No Evidence for Evolution in the Far-Infrared-Radio Correlation out to z ~ 2 in the eCDFS

We investigate the 70 um Far-Infrared Radio Correlation (FRC) of star-forming galaxies in the Extended Chandra Deep Field South (ECDFS) out to z > 2. We use 70 um data from the Far-Infrared Deep Extragalactic Legacy Survey (FIDEL), which comprises the most sensitive (~0.8 mJy rms) and extensive far-infrared deep field observations using MIPS on the Spitzer Space Telescope, and 1.4 GHz radio data (~8 uJy/beam rms) from the VLA. In order to quantify the evolution of the FRC we use both survival analysis and stacking techniques which we find give similar results. We also calculate the FRC using total infrared luminosity and rest-frame radio luminosity, qTIR, and find that qTIR is constant (within 0.22) over the redshift range 0 - 2. We see no evidence for evolution in the FRC at 70 um which is surprising given the many factors that are expected to change this ratio at high redshifts.Comment: 18 pages, 13 figures. Accepted for publication in Ap

Short-time Gibbsianness for Infinite-dimensional Diffusions with Space-Time Interaction

We consider a class of infinite-dimensional diffusions where the interaction between the components is both spatial and temporal. We start the system from a Gibbs measure with finite-range uniformly bounded interaction. Under suitable conditions on the drift, we prove that there exists $t_0>0$ such that the distribution at time $t\leq t_0$ is a Gibbs measure with absolutely summable interaction. The main tool is a cluster expansion of both the initial interaction and certain time-reversed Girsanov factors coming from the dynamics

Understanding Lyman-alpha emitters

This publication contains the conference summary of the Understanding Lyman-alpha Emitters conference held at the Max Planck Institute for Astronomy in Heidelberg October 6 - 10, 2008. The scope of the conference was to bring together most of the scientists working in the field of Lyman-alpha emitters, whether at low or high redshift, or on observational or theoretical aspects, and to summarise how far the field of study of galaxies with Lyman-alpha emission has come. An outlook towards the future of the field was also desired. As part of the conference, two days were dedicated to in total six discussion sessions. The topics were i) new methods and selection methods, ii) morphology, iii) what can the local Universe observations tell us about the high redshift Universe?, iv) clustering, v) SED fitting and vi) Ly-alpha blobs. The chairs of those sessions were asked to summarise the discussions, as presented in these proceedings.Comment: Workshop summary of the "Understanding Lyman-alpha Emitters" meeting in Heidelberg, Oct. 2008, 49 pages (seven contributions), to be published in New Astronomy Review. Conference home-page, with presentations, is http://www.mpia.de/Public/Aktuelles/Tagungen/lae08/lae08.htm

A novel liposomal S-propargyl-cysteine: a sustained release of hydrogen sulfide reducing myocardial fibrosis via TGF-β1/Smad pathway

Purpose: S-propargyl-cysteine (SPRC; alternatively known as ZYZ-802) is a novel modulator of endogenous tissue H2S concentrations with known cardioprotective and anti-inflammatory effects. However, its rapid metabolism and excretion have limited its clinical application. To overcome these issues, we have developed some novel liposomal carriers to deliver ZYZ-802 to cells and tissues and have characterized their physicochemical, morphological and pharmacological properties. Methods :Two liposomal formulations of ZYZ-802 were prepared by thin-layer hydration and the morphological characteristics of each liposome system were assessed using a laser particle size analyzer and transmission electron microscopy. The entrapment efficiency and ZYZ-802 release profiles were determined following ultrafiltration centrifugation, dialysis tube and HPLC measurements. LC-MS/MS was used to evaluate the pharmacokinetic parameters and tissue distribution profiles of each formulation via the measurements of plasma and tissues ZYZ-802 and H2S concentrations. Using an in vivo model of heart failure (HF), the cardio-protective effects of liposomal carrier were determined by echocardiography, histopathology, western blot and the assessment of antioxidant and myocardial fibrosis markers.Results: Both liposomal formulations improved ZYZ-802 pharmacokinetics and optimized H2S concentrations in plasma and tissues. Liposomal ZYZ-802 showed enhanced cardioprotective effects in vivo. Importantly, liposomal ZYZ-802 could inhibit myocardial fibrosis via the inhibition of the TGF-β1/Smad signaling pathway. Conclusion: The liposomal formulations of ZYZ-802 have enhanced pharmacokinetic and pharmacological properties in vivo. This work is the first report to describe the development of liposomal formulations to improve the sustained release of H2S within tissues.Key word: Liposome; S-Propargyl-cysteine (SPRC, ZYZ-802); Hydrogen sulfide; Heart failure; Myocardial fibrosis; TGF-β1/Smad pathwa

