Precision Primordial 4^4He Measurement with CMB Experiments

Big bang nucleosynthesis (BBN) and the cosmic microwave background (CMB) are two major pillars of cosmology. Standard BBN accurately predicts the primordial light element abundances ($^4$He, D, $^3$He and $^7$Li), depending on one parameter, the baryon density. Light element observations are used as a baryometers. The CMB anisotropies also contain information about the content of the universe which allows an important consistency check on the Big Bang model. In addition CMB observations now have sufficient accuracy to not only determine the total baryon density, but also resolve its principal constituents, H and $^4$He. We present a global analysis of all recent CMB data, with special emphasis on the concordance with BBN theory and light element observations. We find $\Omega_{B}h^{2}=0.025+0.0019-0.0026$ and $Y_{p}=0.250+0.010-0.014$ (fraction of baryon mass as $^4$He) using CMB data alone, in agreement with $^4$He abundance observations. With this concordance established we show that the inclusion of BBN theory priors significantly reduces the volume of parameter space. In this case, we find $\Omega_{B}h^2=0.0244+0.00137-0.00284$ and $Y_p = 0.2493+0.0006-0.001$. We also find that the inclusion of deuterium abundance observations reduces the $Y_p$ and $\Omega_{B}h^2$ ranges by a factor of $\sim$2. Further light element observations and CMB anisotropy experiments will refine this concordance and sharpen BBN and the CMB as tools for precision cosmology.Comment: 7 pages, 3 color figures made minor changes to bring inline with journal versio

Constraining slow-roll inflation with WMAP and 2dF

We constrain slow-roll inflationary models using the recent WMAP data combined with data from the VSA, CBI, ACBAR and 2dF experiments. We find the slow-roll parameters to be $0 < \epsilon_1 < 0.032$ and $\epsilon_2 + 5.0 \epsilon_1 = 0.036 \pm 0.025$. For inflation models $V \propto \phi^{\alpha}$ we find that $\alpha< 3.9, 4.3$ at the 2$\sigma$ and $3\sigma$ levels, indicating that the $\lambda\phi^4$ model is under very strong pressure from observations. We define a convergence criterion to judge the necessity of introducing further power spectrum parameters such as the spectral index and running of the spectral index. This criterion is typically violated by models with large negative running that fit the data, indicating that the running cannot be reliably measured with present data.Comment: 8 pages RevTeX4 file with six figures incorporate

Fibroblast senescence in the pathology of idiopathic pulmonary fibrosis

Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing interstitial pneumonia of unknown cause with a median survival of only three years. Little is known about the mechanisms that precede the excessive collagen deposition seen in IPF, but cellular senescence has been strongly implicated in disease pathology. Senescence is a state of irreversible cell-cycle arrest accompanied by an abnormal secretory profile and is thought to play a critical role in both development and wound repair. Normally, once a senescent cell has contributed to wound repair, it is promptly removed from the environment via infiltrating immune cells. However, if immune clearance fails, the persistence of senescent cells is thought to drive disease pathology through their altered secretory profile. One of the major cell types involved in wound healing is fibroblasts, and senescent fibroblasts have been identified in the lungs of patients with IPF and in fibroblast cultures from IPF lungs. The question of what is driving abnormally high numbers of fibroblasts into senescence remains unanswered. The transcription factor signal transducer and activator of transcription 3 (STAT3) plays a role in a myriad of processes, including cell-cycle progression, gene transcription, as well as mitochondrial respiration, all of which are dysregulated during senescence. Activation of STAT3 has previously been shown to correlate with IPF progression and therefore is a potential molecular target to modify early-stage senescence and restore normal fibroblast function. This review summarizes what is presently known about fibroblast senescence in IPF and how STAT3 may contribute to this phenotype

STAT3 Reinforces the Senescent Phenotype in Human Lung Fibroblasts

American Thoracic Society International Conference Abstracts > C73. FIBROBLAST BIOLOG

STAT3 Regulates the Onset of Oxidant-induced Senescence in Lung Fibroblasts

Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease of unknown cause with a median survival of only 3 years. Other investigators and we have shown that fibroblasts derived from IPF lungs display characteristics of senescent cells, and that dysregulated activation of the transcription factor signal transducer and activator of transcription 3 (STAT3) correlates with IPF progression. The question of whether STAT3 activation is involved in fibroblast senescence remains unanswered. We hypothesized that inhibiting STAT3 activation after oxidant-induced senescence would attenuate characteristics of the senescent phenotype. We aimed to characterize a model of oxidant-induced senescence in human lung fibroblasts and to determine the effect of inhibiting STAT3 activity on the development of senescence. Exposing human lung fibroblasts to 150 μM hydrogen peroxide (H2O2) resulted in increased senescence-associated β-galactosidase content and expression of p21 and IL-6, all of which are features of senescence. The shift into senescence was accompanied by an increase of STAT3 translocation to the nucleus and mitochondria. Additionally, Seahorse analysis provided evidence of increased mitochondrial respiration characterized by increased basal respiration, proton leak, and an associated increase in superoxide (O2−) production in senescent fibroblasts. Targeting STAT3 activity using the small-molecule inhibitor STA-21 attenuated IL-6 production, reduced p21 levels, decreased senescence-associated β-galactosidase accumulation, and restored normal mitochondrial function. The results of this study illustrate that stress-induced senescence in lung fibroblasts involves the activation of STAT3, which can be pharmacologically modulated

PRISM (Polarized Radiation Imaging and Spectroscopy Mission): an extended white paper

Contains fulltext : 126057.pdf (preprint version ) (Open Access