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Biomedical subjects

P Deprez

Publications and source records attributed to P Deprez.

At least 91 records · Page 5Linked to original sources
PubMed1995

Evaluation of the nebulisation of sodium ceftiofur in the treatment of experimental Pasteurella haemolytica bronchopneumonia in calves.

Severe acute bronchopneumonia was induced in 24 conventional Friesian Holstein calves by inoculating them intratracheally with Pasteurella haemolytica type A1. Twelve of the calves were treated intramuscularly with sodium ceftiofur and 12 were treated with an aerosol of sodium ceftiofur. The mortality rate in the group of calves treated with the aerosol was significantly lower, and their clinical and haematological parameters returned to normal significantly faster than in the calves treated intramuscularly.

Aerosols↗
PubMed1995

Larval cyathostomiasis as a cause of death in two regularly dewormed horses.

Two horses were presented with complaints of chronic weight loss and subcutaneous oedema, one of them presenting diarrhoea. Both animals were grazed with other unaffected horses, all of them being regularly dewormed. Blood chemistry revealed hypoalbuminaemia and a low albumin-globulin ratio. Faecal egg counts were negative and no cyathostome larvae could be found in the faeces. Neither of these horses could be saved, despite intensive treatment. Postmortem examination revealed severe typhlitis and colitis due to numerous inhibited cyathostome larvae.

Animals↗
PubMed1995

Stimulatory effects of 5HT1A receptor agonists on luteinizing hormone-releasing hormone release from cultured fetal rat hypothalamic cells: interactions with progesterone.

Previous works have suggested an interactive stimulatory effect of progesterone (P) and serotonin (5-HT) on luteinizing hormone release. The purpose of the present study was to determine whether 5-HT via 5-HT1A receptors interacts with P in the process of luteinizing hormone-releasing hormone (LHRH) release. Using fetal hypothalamic neurons in primary cell cultures the first goal of this study was to determine the effects of 5-HT1A receptor agonists on LHRH secretion. 8-Hydroxy-2 (di-n-propylamino) tetralin (8-OH-DPAT) or ipsapirone (10(-5) M) significantly stimulated LHRH release. Pharmacological studies have allowed to rule out the possible involvement of alpha 2- or beta-adrenoreceptors, or 5-HT uptake sites, in the stimulatory effect of 8-OH-DPAT on LHRH release, thus demonstrating the specific involvement of 5-HT1A receptors in the stimulation of LHRH release. The second goal was to test the ability of P to stimulate LHRH release from fetal hypothalamic neurons. P (10(-6) M) applied for 30 or 120 min significantly stimulated LHRH secretion. The maintenance of the stimulation of LHRH release by P after a cycloheximide treatment or by an impermeable analog of P, P-3-BSA, has suggested a nongenomic effect of P on LHRH release. The effects of a pretreatment of cells by P on 8-OH-DPAT-induced LHRH release were tested. While 10(-7) M P alone did not stimulate LHRH release, this concentration of steroid potentiated the LHRH response to 10(-5) M 8-OH-DPAT. These findings led to the conclusion that P acting at the level of the plasma membrane potentiates the stimulatory effect of 5-HT1A receptor agonists on LHRH release.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1994

Effect of drug formulation and feeding on the pharmacokinetics of orally administered quinidine in the horse.

Quinidine is the drug of choice for the treatment of cardiac arrhythmias in horses. The plasma concentrations vs. time profiles following oral administration of two formulations of quinidine sulphate, an oral solution and an oral suspension paste, were evaluated in nine horses. They received multiple administrations of the oral solution under fed and non-fed conditions and of the paste under non-fed conditions. A loading dose of 20 mg.kg-1 and a maintenance dose of 10 mg.kg-1 quinidine with dosing interval of 6 h were used. The relative bioavailability of the oral solution under fed conditions in comparison to the solution under non-fed conditions was 75.0 +/- 10.2% for the loading dose and 97.18 +/- 31.66% after the fourth dose. For the paste formulation the relative bioavailability values are not reported, as steady-state levels were not reached. There was a large variation in plasma quinidine levels when the paste formulation was administered. Feeding conditions had a significant influence on the Cmax values after administration of the loading dose. The Tmax values were not affected by food intake. It was concluded that an oral solution has to be preferred because of the variable drug bioavailability from the paste formulation and the poor acceptability of the paste by the horse.

