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Biomedical subjects

G Thomas

Publications and source records attributed to G Thomas.

At least 757 records · Page 42Linked to original sources
PubMed1984

Effects of sodium ipodate and propylthiouracil in athyreotic human subjects, role of triiodothyronine and pituitary thyroxine monodeiodination in thyrotrophin regulation.

To investigate the respective role of triiodothyronine (T3) and thyroxine (T4) in the regulation of TSH secretion, we studied the action of sodium ipodate and propylthiouracil (PTU) in 11 athyreotic patients. The LT4 replacement dose was adjusted to obtain, in each patient, a normal basal TSH level and a normal TSH response to TRH. In the 5 ipodate-treated patients (single 6 g oral dose), the mean serum T3 level fell by 64% below the baseline value and serum rT3 rose 180% above the baseline. The free T4 index (FT4I) did not change whereas the mean serum TSH concentration increased 280% above baseline values. In the 6 PTU-treated patients (250 mg orally every 6 h for 10 days), serum T3 levels fell 33%, serum rT3 increased up to 82% and the FT4I did not change. The mean serum TSH concentration increased 68% above the baseline value. Thus, the mean percentage increase in serum TSH was less in PTU- than in ipodate-treated patients (68% vs 280%). Statistical analysis of the correlation between the serum T3 decrease (delta T3) and the serum TSH (delta TSH) increase demonstrated that for the same T3 diminution, the ipodate-treated group displayed higher increase of TSH than the PTU-treated patients. In the rat, PTU interferes with the 5'-deiodination of T4 in the liver and kidney but not in the pituitary, while ipodate appears to have the same effect in all tissues. If this holds true for human subjects, our data strongly suggest that circulating T4 (through its intrapituitary conversion to T3) shares with serum T3 the capacity to regulate TSH secretion in man.

Adult↗
PubMed1984

Inhibitors of the rate of carbohydrate and lipid absorption by the intestine.

The rate of energy storage in adipose tissues is, at least in part, dependent on the concentration of nutrients and hormones in the blood. A delayed absorption of ingesta from the intestine should cause lower concentrations of fat, glucose and insulin and, thus, reduce the triglyceride storage rate. Non-selective agents retard the absorption irrespective of composition of food. Inhibitors of intestinal alpha-glucosidases delay the degradation of complex carbohydrates to absorbable monosaccharides and thus decrease the rate of their absorption. Inhibitors of pancreatic lipase interfere with the degradation of dietary triglycerides and decrease the postprandial triglyceride increment in blood and tissues. Recently a compound was found which inhibits the absorption of carbohydrates as well as triglycerides.

Acarbose↗
PubMed1983

Phagocytosis and onset of human labor.

An in vitro experimental model has been developed which allows the study of amnion lysosomal enzyme release under controlled conditions. Briefly, a layer of human amnion membrane mounted on a specially designed reaction vessel serves as the reaction surface. We have noted that the addition of particulate material to these membranes incubating in pseudoamniotic fluid results in an increased release of the lysosomal marker enzyme N-acetylglucosaminidase when compared to the release in the absence of particles. This release is completely inhibited by iodoacetate and slightly by azide. A similar increased release is also noted with the use of term amniotic fluid as incubation medium when compared to centrifuged (30,000 g/20 min) amniotic fluid. Lecithin and lysolecithin were effective in releasing increasing amounts of enzyme. This increased release was noted only from membranes of placentas collected from subjects who had undergone cesarean section prior to labor. Membranes collected from vaginal deliveries after labor showed a baseline increased release but no further stimulation upon the addition of any of the substances. These results suggest that the release of lysosomal enzymes from amnion membranes is brought about by substance(s) present in amniotic fluid. Very probably, these are surfactants. The interaction of these substances with amnion cells would eventually result in an exponential burst of prostaglandin synthesis, which would result in labor.

Acetylglucosaminidase↗
PubMed1983

Ordered phosphorylation of 40S ribosomal protein S6 after serum stimulation of quiescent 3T3 cells.

