The Ultra-Fast Outflow of the Quasar PG 1211+143 as Viewed by Time-Averaged Chandra Grating Spectroscopy

This is an author-created, un-copyedited version of an article published in The Astrophysical Journal. The Version of Record is available online at https://doi.org/10.3847/1538-4357/aaa427We present a detailed X-ray spectral study of the quasar PG 1211+143 based on Chandra High Energy Transmission Grating Spectrometer (HETGS) observations collected in a multi-wavelength campaign with UV data using the Hubble Space Telescope Cosmic Origins Spectrograph (HST-COS) and radio bands using the Jansky Very Large Array (VLA). We constructed a multi-wavelength ionizing spectral energy distribution using these observations and archival infrared data to create xstar photoionization models specific to the PG 1211+143 flux behavior during the epoch of our observations. Our analysis of the Chandra-HETGS spectra yields complex absorption lines from H-like and He-like ions of Ne, Mg, and Si, which confirm the presence of an ultra-fast outflow (UFO) with a velocity of approximately -17,300 km s -1 (outflow redshift z out ∼ -0.0561) in the rest frame of PG 1211+143. This absorber is well described by an ionization parameter and column density. This corresponds to a stable region of the absorber's thermal stability curve, and furthermore its implied neutral hydrogen column is broadly consistent with a broad Lyα absorption line at a mean outflow velocity of approximately -16,980 km s -1 detected by our HST-COS observations. Our findings represent the first simultaneous detection of a UFO in both X-ray and UV observations. Our VLA observations provide evidence for an active jet in PG 1211+143, which may be connected to the X-ray and UV outflows; this possibility can be evaluated using very-long-baseline interferometric observations.Peer reviewedFinal Accepted Versio

Complement activates Kupffer cells and neutrophils during reperfusion after hepatic ischemia

The hypothesis that complement factors may be involved in the postischemic activation of Kupffer cells (KC) and polymorphonuclear neutrophils (PMN) was investigated in a model of hepatic ischemia (45 min) and reperfusion in male Fischer rats in vivo. Depletion of serum complement before ischemia resulted in a significant attenuation of the KC-induced oxidant stress (enhanced oxidation of plasma glutathione) and also prevented the accumulation of PMNs in the liver during the initial reperfusion period of 1 h. Complement activation through injection of cobra venom factor (CVF; 75 μg CVF/kg) also induced enhanced oxidation of plasma glutathione and accumulation of PMNs in the liver. Isolation of KC and PMNs from the liver 1 h after CVF treatment demonstrated a similar priming effect for stimulation with phorbol myristate acetate and opsonized zymosan as was observed in the postischemic liver. Complement-depleted animals and animals pretreated with the soluble human complement receptor type 1 (BRL 55730; 22.5 mg/kg) accumulated significantly less PMNs in the postischemic livers during longer reperfusion periods (24 h) and sustained significantly less injury. It is concluded that complement is involved in the induction of a KC-induced oxidant stress, the priming of KC and PMNs for enhanced reactive oxygen generation, and the continuous accumulation of PMNs in the liver during reperfusion

Complement activates Kupffer cells and neutrophils during reperfusion after hepatic ischemia

The hypothesis that complement factors may be involved in the postischemic activation of Kupffer cells (KC) and polymorphonuclear neutrophils (PMN) was investigated in a model of hepatic ischemia (45 min) and reperfusion in male Fischer rats in vivo. Depletion of serum complement before ischemia resulted in a significant attenuation of the KC-induced oxidant stress (enhanced oxidation of plasma glutathione) and also prevented the accumulation of PMNs in the liver during the initial reperfusion period of 1 h. Complement activation through injection of cobra venom factor (CVF; 75 μg CVF/kg) also induced enhanced oxidation of plasma glutathione and accumulation of PMNs in the liver. Isolation of KC and PMNs from the liver 1 h after CVF treatment demonstrated a similar priming effect for stimulation with phorbol myristate acetate and opsonized zymosan as was observed in the postischemic liver. Complement-depleted animals and animals pretreated with the soluble human complement receptor type 1 (BRL 55730; 22.5 mg/kg) accumulated significantly less PMNs in the postischemic livers during longer reperfusion periods (24 h) and sustained significantly less injury. It is concluded that complement is involved in the induction of a KC-induced oxidant stress, the priming of KC and PMNs for enhanced reactive oxygen generation, and the continuous accumulation of PMNs in the liver during reperfusion