VLBI Observations of a sample of Palomar-Green quasars II: characterising the parsec-scale radio emission

This study uses multi-frequency Very Long Baseline Interferometry (VLBI) to study the radio emission from 10 radio-quiet quasars (RQQs) and four radio-loud quasars (RLQs). The diverse morphologies, radio spectra, and brightness temperatures observed in the VLBI images of these RQQs, together with the variability in their GHz spectra and VLBI flux densities, shed light on the origins of their nuclear radio emission. The total radio emission of RQQs appears to originate from non-thermal synchrotron radiation due to a combination of active galactic nuclei and star formation activities. However, our data suggest that the VLBI-detected radio emission from these RQQs is primarily associated with compact jets or corona, with extended emissions such as star formation and large-scale jets being resolved by the high resolution of the VLBI images. Wind emission models are not in complete agreement the VLBI observations. Unlike RLQs, where the parsec-scale radio emission is dominated by a relativistically boosted core, the radio cores of RQQs are either not dominant or are mixed with significant jet emission. RQQs with compact cores or core-jet structures typically have more pronounced variability, with flat or inverted spectra, whereas jet-dominated RQQs have steep spectra and unremarkable variability. Future high-resolution observations of more RQQs could help to determine the fraction of different emission sources and their associated physical mechanisms.Comment: This paper has been accepted by MNRA

VLBI observations of a sample of Palomar-Green quasars - I. Parsec-scale morphology

We observed 20 Palomar-Green quasars at low redshi ft (z < 0.5) with total flux density >1 mJy, including four radio-loud quasars (RLQs) and 16 radio-quiet quasars (RQQs), using the Very Long Baseline Array (VLBA) at 5 GHz. 10 RQQs are clearly detected in the VLBA images, and a compact radio core is identified in eight of them, indicating the prevalence of active galactic nucleus (AGN)-related radio emission in this flux-density-limited RQQ sample. The RQQs and RLQs in our sample have a division at similar to 30 mJy. The radio emission from RQQs appears to be the result of a combination of star formation and AGN-associated activities. All RQQs in our sample have a 5 GHz flux density ratio of Very Large Array (VLA) A-array to D-array f(c) = S-A(VLA)/S-D(VLA) above 0.2. The RQQs with f(a)(VLBA and VLA flux density ratio S-VLBA/S-A(VLA)) > 0.2 versus f(a) < 0.2 show significant differences in morphology, compactness, and total flux density. f(a) of RQQs is systematically lower than that of RLQs, probably due to the extended jets or relic jets of RQQs on tens to hundreds parsecs that are resolved out in VLBA images. Future larger samples, especially with the addition of milliarcsec resolution radio images of RQQs with total flux densities below 1 mJy, can test the conclusions of this paper and contribute to the understanding of the radio emission mechanism of RQQs, and the dichotomy and physical connection between RQQs and RLQs

Serum Amyloid A Is Not Incorporated into HDL during HDL Biogenesis

Liver-derived serum amyloid A (SAA) is present in plasma where it is mainly associated with HDL and from which it is cleared more rapidly than are the other major HDL-associated apolipoproteins. Although evidence suggests that lipid-free and HDL-associated forms of SAA have different activities, the pathways by which SAA associates and disassociates with HDL are poorly understood. In this study, we investigated SAA lipidation by hepatocytes and how this lipidation relates to the formation of nascent HDL particles. We also examined hepatocyte-mediated clearance of lipid-free and HDL-associated SAA. We prepared hepatocytes from mice injected with lipopolysaccharide or an SAA-expressing adenoviral vector. Alternatively, we incubated primary hepatocytes from SAA-deficient mice with purified SAA. We analyzed conditioned media to determine the lipidation status of endogenously produced and exogenously added SAA. Examining the migration of lipidated species, we found that SAA is lipidated and forms nascent particles that are distinct from apoA-I-containing particles and that apoA-I lipidation is unaltered when SAA is overexpressed or added to the cells, indicating that SAA is not incorporated into apoA-I-containing HDL during HDL biogenesis. Like apoA-I formation, generation of SAA-containing particles was dependent on ABCA1, but not on scavenger receptor class B type I. Hepatocytes degraded significantly more SAA than apoA-I. Taken together, our results indicate that SAA\u27s lipidation and metabolism by the liver is independent of apoA-I and that SAA is not incorporated into HDL during HDL biogenesis

Serum Amyloid A3 is a High Density Lipoprotein-Associated Acute-Phase Protein

Serum amyloid A (SAA) is a family of acute-phase reactants. Plasma levels of human SAA1/SAA2 (mouse SAA1.1/2.1) can increase ≥ 1,000-fold during an acute-phase response. Mice, but not humans, express a third relatively understudied SAA isoform, SAA3. We investigated whether mouse SAA3 is an HDL-associated acute-phase SAA. Quantitative RT-PCR with isoform-specific primers indicated that SAA3 and SAA1.1/2.1 are induced similarly in livers (∼2,500-fold vs. ∼6,000-fold, respectively) and fat (∼400-fold vs. ∼100-fold, respectively) of lipopolysaccharide (LPS)-injected mice. In situ hybridization demonstrated that all three SAAs are produced by hepatocytes. All three SAA isoforms were detected in plasma of LPS-injected mice, although SAA3 levels were ∼20% of SAA1.1/2.1 levels. Fast protein LC analyses indicated that virtually all of SAA1.1/2.1 eluted with HDL, whereas ∼15% of SAA3 was lipid poor/free. After density gradient ultracentrifugation, isoelectric focusing demonstrated that ∼100% of plasma SAA1.1 was recovered in HDL compared with only ∼50% of SAA2.1 and ∼10% of SAA3. Thus, SAA3 appears to be more loosely associated with HDL, resulting in lipid-poor/free SAA3. We conclude that SAA3 is a major hepatic acute-phase SAA in mice that may produce systemic effects during inflammation