The amino acids and tryptic peptides that become phosphorylated in 40S ribosomal protein S6 after serum stimulation of quiescent 3T3 cells were examined by two-dimensional thin-layer electrophoresis. In the maximally phosphorylated form of the protein, most of the phosphate was incorporated into serine and a small amount, into threonine. Digestion of this form of the protein with trypsin revealed 10 major phosphopeptides. All 10 contained phosphoserine and 2 of the 10 also contained phosphothreonine. Next, the five forms of increasingly phosphorylated S6 were individually separated on two-dimensional polyacrylamide gels or total S6 was isolated from cells that were stimulated for only a short time and their phosphotryptic maps were analyzed. The results showed that, as larger amounts of phosphate were added to S6, the phosphopeptides appeared in a specific order.

Animals↗
PubMed1983

Kinase II-dependent formation of angiotensins II and III in the hepatic circulation.

Experiments were performed in 14 pentobarbital-anesthetized dogs to 1) determine if the hepatic arterial vasoconstrictor effects of [des-Asp1]angiotensin I [( des-Asp1]ANG I) were due to its local conversion to angiotensin III (ANG III) and 2) to evaluate the magnitude of conversion of ANG I to angiotensin II (ANG II) and of [des-Asp1]ANG I to ANG III in the hepatic arterial vascular bed. Graded doses of these peptide agonists were administered as bolus injections directly into the hepatic artery; hepatic arterial blood flow was measured with an electromagnetic flow probe. Dose-response relationships were determined before and during the inhibition of kinase II activity with captopril (2-D-methyl-3-mercaptopropanoyl-L-proline) and antagonism of angiotensin receptor sites with [Ile7]angiotensin III [( Ile7]ANG III). ANG I and [des-Asp1]ANG I were equipotent at all doses tested, as were ANG II and III. At all doses tested, ANG II and III were approximately three times more potent than ANG I and [des-Asp1]-ANG I. Captopril attenuated the vasoconstrictor responses to ANG I and [des-Asp1]ANG I only, whereas [Ile7]ANG III inhibited the responses to all four angiotensin peptides. These data indicate that the hepatic arterial vasoconstrictor responses to [des-Asp1]ANG I were due to the intrahepatic formation of ANG III. The extent of intrahepatic conversion of [des-Asp1]-ANG I to ANG III that occurred in one transit through the hepatic arterial vascular bed was estimated to be 33%, which was similar to the estimated 38% conversion of ANG I to ANG II.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1983

Activation of calcium channels by novel 1,4-dihydropyridines. A new mechanism for positive inotropics or smooth muscle stimulants.

The effects of the novel, 1,4-dihydropyridine derivative methyl 1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl) -pyridine-5-carboxylate (Bay k 8644) are reported. In contrast to the nifedipine-like dihydropyridines, which have calcium antagonistic actions. Bay k 8644 has positive inotropic and vasoconstrictor effects. The effects and mechanism of action of Bay k 8644 have been examined in the anaesthetised dog, on the isolated perfused guinea-pig heart, and on the isolated rabbit aortic strip. In these preparations Bay k 8644 is active in the same dose range as nifedipine, but has effects diametrically opposite to those of nifedipine. There is a competitive antagonism between Bay k 8644 and nifedipine, whereas verapamil and diltiazem produce only a functional, non-competitive inhibition of the effects of Bay k 8644. We conclude that a specific dihydropyridine receptor exists, which may bind both nifedipine and Bay k 8644. In contrast to nifedipine Bay k 8644 stimulates the calcium influx into the cell.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1983

[Effect of adjuvants on the pharmaceutical and biological availability of chlorpromazine hydrochloride].

It is reported of the influence of adjuvants upon the pharmaceutical and biological availability of chlorpromazine hydrochloride from tablets. Sodium carboxymethyl cellulose, microcrystalline cellulose (Heweten 40) and potato starch have been used for tabletting. The adjuvants added act on the pharmaceutical availability, certain differences being due to a discriminate swelling behaviour. The differences observed in vitro exert no effect on the bioavailability of the drug in the rabbit. Thus, the tablets produced with the adjuvants mentioned have proved to be preparations of almost equivalent similar biopharmaceutical behaviour.

Animals↗
PubMed1983

[Effects of the pH value and of drug-adjuvant interactions on the dissolution rate and the liberation of drugs].

