Unshifted Metastable He I* Mini-Broad Absorption Line System in the Narrow Line Type 1 Quasar SDSS J080248.18++551328.9

We report the identification of an unusual absorption line system in the quasar SDSS J080248.18$+$551328.9 and present a detailed study of the system, incorporating follow-up optical and NIR spectroscopy. A few tens of absorption lines are detected, including He I*, Fe II* and Ni II* that arise from metastable or excited levels, as well as resonant lines in Mg I, Mg II, Fe II, Mn II, and Ca II. All of the isolated absorption lines show the same profile of width $\Delta v\sim 1,500$km s$^{-1}$ centered at a common redshift as that of the quasar emission lines, such as [O II], [S II], and hydrogen Paschen and Balmer series. With narrow Balmer lines, strong optical Fe II multiplets, and weak [O III] doublets, its emission line spectrum is typical for that of a narrow-line Seyfert 1 galaxy (NLS1). We have derived reliable measurements of the gas-phase column densities of the absorbing ions/levels. Photoionization modeling indicates that the absorber has a density of $n_{\rm H} \sim (1.0-2.5)\times 10^5~ {\rm cm}^{-3}$ and a column density of $N_{\rm H} \sim (1.0-3.2)\times 10^{21} \sim {\rm cm}^{-2}$, and is located at $R\sim100-250$ pc from the central super-massive black hole. The location of the absorber, the symmetric profile of the absorption lines, and the coincidence of the absorption and emission line centroid jointly suggest that the absorption gas is originated from the host galaxy and is plausibly accelerated by stellar processes, such as stellar winds \zhy{and/or} supernova explosions. The implications for the detection of such a peculiar absorption line system in an NLS1 are discussed in the context of co-evolution between super-massive black hole growth and host galaxy build-up.Comment: 28 pages, 16 figures; accepted for publication in Astrophysical Journa

Ultraviolet and Optical Emission Line Outflows in the Heavily Obscured Quasar SDSS J000610.67+121501.2: At the Scale of the Dusty Torus and Beyond

Broad emission line outflows of active galactic nuclei have been proposed for many years but are very difficult to quantitatively study because of the coexistence of the gravitationally bound and outflow emission. We present detailed analysis of a heavily reddened quasar, SDSS J000610.67+121501.2, whose normal ultraviolet broad emission lines (BELs) are heavily suppressed by the dusty torus as a natural "coronagraph," and thus the blueshifted BELs (BBELs) can be reliably measured. The physical properties of the emission-line outflows are derived as follows: ionization parameter U ~ 10^(-0.5), column density N_H ~ 10^(22.0) cm^(−2), covering fraction of ~0.1, and upper limit density of n_H ~ 10^(5.8) cm^(−3). The outflow gases are located at least 41 pc away from the central engine, which suggests that they have expanded to the scale of the dust torus or beyond. Besides, Lyα shows a narrow symmetric component, to our surprise, which is undetected in any other lines. After inspecting the narrow emission line region and the star-forming region as the origin of the Lyα narrow line, we propose that the end result of outflows, diffusing gases in the larger region, acts as the screen of Lyα photons. Future high spatial resolution spectrometry and/or spectropolarimetric observations are needed to make a final clarification

Overexpression of MET4 Leads to the Upregulation of Stress-Related Genes and Enhanced Sulfite Tolerance in Saccharomyces uvarum

Saccharomyces uvarum is one of the few fermentative species that can be used in winemaking, but its weak sulfite tolerance is the main reason for its further use. Previous studies have shown that the expression of the methionine synthase gene (MET4) is upregulated in FZF1 (a gene encoding a putative zinc finger protein, which is a positive regulator of the transcription of the cytosolic sulfotransferase gene SSU1) overexpression transformant strains, but its exact function is unknown. To gain insight into the function of the MET4 gene, in this study, a MET4 overexpression vector was constructed and transformed into S. uvarum strain A9. The MET4 transformants showed a 20 mM increase in sulfite tolerance compared to the starting strain. Ninety-two differential genes were found in the transcriptome of A9-MET4 compared to the A9 strain, of which 90 were upregulated, and two were downregulated. The results of RT-qPCR analyses confirmed that the expression of the HOMoserine requiring gene (HOM3) in the sulfate assimilation pathway and some fermentation-stress-related genes were upregulated in the transformants. The overexpression of the MET4 gene resulted in a significant increase in sulfite tolerance, the upregulation of fermentation-stress-related gene expression, and significant changes in the transcriptome profile of the S. uvarum strain

Metabolite discovery of helicidum in rat urine with XCMS based on the data of ultra performance liquid chromatography coupled to time-of-flight mass spectrometry

