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Biomedical subjects

P Bouchard

Publications and source records attributed to P Bouchard.

At least 181 records · Page 10Linked to original sources
PubMed1985

Membrane lectins on human monocytes. Maturation-dependent modulation of 6-phosphomannose and mannose receptors.

Freshly isolated human monocytes, which do not contain cell-surface mannose-specific receptors, bind mannose 6-phosphate and actively endocytose mannose 6-phosphate-bearing neoglycoproteins (6-P-Man-F-BSA). Three days after isolation, human monocytes endocytose very actively 6-P-Man-F-BSA as well as Man-F-BSA, and the endocytosed neoglycoproteins are rapidly degraded. These results were obtained in quantitative flow cytofluorometry by using a panel of fluoresceinylated sugar-substituted serum albumins (neoglycoproteins). Thus, in contrast to mannose receptors which appear only after maturation, mannose 6-phosphate receptors are already present on freshly isolated human monocytes.

Carrier Proteins↗
PubMed1985

Gonadotropin-releasing hormone pulsatile administration restores luteinizing hormone pulsatility and normal testosterone levels in males with hyperprolactinemia.

Hyperprolactinemia in men is frequently associated with hypogonadism. Normalization of serum PRL levels is generally associated with an increase in serum testosterone (T) to normal. To determine the mechanism of the inhibitory effect of hyperprolactinemia on the hypothalamic-pituitary-gonadal axis, we studied the effect of intermittent pulsatile GnRH administration on LH pulsatility and T levels in four men with prolactinomas. All patients had high PRL values (100-3000 ng/ml), low LH (mean +/- SEM, 2.2 +/- 0.1 mIU/ml), and low T values (2.3 +/- 0.3 ng/ml), with no other apparent abnormality of pituitary function. GnRH was administered iv using a pump delivering a bolus dose of 10 micrograms every 90 min for 12 days. No LH pulses were detected before treatment. Pulsatile GnRH administration resulted in a significant increase in basal LH levels (6.7 +/- 0.6 mIU/ml; P less than 0.001) and restored LH pulsatility. In addition, T levels increased significantly to normal values in all patients (7.8 +/- 0.4 ng/ml; P less than 0.001) and were normal or supranormal as long as the pump was in use, although PRL levels remained elevated. These data, therefore, suggest that hyperprolactinemia produces hypogonadism primarily by interfering with pulsatile GnRH release.

Adult↗
PubMed1985

Elevated metabolic clearance rate of 1 alpha,25-dihydroxyvitamin D3 in hyperthyroidism.

Metabolic clearance rate (MCR) and daily production rate (DPR) of 1 alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3) were measured in 7 hyperthyroid patients and 8 control subjects after a single injection of tritiated 1,25(OH)2D3. Using a bicompartmental analysis, MCR of 1,25(OH)2D3 was found to be significantly higher in hyperthyroid than in control subjects (11.5 +/- 4.4 vs 5.9 +/- 2.4 ml/min (SD), P less than 0.01). No significant difference in plasma 1,25(OH)2D and DPR of 1,25(OH)2D3 was demonstrated. MCR was again measured 1 month after initiation of treatment in 4 hyperthyroid patients and remained elevated. In 2 of these patients, MCR was once more determined 6 months later and had declined towards normal. No correlation was found between MCR and DPR and either plasma calcium, phosphate, immunoreactive PTH, 1,25(OH)D and T3 values. In conclusion, MCR of 1,25(OH)2D3 is elevated in hyperthyroidism, but this finding is probably unrelated to the effect of thyroid hormones on bone metabolism.

Adult↗
PubMed1984

[Anovulation of hypothalamic origin. Treatment by pulsatile injection of hypothalamic gonadotropin releasing hormone].

In two patients with severe hypogonadotrophic hypogonadism intermittent pulsatile delivery of gonadotrophin hormone (LHRH) 5 to 20 micrograms every 90 minutes by means of the Zyklomat pump promptly resulted in ovulation and pregnancy. The comparative effectiveness of the intravenous and subcutaneous routes was evaluated by radioimmuno assay of LHRH in plasma. The pulsatile patterns of LH was satisfactory with both routes, but plasma levels of LHRH were about 7 times lower with the subcutaneous route. The dosage range (5-20 micrograms) of LHRH must be adjusted to the severity of the hypothalamic deficiency and to the route of administration. The use of the pump, the monitoring of ovulation and the indications for this type of treatment are discussed.

