Conformal anomaly from gauge fields without gauge fixing
We show how the Weyl anomaly generated by gauge fields, can be computed from manifestly gauge invariant and diffeomorphism invariant exact renormalization group equations, without having to fix the gauge at any stage. Regularisation is provided by covariant higher derivatives and by embedding the Maxwell field into a spontaneously broken $U(1|1)$ supergauge theory. We first provide a realisation that leaves behind two versions of the original $U(1)$ gauge field, and then construct a manifestly $U(1|1)$ supergauge invariant flow equation which leaves behind only the original Maxwell field in the spontaneously broken regime.
The gauge invariant ERG
We sketch the construction of a gauge invariant Exact Renormalization Group (ERG). Starting from Polchinski's equation, the emphasis is on how a series of ideas have combined to yield the gauge invariant formalism. A novel symmetry of the ERG allows the flow equation to be modified, in such a way that it is suitable for the computation of the (universal) two-loop beta-function. This computation has now been performed, within the framework of the ERG and, as such, in a manifestly gauge invariant way for the very first time.
Influence of inducers and inhibitors on the metabolism in vitro and neurochemical effects in vivo of MDMA.
(S)-(+)- and (R)-(-)-3,4-methylenedioxymethamphetamine (MDMA) were metabolized in vitro by rat liver microsomes via N-demethylation to 3,4-methylenedioxyamphetamine (MDA). Whereas no difference was found in the biotransformation of the two enantiomers in the male rat or in the phenobarbital (PB) treated animals of either sex, more than twice as much MDA was formed from (S)-(+)- than from (R)-(-)-MDMA in the untreated female rat. Although 3-methylcholanthrene (3MC) pretreated rat liver microsomes were less active than those from the untreated rats of the same sex, they formed more MDA from (+)- than from (-)-MDMA. The enantioselective metabolism thus appears to be associated with the relative abundance of individual cytochrome P-450 isozymes. (S)-(+)- and (R)-(-)-MDMA.HCl (20 mg/kg) were about equipotent in depleting serotonin (5-HT) levels in the frontal cortex at 3 hrs and 1 wk following oral administration to female rats. Pretreatment of rats with SKF-525A attenuated and that with PB enhanced the 5-HT depleting potential of either isomer at 3 hrs. The 5-HT depleting potency of (+)-MDMA was significantly greater than that of its (-)-antipode at 3 hr in PB pretreated, but not in SKF-525A pretreated animals. The results suggest that the neurochemical effects of MDMA are caused by the formation of an active metabolite in vivo, and since both enantiomers were N-demethylated in vitro to approximately the same extent by PB pretreated rat liver microsomes, the active metabolite may be other than MDA.