The BRAHMS probes the hot and dense nuclear matter at the RHIC which has reached its design
energy of psNN = 200 GeV for Au + Au collisions. The BRAHMS uses magnetic spectrometers
for hadrons ...covering a large phase space 0 < y < 4 with good particle identification and momentum
resolution. A comprehensive investigation of multiplicity distributions of emitted charged particles
is carried out. Ratios of yields of antiparticles to particles are also measured as a function of rapidity.
Rapidity dependent net-proton yield indicates that substantial transparency has been achieved in
these collisions. Transverse momentum spectra of charged hadrons are measured up to 5 GeV/c
which indicates a significant medium eect when compared to nucleon + nucleon reference spectra. KCI Citation Count: 3
We present spectra of charged pions and protons in 0–10% central Au+Au collisions at sNN=200 GeV at mid-rapidity (y=0) and forward pseudorapidity (η=2.2) measured with the BRAHMS experiment at RHIC. ...The spectra are compared to spectra from p+p collisions at the same energy scaled by the number of binary collisions. The resulting nuclear modification factors for central Au+Au collisions at both y=0 and η=2.2 exhibit suppression for charged pions but not for (anti-) protons at intermediate pT. The p¯/π− ratios have been measured up to pT∼3 GeV/c at the two rapidities and the results indicate that a significant fraction of the charged hadrons produced at intermediate pT range are (anti-) protons at both mid-rapidity and η=2.2.
A reproducible method for dissociation and culture of rat luteal cells is described. The concentration of LH required to produce half-maximal stimulation of progesterone secretion was 50 ng/ml. The ...effects of prostaglandin E2(PGE2) and prostaglandin F2α(PGF2α) on basal and luteinizing hormone (LH)-stimulated progesterone production were examined. Both prostaglandins stimulated basal progesterone production but PGE2was about twice as active, showing a 2-fold maximal stimulation at 0.75 μ M. When either prostaglandin was incubated simultaneously with LH, a dose-dependent inhibition of progesterone secretion occurred; PGF2αwas 4 times more active than PGE2, showing 50% inhibition at a concentration of 40 × nM. Thus, both prostaglandins are more active as antagonists than as agonists of LH with respect to progesterone secretion. PGF2αalso inhibited LH-stimulated adenylate cyclase activity and cyclic AMP accumulation. The block in progesterone secretion was reversed by addition of dibutyryl cyclic AMP (1 mM) but not by theophylline (5 mM) alone. These data and the finding that PGF2α did not affect the specific binding activity of the LH receptor in intact luteal cells indicate that the rapid action of prostaglandins in luteal cells is due to a block of LH-dependent production of cyclic AMP which results in a decrease in progesterone secretion.
Both prostaglandin F2 alpha (PGF2 alpha) and LHRH inhibit LH-stimulated cAMP accumulation and progesterone secretion in the intact luteal cell, but have no effect on LH-sensitive adenylate cyclase ...activity in isolated membranes. The present studies were conducted to assess the possibility that calcium (Ca2+) may mediate the inhibitory activity of PGF2 alpha and LHRH in the rat luteal cell. Removal of extracellular Ca2+ significantly enhanced cAMP accumulation in response to LH by about 2-fold, but blunted LH-stimulated progesterone secretion. Incubation of luteal cells with A23187 caused a highly significant and dose-related decrease in LH-stimulated cAMP accumulation with a concentration for half-maximal inhibition (IC50) of about 1 microM. No effect of A23187 was seen on LH-sensitive adenylate cyclase activity, but the ionophore elicited significant inhibition of LH-stimulated intracellular cAMP accumulation in the presence of isobutyl-methylxanthine (MIX), a phosphodiesterase inhibitor. Inhibition by A23187 was Ca2+ dependent, since a decrease in extracellular Ca2+ to less than 100 microM completely blocked the effect of the ionophore. A23187 also significantly inhibited LH-stimulated progesterone secretion in response to LH or cholera toxin and inhibited cholera toxin-stimulated cAMP accumulation in the absence or presence of MIX. In incubations of isolated luteal membranes, Ca2+ produced a dose-dependent inhibition of LH-stimulated adenylate cyclase activity in the absence or presence of MIX at free Ca2+ levels between 5-20 microM (IC50, approximately 10 microM). Depletion of extracellular Ca2+ had no effect on inhibition of LH-stimulated cAMP accumulation by PGF2 alpha in the intact cell, and the inhibitory activity of LHRH was slightly reduced, but not abolished, by depletion of extracellular Ca2+. Verapamil, a Ca2+ channel blocker, had no effect on inhibition of LH-stimulated cAMP accumulation by PGF2 alpha or LHRH. It is concluded that an acute increase in intracellular Ca2+ inhibits activation of adenylate cyclase by LH in the rat luteal cell. This conclusion is based on studies that showed enhanced cAMP accumulation by LH in Ca2+-depleted media, Ca2+-dependent inhibition of LH-stimulated cAMP production by a Ca2+ ionophore, and direct inhibition of LH-sensitive adenylate cyclase activity by Ca2+ in luteal membranes. It is suggested that a similar effect occurs in response to PGF2 alpha or LHRH in the luteal cell, but inhibition by these luteolytic agents is not dependent on an influx of extracellular Ca2+, but, rather, is due to an increase in intracellular Ca2+ by other mechanisms.
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