The Space Density of Intermediate-redshift, Extremely Compact, Massive Starburst Galaxies

© 2022. The Author(s). Published by the American Astronomical Society. This is an open access article distributed under the Creative Commons Attribution License, to view a copy of the license, see: https://creativecommons.org/licenses/by/4.0/https://creativecommons.org/licenses/by/4.0/We present a measurement of the intrinsic space density of intermediate-redshift (z ∼ 0.5), massive (M * ∼ 1011 M ⊙), compact (R e ∼ 100 pc) starburst (ΣSFR ∼ 1000 M ⊙ yr−1 kpc−1) galaxies with tidal features indicative of them having undergone recent major mergers. A subset of them host kiloparsec-scale, > 1000 km s−1 outflows and have little indication of AGN activity, suggesting that extreme star formation can be a primary driver of large-scale feedback. The aim for this paper is to calculate their space density so we can place them in a better cosmological context. We do this by empirically modeling the stellar populations of massive, compact starburst galaxies. We determine the average timescale on which galaxies that have recently undergone an extreme nuclear starburst would be targeted and included in our spectroscopically selected sample. We find that massive, compact starburst galaxies targeted by our criteria would be selectable for ∼148−24+27 Myr and have an intrinsic space density nCS∼(1.1−0.3+0.5)×10−6Mpc−3 . This space density is broadly consistent with our z ∼ 0.5 compact starbursts being the most extremely compact and star-forming low-redshift analogs of the compact star-forming galaxies in the early universe, as well as them being the progenitors to a fraction of intermediate-redshift, post-starburst, and compact quiescent galaxies.Peer reviewe

Kinematics, Structure, and Mass Outflow Rates of Extreme Starburst Galactic Outflows

We present results on the properties of extreme gas outflows in massive ($\rm M_* \sim$10$^{11} \ \rm M_{\odot}$), compact, starburst ($\rm SFR \sim$$200 \, \rm M_{\odot} \ yr^{-1}$) galaxies at z = $0.4-0.7$ with very high star formation surface densities ($\rm \Sigma_{SFR} \sim$$2000 \,\rm M_{\odot} \ yr^{-1} \ kpc^{-2}$). Using optical Keck/HIRES spectroscopy of 14 HizEA starburst galaxies we identify outflows with maximum velocities of$820 - 2860 \kmps. High-resolution spectroscopy allows us to measure precise column densities and covering fractions as a function of outflow velocity and characterize the kinematics and structure of the cool gas outflow phase (T \sim$10$^4 K). We find substantial variation in the absorption profiles, which likely reflects the complex morphology of inhomogeneously-distributed, clumpy gas and the intricacy of the turbulent mixing layers between the cold and hot outflow phases. There is not a straightforward correlation between the bursts in the galaxies' star formation histories and their wind absorption line profiles, as might naively be expected for starburst-driven winds. The lack of strong \mgii \ absorption at the systemic velocity is likely an orientation effect, where the observations are down the axis of a blowout. We infer high mass outflow rates of \rm \sim$50$-$2200$\rm M_{\odot} \, yr^{-1}$, assuming a fiducial outflow size of 5 kpc, and mass loading factors of$\eta\sim$5 for most of the sample.$\eta\sim$20 for two galaxies. While these values have high uncertainties, they suggest that starburst galaxies are capable of ejecting very large amounts of cool gas that will substantially impact their future evolution.Comment: Accepted for publication in The Astrophysical Journa

