String theory of the Regge intercept.

Using the Polchinski-Strominger effective string theory in the covariant gauge, we compute the mass of a rotating string in D dimensions with large angular momenta J, in one or two planes, in fixed ratio, up to and including first subleading order in the large J expansion. This constitutes a first-principles calculation of the value for the order-J(0) contribution to the mass squared of a meson on the leading Regge trajectory in planar QCD with bosonic quarks. For open strings with Neumann boundary conditions, and for closed strings in D≥5, the order-J(0) term in the mass squared is exactly calculated by the semiclassical approximation. This term in the expansion is universal and independent of the details of the theory, assuming only D-dimensional Poincaré invariance and the absence of other infinite-range excitations on the string world volume, beyond the Nambu-Goldstone bosons.

Phytoestrogens and gonadotropin-releasing hormone pulse generator activity and pituitary luteinizing hormone release in the rat.

Phytoestrogens can produce inhibitory effects on gonadotropin secretion in both animals and humans. The aims of this study were 2-fold: 1) to determine in vivo whether genistein and coumestrol act on the GnRH pulse generator to suppress hypothalamic multiunit electrical activity volleys and associated LH pulses and/or on the pituitary to suppress the LH response to GnRH; and 2) to examine the effect of these phytoestrogens on GnRH-induced pituitary LH release in vitro and to determine whether estrogen receptors are involved. Wistar rats were ovariectomized and chronically implanted with recording electrodes and/or indwelling cardiac catheters, and blood samples were taken every 5 min for 7--11 h. Intravenous infusion of coumestrol (1.6-mg bolus followed by 2.4 mg/h for 8.5 h) resulted in a profound inhibition of pulsatile LH secretion, a 50% reduction in the frequency of hypothalamic multiunit electrical activity volleys, and a complete suppression of the LH response to exogenous GnRH. In contrast, both genistein (1.6-mg bolus followed by 2.4 mg/h for 8.5 h) and vehicle were without effect on pulsatile LH secretion. Coumestrol (10(-5) M; over 2 or 4 h) suppressed GnRH-induced pituitary LH release in vitro, an effect blocked by the antiestrogen ICI 182,780. It is concluded that coumestrol acts centrally to reduce the frequency of the hypothalamic GnRH pulse generator. In addition, the inhibitory effects of coumestrol on LH pulses occur at the level of the pituitary by reducing responsiveness to GnRH via an estrogen receptor-mediated process.