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Biomedical subjects

M Robillard

Publications and source records attributed to M Robillard.

At least 19 recordsLinked to original sources
PubMed1992

Inhibition of vasopressin-induced formation of diradylglycerols in vascular smooth muscle cells by incorporation of eicosapentaenoic acid in membrane phospholipids.

OBJECTIVE: Eicosapentaenoic acid and linoleic acid exert antihypertensive effects by an unknown mechanism unrelated to prostanoids, a property which is not shared by arachidonic acid. This study investigated the influence of these three acids on the formation of diradylglycerols and phosphatidic acid, key intracellular messengers involved in the mediation of agonist-induced vascular smooth muscle cell contraction. DESIGN: Rat mesenteric artery vascular smooth muscle cells in culture were pre-incubated for 24 h with eicosapentaenoic acid, linoleic acid or arachidonic acid. After thorough washing the cells were then incubated for 20 min in the presence of arginine vasopressin or vehicle, either immediately or following cell labelling with 32P-orthophosphate. METHODS: The fatty acid composition of cell lipids was determined by gas chromatography after transesterification in the presence of boron trifluoride and methanol. Diradylglycerols and 32P-phosphatidic acid were purified from cell lipid extracts by thin-layer chromatography and diradylglycerols were analysed. RESULTS: Incubation of vascular smooth muscle cells with eicosapentaenoic acid, linoleic acid or arachidonic acid resulted in the incorporation of these fatty acids at the sn-2 position of membrane phospholipids, mainly phosphatidylcholine and phosphatidylethanolamine. Eicosapentaenoic acid treatment was associated with a reduction, and linoleic acid treatment with an increase in the relative proportions of arachidonic acid found in cell phospholipids. Arginine vasopressin stimulated the formation of both diradylglycerols and 32P-phosphatidic acid. The arginine vasopressin-induced stimulation of diradylglycerols accumulation was almost completely abolished in eicosapentaenoic acid-treated cells, whereas it was not modified by linoleic acid or by arachidonic acid treatment. The arginine vasopressin-stimulated formation of 32P-phosphatidic acid was significantly inhibited by linoleic acid treatment but was not influenced by eicosapentaenoic acid or arachidonic acid treatment. CONCLUSION: The incorporation of eicosapentaenoic acid or linoleic acid at the sn-2 position of membrane phospholipids leads to an inhibition of arginine vasopressin-induced formation of diradylglycerols or phosphatidic acid, respectively, in rat mesenteric artery vascular smooth muscle cells in culture. These properties may contribute to the antihypertensive effects in these fatty acids in vitro.

Animals↗
PubMed1991

Arachidonic acid does not share the antihypertensive properties of linoleic acid and fish oil omega-3 fatty acids in a model of angiotensin II-induced hypertension in the rat.

Linoleic acid and fish oil omega-3 fatty acids, but not arachidonic acid, exerted antihypertensive effects in a model of angiotensin II-induced hypertension in rats. Indomethacin did not influence the systolic arterial pressure of arachidonic acid-treated hypertensive rats whereas compound L-641,953, a prostaglandin H2/thromboxane A2 receptor antagonist, caused a notable but statistically nonsignificant decrease in blood pressure in these animals. Although these results do not exclude entirely the possibility that the lack of antihypertensive effect of arachidonic acid may be due, in part, to the concomitant formation of vasoconstrictor prostanoids, they do not support it. These observations, as well as those of a previous study, indicate that linoleic acid and fish oil omega-3 fatty acids exert antihypertensive effects of their own, independently of the prostanoid system, and that these properties are not shared by arachidonic acid.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

[Primary pulmonary choriocarcinoma].

The authors report a case of a young woman who had been found to have a chorio-carcinoma in the apex of the left lower lobe, following a major and recurrent haemothorax. A study of her past history and a gynaecological examination had not revealed any evidence of a primary tumour. Following this observation the possibility of a primary pulmonary carcinoma was considered and also the usual aetiological hypothesis, namely the migration of trophoblastic cells during an abortion even followed by a normal pregnancy and a degeneration after several years of these cells blocked in the pulmonary capillaries.

Adult↗
PubMed1988

[Reduction using an immunomodulator of the level of respiratory infections in chronic bronchitis].

Fifty-six patients with recurrent bronchopulmonary infections associated with chronic bronchitis were randomly allocated to 2 groups, to assess whether treatment with an immunomodulator, Diribiotin CK, could enhance resistance to infection. The double-blind, placebo-controlled prospective trial over a 9 month period showed that this immunomodulator was well tolerated and significantly reduced the rate of respiratory tract infection. The drug also significantly reduced the prescribing of antibiotic medication and the rate of absenteism from work. These effects have been demonstrated in a rigorously designed clinical study. This is the first time that a clear clinical activity has been attributed to an inducer of soluble mediators of immunity.

Adjuvants, Immunologic↗
PubMed1986

[Respiratory complications of anticancer chemotherapy].

Pulmonary toxicity associated with chemotherapy is still rare, but its incidence may increase with intensive and iterative regimens. Following a review of the four main drugs responsible for lung toxicity (bleomycin, methotrexate, busulfan and BCNU), the authors underline the risk of combined chemotherapy and radiotherapy. To recognize, at an early stage, the signs suggesting lung toxicity is essential to reduce its extent and, above all, to exclude other pathologies which often have the same clinical and radiological features. Only histological studies provide evidence of toxicity. Treatment is frequently disappointing; the only hope of regression lies in withdrawal of the responsible drug and corticosteroid therapy.

