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At least 55 records · Page 3Linked to original sources
PubMed1975

[Estrus synchronization in cattle using chlormadinone acetate ("Bovisynchron" Jenapharm) in the tropics. 1. On the effect of blocking the cycle using chlormadinone acetate and on the introduction of this biotechnical method in the Republic of Mali].

The oestrus synchronization in cattle is being tested as a biotechnical method supporting the implementation of the crossing programme in the Republic of Mali Using the latest results of sexual physiology, the effect is described of Bovisynchron Jenapharm (chlormadinonacetate). Bovisynchron is characterised by a high certainty of synchronization and a good toleration. It leads to a highly fertile oestrus of all animals and to a high rate of conception. An analysis of the situation in the Republic of Mali is used to discuss the advantages of this method.

Animals↗
PubMed1976

Stimulation of cell proliferation in rat liver by alpha-hexachlorocyclohexane or partial hepatectomy and end points during G1 of the inhibitory action of beta-diethyl-aminoethylphenyldiallyl acetate-HC1 (CFT 1201), beta-diethylaminoethyldiphenylpropyl acetate. HC1 (SKF 525-A) and actinomycin D.

The present work was designed to study the nature, sequence and temporal position of some inhibitor-sensitive events of the replicative cycle in rat liver. Hepatocyte proliferation was induced by alpha-hexachlorocyclohexane and by partial hepatectomy; the onset of DNA synthesis and of mitotic activity were determined and used as reference points in the cell cycle. Inhibition of cell proliferation was achieved by CFT 1201, SKF 525-A, and actinomycin D. It was found that the inhibitory action of the three agents ends at the same stage of the replicative cycle, 0--2 h before the G1/S transition, in both alpha-hexachlorocyclohexane-stimulated and regenerating rat liver. It is concluded that the molecular events sensitive to CFT 1201, SKF 525-A or actinomycin D are either identical or temporally closely associated; they do not figure in the metabolic activation of alpha-hexachlorocyclohexane.

Cell Division↗
PubMed1978

[Human-pharmacokinetic Studies on Penetration Kinetics of a 6 alpha-Fluoro-9 alpha-chloro-16 alpha-methyl-delta 1,4-pregnadiene-11 beta-dihydroxy-3,20-dione-21-trimethyl-acetic acid (Clocortolone Trimethyl-acetic acid) after e picutaneous application].

Investigation on 6 alpha-fluoro-9 alpha-chloro-16 alpha-methyl-delta 1,4-pregnadiene-11 beta-dihydroxy-3,20-dione-21-trimethylacetic acid (clocortolone trimethylacetic acid) are reported. The aim of the trial was to prove the penetration kinetics of the steriod into the skin. Three healthy female subjects took part in the investigations. They were treated with an oil-water emulsion of the substance on two spots on the back, after having observed alcohol abstinence. One of the treated spots was stripped after 30 min, the second after 60 min using the "Tesafilm" stripping method. The strips were then analysed gaschromatographically on the presence of clocortolone-trimethylacetic acid. It could be shown that the steroid penetrates into the skin up to the 12th-14th strips, building up a certain congestion of the substance at this time because of reaching the stratum corneum, as we suppose. At this place a depot is built of which probably only a very small or no permeation into the system occurs, as clocortolone could not be detected either in the subjects' serum nor in the urine.

Administration, Topical↗
PubMed1979

Plasma acetate turnover and oxidation.

Plasma acetate turnover and oxidation were determined in 11 healthy subjects by the constant infusion of a trace amount of [1-14C]acetate for 6 h. The subjects ages ranged from 22 to 57 yr. There was a positive correlation (P less than 0.001) between plasma acetate concentration and turnover rate, and a negative correlation (P less than 0.001) between turnover and age. The plasma acetate concentration in the subjects 22--28 yr old was 0.17 vs. 0.13 mM (P less than 0.02) in subjects 40--57 yr old. The plasma acetate turnover rate was also greater in the younger age group (8.23 +/- 0.66 vs. 4.98 +/- 0.64 mumol/min . kg, P less than 0.01). Approximately 90% of the plasma acetate turnover was immediately oxidized to CO2 in both age groups, however, 13.2 +/- 0.89% of the CO2 output in the younger group was derived from plasma acetate oxidation compared to 7.9 +/- 0.94% in the older group (P less than 0.01). The mean plasma acetate concentration, turnover, and oxidation in six cancer patients 47--63 yr old were similar to the values observed in the age-matched healthy subjects. Uptake or output of acetate by various tissues was measured by arterial-venous plasma acetate concentration differences. In seven of eight subjects undergoing elective surgery, the arterial-portal venous concentration difference was negative, which indicated that the gastrointestinal tract can contribute to plasma acetate production. Uptake of plasma acetate by both the leg and liver appeared to be dictated by the arterial acetate concentration. Net production of acetate by both the leg and liver was most often observed at arterial plasma acetate concentrations less than 0.08 mM.

Acetates↗
PubMed1978

Growth and methanogenesis by Methanosarcina strain 227 on acetate and methanol.

