon both allergen and ionophore challenge was inhibited by nordihydroguaiaretic acid (NDGA) (ID50, 2 X 10(-6)M).(ABSTRACT TRUNCATED AT 400 WORDS)

Adjuvants, Immunologic↗
PubMed1985

Increased susceptibility to mouse hepatitis virus 3 of peritoneal macrophages exposed to dieldrin.

Interaction of a single dose (36 mg/kg body wt) of the organochlorine pesticide dieldrin with mouse peritoneal macrophages was examined in C57Bl/6, (C57Bl/6 X A/J)F1, and A/J strains of different genetic resistance to mouse hepatitis virus 3 (MHV3) infection. In vivo studies showed increased susceptibility to MHV3 acute disease of C57Bl/6 and (C57Bl/6 X A/J)F1 animals challenged with the pesticide. Significant decrease of mean time of death in dieldrin-exposed, MHV3-infected susceptible C57Bl/6 mice was observed similarly upon po or ip administration of a single, sublethal dose of dieldrin. In addition, decrease of humoral response to the virus was quantified by determination of anti-MHV3 IgG antibodies in spleen cell supernatant fractions and in blood sera of dieldrin-exposed C57Bl/6 mice. A single dose of dieldrin did not alter the in vivo resistance of A/J animals to acute MHV3 disease. The resistant A/J mice, however, showed increased mortality upon two subsequent exposures to dieldrin followed by infection with high lethal doses of MHV3. Phagocytic activity, cell adherence capacity, and attachment and uptake of 3H-radiolabeled MHV3 by C57Bl/6 peritoneal macrophages were determined by in vitro studies. These affector activities of peritoneal macrophages were slightly decreased or unchanged in cells originating from animals exposed to the pesticide. However, the intrinsic activity of MHV3 restriction appeared to be affected in macrophages derived from dieldrin-treated animals: (i) peritoneal C57Bl/6 macrophages collected from the early phase of acute MHV3 disease contained increased MHV3 antigen and (ii) increased cytolysis was observed after in vitro MHV3 infection of macrophages originating from dieldrin-exposed C57Bl/6 mice.

Animals↗
PubMed1985

Electroencephalographic study of SR 95103, a GABAA antagonist: interaction with inhibitory amino acids and muscimol.

SR 95103 has recently been described as a selective GABAA antagonist. In this study, the electroencephalographic (EEG) effects of SR 95103 were investigated as well as its central interaction with inhibitory amino acids and muscimol. Slow intravenous infusions of SR 95103 in rats induced epileptiform EEG activities which were antagonized by intracerebroventricularly injected muscimol, GABA and taurine whereas glycine did not modify and even facilitated the effects of SR 95103. These results suggest that the EEG effects of SR 95103 are due to the specific GABAA antagonistic properties of this compound.

Animals↗
PubMed1985

EEG effects of i.v. infusion of pentylenetetrazol in rats: a model for screening and classifying antiepileptic compounds.

In order to validate a new animal model predictive of the profile of antiepileptic drugs, we studied the antagonism by standard antiepileptics of the EEG modifications induced by low-speed IV infusion of pentylenetetrazol (PTZ) in rats. The activity of the drugs was measured by their effects on temporal characteristics of the PTZ-induced EEG paroxysms. Most compounds had moderate to potent anti-PTZ effects, as shown by the changes in the EEG temporal parameters. However, these effects depended on the drugs and doses. Cluster analysis showed that drugs and doses which evoked similar changes were closely related and were included in separate clusters with respect to one another. In particular, the present results showed that benzodiazepines and antiepileptics cluster differently in their effects. Thus, this model could be a useful tool for assessing new antiepileptic drugs.

Animals↗
PubMed1985

[Not Available].

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Anatomy↗
PubMed1985

[Effect of glucocorticoids in chronic dyspneic asthma: histological and immunohistochemical study of the bronchial mucosa].

