Current directions in research on understanding and preventing intoxicated aggression

The present paper describes promising research directions that emerged from a recent international conference on intoxication and aggression and from the scientific literature generally. In this overview, intoxicated aggression is seen as arising from an interactional process involving multiple contributing factors or causes. This model helps to define research directions that can further understanding and prevention. First, the societal/cultural framing of intoxication and aggression exerts a powerful influence on drinking behaviour and needs to be better understood. Another important area for research is the moderating role on alcohol-related aggression of personal factors such as predisposition to aggression and individual differences in expectations about alcohol and aggression. Research on the role of basic pharmacological effects of alcohol in increasing the likelihood of aggressive behaviour is also a critical aspect of understanding intoxicated aggression. Drinking contexts and environments play a considerable role in the relationship between intoxication and aggressive behaviour and need to be better understood. Another critical direction for future research is the study of intoxicated aggression as a process involving the interaction of the person, the situation and the effects of alcohol in natural and experimental settings. Finally, the paper highlights promising directions for research on interventions to prevent intoxicated aggression and violence.     

Phenylalanine and tyrosine metabolism in neonates receiving parenteral nutrition differing in pattern of amino acids

Tyrosine is considered to be an indispensable dietary amino acid in the neonate, yet achieving adequate parenteral tyrosine intake is difficult due to its poor solubility. Increasing the supply of phenylalanine is the most common means of compensating for low tyrosine levels. Unfortunately, plasma phenylalanine concentrations are sometimes elevated in infants receiving high phenylalanine intake. This led us to study the phenylalanine and tyrosine metabolism in 16 neonates randomized to receive total parenteral nutrition with either a high or a moderate phenylalanine-containing amino acid solution. A primed, 24-h continuous stable isotope infusion of L-[1-13C]phenylalanine and L-[3,3-2H2]tyrosine was given to enable the measurement of phenylalanine and tyrosine kinetics. Results demonstrated that 1) phenylalanine hydroxylation was significantly greater in infants receiving high phenylalanine, 2) phenylalanine oxidation and percent dose oxidized was also significantly greater in infants receiving high phenylalanine, 3) apparent phenylalanine retention was greater in neonates receiving high phenylalanine, and 4) alternate catabolites of phenylalanine and tyrosine metabolism were significantly greater in infants receiving high phenylalanine compared with moderate phenylalanine. We conclude that neonates respond to increased parenteral phenylalanine intake by increasing their hydroxylation and oxidation rates. The greater oxidation of phenylalanine in infants receiving high phenylalanine in conjunction with the urinary excretion of alternate catabolites of phenylalanine and tyrosine suggests that the high phenylalanine intake may be in excess of needs. However, the lower apparent phenylalanine retention observed in infants receiving moderate phenylalanine suggests that the total aromatic amino acid level of moderate phenylalanine may be deficient for neonatal needs.     

Mechanisms of isoniazid resistance in Mycobacterium tuberculosis: enzymatic characterization of enoyl reductase mutants identified in isoniazid-resistant clinical isolates

Hepatocyte growth factor (HGF) decreases transforming growth factor beta1 (TGFbeta1) levels in the liver and attenuates hepatic fibrosis caused by dimethylnitrosamine in rats. In the liver, HGF is presumed to act predominantly on parenchymal cells, and TGFbeta1 is produced mainly by mesenchymal cells. In hepatic fibrosis, stellate cells play a central role with undergoing activation, which also occurs when the cells are cultured on plastic. Thus, we wondered if HGF could act directly on stellate cells. c-Met was detected in rat stellate cells activated by culture for 10 days, but not in the cells cultured for 3 days. Specific binding of HGF to the activated cells was determined, and Scatchard analysis indicated an apparent Kd of 1.5 nM. c-Met mRNA was detected in freshly isolated stellate cells from rats treated with carbon tetrachloride for 8 weeks, but not in those cells from normal rats. These results indicate that stellate cells express c-met when activated in vitro and in vivo. HGF enhanced TGFbeta1 production and DNA synthesis in the activated cells.     

The discrimination of marijuana intoxication

Forty Ss, 20 males and 20 females, observed a videotape that showed four males interacting in a social setting under four different drug conditions; coltsfoot, placebo, marijuana low dose, and marijuana high dose. The observers attempted to discriminate the level of intoxication of the four males in each condition. The observers accurately detected the level of intoxication in the high dose condition. While marijuana experienced users were more successful in detecting levels of intoxication, the sex of the observer was not significant. Behaviors used to discriminate intoxication and the implications of these results to defining intoxication are discussed.