A simple cosmological model with only six parameters (matter density, Omega_m h^2, baryon density, Omega_b h^2, Hubble Constant, H_0, amplitude of fluctuations, sigma_8, optical depth, tau, and a ...slope for the scalar perturbation spectrum, n_s) fits not only the three year WMAP temperature and polarization data, but also small scale CMB data, light element abundances, large-scale structure observations, and the supernova luminosity/distance relationship. Using WMAP data only, the best fit values for cosmological parameters for the power-law flat LCDM model are (Omega_m h^2, Omega_b h^2, h, n_s, tau, sigma_8) = 0.1277+0.0080-0.0079, 0.02229+-0.00073, 0.732+0.031-0.032, 0.958+-0.016, 0.089+-0.030, 0.761+0.049-0.048). The three year data dramatically shrink the allowed volume in this six dimensional parameter space. Assuming that the primordial fluctuations are adiabatic with a power law spectrum, the WMAP data_alone_ require dark matter, and favor a spectral index that is significantly less than the Harrison-Zel'dovich-Peebles scale-invariant spectrum (n_s=1, r=0). Models that suppress large-scale power through a running spectral index or a large-scale cut-off in the power spectrum are a better fit to the WMAP and small scale CMB data than the power-law LCDM model; however, the improvement in the fit to the WMAP data is only Delta chi^2 = 3 for 1 extra degree of freedom. The combination of WMAP and other astronomical data yields significant constraints on the geometry of the universe, the equation of state of the dark energy, the gravitational wave energy density, and neutrino properties. Consistent with the predictions of simple inflationary theories, we detect no significant deviations from Gaussianity in the CMB maps.
A close association between pericytes and endothelial cells (ECs) is crucial to the stability and function of capillary blood vessels and microvessels. The loss or dysfunction of pericytes results in ...significant disruption of these blood vessels as observed in pathological conditions, including cancer, diabetes, stroke, and Alzheimer's disease. Prostaglandin E2 (PGE2) is a lipid mediator of inflammation, and its tissue concentration is elevated in cancer and neurological disorders. Here, we show that the exposure to PGE2 switches pericytes to a fast-migrating, loosely adhered phenotype that fails to intimately interact with ECs. N-cadherin and connexin-43 in adherens junction and gap junction between pericytes and ECs are downregulated by EP-4 and EP-1-dependent mechanisms, leading to breakdown of the pericyte-EC interaction. Furthermore, R-Ras, a small GTPase important for vascular normalization and vessel stability, is transcriptionally repressed by PGE2 in an EP4-dependent manner. Mouse dermal capillary vessels lose pericyte coverage substantially upon PGE2 injection into the skin. Our results suggest that EP-mediated direct disruption of pericytes by PGE2 is a key process for vascular destabilization. Restoring pericyte-EC interaction using inhibitors of PGE2 signaling may offer a therapeutic strategy in cancer and neurological disorders, in which pericyte dysfunction contributes to the disease progression.
Myocardial ischemia interrupts neurotransmission and causes the depression of norepinephrine release. However, the effects of sympathetic nerve stimulation on neurotransmission and norepinephrine ...release in post-ischemic myocardium are not well defined. We measured regional myocardial length and nor-epinephrine (NE) release during sympathetic nerve stimulation in anesthetized dogs. Dogs were divided into 2 groups: Group I (n=14); sympathetic nerve stimulation, Group 2 (n=9); pre-treatment with α-blockade yohimbine hydrochloride (0.2 mg/kg) followed by sympathetic nerve stimulation. The left anterior descending artery was occluded for 15 min. Sympathetic nerve stimulation was performed before coronary occlusion and after reperfusion. In group 1, the decrease in systolic shortening in the ischemic region persisted for more than 60 min. Although sympathetic nerve stimulation caused an increase in systolic shortening, it was lower than the pre-ischemic value. NE release from the post-ischemic myocardium remained decreased for 60 min. The decrease in the post-ischemic myocardial response to sympathetic nerve stimulation was associated with diminished NE release. When the cardiac sympathetic nerve was denervated with an epicardial phenol application, NE release decreased even further. In group 2, NE release did not decrease following reperfusion. These results suggest that sympathetic nerve conduction is not completely impaired in post-ischemic myocardium and that pre-synaptic a -2 receptors might play an important role in diminished NE release.