Administration, Oral↗
PubMed1993

Evidence for the presence of noradrenergic neurons and their inhibitory action on luteinizing hormone-releasing hormone release in cultured fetal rat hypothalamic cells.

The control of LHRH release by catecholamine systems during fetal life (embryonic stages) was studied using hypothalamic neurons in primary cell cultures and an attempt was made to characterize the receptor type involved. Phenylephrine and clonidine, respectively alpha 1 an alpha 2 adrenoreceptor agonists, both inhibited LHRH release. These agonist inhibitory induced-effects were antagonized by the respective alpha 1 and alpha 2 adrenoreceptor antagonists (prazosin and rauwolscine). Both prazosin and rauwolscine applied alone induced a marked increase in LHRH release. Similarly, inhibition of catecholamine synthesis obtained by alpha-methyl-para-tyrosine (alpha-MT) led to a significant increase in LHRH release. The stimulatory effects induced by alpha 1 and alpha 2 adrenoreceptor antagonists or by alpha-MT on LHRH release suggest the presence of noradrenergic and/or adrenergic cells in fetal hypothalamic cultures. Therefore, catecholamine contents were measured in fetal hypothalamic cells in culture. Measurable amounts of norepinephrine and dopamine were found in cells, although epinephrine was undetectable. These results show: 1--noradrenergic cells are present in primary culture of fetal hypothalamic cells. 2--This intrinsic hypothalamic noradrenergic system exerts an inhibitory control on LHRH release at an early stage of development through alpha 1 and alpha 2 adrenoreceptors.

Adrenergic alpha-Agonists↗
PubMed1993

Glutamate, GABA, glycine and taurine modulate serotonin synthesis and release in rostral and caudal rhombencephalic raphe cells in primary cultures.

Control of serotonin release and synthesis by amino acid neurotransmitters was investigated in rat rostral and caudal rhombencephalic raphe cells in primary cultures respectively. Endogenous amounts of taurine, glycine, GABA and glutamate were measured in both types of cultures. These amino acids were spontaneously released to the incubating medium. Exogenous taurine (10(-4) M) inhibited release and synthesis of newly formed [3H]serotonin [3H]5-HT from [3H]-tryptophan only in rostral raphe cells. Glycine (10(-3) M) decreased [3H]5-HT release in both types of cells, synthesis being diminished only in rostral raphe cells. Glycine inhibitory effect was totally blocked by strychnine (5 x 10(-5) M). GABA (10(-4) M) reduced [3H]5-HT metabolism in rostral as well as caudal raphe cells. This effect was totally antagonized in caudal and partially in rostral raphe cells by bicuculline (5 x 10(-5) M) a GABAA receptor antagonist. Baclofen (5 x 10(-5) M), a GABAB receptor agonist, induced a decrease of 5-HT release in rostral raphe cells. These observations suggest that monoamine release was entirely mediated by GABAA receptors in caudal raphe cells although GABAA and GABAB receptors were involved in control of 5-HT metabolism in rostral raphe cells. L-glutamate (10(-4) M) stimulated 5-HT metabolism in both types of cells, effect totally blocked by PK26124 (10(-6) M). N-methyl-D-aspartate (10(-4) M) enhanced 5-HT metabolism and the induced-effect was antagonized by the selective N-methyl-D-aspartate receptor antagonist D,L-2 amino-5-phosphonovaleric acid. Quisqualate (10(-5) M) stimulated [3H]5-HT release only in caudal raphe cells. This effect was mimicked by (RS)-a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, a quisqualate "ionotropic" receptor agonist, this increase being blocked by 6,7-dinitroquinoxaline 2,3-dione. These observations suggest that the glutamate stimulating-induced effect on serotonin metabolism is entirely mediated by N-methyl-D-aspartate receptor-type in rostral raphe cells and that quisqualate "ionotropic" receptors are also involved in caudal raphe cells. Taken together these results show that [3H]5-HT metabolism is controlled by taurine, glycine, GABA and glutamate in rhombencephalic raphe cells in primary cultures. However, some difference in amino acid receptor-types involved in the control of serotonin metabolism are observed according to the rostral or caudal origin of raphe cells.

