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Biomedical subjects

A Fournier

Publications and source records attributed to A Fournier.

At least 127 records · Page 7Linked to original sources
PubMed1998

The neurotrophic activity of PACAP on rat cerebellar granule cells is associated with activation of the protein kinase A pathway and c-fos gene expression.

In vitro studies have shown that PACAP promotes cell survival and neurite outgrowth in immature cerebellar granule cells. In the present study, we have examined the transduction pathways involved in the neurotrophic activity of PACAP. Incubation of cultured granule cells with graded concentrations of PACAP produced a dose-dependent increase in c-fos mRNA level. The effects of PACAP on c-fos gene expression and granule cell survival were both mimicked by dbcAMP but not by PMA. The maximum effect of PACAP on c-fos gene expression was observed after 1 h of treatment. Similar effects of the peptide on granule cell survival were observed whether the cells were continuously incubated with PACAP for 48 h or only exposed to PACAP during 1 h. The PKA inhibitor H89 significantly reduced the effect of PACAP on c-fos mRNA level, whereas the specific PKC inhibitor chelerytrine had no effect. These data indicate that the action of PACAP on cerebellar granule cell survival and c-fos gene expression are both mediated through the adenylyl cyclase/PKA pathway.

Animals↗
PubMed1998

Use of muscle exudates for the detection of anti-gE antibodies to Aujeszky's disease virus.

A commercial ELISA test to detect serum anti-gE antibodies to Aujeszky's disease virus was adapted for use with muscle exudates. The muscle samples were taken from the diaphragm of pig carcasses at the slaughterhouse. Three hundred and eighty-nine pairs of samples of serum and muscle exudate were compared to determine the possibility of using muscle exudate samples in a programme to control Aujeszky's disease. Taking the serum samples as the reference, the individual sensitivity of the test was 93.2 per cent and the individual specificity was 98.3 per cent. The concentration of antibodies in the muscle exudates was on average 20 times lower than that in the serum samples.

Animals↗
PubMed1998

Expression and characterization of the neuropeptide Y Y5 receptor subtype in the rat brain.

The neuropeptide Y Y5 receptor subtype has generated great interest, especially regarding its possible involvement in feeding behaviors. However, its distribution and sites of expression in the mammalian brain are, in large part, unknown because of the lack of selective tools. We demonstrate in this study that specific [125I][Leu31, Pro34]PYY binding is competed in a biphasic manner by BIBP3226, a Y1 receptor antagonist, demonstrating the existence of sensitive and insensitive sites to BIBP3226. Assays performed by using [125I][Leu31,Pro34]PYY in the presence of 1 microM BIBP3226 to block the Y1 receptor subtype revealed a pharmacological profile highly similar to the cloned Y5 receptor. Moreover, results obtained with GW1229 suggest that the Y4 subtype represents only a very small proportion of the total population of NPY receptors in the rat brain. Quantitative receptor autoradiographic data revealed the discrete distribution of [125I][Leu31,Pro34]PYY/BIBP3226-insensitive Y5 sites in the rat brain, with the external plexiform layer of the olfactory bulb, the lateral septum, the anteroventral thalamic nucleus, the CA3 subfield of the ventral hippocampus, the nucleus tractus solitarius, and the area postrema being most enriched. Rather surprisingly, in the hypothalamus, a key structure modulating food intake, only low densities of Y5 binding sites were detected as well as in most other regions of the rat brain. These data suggest that the Y5 receptor protein is expressed and translated by a small percentage of hypothalamic neurons and that the effect of NPY on feeding behaviors likely is mediated by more than one class of NPY receptors. It also indicates that the Y5 receptor may be involved in other biological actions induced by NPY. Taken together, these data represent the first pharmacological demonstration of the expression and discrete localization of the Y5 receptor protein in the rat brain.

Animals↗
PubMed1998

[Long-term stability of bone mineral density in patients with renal transplant treated with cyclosporine and low doses of corticoids. Protective role of cyclosporine?].