The present study demonstrates the use of XCMS (various forms (X) of chromatography coupled to mass spectrometry), an open-source software tool primarily used in bioinformatics, on the data of ultra-performance liquid chromatography connected online with a mass spectrometer (UPLC/MS) for the discovery of the metabolites of helicidum in urine after oral single dosage to rats. Helicidum (formaldehydephenyl-O-β-d-pyranosyl alloside) is the major active component of the fruits of Helicid hilagirica Beed. In China, it is often used in the clinic to treat neurasthenic syndromes, vascular headache, and trigeminal neuralgia with high efficacy and low side effect and toxicity. The urine samples of five rats were collected during 0–4, 4–8, 8–12, 12–16, 16–20, 20–24, 24–32, 32–40, and 40–48 h, respectively, after oral administration of helicidum at a dosage of 25.0 mg/kg. A UPLC coupled to time-of-flight MS (UPLC/TOF MS) was used to analyze the samples. Concerning XCMS, the “.raw” format files were preliminarily converted to the open mzXML format using massWolf-4.3.1 (http://sourceforge.net/projects/sashimi/files/massWolf%20(MassLynx%20converter)/). For converting lots of files a time, we wrote a tool rawTomzXML which also uses massWolf-4.3.1. The data were processed using XCMS version l.26.0 (http://www.bioconductor.org/packages/2.8/bioc/html/xcms.html) running under R version 2.13 (http://http://www.r-project.org/) which provided the running platform for XCMS. The “centWave” method from XCMS was used for chromatographic peak detection. Based on the m/z data of the metabolites obtained by XCMS, MS was used to identify the molecular formula. Nine metabolites were finally found and identified. For six of them, the bio-transformation mechanisms of the parent compound was elucidated: glucuronide conjugation (C19H24O14), reduction (C13H18O7), oxidation (C13H16O8), methylation (C14H18O7), and the mixed transformation of reduction, methylation, and acetylation (C16H22O8). For the other three metabolites, C11H19N3O9, C11H21N3O9, and C14H15NO7, the bio-transformation mechanisms remain unknown and need further investigation. Calculated as mass of helicidum, the cumulative urine excretion rate of the metabolites was 8.39%. The amount of oxidized helicidum was more than 50% among the metabolites while the parent compound helicidum was 13.28% and the reduced helicidum 11.72%, indicating that oxidation was the major bio-transformation that occurred in vivo

Extension of Drosophila Lifespan by Astragalus polysaccharide through a Mechanism Dependent on Antioxidant and Insulin/IGF-1 Signaling

Historical literature and pharmacological studies demonstrate that Astragalus polysaccharide (APS) has anti-inflammatory and antioxidative effects. Studies into the longevity effects of APS are limited, and the molecular mechanism of lifespan extension by APS is not elucidated yet. Here, the longevity effect of APS was investigated in Drosophila melanogaster by feeding dose-dependent APS. APS significantly extended the lifespan and improved the reproduction. Meanwhile, APS increased locomotion, TAG level, and starvation resistance and reduced the mortality rate induced by hydrogen peroxide. The activities of superoxide dismutase (SOD) and catalase (CAT) were increased in flies treated with APS diet. Moreover, APS significantly enhanced expressions of antioxidant genes (Sod1, Sod2, and Cat), dFoxO, and 4E − BP, decreased the expressions of insulin-like peptides (dilp2, dilp3, and dilp5), and longevity gene MTH. Together, these results indicate that APS can prolong the lifespan by regulating antioxidant ability and insulin/IGF-1 signaling and also enhance the reproduction ability in Drosophila. APS may be explored as a novel agent for slowing the aging process and improving reproduction

Exercise protects aged mice against coronary endothelial senescence via FUNDC1-dependent mitophagy

Vascular aging contributes to adverse changes in organ function and is a significant indicator of major cardiac events. Endothelial cells (ECs) participate in aging-provoked coronary vascular pathology. Regular exercise is associated with preservation of arterial function with aging in humans. However, the molecular basis is not well understood. The present study was aimed to determine the effects of exercise on coronary endothelial senescence and whether mitochondrial clearance regulator FUN14 domain containing 1 (FUNDC1)-related mitophagy and mitochondrial homeostasis were involved. In mouse coronary arteries, FUNDC1 levels showed gradually decrease with age. Both FUNDC1 and mitophagy levels in cardiac microvascular endothelial cells (CMECs) were significantly reduced in aged mice and were rescued by exercise training. Exercise also alleviated CMECs senescence as evidenced by senescence associated β-galactosidase activity and aging markers, prevented endothelial abnormal cell migration, proliferation, and eNOS activation in CMECs from aged mice, and improved endothelium-dependent vasodilation of coronary artery, reduced myocardial neutrophil infiltration and inflammatory cytokines evoked by MI/R, restored angiogenesis and consequently alleviated MI/R injury in aging. Importantly, FUNDC1 deletion abolished the protective roles of exercise and FUNDC1 overexpression in ECs with adeno-associated virus (AAV) reversed endothelial senescence and prevented MI/R injury. Mechanistically, PPARγ played an important role in regulating FUNDC1 expressions in endothelium under exercise-induced laminar shear stress. In conclusion, exercise prevents endothelial senescence in coronary arteries via increasing FUNDC1 in a PPARγ-dependent manner, and subsequently protects aged mice against MI/R injury. These findings highlight FUNDC1-mediated mitophagy as potential therapeutic target that prevents endothelial senescence and myocardial vulnerability