Adult↗
PubMed1984

The hormonal control of adenylate cyclase in rabbit myometrium: in vitro inhibition by adenosine and lack of effect of progesterone.

The mechanism by which progesterone modifies uterine smooth muscle cell contraction is still unknown. We investigated the biochemical basis of progesterone effects on myometrium of estradiol-primed rabbits. Progesterone did not affect adenylate cyclase basal activity and displayed no interaction with stimulators of myometrium adenylate cyclase (NaF, guanylyl nucleotides, beta-adrenoreceptor agonists, prostaglandins, forskolin) or with adenosine. On the other hand, adenosine inhibited myometrial adenylate cyclase, which correlates with its contracting properties in vivo; this inhibition is mediated through interaction at 'P sites'. We conclude that whilst adenosine inhibits myometrial adenylate cyclase by acting at 'P sites', progesterone does not interact directly with adenylate cyclase to regulate myometrial contractility.

Adenosine↗
PubMed1984

[Spinal anesthesia and multiple sclerosis].

Spinal anaesthesia was performed in 9 patients with multiple sclerosis for 14 surgical procedures: urological surgery 13 times and plastic surgery once. No complication was observed. except for a transient exacerbation in one case. Spinal anaesthesia appeared to be an innocuous procedure in multiple sclerosis as no neurotoxicity was observed. Exacerbation of multiple sclerosis was similar to that seen with general anaesthesia. Moreover, spinal anaesthesia improved the operating conditions by relieving bladder spasticity; it was also often asked for by patients who feared the loss of consciousness of general anaesthesia.

Adult↗
PubMed1984

Absence of a direct inhibitory effect of the gonadotropin-releasing hormone (GnRH) agonist D-Ser (TBU)6, des-Gly-NH2(10) GnRH ethylamide (Buserelin) on testicular steroidogenesis in men.

The antigonadal effects of GnRH agonists (GnRH-A) are mediated both through pituitary and testicular inhibitory mechanisms in the rat. To investigate these effects in men, we studied patients having no gonadotropin secretion and compared their testicular response to hCG in the absence or in the presence of GnRH-A. Thirteen patients with acquired pituitary hypogonadotropism had plasma testosterone levels below 1.5 ng/ml and no gonadotropin responses to acute GnRH administration (100 micrograms iv). Testicular responsiveness was evaluated using a single im injection of hCG (5000 IU im). Plasma levels of testosterone, dihydrotestosterone, androstenedione, 17-hydroxyprogesterone (17-OHP), and progesterone were determined before and 4, 12, 24, 48, and 72 h after hCG stimulation. The same protocol was also used in the same patients on day 4 of a 6-day course of treatment with the GnRH-A, D-Ser-(TBU)6, des-Gly NH2 GnRH ethylamide (Buserelin) (3 sc injections of 250 micrograms/day). During the first 4 days of GnRH-A administration, plasma LH, FSH, and testosterone levels were measured daily in order to establish the completeness of the gonadotropin deficiency. Before treatment with hCG, plasma testosterone levels were 0.56 +/- 0.15 and 0.96 +/- 0.22 ng/ml (mean +/- SE) in the absence of GnRH-A and during GnRH-A administration, respectively. The administration of hCG elicited a significant increase in plasma testosterone in both situations; integrated testosterone concentrations were 123.7 +/- 24.9 and 155.5 +/- 27.9 ng/ml . 72 h (P greater than 0.1) in the absence of GnRH-A and during GnRH-A administration, respectively. Likewise the ratios of 17-OHP to progesterone, androstenedione to 17-OHP, and dihydrotestosterone to testosterone after hCG injection were similar in the presence or absence of GnRH-A. Since short term administration of buserelin did not inhibit hCG-induced testosterone secretion in patients with gonadotropin deficiency, we suggest that Buserelin does not grossly modify the function of testicular steroidogenesis enzymes. The antigonadal effects of GnRH-A in man appear to be mediated exclusively through the pituitary.

Buserelin↗
PubMed1984

Effect of carbimazole treatment on specific and non-specific immunological parameters in patients with Graves' disease.