We present limits to the amplitude of non-Gaussian primordial fluctuations in the WMAP 1-year cosmic microwave background sky maps. A non-linear coupling parameter, f_NL, characterizes the amplitude ...of a quadratic term in the primordial potential. We use two statistics: one is a cubic statistic which measures phase correlations of temperature fluctuations after combining all configurations of the angular bispectrum. The other uses the Minkowski functionals to measure the morphology of the sky maps. Both methods find the WMAP data consistent with Gaussian primordial fluctuations and establish limits, -58<f_NL<134, at 95% confidence. There is no significant frequency or scale dependence of f_NL. The WMAP limit is 30 times better than COBE, and validates that the power spectrum can fully characterize statistical properties of CMB anisotropy in the WMAP data to high degree of accuracy. Our results also validate the use of a Gaussian theory for predicting the abundance of clusters in the local universe. We detect a point-source contribution to the bispectrum at 41 GHz, b_src = (9.5+-4.4) X 1e-5 uK^3 sr^2, which gives a power spectrum from point sources of c_src = (15+-6) X 1e-3 uK^2 sr in thermodynamic temperature units. This value agrees well with independent estimates of source number counts and the power spectrum at 41 GHz, indicating that b_src directly measures residual source contributions.
The local expansion rate of the Universe is parametrized by the Hubble constant, Formula: see text, the ratio between recession velocity and distance. Different techniques lead to inconsistent ...estimates of Formula: see text Observations of Type Ia supernovae (SNe) can be used to measure Formula: see text, but this requires an external calibrator to convert relative distances to absolute ones. We use the angular diameter distance to strong gravitational lenses as a suitable calibrator, which is only weakly sensitive to cosmological assumptions. We determine the angular diameter distances to two gravitational lenses, Formula: see text and Formula: see text megaparsec, at redshifts Formula: see text and 0.6304. Using these absolute distances to calibrate 740 previously measured relative distances to SNe, we measure the Hubble constant to be Formula: see text kilometers per second per megaparsec.
We confront predictions of inflationary scenarios with the WMAP data, in combination with complementary small-scale CMB measurements and large-scale structure data. The WMAP detection of a ...large-angle anti-correlation in the temperature--polarization cross-power spectrum is the signature of adiabatic superhorizon fluctuations at the time of decoupling. The WMAP data are described by pure adiabatic fluctuations: we place an upper limit on a correlated CDM isocurvature component. Using WMAP constraints on the shape of the scalar power spectrum and the amplitude of gravity waves, we explore the parameter space of inflationary models that is consistent with the data. We place limits on inflationary models; for example, a minimally-coupled lambda phi^4 is disfavored at more than 3-sigma using WMAP data in combination with smaller scale CMB and large scale structure survey data. The limits on the primordial parameters using WMAP data alone are: n_s(k_0=0.002 Mpc^{-1})=1.20_{-0.11}^{+0.12}, dn/dlnk=-0.077^{+0.050}_{- 0.052}, A(k_0=0.002 Mpc}^{-1})=0.71^{+0.10}_{-0.11} (68% CL), and r(k_0=0.002 Mpc^{-1})<1.28 (95% CL).
To clarify the relationship between post-ischemic myocardial dysfunction and local cardiac sympathetic nerve function, we measured regional myocardial length and norepinephrine (NE) release during ...sympathetic nerve stimulation in 32 mongrel dogs. Coronary occlusion was produced by balloon occluder for 15 min and reperfused for 60 min. Dogs were divided into 3 groups as follows; Group 1 (n = 14): Sympathetic nerve stimulation, Group 2 (n = 9): Pre-treatment with yohimbine hydrochloride (0.2 mg/kg) and sympathetic nerve stimulation, Group 3 (n = 9): Exogenous NE administration. Sympathetic nerve stimulation or NE infusion were performed before occlusion and after reperfusion. In group 1, the extent of the increase in systolic shortening during sympathetic nerve stimulation (delta - shortening) lowered at 5 min after reperfusion and augmented progressively. But, delta-shortening at an early reperfusion period did not reduce in group 2 and 3. NE release from the ischemic myocardium decreased in group 1 and did not recover for 60 min. When the cardiac sympathetic nerve was denervated with 90% phenol solution, NE release further decreased in group 1. On the other hand, NE release did not decrease in group 2. These results indicate that the response to sympathetic nerve stimulation decreased in post-ischemic reperfused myocardium and this was due to diminished NE release. It was considered that sympathetic nerve conduction was not completely impaired in post-ischemic myocardium and pre-synaptic alpha-2 receptor mediated negative feedback mechanism would play an important role in these diminished NE release.
PDF
