Moduli Inflation from Dynamical Supersymmetry Breaking

Moduli fields, which parameterize perturbative flat directions of the potential in supersymmetric theories, are natural candidates to act as inflatons. An inflationary potential on moduli space can result if the scale of dynamical SUSY breaking in some sector of the theory is determined by a moduli dependent coupling. The magnitude of density fluctuations generated during inflation then depends on the scale of SUSY breaking in this sector. This can naturally be hierarchically smaller than the Planck scale in a dynamical model, giving small fluctuations without any fine tuning of parameters. It is also natural for SUSY to be restored at the minimum of the moduli potential, and to leave the universe with zero cosmological constant after inflation. Acceptable reheating can also be achieved in this scenario.Comment: 14 pages, latex, improved discussion of reheating for composite inflaton

False Vacuum Inflation with Einstein Gravity

We investigate chaotic inflation models with two scalar fields, such that one field (the inflaton) rolls while the other is trapped in a false vacuum state. The false vacuum becomes unstable when the inflaton field falls below some critical value, and a first or second order transition to the true vacuum ensues. Particular attention is paid to Linde's second-order `Hybrid Inflation'; with the false vacuum dominating, inflation differs from the usual true vacuum case both in its cosmology and in its relation to particle physics. The spectral index of the adiabatic density perturbation can be very close to 1, or it can be around ten percent higher. The energy scale at the end of inflation can be anywhere between $10^{16}$\,GeV and $10^{11}$\,GeV, though reheating is prompt so the reheat temperature can't be far below $10^{11}\,$GeV. Topological defects are almost inevitably produced at the end of inflation, and if the inflationary energy scale is near its upper limit they can have significant effects. Because false vacuum inflation occurs with the inflaton field far below the Planck scale, it is easier to implement in the context of supergravity than standard chaotic inflation. That the inflaton mass is small compared with the inflationary Hubble parameter is still a problem for generic supergravity theories, but remarkably this can be avoided in a natural way for a class of supergravity models which follow from orbifold compactification of superstrings. This opens up the prospect of a truly realistic, superstringComment: 37 pages, LaTeX (3 figures available as hard copies only), SUSSEX-AST 94/1-

Alteration in voltage-dependent calcium channels in dog basilar artery after subarachnoid hemorrhage: Laboratory investigation

Object. The L-type Ca++ channel antagonists like nimodipine have limited efficacy against vasospasm after subarachnoid hemorrhage (SAH). The authors tested the hypothesis that this is because SAH alters these channels, rendering them less responsible for contraction. Methods. Basilar artery smooth muscle cells were isolated 4, 7, and 21 days after SAH in dogs, and Ca ++ channel currents were recorded in 10-mmol/L barium. Proteins for α1 subunits of L-type Ca++ channels were measured by immunoblotting and isometric tension recordings done on rings of the basilar artery. Results. High voltage - activated (HVA) Ca++ channel currents were significantly decreased and low voltage - activated (LVA) currents increased during vasospasm 4, 7, and 21 days after SAH (p \u3c 0.05). Vasospasm was associated with a significant decrease in the number of cells with negligible LVA current while the number of cells in which the LVA current formed greater than 50% of the maximal current increased (p \u3c 0.01). Window currents through LVA and HVA channels were significantly reduced. All changes correlated with the severity of vasospasm. There was an increase in protein for Cav3.1 and Cav3.3 α1 subunits that comprise T-type Ca++ channels, a decrease in L-type (Ca v1.2 and Cav1.3) and an increase in R-type (Ca v2.3) Ca++ channel α1 subunits. Functionally, however, isometric tension studies showed vasospastic arteries still relaxed with nimodipine. Conclusions. Voltage-dependent Ca++ channels are altered in cerebral arteries after SAH. While decreased L-type channels may account for the lack of efficacy of nimodipine clinically, there may be other reasons such as inadequate dose, effect of nimodipine on other cellular targets, and mechanisms of vasospasm other than smooth muscle contraction mediated by activation of L-type Ca++ channels

Alteration in voltage-dependent calcium channels in dog basilar artery after subarachnoid hemorrhage: Laboratory investigation

Object. The L-type Ca++ channel antagonists like nimodipine have limited efficacy against vasospasm after subarachnoid hemorrhage (SAH). The authors tested the hypothesis that this is because SAH alters these channels, rendering them less responsible for contraction. Methods. Basilar artery smooth muscle cells were isolated 4, 7, and 21 days after SAH in dogs, and Ca ++ channel currents were recorded in 10-mmol/L barium. Proteins for α1 subunits of L-type Ca++ channels were measured by immunoblotting and isometric tension recordings done on rings of the basilar artery. Results. High voltage - activated (HVA) Ca++ channel currents were significantly decreased and low voltage - activated (LVA) currents increased during vasospasm 4, 7, and 21 days after SAH (p \u3c 0.05). Vasospasm was associated with a significant decrease in the number of cells with negligible LVA current while the number of cells in which the LVA current formed greater than 50% of the maximal current increased (p \u3c 0.01). Window currents through LVA and HVA channels were significantly reduced. All changes correlated with the severity of vasospasm. There was an increase in protein for Cav3.1 and Cav3.3 α1 subunits that comprise T-type Ca++ channels, a decrease in L-type (Ca v1.2 and Cav1.3) and an increase in R-type (Ca v2.3) Ca++ channel α1 subunits. Functionally, however, isometric tension studies showed vasospastic arteries still relaxed with nimodipine. Conclusions. Voltage-dependent Ca++ channels are altered in cerebral arteries after SAH. While decreased L-type channels may account for the lack of efficacy of nimodipine clinically, there may be other reasons such as inadequate dose, effect of nimodipine on other cellular targets, and mechanisms of vasospasm other than smooth muscle contraction mediated by activation of L-type Ca++ channels