Animals↗
PubMed1993

N-methyl-D-aspartic acid/glycine interactions on the control of 5-hydroxytryptamine release in raphe primary cultures.

Glutamic acid and glycine were quantified in cells and medium of cultured rostral rhombencephalic neurons derived from fetal rats. In the presence of 1 mM Mg2+, NMDA (50 microM) significantly stimulated (by 69%) release of newly synthesized 5-[3H]hydroxytryptamine ([3H]5-HT). D-2-Amino-5-phosphonopentanoate (AP-5; 50 microM) blocked the stimulatory effect of NMDA. AP-5 by itself inhibited [3H]5-HT release (by 25%), suggesting a tonic control of 5-HT by glutamate. In the absence of Mg2+, basal [3H]5-HT release was 60% higher as compared with release with Mg2+. AP-5 blocked the increased [3H]5-HT release observed without Mg2+, suggesting that this effect was due to the stimulation of NMDA receptors by endogenous glutamate. Glycine (100 microM) inhibited [3H]5-HT release in the absence of Mg2+. Strychnine (50 microM) blocked the inhibitory effect of glycine, indicating an action through strychnine-sensitive inhibitory glycine receptors. The [3H]5-HT release stimulated by NMDA was unaffected by glycine. In contrast, when tested in the presence of strychnine, glycine increased NMDA-evoked [3H]5-HT release (by 22%), and this effect was prevented by a selective antagonist of the NMDA-associated glycine receptor, 7-chlorokynurenate (100 microM). 7-Chlorokynurenate by itself induced a drastic decrease in [3H]5-HT release, indicating that under basal conditions these sites were stimulated by endogenous glycine. These results indicate that NMDA stimulated [3H]5-HT release in both the presence or absence of Mg2+. Use of selective antagonists allowed differentiation of a strychnine-sensitive glycine response (inhibition of [3H]5-HT release) from a 7-chlorokynurenate-sensitive response (potentiation of NMDA-evoked [3H]5-HT release).

Animals↗
PubMed1992

Effect of chymotrypsin on human cholecystokinin release: use of clostripain in the validation of a new radioimmunoassay.

We have developed and validated a new radioimmunoassay for cholecystokinin. In order to establish that the antiserum binds large and small forms of CCK to an equal extent, we used the microbial enzyme clostripain, which cleaves large forms of CCK yielding CCK 8. Cleavage by clostripain of synthetic and purified forms of CCK, and CCK extracted at from human jejunum and CCK in human plasma was found not to affect immunoactivity, indicating that the antiserum reacts similarly with all forms of CCK. There is controversy over whether intraduodenal trypsin inhibits release of CCK in man. We used our radioimmunoassay to investigate whether chymotrypsin, rather than trypsin, could be the major mediator of negative feedback control of CCK release. Six normal subjects received an intraduodenal infusion of L-phenylalanine and L-tryptophan on two occasions, with the addition of either 1 g/l bovine chymotrypsin or 1 g/l albumin. Plasma CCK concentrations rose in response to the amino acid infusion, but were not affected by the addition of chymotrypsin, indicating that this enzyme is not a mediator of CCK feedback regulation in man.

Antibody Specificity↗
PubMed1992

Evaluation of the effect of 3 probiotics on experimental Escherichia coli enterotoxaemia in weaned piglets.

In this report the efficacy of 3 different probiotics (Bacillus cereus "toyoi", Lactobacillus spp. and Streptococcus faecium) was investigated. They were supplemented in the food of recently weaned piglets that were orally infected with E. coli O141 K85ab. Supplementation could not prevent mortality and clinical symptoms nor reduce the faecal excretion of hemolytic E. coli. The possible explanations for the unsatisfying results are various.

Animal Feed↗
PubMed1992

Effect of chronic active immunization anti-corticotropin-releasing factor on the pituitary-adrenal function in the sheep.