This prospective study was done in 8 patients with chronic asthma, hospitalised for an exacerbation of their illness without any evidence of airway infection. The intention was to measure both qualitatively and quantitatively the impact of high dosage glucocorticoids on the inflammatory changes of the bronchial mucus in such patients. Biopsies of the proximal bronchi by fibreoscopy were taken before and after 6 to 9 days of Prednisolone (0.5-0.75 mg/kg per day), this treatment led to a relative rise in the FEV1 (VEMS) of at least 15%. These biopsies were fixed in Bouin and Paraffin, and the sections simultaneously processed for qualitative identification (histochemical and immuno-peroxidasic) of cells infiltrating the bronchial mucosa and for a count of these cells in a pre-determined sub-epithelial zone. It was noted: In all patients at the entry to the study: an essentially lympho-monocytic cellular infiltrate of the bronchial mucosa, a virtual absence of neutrophils, and various abnormalities of the surface epithelium. After 6 to 9 days of steroids there was a persistence of epithelial lesions and in 6 out of 8 patients a statistically significant fall in the density of the inflammatory infiltrate. In 75% patients suffering from exacerbations of chronic asthma, the improvement in the ventilatory function with dosage corticotherapy was accompanied by a fall in the level of inflammatory infiltrate in the proximal bronchi.

Adult↗
PubMed1984

Enzymatic conversion of adenosine to inosine in the wobble position of yeast tRNAAsp: the dependence on the anticodon sequence.

We have investigated the specificity of the tRNA modifying enzyme that transforms the adenosine at position 34 (wobble position) into inosine in the anticodon of several tRNAs. For this purpose, we have constructed sixteen recombinants of yeast tRNAAsp harboring an AXY anticodon (where X or Y was one of the four nucleotides A, G, C or U). This was done by enzymatic manipulations in vitro of the yeast tRNAAsp, involving specific hydrolysis with S1-nuclease and RNAase A, phosphorylation with T4-polynucleotide kinase and ligation with T4-RNA ligase: it allowed us to replace the normal anticodon GUC by trinucleotides AXY and to introduce simultaneously a 32P-labelled phosphate group between the uridine at position 33 and the newly inserted adenosine at position 34. Each of these 32P-labelled AXY "anticodon-substituted" yeast tRNAAsp were microinjected into the cytoplasm of Xenopus laevis oocytes and assayed for their capacity to act as substrates for the A34 to I34 transforming enzyme. Our results indicate that: 1/ A34 in yeast tRNAAsp harboring the arginine anticodon ACG or an AXY anticodon with a purine at position 35 but with A, G or C but not U at position 36 were efficiently modified into I34; 2/ all yeast tRNAAsp harboring an AXY anticodon with a pyrimidine at position 35 (except ACG) or uridine at position 36 were not modified at all. This demonstrates a strong dependence on the anticodon sequence for the A34 to I34 transformation in yeast tRNAAsp by the putative cytoplasmic adenosine deaminase of Xenopus laevis oocytes.

Adenosine↗
PubMed1984

Ultrastructural localization of acetylcholinesterase activity by means of the electron dense precipitate derived from Koelle's cuprous thiocholine iodide by treatment with phosphomolybdic acid and osmium tetroxide.

An osmium resistant, thermostable and electron dense precipitate was obtained from cuprous thiocholine iodide (Koelle's precipitate) by a joint interaction with phosphomolybdic acid and OsO4. No diffusion artifact due to the conversion of the primary precipitate to the secondary precipitate was observed, contrary to that seen after (NH4)2S or K3Fe (CN)6 posttreatment of the cuprous thiocholine iodide. In addition, phosphomolybdic acid and OsO4 provided a counterstain effect on the ultrastructural background. By the present modification, Koelle's histochemical method becomes a useful cytochemical method for ultrastructural localization of acetylcholinesterase activity.

Acetylcholinesterase↗
PubMed1984

[Not Available].

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Canada↗
PubMed1983

Post-transcriptional modification of the wobble nucleotide in anticodon-substituted yeast tRNAArgII after microinjection into Xenopus laevis oocytes.

An enzymatic procedure for the replacement of the ICG anticodon of yeast tRNAArgII by NCG trinucleotide (N = A, C, G or U) is described. Partial digestion with S1-nuclease and T1-RNAase provides fragments which, when annealed together, form an "anticodon-deprived" yeast tRNAArgII. A novel anticodon, phosphorylated with (32P) label on its 5' terminal residue, is then inserted using T4-RNA ligase. Such "anticodon-substituted" yeast tRNAArgII are microinjected into the cytoplasm of Xenopus laevis oocytes and shown to be able to interact with the anticodon maturation enzymes under in vivo conditions. Our results indicate that when adenosine occurs in the wobble position (A34) in yeast tRNAArgII it is efficiently modified into inosine (I34) while uridine (U34) is transformed into two uridine derivatives, one of which is probably mcm5U. In contrast, when a cytosine (C34) or guanosine (G34) occurs, they are not modified. These results are at variance with those obtained previously under similar conditions with anticodon derivatives of yeast tRNAAsp harbouring A, C, G or U as the first anticodon nucleotide. In this case, guanosine and uridine were modified while adenosine and cytosine were not.

