Testing for Rate-Dependence and Asymmetry in Inflation Uncertainty:Evidence from the G7 Economies

The Friedman-Ball hypothesis implies a link between the inflation rate and inflation uncertainty. In this paper we employ a new test for the joint null hypothesis of no dependence effects and no asymmetry in the G7 inflation volatility. The results show that higher inflationrates operate additively via the conditional variance of inflation to induce greater inflation uncertainty in the U.S., U.K. and Canada. In addition, positive inflationary shocks are found to generate greater inflation uncertainty than negative shocks of a similar magnitude in the U.K. and Canada.Friedman-Ball hypothesis, Asymmetry, Davies’ Problem

Equity Return and Short-Term Interest Rate Volatility : Level Effects and Asymmetric Dynamics

Evidence suggests that short-term interest rate volatility peaks with the level of short rates, while equity volatility responds asymmetrically to positive and negative shocks. We present an LM based test that distinguishes between level effects and asymmetry in volatility which is robust to the presence of unidentified nuisance parameters under the null. There is strong evidence of a level effect and asymmetric response in the relationship between S&P 500 Index returns and 3-month US Treasury Bills. The conditional covariance depends on the level of the short rate which has implications for hedging equity returns against short term interest rate movements.Level Effects; Asymmetry; LM Tests; Davies Problem; Nonlinear Granger Causality

Optimal Estimators for Threshold-Based Quality Measures

We consider a problem in parametric estimation: given n samples from an unknown distribution, we want to estimate which distribution, from a given one-parameter family, produced the data. Following Schulman and Vazirani (2005), we evaluate an estimator in terms of the chance of being within a specified tolerance of the correct answer, in the worst case. We provide optimal estimators for several families of distributions on ℝ. We prove that for distributions on a compact space, there is always an optimal estimator that is translation invariant, and we conjecture that this conclusion also holds for any distribution on ℝ. By contrast, we give an example showing that, it does not hold for a certain distribution on an infinite tree

CANDELS: The Contribution of the Observed Galaxy Population to Cosmic Reionization

We present measurements of the specific ultraviolet luminosity density from a sample of 483 galaxies at 6<z<8. These galaxies were selected from new deep near-infrared HST imaging from the CANDELS, HUDF09 and ERS programs. In contrast to the majority of previous analyses, which assume that the distribution of galaxy ultraviolet (UV) luminosities follows a Schechter distribution, and that the distribution continues to luminosities far below our observable limit, we investigate the contribution to reionization from galaxies which we can observe, free from these assumptions. We find that the observable population of galaxies can sustain a fully reionized IGM at z=6, if the average ionizing photon escape fraction (f_esc) is ~30%. A number of previous studies have measured UV luminosity densities at these redshifts that vary by 5X, with many concluding that galaxies could not complete reionization by z=6 unless a large population of galaxies fainter than the detection limit were invoked, or extremely high values of f_esc were present. The observed UV luminosity density from our observed galaxy samples at z=7-8 is not sufficient to maintain a fully reionized IGM unless f_esc>50%. Combining our observations with constraints on the emission rate of ionizing photons from Ly-alpha forest observations at z=6, we can constrain f_esc<34% (2-sigma) if the observed galaxies are the only contributors to reionization, or <13% (2-sigma) if the luminosity function extends to M_UV = -13. These escape fractions are sufficient to complete reionization by z=6. These constraints imply that the volume ionized fraction of the IGM becomes less than unity at z>7, consistent with a number of complementary reionization probes. If faint galaxies dominate reionization, future JWST observations will probe deep enough to see them, providing an indirect constraint on the ionizing photon escape fraction [abridged].Comment: 16 pages, 7 figures, Submitted to the Astrophysical Journa

Concert recording 2016-04-23a

[Track 01]. Interludes for percussion and trumpet. March ; [Track 02]. Elegy ; [Track 03]. Prayer ; [Track 04]. Finale / Marilyn J. Harris ; Mark E. Wolfram -- [Track 05]. Pastorale / Eric Ewazen -- [Track 06]. Animal ditties. The turtle ; [Track 07]. The python ; [Track 08]. The hog ; [Track 09]. The chipmunk ; [Track 10]. The canary ; [Track 11]. The elk / Anthony Plog -- [Track 12]. La revue de cuisine. Prologue ; [Track 13]. Tango ; [Track 14]. Charleston ; [Track 15]. Finale / Bohuslav Martinů

Graded Nodal/Activin Signaling Titrates Conversion of Quantitative Phospho-Smad2 Levels into Qualitative Embryonic Stem Cell Fate Decisions

Nodal and Activin are morphogens of the TGFbeta superfamily of signaling molecules that direct differential cell fate decisions in a dose- and distance-dependent manner. During early embryonic development the Nodal/Activin pathway is responsible for the specification of mesoderm, endoderm, node, and mesendoderm. In contradiction to this drive towards cellular differentiation, the pathway also plays important roles in the maintenance of self-renewal and pluripotency in embryonic and epiblast stem cells. The molecular basis behind stem cell interpretation of Nodal/Activin signaling gradients and the undertaking of disparate cell fate decisions remains poorly understood. Here, we show that any perturbation of endogenous signaling levels in mouse embryonic stem cells leads to their exit from self-renewal towards divergent differentiation programs. Increasing Nodal signals above basal levels by direct stimulation with Activin promotes differentiation towards the mesendodermal lineages while repression of signaling with the specific Nodal/Activin receptor inhibitor SB431542 induces trophectodermal differentiation. To address how quantitative Nodal/Activin signals are translated qualitatively into distinct cell fates decisions, we performed chromatin immunoprecipitation of phospho-Smad2, the primary downstream transcriptional factor of the Nodal/Activin pathway, followed by massively parallel sequencing, and show that phospho-Smad2 binds to and regulates distinct subsets of target genes in a dose-dependent manner. Crucially, Nodal/Activin signaling directly controls the Oct4 master regulator of pluripotency by graded phospho-Smad2 binding in the promoter region. Hence stem cells interpret and carry out differential Nodal/Activin signaling instructions via a corresponding gradient of Smad2 phosphorylation that selectively titrates self-renewal against alternative differentiation programs by direct regulation of distinct target gene subsets and Oct4 expression