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Biomedical subjects

J C Meunier

Publications and source records attributed to J C Meunier.

160 records · Page 9Linked to original sources
PubMed1969

Compared effects of dithiotreitol on the interaction of an affinity-labeling reagent with acetylcholinesterase and the excitable membrane of the electroplax.

p-(trimethyl ammonium) benzene diazonium difluoroborate (TDF), an affinity-labeling reagent of the acetylcholine receptor site(s), which in the normal cell acts as an irreversible inhibitor becomes a reversible activator after in vivo exposure of the electroplax to dithiothreitol (DTT), a disulfide bond reducing agent. After in vitro exposure of acetylcholinesterase to DTT, TDF becomes a reversible competitive inhibitor of the enzyme, using indophenyl acetate as the substrate. Both acetylcholinesterase and the macromolecular receptor of acetylcholine thus contain disulfide bonds. Additional experiments with DTT suggest that there might exist several different classes of receptor sites for cholinergic agents in the excitable membrane of the electroplax.

Animals↗
PubMedDate not supplied

Pancreatic B-cell response to a test-meal in lean and obese diabetic patients: relation to metabolic control.

We have measured fasting C-peptide reactivity (CPR) as well as CPR responses to a test meal in 83 diabetic patients and 41 non diabetic controls. In comparison to controls, basal CPR was decreased in lean insulin-treated diabetics with stable or brittle diabetes and in obese patients with brittle diabetes. Lean and obese maturity-onset diabetics had increased CPR levels and so had obese insulin-treated patients. Nevertheless, the CPR response to the test meal was clearly inadequate in all diabetics. In control patients, there was a positive correlation between fasting blood glucose and CPR levels. On the contrary, lean diabetics demonstrated a negative correlation between these parameters. Hemoglobin A1 levels were negatively correlated to fasting CPR levels in lean diabetics, indicating the importance of residual B-cell function for diabetes control. These correlations were obscured in obese diabetics. In our patients, circulating insulin antibodies had apparently no deleterious effect on metabolic control.

Adult↗
PubMedDate not supplied

B-cell response to a standardized breakfast in end-stage renal failure.

Twelve uremic patients (U) on regular hemodialysis were submitted to a standardized test meal. In comparison with normal controls (C), U patients demonstrated a slight increase of HbA1 level and a definite elevation of fasting plasma C-peptide immunoreactivity. They showed glucose intolerance at 60 and 120 min. This was associated with an inappropriate insulin response as evidenced by a significantly lower insulin/glucose index at 60 min. U patients were tested again during a hemodialysis session in order to reduce the 60-min glucose intolerance. Six patients (U1) were selected because they exhibited mean fasting and 60-min glucose values similar to those of the controls. In these conditions, the insulin response at 60 min was significantly decreased in comparison to basal conditions and this could not be accounted for by a concomitant decrease of plasma alpha-aminonitrogen values. It is concluded that, in uremic patients, glucose intolerance is associated with an inappropriately low B-cell response.

Adult↗
PubMedDate not supplied

Immobilization as a tool for the stabilization of lignin peroxidase produced by Phanerochaete chrysosporium INA-12.

Lignin peroxidase immobilization was achieved by covalent coupling on CNBr-Sepharose 4B. Protein immobilization yield was around 80%. For veratryl alcohol oxidation, in the presence of hydrogen peroxide, both soluble and bound enzymes exhibited the same pH profile with an optimum near 2.5. Catalytic parameters (kc and Km) were seriously affected by immobilization. On the other hand, immobilization provided a noticeable stabilization of the enzyme against acidic pH and high temperatures. A 15-20 increase in the half-inactivation times at pH 2.2 and 2.7, respectively, could be observed. Bound enzyme was also much more thermostable than soluble.

Basidiomycota↗
PubMedDate not supplied

Mu and kappa opiate binding sites in the rabbit CNS.

We have examined the ability of various opiates to compete with the binding of 3H-etorphine (0.5 nM) in membranes from the rabbit cerebellum and thalamus. Our data suggest that greater than 80% of 3H-etorphine binding occurs at mu receptor sites in cerebellum membranes. In thalamus membranes, D-Ala2, D-Leu5-enkephalin (DADL) resolves binding of 3H-etorphine into two components. The first component accounts for about 50% of binding and may represent interaction of the radioligand with mu receptor sites. The second component is unaffected in the presence of high (1-5 microM) concentrations of DADL. The ranking of potency for opiate inhibition of the second component is ethylketocyclazocine greater than naloxone much greater than morphine much greater than DADL, suggesting it represents binding of 3H-etorphine to a kappa-opiate binding site. In the rabbit brain, the kappa-opiate binding site is particularly abundant in the thalamus followed by frontal cortex and caudate nucleus.

Animals↗
PubMedDate not supplied

[Fom orphan receptor to novel neuropeptide: an example of reverse pharmacology].

Nociceptin, a neuropeptide 17 amino acid residues in length, is the first novel bioactive substance to have been discovered by functional genomics. Nociceptin was isolated from a rat brain extract as the endogenous ligand to an orphan receptor, ORL1 (Opioid Receptor-Like 1), structurally akin to opioid receptors, whose cDNA had been cloned from a human brain stem library. The peptide is processed from a larger precursor polypeptide, prepro-nociceptin, which is widely distributed in the nervous system. Nociceptin is primarily an inhibitory neuropeptide that acts on neurons to depress synaptic transmission. Nociceptin's wide spectrum of pharmacological actions hints at several potential therapeutic applications for ORL1 receptor agonists and/or antagonists, particularly for treating pain states, stress and anxiety, cognitive defects, and drug addiction. A major challenge is now the discovery and pharmacological in vivo profiling of ORL1 receptor ligands that are active by medically practical routes of administration.

Amino Acid Sequence↗
PubMedDate not supplied

Interest of the association clonidine-spironolactone in cirrhotic patients with ascites and activation of sympathetic nervous system.

BACKGROUND: The aim of this study was to examine the effects of spironolactone, clonidine and the association of clonidine-spironolactone on renin-aldosterone and sympathetic systems, renal function, systemic hemodynamics and mobilization of ascites in 32 alcoholic cirrhotic patients with marked increase in sympathetic system. METHODS: Measurements were taken before and after an 8-day treatment with spironolactone (200 mg/day), after an 8-day treatment with clonidine (0.150 mg/day) and 10 days after adjunction of spironolactone (200 mg/day) to clonidine. RESULTS: Three patients abandoned the treatment or were excluded because lack of compliance. Spironolactone alone induced an increase in renin-aldosterone and sympathetic systems without any remarkable increase of natriuresis and body weight loss. Given for 8 days, clonidine alone induced a significant decrease in plasma norepinephrine associated with a significant increase in glomerular filtration rate without effect on natriuresis. In contrast, 10 days after adjunction of spironolactone to clonidine, plasma renin and aldosterone significantly decreased, natriuresis increased (from 7.4 +/- 0.7 to 41.6 +/- 3.2 mEq/24 h) and body weight decreased (from 66.03 +/- 2.3 to 63.5 +/- 2.3 kg) without adverse effects. CONCLUSION: In cirrhotic patients with ascites and marked activation of sympathetic nervous system, spironolactone (200 mg/day) is unable to mobilize ascites. In these patients, after 8 days, clonidine decreases sympathetic activity, increases glomerular filtration rate and after 18 days, decreases plasma renin and aldosterone concentrations allowing a better action of spironolactone. The association clonidine-spironolactone enhances natriuresis and body weight loss.

Adrenergic alpha-Agonists↗