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Haas, Mary Elizabeth

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Haas

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Mary Elizabeth

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Haas, Mary Elizabeth
Author's Publications: search.filters.isAuthorOfPublication.28cc93ef-6bc3-407d-9b3d-ee0b7d1efac0

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Now showing 1 - 3 of 3
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    Mid-Infrared Spectroscopy of High-Redshift 3crr Sources
    (IOP Publishing, 2010) Leipski, C.; Haas, Mary Elizabeth; Willner, Steven; Ashby, Matthew; Wilkes, Belinda; Fazio, Giovanni; Antonucci, R.; Barthel, P.; Chini, R.; Siebenmorgen, R.; Ogle, P.; Heymann, F.
    Using the Spitzer Space Telescope, we have obtained rest-frame 9–16 μm spectra of 11 quasars and 9 radio galaxies from the 3CRR catalog at redshifts 1.0
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    Star formation in z > 1 3CR host galaxies as seen by Herschel
    (EDP Sciences, 2015) Podigachoski, P.; Barthel, P. D.; Haas, Mary Elizabeth; Leipski, C.; Wilkes, Belinda; Kuraszkiewicz, Joanna; Westhues, C.; Willner, Steven; Ashby, Matthew; Chini, R.; Clements, D. L.; Fazio, Giovanni; Labiano, A.; Lawrence, C.; Meisenheimer, K.; Peletier, R. F.; Siebenmorgen, R.; Verdoes Kleijn, G.
    We present Herschel (PACS and SPIRE) far-infrared (FIR) photometry of a complete sample of z> 1 3CR sources, from the Herschel guaranteed time project The Herschel Legacy of distant radio-loud AGN. Combining these with existing Spitzer photometric data, we perform an infrared (IR) spectral energy distribution (SED) analysis of these landmark objects in extragalactic research to study the star formation in the hosts of some of the brightest active galactic nuclei (AGN) known at any epoch. Accounting for the contribution from an AGN-powered warm dust component to the IR SED, about 40% of our objects undergo episodes of prodigious, ULIRG-strength star formation, with rates of hundreds of solar masses per year, coeval with the growth of the central supermassive black hole. Median SEDs imply that the quasar and radio galaxy hosts have similar FIR properties, in agreement with the orientation-based unification for radio-loud AGN. The star-forming properties of the AGN hosts are similar to those of the general population of equally massive non-AGN galaxies at comparable redshifts, thus there is no strong evidence of universal quenching of star formation (negative feedback) within this sample. Massive galaxies at high redshift may be forming stars prodigiously, regardless of whether their supermassive black holes are accreting or not.
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    Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) in Secondary Hyperlipidemias
    (2016-05-16) Haas, Mary Elizabeth; Kreidberg, Jordan; Biddinger, Sudha B.; Greka, Anna; Sacks, Frank; Jacques, Paul
    Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) has emerged over the past decade as an important regulator of plasma cholesterol and cardiovascular disease risk. PCSK9 promotes degradation of low density lipoprotein (LDL) receptors, thereby decreasing LDL clearance. Accordingly, patients with gain-of-function mutations in PCSK9 have increased LDL cholesterol and increased risk of cardiovascular disease. Conversely, PCSK9 inhibitors recently approved by the FDA are effective in reducing LDL cholesterol. While the contribution of PCSK9 to familial hypercholesterolemia is well-established, less is understood about the role of PCSK9 in diseases in which hyperlipidemia results secondary to an initial disease insult. Hormonal regulation of PCSK9 is also incompletely understood. Understanding the regulators of PCSK9 and specific diseases in which it contributes to hypercholesterolemia is important for identifying additional mechanisms via which PCSK9 can be manipulated, and for choosing patient populations in which PCSK9 inhibitors will be effective. Here, we investigate PCSK9 in two diseases of secondary hyperlipidemia. In nephrotic syndrome, damage to kidney podocytes causes extreme proteinuria and hypercholesterolemia of unclear etiology. We show that plasma cholesterol and PCSK9 are dramatically elevated in mice made nephrotic by nephrotoxic serum treatment or podocyte apoptosis. Moreover, knockout of Pcsk9 protects mice from the effects of nephrotic syndrome on plasma lipids, particularly increased LDL cholesterol. Similarly, nephrotic patients show decreased plasma PCSK9 and cholesterol upon disease remission. Second, loss of adipose tissue in lipodystrophy results in low levels of the hormone leptin. Treatment of lipodystrophic patients with leptin reduces LDL cholesterol through unknown mechanisms. We used this background of hypoleptinemia to investigate the effects of leptin on PCSK9. We found that in female lipodystrophic patients, leptin treatment reduced plasma PCSK9, correlating with decreased LDL cholesterol. Similarly, in male leptin-deficient ob/ob mice, leptin also decreased plasma PCSK9 but did not affect plasma lipids. Our data show that PCSK9 is a novel regulator of hypercholesterolemia in nephrotic syndrome, suggesting that PCSK9 inhibitors may be an important therapy for this patient population with ambiguous treatment options. They also show that leptin can suppress PCSK9 expression, which may explain the observed decreases in LDL cholesterol upon leptin treatment of lipodystrophic patients.