Modelling high redshift Lyman-alpha Emitters

We present a new model for high redshift Lyman-Alpha Emitters (LAEs) in the cosmological context which takes into account the resonant scattering of Ly-a photons through expanding gas. The GALICS semi-analytic model provides us with the physical properties of a large sample of high redshift galaxies. We implement a gas outflow model for each galaxy based on simple scaling arguments. The coupling with a library of numerical experiments of Ly-a transfer through expanding or static dusty shells of gas allows us to derive the Ly-a escape fractions and profiles. The predicted distribution of Ly-a photons escape fraction shows that galaxies with a low star formation rate have a f_esc of the order of unity, suggesting that, for those objects, Ly-a may be used to trace the star formation rate assuming a given conversion law. In galaxies forming stars intensely, the escape fraction spans the whole range from 0 to 1. The model is able to get a good match to the UV and Ly-a luminosity function (LF) data at 3 < z < 5. We find that we are in good agreement with both the bright Ly-a data and the faint population observed by Rauch et al. (2008) at z=3. Most of the Ly-a profiles of our LAEs are redshifted by the diffusion in the outflow which suppresses IGM absorption. The bulk of the observed Ly-a equivalent width (EW) distribution is recovered by our model, but we fail to obtain the very large values sometimes detected. Predictions for stellar masses and UV LFs of LAEs show a satisfactory agreement with observational estimates. The UV-brightest galaxies are found to show only low Ly-a EWs in our model, as it is reported by many observations of high redshift LAEs. We interpret this effect as the joint consequence of old stellar populations hosted by UV-bright galaxies, and high HI column densities that we predict for these objects, which quench preferentially resonant Ly-a photons via dust extinction.Comment: 17 pages, 12 figures, 3 tables, accepted for publication in MNRA

Star Formation History up to z = 7.4: Implications for Gamma-Ray Bursts and the Cosmic Metallicity Evolution

The current Swift sample of gamma-ray bursts (GRBs) with measured redshifts allows to test the assumption that GRBs trace the star formation in the Universe. Some authors have claimed that the rate of GRBs increases with cosmic redshift faster than the star formation rate, whose cause is not known yet. In this paper, I investigate the possibility for interpreting the observed discrepancy between the GRB rate history and the star formation rate history by the cosmic metallicity evolution, motivated by the observation that the cosmic metallicity evolves with redshift and GRBs prefer to occur in low metallicity galaxies. First, I derive a star formation history up to redshift z=7.4 from an updated sample of star formation rate densities obtained by adding the new UV measurements of Bouwens et al. and the new UV and infrared measurements of Reddy et al. to the existing sample compiled by Hopkins & Beacom. Then, adopting a simple model for the relation between the GRB production and the cosmic metallicity history as proposed by Langer & Norman, I show that the observed redshift distribution of the Swift GRBs can be reproduced with a fairly good accuracy. Although the results are limited by the small size of the GRB sample and the poorly understood selection biases in detection and localization of GRBs and in redshift determination, they suggest that GRBs trace both the star formation and the metallicity evolution. If the star formation history can be accurately measured with other approaches, which is presumably achievable in the near future, it will be possible to determine the cosmic metallicity evolution with the study on the redshift distribution of GRBs.Comment: 16 pages, 11 figures and 2 tables, accepted for publication in MNRAS. New version contains an updated star formation history and a review on the cosmic metallicity measuremen

The alpha 7 nicotinic receptor agonist PHA-543613 hydrochloride inhibits <i>Porphyromonas gingivalis</i>-induced expression of interleukin-8 by oral keratinocytes

