6 research outputs found
Dynamical Jahn-Teller Effect and Berry Phase in Positively Charged Fullerene I. Basic Considerations
We study the Jahn-Teller effect of positive fullerene ions C
and C. The aim is to discover if this case, in analogy with the
negative ion, possesses a Berry phase or not, and what are the consequences on
dynamical Jahn-Teller quantization. Working in the linear and spherical
approximation, we find no Berry phase in C, and
presence/absence of Berry phase for coupling of one hole to an
/ vibration. We study in particular the special equal-coupling case
(), which is reduced to the motion of a particle on a 5-dimensional
sphere. In the icosahedral molecule, the final outcome assesses the
presence/absence of a Berry phase of for the hole coupled to
/ vibrations. Some qualitative consequences on ground-state symmetry,
low-lying excitations, and electron emission from C are spelled out.Comment: 31 pages (RevTeX), 3 Postscript figures (uuencoded
Surprises in the Orbital Magnetic Moment and g-Factor of the Dynamic Jahn-Teller Ion C_{60}^-
We calculate the magnetic susceptibility and g-factor of the isolated
C_{60}^- ion at zero temperature, with a proper treatment of the dynamical
Jahn-Teller effect, and of the associated orbital angular momentum, Ham-reduced
gyromagnetic ratio, and molecular spin-orbit coupling. A number of surprises
emerge. First, the predicted molecular spin-orbit splitting is two orders of
magnitude smaller than in the bare carbon atom, due to the large radius of
curvature of the molecule. Second, this reduced spin-orbit splitting is
comparable to Zeeman energies, for instance, in X-band EPR at 3.39KGauss, and a
field dependence of the g-factor is predicted. Third, the orbital gyromagnetic
factor is strongly reduced by vibron coupling, and so therefore are the
effective weak-field g-factors of all low-lying states. In particular, the
ground-state doublet of C_{60}^- is predicted to show a negative g-factor of
\sim -0.1.Comment: 19 pages RevTex, 2 postscript figures include
Cardiac chymase: pathophysiological role and therapeutic potential of chymase inhibitors
On release from cardiac mast cells, alpha-chymase converts angiotensin I (Ang I) to Ang II. In addition to Ang II formation, alpha-chymase is capable of activating TGF-beta 1 and IL-1 beta, forming endothelins consisting of 31 amino acids, degrading endothelin-1, altering lipid metabolism, and degrading the extracellular matrix. Under physiological conditions the role of chymase in the mast cells of the heart is uncertain. In pathological situations, chymase may be secreted and have important effects on the heart. Thus, in animal models of cardiomyopathy, pressure overload, and myocardial infarction, there are increases in both chymase mRNA levels and chymase activity in the heart. In human diseased heart homogenates, alterations in chymase activity have also been reported. These findings have raised the possibility that inhibition of chymase may have a role in the therapy of cardiac disease. The selective chymase inhibitors developed to date include TY-51076, SUN-C8257, BCEAB, NK320, and TEI-E548. These have yet to be tested in humans, but promising results have been obtained in animal models of myocardial infarction, cardiomyopathy, and tachycardia-induced heart failure. It seems likely that orally active inhibitors of chymase could have a place in the treatment of cardiac diseases where injury-induced mast cell degranulation contributes to the pathology