Antineoplastic Agents↗
PubMed1985

Urinary levels of 2,3-dinor-6-oxo-PGF1 alpha: a reliable index of the production of PGI2 in the spontaneously hypertensive rat.

The urinary levels of 2,3-dinor-6-oxo-PGF1 alpha (PGI2-M), a major metabolite of PGI2, are determined by the balance between the amount of PGI2 synthesized and the extent of its further metabolic oxidation. The purpose of the present study was to determine if the urinary excretion of PGI2-M can be used as a reliable index of the in vivo production of PGI2 in both normal Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). This involved the exclusion of differences in metabolism between these two strains of rats. In order to do so, we monitored the urinary excretion of PGI2-M during paired intravenous infusions of 6-oxo-PGF1 alpha (the stable product of the spontaneous hydrolysis of PGI2) in conscious, unrestrained SHR and WKY rats aged 12-15 weeks, in doses ranging from 250 to 700 ng. In one experiment, PGI2 was infused instead of 6-oxo-PGF1 alpha. The results of these experiments indicate that SHR and WKY rats are equal with regard to the transformation of 6-oxo-PGF1 alpha and PGI2 into PGI2-M. For both groups, there is a good correlation between the amount of 6-oxo-PGF1 alpha infused and the amount of PGI2-M excreted in urine. These observations confirm the validity of using the urinary levels of 2,3-dinor-6-oxo-PGF1 alpha as an index of PGI2 production in both WKY and SHR. In addition, they support the conclusions drawn from our previous studies, namely that SHR do not produce more PGI2 than WKY rats in vivo, contrary to the situation prevailing in vitro.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Graft-versus-host disease in murine bone marrow transplantation. I. Modification of GVHD by preimmunization of recipients with spleen cells of primary recipients undergoing GVHD.

Lethally irradiated (1000 rad) CBA/J mice were transplanted with anti-Thy 1 treated BALB/c bone marrow. Under these conditions, we uniformly observed the development of pathology suggestive of acute graft-vs.-host disease (GVHD), i.e. weight loss, diarrhoea, hypogammaglobulinemia and thymic hypoplasia. If, 2 wk before irradiation, the recipients were preimmunized with spleen cells taken from mice undergoing acute GVHD, these symptoms were avoided. Instead, such animals seemed to show long term survival either with or without signs of chronic GVHD (hypergammaglobulinemia, splenomegaly, lymphoid hyperplasia). The ability to show long term survival with bone marrow allografts was dependent upon successful immunization of the recipient mice. Long term survivors contain a splenic population not bearing detectable host MHC antigens, which can elicit a memory anti-host cytotoxic response from a population of quiescent donor lymphocytes previously immunized in vitro against host MHC antigens.

Animals↗
PubMed1985

Graft-versus-host disease in murine bone marrow transplantation. II. Modulation of acute and chronic GVHD in mice receiving bone marrow allografts pretreated with immunosuppressive factor derived from a human T cell line.

BALB/c bone marrow treated with monoclonal anti-Thy 1.2 antibody and complement is unable to produce prolonged hemopoietic repopulation and survival when transplanted to lethally-irradiated allogeneic CBA recipient mice. Preincubation of the antibody treated bone marrow cells with an immunosuppressive factor (SAF) derived from a 6-thioguanine resistant cell line, itself derived from the human T cell line CEM, in contrast, allowed those bone marrow cells to produce a state of chimerism and long term survival. Parameters designed to gauge the degree of graft-versus-host reactivity (GVHR) in these animals suggested that acute GVHR was abolished with this procedure. Moreover, defining chronic GVHD as associated with abnormally high spontaneous proliferation of splenic cells, elevated anti-host mixed lymphocyte reactivity, or elevated serum immunoglobulin levels (in all cases when compared with the syngeneically repopulated BALB/c----BALB/c), our data suggest that preincubation with SAF modified chronic GVHD also.

Acute Disease↗
PubMed1982

Microwave thermography--characteristics of waveguide applicators and signatures of thermal structures.

In this paper, we study the problem of the interpretation of the signals provided by microwave thermography, which allows the detection of the thermal gradients in living tissues. These signals correspond to the thermal noise measured by a radiometer when the probe scans the surface of the tissues (passive process). We describe how these signals can be computed by means of a new method based on the antenna reciprocity principle. This process requires a knowledge of the electrical field distribution in the lossy medium when the applicator is radiating a microwave signal (active process). Examples of computations of the thermal signals and experimental verifications are presented. Then, we introduce a new concept of 'thermal signature' and show how it is possible to reach a quantitative interpretation of the thermal signals such as those obtained in clinical investigations (thermal pattern recognition).

Microwaves↗
PubMed1980

Electrical characteristics of waveguide applicators for medical applications.

This work concerns the electrical properties of waveguide applicators consisting of flanged rectangular waveguides filled with a dielectric, used in medical applications (microwave thermography and local hyperthermia). The reflection coefficient and the near field configuration in lossy materials were obtained in some cases analytically and in some other cases numerically. The validity of these methods was verified experimentally. The study shows that the matching of the applicator and the penetration depth in a lossy material, such as a living tissue, depend not only on the tissue characteristics but also on the characteristics of the applicator itself.

Electromagnetic Fields↗