Testing the Blazar Paradigm: ASCA Observations of FSRQs with Steep Soft X-ray Spectra

We present the first observations at medium-hard X-rays with ASCA in 1998 August--November of four Flat Spectrum Radio Quasars (FSRQs), characterized by unusually steep soft X-ray spectra (photon index, \Gamma_{0.2-2.4 keV} \sim 2-2.5), as previously measured with ROSAT. Such steep X-ray slopes are similar to those observed in synchrotron-dominated BL Lacs and are unexpected in the context of the recent blazar paradigm, where sources with strong emission lines (such as FSRQs) are dominated in soft X-rays by a flat inverse Compton tail. We find that the ASCA spectra of the four FSRQs are consistent with a power law model with \Gamma_{2-10 keV} \sim 1.8, flatter than their ROSAT spectra. This indicates the onset of an inverse Compton component at energies \gtrsim 2 keV, in agreement with the blazar unification scheme. However, these objects are still anomalous within the blazar class for their steep soft X-ray continua which, together with non-simultaneous data at longer wavelengths, hint at the possibility that the synchrotron emission extends to soft X-rays. This would imply an anomalously high synchotron peak frequency for a quasar with luminous broad lines, challenging current blazar unification schemes. Alternatively, a plausible explanation for the steep optical-to-soft X-ray continua of the four FSRQs is thermal emission from the accretion disk, similar to the blazars 3C~273 and 3C~345. In the Appendix, we present fits to the SIS data in an effort to contribute to the ongoing calibration of the the time-dependence of the SIS response at low energies.Comment: accepted for publication in The Astrophysical Journa

Alpha-Amino-Beta-Carboxy-Muconate-Semialdehyde Decarboxylase Controls Dietary Niacin Requirements for NAD+ Synthesis

NAD+ is essential for redox reactions in energy metabolism and necessary for DNA repair and epigenetic modification. Humans require sufficient amounts of dietary niacin (nicotinic acid, nicotinamide, and nicotinamide riboside) for adequate NAD+ synthesis. In contrast, mice easily generate sufficient NAD+ solely from tryptophan through the kynurenine pathway. We show that transgenic mice with inducible expression of human alpha-amino-beta-carboxy-muconate-semialdehyde decarboxylase (ACMSD) become niacin dependent similar to humans when ACMSD expression is high. On niacin-free diets, these acquired niacin dependency (ANDY) mice developed reversible, mild-to-severe NAD+ deficiency, depending on the nutrient composition of the diet. NAD deficiency in mice contributed to behavioral and health changes that are reminiscent of human niacin deficiency. This study shows that ACMSD is a key regulator of mammalian dietary niacin requirements and NAD+ metabolism and that the ANDY mouse represents a versatile platform for investigating pathologies linked to low NAD+ levels in aging and neurodegenerative diseases