The quantum information manifold for epsilon-bounded forms

Let H be a self-adjoint operator bounded below by 1, and let V be a small form perturbation such that RVS has finite norm, where R is the resolvent at zero to the power 1/2 +epsilon, and S is the resolvent to the power 1/2-epsilon. Here, epsilon lies between 0 and 1/2. If the Gibbs state defined by H is sufficiently regular, we show that the free energy is an analytic function of V in the sense of Frechet, and that the family of density operators defined in this way is an analytic manifold modelled on a Banach space.Comment: 12 pages, report to Torun Conference, 199

Time Evolution via S-branes

Using S(pacelike)-branes defined through rolling tachyon solutions, we show how the dynamical formation of D(irichlet)-branes and strings in tachyon condensation can be understood. Specifically we present solutions of S-brane actions illustrating the classical confinement of electric and magnetic flux into fundamental strings and D-branes. The role of S-branes in string theory is further clarified and their RR charges are discussed. In addition, by examining ``boosted'' S-branes, we find what appears to be a surprising dual S-brane description of strings and D-branes, which also indicates that the critical electric field can be considered as a self-dual point in string theory. We also introduce new tachyonic S-branes as Euclidean counterparts to non-BPS branes.Comment: 62 pages, 10 figures. v2 references adde

Participation of hepatic α/β-adrenoceptors and AT1 receptors in glucose release and portal hypertensive response induced by adrenaline or angiotensin II

It has been previously demonstrated that the hemodynamic effect induced by angiotensin II (AII) in the liver was completely abolished by losartan while glucose release was partially affected by losartan. Angiotensin II type 1 (AT1) and adrenergic (∝1- and β-) receptors (AR) belong to the G-proteins superfamily, which signaling promote glycogen breakdown and glucose release. Interactive relationship between AR and AT1-R was shown after blockade of these receptors with specific antagonists. The isolated perfused rat liver was used to study hemodynamic and metabolic responses induced by AII and adrenaline (Adr) in the presence of AT1 (losartan) and ∝1-AR and β-AR antagonists (prazosin and propranolol). All antagonists diminished the hemodynamic response induced by Adr. Losartan abolished hemodynamic response induced by AII, and AR antagonists had no effect when used alone. When combined, the antagonists caused a decrease in the hemodynamic response. The metabolic response induced by Adr was mainly mediated by ∝1-AR. A significant decrease in the hemodynamic response induced by Adr caused by losartan confirmed the participation of AT1-R. The metabolic response induced by AII was impaired by propranolol, indicating the participation of β-AR. When both ARs were blocked, the hemodynamic and metabolic responses were impaired in a cumulative effect. These results suggested that both ARs might be responsible for AII effects. This possible cross-talk between β-AR and AT1-R signaling in the hepatocytes has yet to be investigated and should be considered in the design of specific drugs