Vector Mesons and Baryon Resonances in Nuclear Matter

We calculate the effect of many-body interactions in nuclear matter on the spectral function of $\rho$ and $\omega$ meson. In particular, we focus on the role played by baryon resonances in this context.Comment: 4 pages, 4 figures, to be published in proceedings of the Third International Conference on Perspectives on Hadronic Physics, 7 - 11 May 2001, Miramare-Trieste, Ital

Vector Meson Decay of Baryon Resonances

We investigate the coupling of vector mesons with nucleons to nucleon resonances in an isospin-selective VMD approach and explore the in-medium properties of vector mesons.Comment: 8 pages, 2tables, 4 figures, invited talk at NSTAR 2001, Workshop on the Physics of Excited Nucleons, University of Mainz, Germany, March 7-10, 2001. To be published in World Scientifi

Coupling of Baryon Resonances to the NωN \omega channel

We estimate the resonance coupling strength $f_{RN\omega}$ and $f_{RN\rho}$ from a Vector Meson Dominance (VMD) analysis. The isoscalar and isovector part of the photon coupling are obtained separately from helicity amplitudes. The reliability of this approach is tested by comparing VMD predictions for $f_{RN\rho}$ with values obtained from fitting the hadronic decay widths into $N \rho$. A reasonable agreement is found, but VMD tends to underestimate the coupling constants. In order to confirm consistency with experimental data, we calculate the cross-sections for photon-and pion induced reactions within a {\it Breit-Wigner} model. Finally, we study how the properties of $\omega$ mesons in nuclear matter are affected from the excitation of resonance-hole loops. For an $\omega$ at rest, we find a broadening of about 40 MeV, while at higher momenta the effect of resonance excitations is reduced.Comment: 21 pages, 5 ps figures, misprints corrected, discussion added, improved calculation of gamma N -> omega N, revised version to be published in Nuclear Physics

Tolerance to the Prophylactic Effects of Carbamazepine and Related Mood Stabilizers in the Treatment of Bipolar Disorders

Tolerance development after successful long-term treatment of bipolar disorder is under recognized, as are ways to prevent or show its occurrence or reverse it once it has occurred. We review the clinical literature which suggests that tolerance can develop to most treatment approaches in bipolar illness and present an animal model of tolerance development to anticonvulsant effects of carbamazepine or lamotrigine on amgydala-kindled seizures. In this model tolerance does not have a pharmacokinetic basis, but is contingent upon the drug being present in the brain at the time of amygdala stimulation. The occurrence of seizures in the absence of drug is sufficient to reverse tolerance and re-establish anticonvulsant efficacy. Based on the model, we hypothesize that some episode-induced compensatory adaptive changes in gene expression fail to occur in tolerant subjects and that episodes off medication re-induce these changes and renew drug effectiveness. Approaches that slow or reverse tolerance development in the animal model are reviewed so that they can be tested for their applicability in the clinic. Criteria for assessing tolerance development are offered in the hope that this will facilitate a more systemic literature about its prevalence, prevention, and reversal. Careful longitudinal monitoring of episode occurrence is essential to understanding tolerance development in the affective disorder and its treatment