Methanosarcina strain 227 exhibited exponential growth on sodium acetate in the absence of added H(2). Under these conditions, rates of methanogenesis were limited by concentrations of acetate below 0.05 M. One mole of methane was formed per mole of acetate consumed. Additional evidence from radioactive labeling studies indicated that sufficient energy for growth was obtained by the decarboxylation of acetate. Diauxic growth and sequential methanogenesis from methanol followed by acetate occurred in the presence of mixtures of methanol and acetate. Detailed studies showed that methanol-grown cells did not metabolize acetate in the presence of methanol, although acetate-grown cells did metabolize methanol and acetate simultaneously before shifting to methanol. Acetate catabolism appeared to be regulated in response to the presence of better metabolizable substrates such as methanol or H(2)-CO(2) by a mechanism resembling catabolite repression. Inhibition of methanogenesis from acetate by 2-bromoethanesulfonate, an analog of coenzyme M, was reversed by addition of coenzyme M. Labeling studies also showed that methanol may lie on the acetate pathway. These results suggested that methanogenesis from acetate, methanol, and H(2)-CO(2) may have some steps in common, as originally proposed by Barker. Studies with various inhibitors, together with molar growth yield data, suggest a role for electron transport mechanisms in energy metabolism during methanogenesis from methanol, acetate, and H(2)-CO(2).

Acetates↗
PubMed1978

Metabolic control of the circulation. Effects of acetate and pyruvate.

Chloralose-anesthetized dogs were infused intravenously with either Tris-acetate or Tris-pyruvate at 0.0375, 0.075, and 0.15 mmol/kg per min successively, each for 20 min. Acetate infusion increased cardiac output, left ventricular dP/dt and dP/dt/P, and coronary blood flow, while pyruvate infusion did not. Infusions of either substance increased arterial blood and skeletal muscle concentrations of citrate and malate, but only acetate infusion increased the tissue AMP content and decreased the ATP:AMP ratio. The increase in cardiac output produced by acetate was accompanied by an increase in total body oxygen consumption and a decrease in the difference between arterial and mixed venous blood oxygen. Myocardial oxygen consumption increased during acetate infusion, but the decrease in myocardial oxygen extraction and the increase in coronary sinus blood oxygen saturation suggest that an active coronary vasodilation which was not a result of the increased cardiac work, occurred. The concentration of hypoxanthine in the coronary sinus and the content of myocardial adenosine increased, which suggests that the increase in coronary blood flow was caused by the vasodilator action of adenosine released from the myocardium, and that adenosine production is not necessarily tied to PO(2). These systemic and coronary hemodynamic changes also occurred when acetate (0.075 mmol/kg per min) was infused into conscious dogs. Acetate infusion also increased blood flow to the gastrointestinal tract, kidneys, intercostal muscle, and diaphragm. These changes were not affected by propranolol pretreatment, but were abolished by pretreatment with fluoroacetate which reduced acetate oxidation. These results suggest that the circulatory stimulation produced by acetate was not caused by increases in tricarboxylic acid cycle intermediates. Instead, it was probably related to the increased cleavage of ATP to AMP that accompanies activation of acetate to acetyl CoA, and was not mediated via beta-adrenergic receptors. It is speculated that hemodynamic changes may occur in patients who undergo hemodialysis with acetate-containing dialysate. Hemodynamic changes of ethanol may also be brought about by acetate, which is one of the intermediates that accumulates during ethanol metabolism.

Acetates↗
PubMed1979

Measurement of acetate in human blood by gas chromatography: effects of sample preparation, feeding, and various diseases.

We measured acetate concentrations in whole blood, serum, and plasma by a modification of a previously described method involving vacuum distillation and gas chromatography. The mean acetate concentration of fresh venous plasma from 27 normal subjects was 51 +/- 5 mumol/L (95% confidence limits ranged from 0 to 103 mumol/L). The acetate concentrations of serum and plasma incubated for 2 h at either 4 degrees C or 27 degrees C were the same. The acetate concentration of whole blood incubated at 27 degrees C was significantly greater than that of blood incubated at 4 degrees C. This change may have resulted from the production of acetate by erythrocytes or from the hydrolysis of acetate esters. Storage of plasma at -20 degrees C for 24 h significantly increased acetate concentrations from 26 +/- 6 mumol/L to 63 +/- 4 mumol/L. After the subjects consumed a standard breakfast, venous plasma acetate concentrations increased from 58 to 97 mumol/L at 30 min. Acetate concentrations in arterial plasma exceeded those in venous plasma. Plasma acetate concentrations were not significantly altered in patients with malignancy or diabetes mellitus, but severe liver disease and severe acidosis were both associated with increased acetate concentrations. These preliminary observations suggest that plasma acetate concentrations may be altered in several disease states.

Acetates↗
PubMed1976

Production of endogenous acetate by the liver in lactating ewes.

The production of endogenous acetate by the liver has been investigated in lactating ewes using animals with indwelling arterial, and portal and hepatic venous cannulae. The capacity of the liver to produce acetate from acetyl-CoA in vitro has also been examined using homogenates prepared from liver biopsy samples. Mean arterial, portal and hepatic venous blood acetate concentrations in four ewes at 4 weeks lactation were 0.40, 1.00 and 1.46 mM respectively. The mean exogenous and endogenous acetate production rates were 56 and 54 mmol/h respectively, giving a total of 110 MMOL/h. The mean portal-hepatic venous difference in free fatty acid concentration was 81 muM. Converting this uptake of free fatty acids by the liver (based on palmitate as a standard) to 2-carbon equivalents, the acetate produced accounted for 70% of the fatty acids taken up. The correlation coefficient (r2) between uptake of free fatty acids and production of acetate by the liver was 0.83 (P less than 0.01). Calculation of the net acetate production in vivo gave a mean value for the production of acetate of 0.75 nmol/min. Calculation of the in vitro enzymic capacity of the liver to produce acetate from acetyl-CoA gave a mean of 0.94 mmol/min. These results indicate that enzymic production of acetate from acetyl-CoA, via carnitine acetyltransferase and acetylcarnitine hydrolase (see Costa and Snoswell 1975a), can adequately account for the substantial production of acetate by the liver in lactating ewes.

Acetates↗