Twenty-two patients with newly diagnosed Graves' disease (GD) were treated with carbimazole (CBZ) for 6 months. Thyroid stimulating immunoglobulins (TSI) and T cell subsets were studied prior to treatment and after 3 and 6 months of therapy. TSI were measured on human thyroid epithelial cell monolayers by the cAMP production after the addition of highly purified GD IgG. Before treatment, serum IgG from 20 out of the 22 patients (91%) stimulated cAMP production significantly compared to normal IgG. The mean index of cAMP production (GD IgG relative to normal IgG) was 2.15. After 3 months of CBZ treatment, a non-significant decrease of the mean cAMP production index was observed, whereas it was significantly decreased at the end of the 6 month course of therapy. Before treatment, total T cells (OKT3+), helper/inducer T cells (OKT4+) and suppressor/cytotoxic T cells (OKT8+) were all significantly decreased compared with controls. After 3 or 6 months of CBZ therapy, both total T cells and helper/inducer T cells returned to a normal level, while cytotoxic/suppressor T cells remained at the same low level. Taken together, these data indicate that treatment with CBZ leads to an early increase of helper/inducer T cells followed 3 months later by a decrease of the TSI level with no change in decreased suppressor/cytotoxic T cells. The disappearance of TSI following the increased helper/inducer T cell level suggests that an anti-idiotypic reaction may have occurred, and the persistent decrease of the suppressor/cytotoxic T subset that CBZ therapy does not act upon the underlying autoimmune disease.

Adult↗
PubMed1983

Endogenous protein carboxyl methylation in hamster spermatozoa: changes associated with capacitation in vitro.

Protein carboxyl methylase (PCM) and its substrate(s), methyl acceptor protein(s) (MAP), are present in the spermatozoa of rat, rabbit and man. In the present study, PCM activity and MAP capacity were measured in homogenates of hamster testes and isolated spermatozoa, and found to be similar to those of other species. Using solubilized preparations of spermatozoa from the cauda epididymis of hamster, PCM activity was twice as high in sperm tails as in heads while the reverse was true for MAP capacity. Since in this and in previous studies this enzyme reaction has been measured in broken cells, we thought it pertinent to measure methylation under physiological conditions (i.e., in motile spermatozoa). To accomplish this, an assay was developed which depends upon the conversion of [3H-methyl]methionine to S-adenoxyl-L [methyl-3H]methionine which, in turn, serves as a methyl donor for PCM. In sperm that had been labelled with [3H]methionine the MAP for the endogenous methylation reaction was not solubilized with Triton X-100, and was found primarily in sperm tails. When hamster spermatozoa were incubated in medium containing taurine, epinephrine and bovine serum albumin to induce capacitation, endogenous methylation was stimulated 8- to 9-fold; when taurine was omitted from this medium, methylation was stimulated 14-fold. Taurine, however, was essential for in vitro fertilization as the number of eggs fertilized declined from 92% in complete medium to 0% in medium minus taurine. The decrease in fertilization rate was also associated with a decrease in sperm motility. In previous studies we have demonstrated an association between PCM and sperm motility, and have suggested that this enzyme system could be involved in other functions such as the acrosome reaction. From the results in the present study we conclude that the conditions that lead to capacitation in vitro are associated with a marked change in endogenous protein carboxyl methylation.

Animals↗
PubMed1982

Diabetes mellitus following pentamidine-induced hypoglycemia in humans.

Four patients, treated with pentamidine because of Pneumocystis carinii pneumonitis, displayed severe fasting hypoglycemia during this treatment. Diabetes mellitus appeared later, requiring insulin therapy in the three of them who survived more than a few weeks. The metabolic study, performed in two cases during the hypoglycemic period, demonstrated inappropriately high insulin levels in the postabsorptive state. 28 +/- 1 microunits/ml (blood glucose 41 +/- 4 mg/dl) and 86 +/- 5 microunits/ml (blood glucose 15 +/- 5 mg/dl) vs. 15 +/- 3 microunits/ml in 10 control subjects and 55 +/- 3 microunits/ml in 6 patients with a verified B-cell tumor, respectively. Poor B-cell secretory responses followed the stimulations by oral glucose (maximal increment over basal: +5 microunits/ml vs. + 40 microunits/ml in control group and +77 microunits/ml in the insulinoma group), by i.v. arginine (maximal increment + 10 and +28 microunits/ml, respectively, vs. +55 in the controls and +90 microunits/ml in the insulinoma group) and by i.v. glucagon (+10 and +23 microunits/ml, respectively) vs. +40 microunits/ml in both the control and the insulinoma groups). Plasma cortisol and glucagon, and the A-cell response to arginine were higher than normal. These high, nonsuppressible, nonstimulable insulin levels and the sequence of hypoglycemia followed by insulin-dependent diabetes mellitus is consistent with the hypothesis of a selective toxicity turned towards the B-cells. In vitro incubation of islets with pentamidine 10(-10) M produced a passive release of insulin, followed by a significant decrease in B-cell response to glucose + theophylline. It is suggested that pentamidine can induce hypoglycemia because of an early cytolytic release of insulin, and then diabetes mellitus because of B-cell destruction and insulin deficiency.