Animals↗
PubMed1983

[Bronchopulmonary antigenic information].

Only a small part of those antigenic compounds that pass through the rhinopharyngeal filter and reach the lower airways or the lung crosses the bronchial or alveolar epithelial barrier. The crossing, which is directly or indirectly mediated by macrophage phagocytosis, provides antigenic information which starts off an immune reaction with different impacts on the bronchi and deep lung. Normally (infections excluded), the lung is quiescent, with a probably weak immune activity. In contrast, the level of immune activity in the bronchial lymphoid tissue, although inferior to that of the rhinopharynx, is high. This gradient of immune activity decreasing from the upper airways to the alveoli may be compared to the gradient of saprophytic bacteria which are numerous in the nose, mouth and pharynx, and absent in the deep lung.

Animals↗
PubMed1983

Site-directed in vitro replacement of nucleosides in the anticodon loop of tRNA: application to the study of structural requirements for queuine insertase activity.

We have investigated the specificity of the enzymes Q-insertase and mannosyl-Q transferase that replace the guanosine at position 34 (wobble base) in the anticodon of several tRNAs by Q or mannosyl-Q derivatives. We have restructured in vitro the normal anticodon of yeast tRNA-Asp-GUC, yeast tRNAArgICG and yeast tRNALeuUAG. With yeast tRNA-Asp-GUC, we have replaced one or several nucleotides in the vicinity of G34 by one of the four canonical nucleotides or by pseudouridylic acid; we have also constructed a tRNAAsp with eight bases instead of seven in the anticodon loop. With yeast tRNAArgICG and yeast tRNALeuUAG, we have replaced their anticodon by the trinucleotide GUC, coding for aspartic acid. The chimerical tRNAs were microinjected into the cytoplasm of Xenopus laevis oocytes and after 72 h the amount of Q34 and mannosyl-Q34 incorporated was measured. Our results show that the U33G34U35 sequence, within an anticodon loop of seven bases in chimerical yeast tRNA-Asp-GUC, tRNAArgGUC or tRNALeuGUC, is the main determinant for Q-insertase activity at position 34; the rest of the tRNA sequence has only a slight influence. For mannosyl-Q transferase, however, a much broader structural feature of the tRNA than just the U33G34U35 sequence is important for the efficiency of Q34 transformation into mannosyl-Q34.

Animals↗
PubMed1983

Involvement of tRNA in retrovirus expression: biological implications of reverse transcriptase-primer tRNA interactions.

We have previously studied the topographical and functional implications of the recognition of primer tRNATrp by avian retrovirus reverse transcriptase. Here we have presented evidence that the enzyme is able to deacylate beef liver Trp-tRNATrp, provided that 35-S viral RNA is present in the incubation mixture. No effect of dNTPs on this activity was observed. The extensive modification of tRNATrp with acrylonitrile led to a marked loss of priming activity by tRNATrp if the annealing between primer and template was performed at 37 degrees C, while the annealing of cyanoethylated tRNA with the viral genome at 75 degrees C gave almost normal levels of cDNA synthesis. We have also studied the priming behaviour of tRNATrp, modified by incorporation of various analogs of adenosine. Only tRNATrp-2'dA was active in cDNA initiation; 3'dA, 3'NH2-3'dA, and primer tRNA with formycin in the 3' end showed low or nonexistent priming activity.

Adenosine Triphosphate↗
PubMed1983

Nuclear inclusions in oculopharyngeal dystrophy. An ultrastructural study of six cases.

Nuclear inclusions in striated muscle from patients with oculopharyngeal dystrophy have been detected recently. We carried out ultrastructural examinations of biopsy specimens on 5 patients with oculopharyngeal dystrophy and we also reexamined a former case. In these 6 cases we found filamentous inclusions in a few nuclei. These inclusions seem to be characteristic of this disease as they have never been seen elsewhere.

Aged↗
PubMed1983

[Not Available].

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History, Modern 1601-↗