OBJECTIVES: Cyclosporine has been thought to have a deleterious effect on bone in transplant recipients because of high turnover osteopenia observed in humans after transplantation. However, varying confounding factors such as renal and parathyroid function, cumulative steroid doses and previous exposure to aluminium, also play a role and hinder interpretation of the cyclosporine effect on bone mineral density (BMD). PATIENTS AND METHODS: A 2-year prospective study was conducted to measure BMD starting 3 months after transplantation and bone remodeling markers from the first post-transplantation day in 52 kidney recipients with no prior exposure to aluminum. None of the patients experienced rejection and at 3 months all had good stable renal function (serum creatinine 137 mumol/l) and mildly elevated parathyroid hormone levels (1.5 times the upper limit of normal). All patients were given the same low dose steroid treatment (10 mg/day) and at 6 months cyclosporine was decreased from 7 to 4.8 mg/kg/day. RESULTS: BMD measured by double energy X-ray absorptiometry, (DEXA) and expressed in Z score, was moderately decreased at 3 months for the vertebrae (-1.40), the femoral neck (-1.34) and the ultradistal radius (-0.95) which have predominantly cancellous bone and was significantly less decreased (p < 0.05) for the lower third of the radius (-0.6) which is mainly cortical bone. BMD measurements were comparable at 6, 12 and 24 months. When measured by axial computerized tomography (ACT) BMD of the vertebrae showed a non-significant increase of Z score from -1.37 to -1.19 at 2 years. Bone remodeling markers was observed up to month 6 (from month 3 for osteocalcine and from month 1 for total and bone alkaline phosphatase and urinary pyridinoline), then returned to baseline levels at 2 years in parallel with decreased cyclosporine dosage. The increase of vertebral BMD measured by ACT at 1 year was correlated both to cyclosporine dose at 1 year and to bone alkaline phosphatase at 6 months. CONCLUSION: Our data confirm the presence of moderate osteopenia 3 months after transplantation, predominantly in trabecular bone, logically linked to the initial high doses of corticosteroids. The long-term stability of BMD measured by DEXA and the correlation of vertebral BMD increase measured by ACT with cyclosporine dose and bone alkaline phosphate suggest that cyclosporine had a beneficial immunosuppressor effect by stimulating bone remodeling and thus counterbalancing the suppressive effect of corticosteroids.

Adrenal Cortex Hormones↗
PubMed1998

Pituitary adenylate cyclase-activating polypeptide stimulates both c-fos gene expression and cell survival in rat cerebellar granule neurons through activation of the protein kinase A pathway.

A high density of pituitary adenylate cyclase-activating polypeptide (PACAP) receptors coupled to both adenylyl cyclase and phospholipase C is found in the external granule cell layer of the rat cerebellum during postnatal development. It has recently been reported that synthetic PACAP promotes cell survival and neurite outgrowth in immature granule cells. In the present study, we have investigated the transduction pathways that mediate the neurotrophic activity of PACAP in cultured granule cells from eight-day-old rat cerebellum. The effect of PACAP on cell survival was mimicked by dibutyryladenosine 3',5'-cyclic-monophosphate but not phorbol 12-myristate 13-acetate suggesting that only the adenylyl cyclase pathway is involved in the neurotrophic activity of PACAP. PACAP also induced a transient increase in c-fos messenger RNA level. The ability of PACAP to stimulate c-fos gene expression was mimicked by dibutyryladenosine 3',5'-cyclic-monophosphate but not phorbol 12-myristate 13-acetate. Similar effects of PACAP on granule cell survival were observed whether the cells were continuously incubated with PACAP for 48 h or only exposed to PACAP during 1 h. The protein kinase A inhibitor H89 significantly reduced the effect of PACAP on c-fos messenger RNA level whereas the specific protein kinase C inhibitor chelerythrine did not modify c-fos gene expression. These data indicate that the action of PACAP on cerebellar granule cell survival and c-fos gene expression are both mediated through the adenylyl cyclase/protein kinase A pathway. The observation that a short-term stimulation by PACAP can be converted into a long-lasting response indicates that the effect of the peptide on cell survival must involve immediate-early gene activation. The fact that a brief exposure to PACAP causes both c-fos gene expression and promotes cell survival strongly suggests that c-fos is involved in the trophic effect of PACAP on immature cerebellar granule cells.

Adenylyl Cyclases↗