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J Durlach

Publications and source records attributed to J Durlach.

At least 127 records · Page 7Linked to original sources
PubMedDate not supplied

Dose-dependent suppression of the high alcohol intake of chronically intoxicated rats by Ca-acetyl homotaurinate.

The effect of taurine derivative, Ca-acetyl homotaurinate, on voluntary alcohol intake was investigated in ethanol-dependent and naive rats. A high 24 hr oral intake of a 10% ethyl alcohol solution (9-10 g/kg) was exhibited by rats following 15 days of intragastric infusions of ethanol (7-8 g/kg/day). In four groups, rats were IG injected by short pulses of isotonic saline or a daily dose of 200, 300 and 450 mg/kg respectively, distributed over six daily infusions during alternating 8 hr presentations of ethanol solution and water. Compared to their respective basal intakes during the first two days of injection, the rats demonstrated a dose-dependent 50 to 70% reduction in alcohol consumption with drug treatment. This suppression effect was specific to the ethanol solution and persisted during 4 days of post-treatment observation. In ethanol-naive rats similarly tested and drinking half the amount of alcohol drunk by their ethanol-dependent counterparts, only the highest dose of drug (450 mg/kg) significantly suppressed their alcohol intake. It is suggested that Ca-acetyl homotaurinate interacts with CNS mechanisms involved in the ethanol tolerance-dependence state, underlying an enhanced reinforcing property of ethanol oral intake. Opioid receptors could be the targets in this action.

Acamprosate↗
PubMedDate not supplied

Lack of effects of Ca-acetyl homotaurinate on chronic and acute toxicities of ethanol in rats.

In a previous study, it was shown that in rats Ca-acetyl homotaurinate suppresses or eliminates the high oral intake of ethanol induced by earlier chronic ethanol administration, and to a lesser degree the spontaneous ethanol intake of ethanol-naive rats. The present study examines the effect of the drug on the chronic and acute toxicity of ethanol as a possible mechanism in its alteration of the reinforcing properties of ethanol intake. In the first experiment, it was demonstrated that chronic administration of the drug (45 mg/kg per day) for 15 days, alone or combined with chronic intragastric administration of high doses of ethanol, did not significantly alter subsequent ethanol intake. In two other experiments, it was shown that the drug did not interfere with acute ethanol toxicity as tested by ethanol-induced hypothermia, motor impairment and taste aversion in ethanol-naive rats. It is concluded that the acute activity of Ca-AOTA on CNS mechanisms presumably involved in the state of tolerance-dependence, other than those concerned in ethanol-induced hypothermia, motor impairment and taste aversion, may explain its action on the reinforcing property of ethanol intake.

Acamprosate↗
PubMedDate not supplied

Ethanol effect on the ionic transfer through isolated human amnion. I. Preventive and antagonistic actions of some nutrients and of their synthetic congeners.

The inhibition of the placental transfer of nutrients was studied in the pathogenesis of the fetal alcohol syndrome. Ethanol reduces the ionic transfer through the human amnion. In this study, the preventive and antagonistic actions of natural nutrients (Mg2+, Ca2+, taurine, homotaurine, gamma-aminobutyric acid) and of their synthetic congeners (Ca2+-taurinate, Ca2+-acetyltaurinate, Ca2+-acetylhomotaurinate) were observed on the amniotic conductance which was modified by ethanol. All the molecules, except Mg, demonstrated protective actions on the fetal side. The effect varied with the molecule and its concentration. An absolute protective effect was obtained on the maternal side with Ca2+-acetylhomotaurinate and Ca2+-taurinate. Some molecules, which have protective actions, had no opposing actions (homotaurine), or inversely (Mg2+), only Ca2+-acetylhomotaurinate exhibited both a preventive and an opposing action against ethanol. These results show the interest of studying synthetic molecules for prevention of fetal alcoholism.

Acamprosate↗
PubMedDate not supplied

EEG effects of a single low dose of ethanol on afternoon sleep in the nonalcohol-dependent adult.

Three polygraphic recordings (PGR) of afternoon sleep (ANS) related to the duration of one sleep cycle, i.e., 90 min, were performed in 14 healthy adult volunteers (7 men and 7 women): two reference PGR, on two consecutive days (before ingestion of alcohol). Only the second being retained: reference PGR = P1; another recording, on day 3, 50 min after the start of single slow oral ingestion of the equivalent of 0.25 g 95% ethyl alcohol (ETOH) per kg body weight. Alcohol was ingested as 40 degrees whiskey, and the volume administered ranged from 34.5 to 66 ml (ETOH polygraphic recording = P2). Analysis of polygraphic traces was carried out according to the criteria of Rechtschaffen and Kales, and results were presented using the parameters adopted by Gross et al. (2). A single low dose of alcohol, leading to a low mean blood alcohol level (below 30 mg/100 ml, range 9 to 29 mg/100 ml), clearly perturbs sleep in the normal nonalcohol-dependent adult. In this context, ETOH does not appear to be a hypnotic since: a) the latencies to onset of sleep and the appearance of stages II, III, and IV of slow-wave sleep (SWS) are not shortened; b) the total duration of sleep, the percentage of delta sleep, and the duration (and percentage) of rapid eye movement sleep (REMS) are decreased; c) the number, duration, and percentages of intrasleep awakenings are increased, as are the number of stage changes. In addition, the study of afternoon sleep has shown itself to be a sensitive and reliable test for the analysis of the effects of a low dose of alcohol on nonalcohol-dependent subjects.