Impact of Individual Acute Phase Serum Amyloid A Isoforms on HDL Metabolism in Mice

The acute phase (AP) reactant serum amyloid A (SAA), an HDL apolipoprotein, exhibits pro-inflammatory activities, but its physiological function(s) are poorly understood. Functional differences between SAA1.1 and SAA2.1, the two major SAA isoforms, are unclear. Mice deficient in either isoform were used to investigate plasma isoform effects on HDL structure, composition, and apolipoprotein catabolism. Lack of either isoform did not affect the size of HDL, normally enlarged in the AP, and did not significantly change HDL composition. Plasma clearance rates of HDL apolipoproteins were determined using native HDL particles. The fractional clearance rates (FCRs) of apoA-I, apoA-II, and SAA were distinct, indicating that HDL is not cleared as intact particles. The FCRs of SAA1.1 and SAA2.1 in AP mice were similar, suggesting that the selective deposition of SAA1.1 in amyloid plaques is not associated with a difference in the rates of plasma clearance of the isoforms. Although the clearance rate of SAA was reduced in the absence of the HDL receptor, scavenger receptor class B type I (SR-BI), it remained significantly faster compared with that of apoA-I and apoA-II, indicating a relatively minor role of SR-BI in SAA’s rapid clearance. These studies enhance our understanding of SAA metabolism and SAA’s effects on AP-HDL composition and catabolism

The Impairment of Macrophage-to-Feces Reverse Cholesterol Transport during Inflammation Does Not Depend on Serum Amyloid A

Studies suggest that inflammation impairs reverse cholesterol transport (RCT). We investigated whether serum amyloid A (SAA) contributes to this impairment using an established macrophage-to-feces RCT model. Wild-type (WT) mice and mice deficient in SAA1.1 and SAA2.1 (SAAKO) were injected intraperitoneally with 3H-cholesterol-labeled J774 macrophages 4 hr after administration of LPS or buffered saline. 3H-cholesterol in plasma 4 hr after macrophage injection was significantly reduced in both WT and SAAKO mice injected with LPS, but this was not associated with a reduced capacity of serum from LPS-injected mice to promote macrophage cholesterol efflux in vitro. Hepatic accumulation of 3H-cholesterol was unaltered in either WT or SAAKO mice by LPS treatment. Radioactivity present in bile and feces of LPS-injected WT mice 24 hr after macrophage injection was reduced by 36% (P \u3c 0.05) and 80% (P \u3c 0.001), respectively. In contrast, in SAAKO mice, LPS did not significantly reduce macrophage-derived 3H-cholesterol in bile, and fecal excretion was reduced by only 45% (P \u3c 0.05). Injection of cholesterol-loaded allogeneic J774 cells, but not syngeneic bone-marrow-derived macrophages, transiently induced SAA in C57BL/6 mice. Our study confirms reports that acute inflammation impairs steps in the RCT pathway and establishes that SAA plays only a minor role in this impairment

Mildly relativistic motion in the radio-quiet quasar PG 1351+640

Measuring the proper motion of the emission component in radio-quiet quasars (RQQs) could help to distinguish between the origins of the radio emission and to understand whether the jet production mechanism is the same in radio-loud quasars and RQQs. PG 1351+640 is one of the few RQQs suitable for proper motion studies: it has two compact components on milli-arcsec scales, a flat-spectrum core and a steep-spectrum jet; both components are ≳2 mJy at 5 GHz and are well suited for Very Long Baseline Array (VLBA) observations. We compare recent VLBA observations with that made seventeen years ago and find no significant change in the core-jet separation between 2005 and 2015 (a proper motion of 0.003 mas yr-1). However, the core-jet separation increased significantly between 2015 and 2022, inferring a jet proper motion velocity of 0.063 mas yr-1, which corresponds to an apparent transverse velocity of. The result suggests that the jet of the RQQ PG 1351+640 is mildly relativistic and oriented at a relatively small viewing angle

Overexpression of CD70 and overstimulation of IgG synthesis by lupus T cells and T cells treated with DNA methylation inhibitors

Objective Generalized DNA hypomethylation contributes to altered T cell function and gene expression in systemic lupus erythematosus (SLE). Some of the overexpressed genes participate in the disease process, but the full repertoire of genes affected is unknown. Methylation-sensitive T cell genes were identified by treating T cells with the DNA methyltransferase inhibitor 5-azacytidine and comparing gene expression with oligonucleotide arrays. CD70, a costimulatory ligand for B cell CD27, was one gene that reproducibly increased. We then determined whether CD70 is overexpressed on T cells treated with other DNA methylation inhibitors and on SLE T cells, and determined its functional significance. Methods Oligonucleotide arrays, real-time reverse transcription–polymerase chain reaction, and flow cytometry were used to compare CD70 expression in T cells treated with 2 DNA methyltransferase inhibitors (5-azacytidine and procainamide) and 3 ERK pathway inhibitors known to decrease DNA methyltransferase expression (U0126, PD98059, and hydralazine). The consequences of CD70 overexpression were tested by coculture of autologous T and B cells with and without anti-CD70 and measuring IgG production by enzyme-linked immunosorbent assay. The results were compared with those of T cells from lupus patients. Results SLE T cells and T cells treated with DNA methylation inhibitors overexpressed CD70 and overstimulated B cell IgG production. The increase in IgG synthesis was abrogated by anti-CD70. Conclusion SLE T cells and T cells treated with DNA methyltransferase inhibitors and ERK pathway inhibitors overexpress CD70. This increased B cell costimulation and subsequent immunoglobulin overproduction may contribute to drug-induced and idiopathic lupus.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/34311/1/20255_ftp.pd