Adult↗
PubMed1981

erythro-9-[3-(2-Hydroxynonyl)]adenine is an inhibitor of sperm motility that blocks dynein ATPase and protein carboxylmethylase activities.

Protein carboxylmethylase (S-adenosyl-L-methionine:protein O-methyltransferase, EC 2.1.1.24.) is believed to be involved in the regulation of sperm motility. To test this hypothesis, we investigated the effects of erythro-9-[3-(2-hydroxynonyl)]adenine (EHNA) which, in combination with adenosine and homocysteine thiolactone, inhibits protein carboxylmethylase activity in monocytes. This group of compounds inhibited sea urchin sperm motility. Unexpectedly, EHNA alone inhibited the motility., This observation was confirmed in intact spermatozoa from rats, rabbits, and humans. EHNA also inhibited the motility of demembranated, reactivated sea urchin and rat spermatozoa from which protein carboxylmethylase had been extracted. In these preparations, motility was restored by ATP. These observations suggested that EHNA arrests sperm motility by inhibiting the axonemal dynein ATPase on which motility depends. Kinetic analysis demonstrated that EHNA produced mixed inhibition of both the axonemal ATPase and the partially purified dynein 1 from sea urchin sperm tails, as well as the axonemal ATPase of rat sperm tails. These observations also provide evidence for the similarity of the active site of the dynein ATPase in sea urchin and rat spermatozoa.

Adenine↗
PubMed1981

Androgen receptor in human skin cytosol.

Human skin, an accessible tissue, is an androgen target organ. We have measured the androgen-binding capacity of human skin cytosol using either 5 alpha[3H]dihydrotestosterone ([3H]DHT) or [3H]methyltrienolone ([3H]R-1881) as ligand. Samples were incubated for 20 h at 0 C, and dextran-coated charcoal was used to separate bound from free steroids. The androgen receptor has a high affinity for both ligands (0.23 +/- 0.04 nM for [3H]DHT; 0.32 +/- 0.16 nM for [3H]R-1881). Testosterone, cyproterone acetate, and, to a lesser extent, estradiol also bind this protein. Progesterone displaces R-1881 from its binding sites, whereas its 5 alpha-reduced metabolite somewhat inhibits DHT binding. The highest binding capacity is measured in cytosol of skin from external genitalia (129.14 +/- 58.0 fmol/g skin; n = 34); it is lower in pubic skin (21.8 +/- 13 fmol/g skin; n = 6). There is no variation as a function of age or sex in genital skin; the higher concentrations observed in the cytosol of pubic skin of women compared to that of men are probably related to lower levels of endogenous steroids. Whereas most patients with the complete form of the testicular feminization syndrome do not have detectable concentrations of androgen receptor, one patient with apparent complete clinical androgen insensitivity had a normal androgen-binding capacity. The parity of values in genital skin from men and women, the absence of variation with age, and the presence of a cytosolic androgen receptor in some androgen-insensitive patients suggest that the androgen receptor in human skin cytosol is not regulated by androgens.

Adolescent↗
PubMed1981

[Bacteriologic study of indwelling central venous catheters. Factors influencing the risk of microbial colonization and sepsis (author's transl)].

The mechanism of microbial colonization and sepsis is disputed. For many authors, catheter contamination results from poor aseptic technic during insertion or removal or from the descent of organisms along the catheter from the skin puncture site; we think with Michel that endogenous colonization of the thrombus at the tip of the catheter must be considered: a statistical correlation between infected foci remote from the catheter allows this hypothesis; tracheostomy may be considered as well as a percutaneous contaminant as a deep infected focus. The correlation between non specific immunity and contamination is another finding which allows the ability of endogenous colonization.

Catheterization↗