In primary cultures of cells from human thyroid cancer, functional activity was investigated by adenylate cyclase responsiveness and radioiodine uptake. In cells from well-differentiated follicular carcinomas (2 cases), TSH stimulation of cAMP accumulation is similar to that of normal thyroid cells. In contrast, in papillary carcinomas (11 cases), the mean dose-response curve is much lower than normal. In thyroid cancers, radioiodine uptake by the cells has been detected in some cases after 3 days of 125I incorporation. As previously observed, our results suggest the existence of a relationship between adenylcyclase responsiveness and 125I uptake by the cells.

Inhibitory effects of Celiptium on the thymidine kinase synthesis induced by oestradiol-17 beta in the rat uterus. In the rat uterus, the synthesis of thymidine kinase specifically induced by oestradiol-17 beta was inhibited by Celiptium. The synthesis was totally inhibited when the drug was administered before the oestrogen and partially when it was administered after. These facts suggested that Celiptium was competitive to the acceptor sites for oestradiol-receptors and inhibited the expression of the thymidine kinase gene.

In uteri from immature female rats, thymidine kinase activity was largely increased by administration of 5-androstene-3 beta, 17 beta-diol. Kinetic studies showed that the enzyme activity reached its maximum level 30 h after hormone administration. That increase in thymidine kinase activity was dose-dependent and could be related to the synthesis of new molecules of enzyme. Moreover, it was exclusively observed in target-organs for estrogens. It was concluded that 5-androstene-3 beta, 17 beta-diol which results from the metabolism of dehydroepiandrosterone had estrogen-like properties with regard to the induction of thymidine kinase.

We have studied strains of enterobacteria which are resistant to first generation cephalosporins, in relation to their cephalosporinase production. Therefore, this is not an epidemiological study. For these selected strains, if a difference in MIC greater than or equal to 2 base 2 logarithms is considered to be significant, Moxalactam appears as more potent than cefotaxim. An appropriate study shows that these findings are related to the production of cephalosporinase. If very little cephalosporinase is produced, cefotaxim is more potent, implying better accession to the lethal target of the bacteria. Conversely, when cephalosporinase production is higher, Moxalactam is more potent. Moxalactam can be shown to be more resistant to hydrolysis by cephalosporinases.

1. Male Wistar rats were treated with tiadenol, 200 mg/kg/ p.o. daily for 7 days. 2. The administration of tiadenol markedly increased the activity of bilirubin glucuronosyl transferase in hepatic microsomes. Cytochrome P 450 levels and ethoxycoumarin deethylase activity were more slightly increased. 3. Electrophoresis of microsomal proteins showed the induction of a protein with a molecular weight of about 72,000. 4. Tiadenol alone only slightly affected the fatty acid composition of microsomal lecithins and cephalins. When given with phenobarbital, however, tiadenol modified the phenobarbital-induced changes in the fatty acid composition of microsomal lipids.

After transformation of Escherichia coli strains with plasmid pBR 322 and growth in rich L medium, the total amount of beta-lactamase produced, strongly decreased when the temperature was raised from 30 to 42 degrees C, but increased after addition of ampicillin or tetracycline to the medium. beta-lactamase was synthesized and exported into the periplasmic space of wild-type strain, but was not significantly released into the extracellular medium, after growth at low temperature. We have identified an E. coli mutant which excreted up to 90% of total amount of beta-lactamase activity, any temperature. This mutant has been used as an indicator strain, for the development of an in situ test allowing the detection of beta-lactamase excretion.

Among the three strains of Clostridium acetobutylicum we investigated: NRRL 592, NCIB 619 and ATCC 824, only the last was shown to contain a NADH: rubredoxin oxidoreductase activity. We report that the biosynthesis rate of this enzyme fluctuated in the proportions of 1 to 50 according to the growth phase and medium composition. These variations reflect a mode of regulation adjusted to the metabolism of bacteria.

Male Wistar rate were treated with benfluorex, 50 mg/kg/p.p. daily for 7 days. The administration of benfluorex markedly increased the activity of ethoxycoumarin deethylase without increase of cytochrome P 450 levels in hepatic microsomes. The activity of bilirubin glucuronosyl transferase is so much increased with benfluorex than phenobarbital but this effects are not additive. Benfluorex alone affected the fatty acid composition of microsomal lecithins and when given with phenobarbital benfluorex modified the phenobarbital-induced changes in the fatty acid composition of microsomal lecithins. Electrophoresis of microsomal proteins showed non sensitive induction of any proteins with benfluorex.

In uteri from adult female rats, Thymidine Kinase activity varied during ovarian cycle and was maximum at metestrus. Subcutaneous injections of 5, 10 or 25 ng of estradiol-17 beta to immature female rats, resulted in a 3, 5 or 10 fold increase of enzyme activity. Moreover, Thymidine Kinase activity was decreased by injection of medroxyprogesterone alone or associated with estradiol-17 beta. From these results it seemed that Thymidine Kinase activity in rats uteri was specifically induced by estradiol-17 beta.

Eight cases of hepatitis induced by amineptine chlorhydrate, a new tricyclic antidepressant are reported. Jaundice and/or biological changes occurred 16 to 75 days after the onset of treatment and with a total oral dose of 3,8 to 26 grams. Biologically, cholestasis and cytolysis have been observed simultaneously in 4 cases, cholestasis alone in 2 cases, and prevalent cytolysis in 2 others. After withdrawal of amineptine, clinical improvement was achieved within 10 to 21 days, whereas biological changes of hepatic function tests lasted for as long as 3 to 12 weeks. Physiopathology of such disorders is not clear : toxicity, enzyme induction, immunoallergy, may be considered as possible mechanisms.

The time course of hepatic Acetyl-CoA carboxylase activity as well as hepatic and plasmatic fatty acids concentrations following a single injection of estradiol benzoate (EB, 0.2 mg/kg) was studied in the quail. Acetyl-CoA carboxylase activity increases rapidly and reaches its peak 3 h after the injection of EB. Similarly, hepatic and plasmatic fatty acids concentrations are significantly increased 6 h after the hormonal injection and attain their highest level 18 h later. These results suggest that estrogen affects the hepatic fatty acids biosynthesis by regulating the conversion of acetyl-CoA to malonyl-CoA.

Diets containing increasing amounts of corn oil (0%, 1,5%, 3%, 4,5%, 6%), diets containing a same quantity (6%) of differents fats (corn oil, coconut oil, fish oil) and one free fat diet containing squalen (1,5%) were fed to rats. The UDP glucuronosyl transferase (UDPGT) activity of hepatic homogenate and cytochrome P 450 concentration of hepatic microsomal fractions were measured without or after phenobarbital treatment. 1. Presence of dietary lipids generally gives a moderate increase of these parameters, but the effect of fish oil is higher than of other fats. 2. With the phenobarbital treatment the induction of hepatic cyt P 450 and UDPGT is higher in the animals fed dietary fats than in animals fed free fat diets. However this difference is more important in the rats fed fish oil, less important with coconut oil and the lowest with corn oil. 3. The addition of squalen in the diet did not give variations of cyt P 450 hepatic concentration and UDPGT hepatic activity. The inducting effect of phenobarbital on microsomal cyt P 450 is unchanged but significantly enhanced in the case of hepatic UDPGT.