ACTH and cortisol diurnal variations and responses to two types of stress (insulin-induced hypoglycemia and isolation-restraint stress) or to an acute injection of lysine-vasopressin were studied in intact and anti-corticotropin-releasing factor (CRF) actively immunized rams. Immunization was obtained by the injection of synthetic ovine CRF coupled to BSA with carbodiimide. All animals developed antibodies anti-CRF and displayed an alteration of their general condition and a body weight reduction. The mean basal ACTH and cortisol secretion as well as the number and mean amplitude of diurnal pulses of these hormones was significantly reduced in the group of anti-CRF immunized rams. However, the reduction in all three parameters was much more pronounced for cortisol than for ACTH. No ACTH and cortisol response to insulin-induced hypoglycemia and isolation-restraint stress was observed. The stimulating action of lysine-vasopressin on ACTH release was significantly reduced as compared to controls. These results indicate that CRF is a major physiological component of the ovine hypothalamo-hypophysial-adrenal axis and participates in the events that regulate ACTH and cortisol diurnal variations and response to stress.

Adrenocorticotropic Hormone↗
PubMed1991

[Angiosarcoma after total knee prosthesis. Apropos of a case].

The authors describe the case of an angiosarcoma associated with a knee prosthesis. The appearance of a malignant tumour in the area of the implantation of a metallic prosthesis is rare. The pathogenesis of this association is still unknown. The authors make an analysis of the problem on the basis of a review of the literature.

Aged↗
PubMed1990

Biochemical profiles in cows with abomasal displacement estimated by blood and liver parameters.

The metabolic status of normal lactating cows and of cows suffering from abomasal dilatation was evaluated by examination of blood parameters and by determination of the fat and glycogen content in liver biopsies. The method for examination of the liver biopsies is described. In clinically normal lactating cows the liver contains less than 20 mg triglycerides (TG) and more than 20 mg glycogen per gram of wet tissue. Cows suffering from abomasal displacement all showed hyperglycemia and in most of them a fatty to very fatty liver was found. The degree of hyperglycemia depends on the amount of liver glycogen and is independent of the liver TG content. The degree of ketonemia also depends on the liver glycogen content.

Abomasum↗
PubMed1989

Detection and identification of pathotypes of verocytotoxigenic Escherichia coli isolated from weaned piglets using gene probes for seven E. coli toxins.

Seventy verocytotoxigenic (VTEC) and sixty-three non VTEC haemolytic Escherichia coli isolated from recently weaned piglets were examined by the colony hybridization assay using gene probes for three verocytotoxins: Edema disease principle (EDP) and Shiga-like toxins I and II (SLTI and SLTII). The results with the EDP and SLTII probes were identical. All VTEC hybridized with these two probes, while non VTEC did not. All 133 E. coli were negative for the SLTI probe. Hybridization of the plasmid content of 14 VTEC did not show any evidence for plasmid localization of the genes coding for the EDP. The 70 VTEC were also assayed with gene probes for heat-stable (STaP, STb) and heat-labile (LT, LTIIa) enterotoxins. Only the STb probe was hybridized by 36 of them. Most STb-positive isolates belonged to serotype O141: K85 biotypes 9 and 13 PC.

Animals↗
PubMed1987

Detection and photoaffinity labeling of the Ca2+-activated K+ channel-associated apamin receptor in cultured astrocytes from rat brain.

Apamin, an 18-amino acid bee venom peptide, is a specific blocker of a class of Ca2+ activated K+ channels. Mono 125I-iodoapamin was used to detect the K+ channel-associated receptor site in cultured astrocytes from rat brain. Specific high-affinity binding to intact glial cells with a Kd of about 90 pM at 1 degree C and pH 7.5 was demonstrated by equilibrium and kinetic methods. The average receptor capacity was 3 fmol/mg cell protein which is 2 to 3-fold lower than in primary cultured neurons. Binding was stimulated by K+ ions, but to a lesser extent than with neuronal receptors. Photoaffinity labeling of receptor/ion channel components using an arylazide derivative of 125I-monoiodoapamin revealed the presence of the 86- and 33-kDa polypeptides, previously detected in neurones. However a 59-kDa peptide which is present in synaptic membrane preparations from adult rat brain, but not in cultured neurons, was also clearly labeled in intact astrocytes. This indicates that the 59-kDa polypeptide is not a proteolytic fragment of the 86-kDa chain but an associated subunit which is only accessible to photolabeling in certain apamin receptor preparations. Apamin-sensitive Ca2+-activated K+ channels in astrocytes may be one of the pathways by which glial cells redistribute K+ in the central nervous system (CNS).

Affinity Labels↗