It is reported of the effects of the pH value and of drug-adjuvant interactions on the dissolution profile of chlorpromazine hydrochloride and theophylline, as well as on their liberation from triturations with sodium carboxy-methylcellulose and microcrystalline celluloses. The binding of chlorpromazine hydrochloride to sodium carboxymethylcellulose and (less markedly) to micro-crystalline celluloses acts on the drug liberation only in those pH ranges where the dissolution rate of the drug remains constant. In a pH range where the dissolution rate decreases, the binding is of negligible significance. A prolongation of the dissolution time is sufficient to dissolve out the sodium carboxymethylcellulose-bound chlorpromazine hydrochloride from the associate and to produce an increase in liberation. The binding of the drug to the adjuvant weakens with increasing ionic strength of the liberation medium, which leads to a considerable rise of the liberation rate. Owing to the slight sorption of the drug on microcrystalline celluloses, the drug liberation equalizes the dissolution rate in pH ranges greater than 4.8. The dissolution rate of theophylline and the rate of its liberation from triturations showed no differences since there were no drug-adjuvant interactions.

Adjuvants, Pharmaceutic↗
PubMed1982

[Unusual concentrations of triiodothyronine in the serum due to anti-T3 autoantibodies].

Abnormally high T3 serum concentrations incompatible with the patients' clinical thyroid status were observed in a case of Graves' disease and in a euthyroid patient with hyperlipaemia. T3 was in the form of immune complexes precipitable by polyethyleneglycol. Specific anti-T3 autoantibodies were detected in the serum gammaglobulin fraction. The T3 affinity constants of these autoantibodies were found to be as high as 1.10(10) and 7.2.10(10)l/mol respectively. The antibodies interfered with radioimmunological T3 determination, resulting in an apparent increase of T3. However, after extraction, true T3 serum levels remained higher than expected. These findings illustrate the importance of hormone concentrations, affinity constants of binding proteins and equilibrium between free and bound forms in the resulting hormonal effect.

Adult↗
PubMed1982

The phosphorylation of ribosomal protein S6 in rat tissues following cycloheximide injection, in diabetes, and after denervation of diaphragm. A simple immunological determination of the extent of S6 phosphorylation on protein blots.

The extent of phosphorylation of S6 was measured in a variety of cells, organs, and tissues using a simplified procedure. Ribosomal proteins were separated by electrophoresis on a one-dimensional urea-sodium dodecyl sulfate gel. They were transferred electrophoretically to nitrocellulose, and S6 was specifically stained by means of its reaction with a monoclonal antibody. The mobility of the stained protein was shown to be a measure of the extent of its phosphorylation. Using this method, we found that cycloheximide injection of rats gives rise to the phosphorylation of S6 in a variety of organs and tissues: diaphragm, heart and skeletal muscle liver and kidney, but not brain. Diabetes induced with alloxan did not result in the phosphorylation of S6 in any of the tissues examined, and subsequent insulin injection resulted in a slight increase in the phosphorylation of S6 in liver. Insulin injection in normal rats also caused the phosphorylation of liver S6. Unilateral denervation of rat diaphragm resulted in phosphorylation of S6 in the denervated portion but not in the innervated portion of the diaphragm.

Animals↗
PubMed1982

[Sensitivity and specificity of lead poisoning detection tests].

The results of biochemical tests used for the supervision of factory workers exposed to lead (notably lead serum levels, urinary aminolevulinic acid (ALA) and punctuated red cells) were compared in 90 patients. The reference test used to evaluate the sensitivity and specificity of these examinations was EDTA-induced lead urinary excretion. Lead serum levels and urinary ALA were about equally effective in providing information. However, these two tests were more sensitive when performed simultaneously than when performed separately. It is suggested that both should be requested when trying to prevent lead poisoning.

Adult↗
PubMed1982

Mechanism of ionophore A23187 induction of plasma protein leakage and of its inhibition by indomethacin.

Calcium ionophore A23187 produced a dose-dependent increase in plasma protein leakage on intradermal injection in rats. Studies with mepyramine and cyproheptadine indicated that histamine and 5-hydroxytryptamine (5-HT) partially contribute to the ionophore action and experiments with compound 48/80 supported these findings. Depletion of plasma kininogen levels with cellulose sulphate administered indomethacin inhibited the ionophore response in a dose-dependent manner. The inhibition was not reversed by intradermally injected prostaglandin E2 (PGE2) in doses up to 50 ng/site, suggesting that PGE2 also may not be an important mediator. It is proposed that the ionophore produces plasma protein leakage by an indirect (through histamine and 5-HT release) and a direct action on vascular endothelial cells and that indomethacin antagonises both actions by inhibiting calcium transport processes.

Animals↗