Adult↗
PubMedDate not supplied

Magnesium and thermoregulation. I. Newborn and infant. Is sudden infant death syndrome a magnesium-dependent disease of the transition from chemical to physical thermoregulation?

The sudden infant death syndrome (SIDS) remains a leading cause of death during the first year. The common epidemiological and pathological data which characterize SIDS include the curve for age at death (with 3 months as modal age), the stigmata of early maternal intrauterine injury, the seasonal predominance in winter, and the absence of an adequate cause of death at autopsy. Some data characterize risk factor subgroups: for example low socioeconomic level, environmental pollution, stress, and mistakes in baby care. Symptoms before death may be lacking, they may be common and non-specific, or rarely they may be acute, corresponding to "apparent life-threatening events" (ALTE). SIDS may be a magnesium-dependent disease of the transition from chemical to physical thermoregulation. This theory originates from a synthesis of our present knowledge of SIDS, maternal magnesium status, and thermoregulation in the baby. It is consistent with all the epidemiological and pathological prerequisites characterizing SIDS. It eliminates the hiatus between relatively minor thermal stress and induced lethal thermal stroke. Logical scepticism about the role of an implausible lethal superacute magnesium deficiency is no longer justified with regard to well established chronic marginal magnesium deficiency. Further experimental and clinical research will be interesting, i.e. ex vivo studies on brown adipose tissue (BAT) and magnesium deficiency under various conditions of thermal exposure. But even now the theory leads to three therapeutic consequences: (1) the need to define the importance of magnesium deficiency in diagnosis and treatment of ALTE; (2) an assessment of the use of new techniques of rewarming (i.e. extracorporeal circulation) in hypothermia cases to distinguish cot death from "apparent death"; (3) investigation of the prevention of SIDS with magnesium through a blinded and randomized multicentre prospective cooperative study of magnesium supplementation in pregnant and lactating women, followed not only in the mother, fetus, and neonate at birth, but also through the first year of life.

Body Temperature Regulation↗
PubMedDate not supplied

Magnesium and extinction of dinosaurs. Was magnesium deficit a major cause?

Chinese researchers have recently demonstrated that, before the extinction of dinosaurs, there was an impressive lowering in the magnesium concentration of fossil dinosaur eggshell. The structural and functional importance of eggshell magnesium--mainly in the cone layer--for embryonic viability and hatchability of oviparous species supports the hypothesis that magnesium deficit may have had a direct role in dinosaur extinction. Conversely this low magnesium concentration seems a questionable marker of magnesium deficit. The natural forces involved in the extinction of dinosaurs are more likely to induce magnesium depletion than magnesium deficiency. These very interesting preliminary data call for further research.

Animals↗
PubMedDate not supplied

Relationship between magnesium, cancer and carcinogenic or anticancer metals.

It is known that carcinogenesis induces Mg distribution disturbances which cause Mg mobilization through blood cells and Mg depletion in non-neoplastic tissues. Mg deficiency seems to be carcinogenic in cases of some particular haemolymphoreticular diseases only, more often, in cases of solid tumors, it inhibits carcinogenesis. Both carcinogenesis and Mg deficiency increase the plasma membrane permeability and fluidity. The regulation of Mg cellular and subcellular distribution is very important in cancer research. If the Mg level is normal in histones, and particularly in H1 and in nucleic acids on the N7 site of the guanine, it can protect against carcinogenesis. On the other hand, if it is abnormally high it can generate the left-handed Z DNA which is correlated with carcinogenesis. The carcinogenic action of Mg may be linked with some effects on sulfur amino-acid metabolism, growth and the immune system. Although Mg antagonizes certain carcinogenic metals, this is not one of its general properties. Our studies on human amniotic membranes show that Mg acts as a competitive antagonist on 2 or 3 weak carcinogens, Pb and Cd, but not on Co. Mg is a non-competitive antagonist of Ni and is devoid of action on As, both of which are powerful carcinogens. All carcinogenic metals (As, Ni, Cr, Cd, Co, Pb, except Be) reduce the total conductance (Gt). Reversibly all cocarcinogens increase Gt or do not modify it. However, both anticancer and carcinogenic metals reduce Gt. Thus the main target in the relationship between Mg and metals in carcinogenesis is either membrane as regards Pb and Cd, or nucleus as regards Pt, Ga, Co and Ni. The ideal treatment of Mg disturbances in carcinogenesis should control the factors which regulate cellular and subcellular Mg distribution in neoplastic tissues as well as those which avoid Mg depletion in extra malignant tissues.

Animals↗