Objective: The alpha 7 nicotinic receptor (α7nAChR) is expressed by oral keratinocytes. α7nAChR activation mediates anti-inflammatory responses. The objective of this study was to determine if α7nAChR activation inhibited pathogen-induced interleukin-8 (IL-8) expression by oral keratinocytes.&lt;p&gt;&lt;/p&gt; Materials and methods: Periodontal tissue expression of α7nAChR was determined by real-time PCR. OKF6/TERT-2 oral keratinocytes were exposed to &lt;i&gt;Porphyromonas gingivalis&lt;/i&gt; in the presence and absence of a α7nAChR agonist (PHA-543613 hydrochloride) alone or after pre-exposure to a specific α7nAChR antagonist (α-bungarotoxin). Interleukin-8 (IL-8) expression was measured by ELISA and real-time PCR. Phosphorylation of the NF-κB p65 subunit was determined using an NF-κB p65 profiler assay and STAT-3 activation by STAT-3 in-cell ELISA. The release of ACh from oral keratinocytes in response to &lt;i&gt;P. gingivalis&lt;/i&gt; lipopolysaccharide was determined using a GeneBLAzer M3 CHO-K1-blacell reporter assay.&lt;p&gt;&lt;/p&gt; Results: Expression of α7nAChR mRNA was elevated in diseased periodontal tissue. PHA-543613 hydrochloride inhibited &lt;i&gt;P. Gingivalis&lt;/i&gt;-induced expression of IL-8 at the transcriptional level. This effect was abolished when cells were pre-exposed to a specific α7nAChR antagonist, α-bungarotoxin. PHA-543613 hydrochloride downregulated NF-κB signalling through reduced phosphorylation of the NF-κB p65-subunit. In addition, PHA-543613 hydrochloride promoted STAT-3 signalling by maintenance of phosphorylation. Furthermore, oral keratinocytes upregulated ACh release in response to &lt;i&gt;P. Gingivalis&lt;/i&gt; lipopolysaccharide.&lt;p&gt;&lt;/p&gt; Conclusion: These data suggest that α7nAChR plays a role in regulating the innate immune responses of oral keratinocytes.&lt;p&gt;&lt;/p&gt

DNA strand break repair and neurodegeneration.

A number of DNA repair disorders are known to cause neurological problems. These disorders can be broadly characterised into early developmental, mid-to-late developmental or progressive. The exact developmental processes that are affected can influence disease pathology, with symptoms ranging from early embryonic lethality to late-onset ataxia. The category these diseases belong to depends on the frequency of lesions arising in the brain, the role of the defective repair pathway, and the nature of the mutation within the patient. Using observations from patients and transgenic mice, we discuss the importance of double strand break repair during neuroprogenitor proliferation and brain development and the repair of single stranded lesions in neuronal function and maintenance

WNT signaling regulates self-renewal and differentiation of prostate cancer cells with stem cell characteristics

Prostate cancer cells with stem cell characteristics were identified in human prostate cancer cell lines by their ability to form from single cells self-renewing prostaspheres in non-adherent cultures. Prostaspheres exhibited heterogeneous expression of proliferation, differentiation and stem cell-associated makers CD44, ABCG2 and CD133. Treatment with WNT inhibitors reduced both prostasphere size and self-renewal. In contrast, addition of Wnt3a caused increased prostasphere size and self-renewal, which was associated with a significant increase in nuclear Β-catenin, keratin 18, CD133 and CD44 expression. As a high proportion of LNCaP and C4-2B cancer cells express androgen receptor we determined the effect of the androgen receptor antagonist bicalutamide. Androgen receptor inhibition reduced prostasphere size and expression of PSA, but did not inhibit prostasphere formation. These effects are consistent with the androgen-independent self-renewal of cells with stem cell characteristics and the androgen-dependent proliferation of transit amplifying cells. As the canonical WNT signaling effector Β-catenin can also associate with the androgen receptor, we propose a model for tumour propagation involving a balance between WNT and androgen receptor activity. That would affect the self-renewal of a cancer cell with stem cell characteristics and drive transit amplifying cell proliferation and differentiation. In conclusion, we provide evidence that WNT activity regulates the self-renewal of prostate cancer cells with stem cell characteristics independently of androgen receptor activity. Inhibition of WNT signaling therefore has the potential to reduce the self-renewal of prostate cancer cells with stem cell characteristics and improve the therapeutic outcome.Peer reviewe