The Ionization and Dynamics of the Makani Galactic Wind

© 2023 The Author(s). Published by the American Astronomical Society. This is an open access article distributed under the Creative Commons Attribution License, to view a copy of the license, see: https://creativecommons.org/licenses/by/4.0/The Makani galaxy hosts the poster child of a galactic wind on scales of the circumgalactic medium. It consists of a two-episode wind in which the slow, outer wind originated 400 Myr ago (Episode I; R I = 20 − 50 kpc) and the fast, inner wind is 7 Myr old (Episode II; R II = 0 − 20 kpc). While this wind contains ionized, neutral, and molecular gas, the physical state and mass of the most extended phase—the warm, ionized gas—are unknown. Here we present Keck optical spectra of the Makani outflow. These allow us to detect hydrogen lines out to r = 30–40 kpc and thus constrain the mass, momentum, and energy in the wind. Many collisionally excited lines are detected throughout the wind, and their line ratios are consistent with 200–400 km s−1 shocks that power the ionized gas, with v shock = σ wind. Combining shock models, density-sensitive line ratios, and mass and velocity measurements, we estimate that the ionized mass and outflow rate in the Episode II wind could be as high as those of the molecular gas: MIIHII∼MIIH2=(1−2)×109M⊙ and dM/dtIIHII∼dM/dtIIH2=170−250M⊙ yr−1. The outer wind has slowed, so that dM/dtIHII∼10M⊙ yr−1, but it contains more ionized gas, MIHII=5×109 M ⊙. The momentum and energy in the recent Episode II wind imply a momentum-driven flow (p “boost” ∼7) driven by the hot ejecta and radiation pressure from the Eddington-limited, compact starburst. Much of the energy and momentum in the older Episode I wind may reside in a hotter phase, or lie further into the circumgalactic medium.Peer reviewe

Physical Properties of Massive Compact Starburst Galaxies with Extreme Outflows

© 2021. The Author(s). Published by the American Astronomical Society. This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 licence. https://creativecommons.org/licenses/by/4.0/We present results on the nature of extreme ejective feedback episodes and the physical conditions of a population of massive (M * ∼ 1011 M ⊙), compact starburst galaxies at z = 0.4–0.7. We use data from Keck/NIRSPEC, SDSS, Gemini/GMOS, MMT, and Magellan/MagE to measure rest-frame optical and near-IR spectra of 14 starburst galaxies with extremely high star formation rate surface densities (mean ΣSFR ∼ 2000 M ⊙ yr−1 kpc−2) and powerful galactic outflows (maximum speeds v 98 ∼ 1000–3000 km s−1). Our unique data set includes an ensemble of both emission ([O ii] λλ3726,3729, Hβ, [O iii] λλ4959,5007, Hα, [N ii] λλ6549,6585, and [S ii] λλ6716,6731) and absorption (Mg ii λλ2796,2803, and Fe ii λ2586) lines that allow us to investigate the kinematics of the cool gas phase (T ∼ 104 K) in the outflows. Employing a suite of line ratio diagnostic diagrams, we find that the central starbursts are characterized by high electron densities (median n e ∼ 530 cm−3), and high metallicity (solar or supersolar). We show that the outflows are most likely driven by stellar feedback emerging from the extreme central starburst, rather than by an AGN. We also present multiple intriguing observational signatures suggesting that these galaxies may have substantial Lyman continuum (LyC) photon leakage, including weak [S ii] nebular emission lines. Our results imply that these galaxies may be captured in a short-lived phase of extreme star formation and feedback where much of their gas is violently blown out by powerful outflows that open up channels for LyC photons to escape.Peer reviewedFinal Published versio

Elevated frequencies of leukemic myeloid and plasmacytoid dendritic cells in acute myeloid leukemia with the FLT3 internal tandem duplication

Some 30% of acute myeloid leukemia (AML) patients display an internal tandem duplication (ITD) mutation in the FMS-like tyrosine kinase 3 (FLT3) gene. FLT3-ITDs are known to drive hematopoietic stem cells towards FLT3 ligand independent growth, but the effects on dendritic cell (DC) differentiation during leukemogenesis are not clear. We compared the frequency of cells with immunophenotype of myeloid DC (mDC: Lin−, HLA-DR+, CD11c+, CD86+) and plasmacytoid DC (pDC: Lin−, HLA-DR+, CD123+, CD86+) in diagnostic samples of 47 FLT3-ITD− and 40 FLT3-ITD+ AML patients. The majority of ITD+ AML samples showed high frequencies of mDCs or pDCs, with significantly decreased HLA-DR expression compared with DCs detectable in ITD− AML samples. Interestingly, mDCs and pDCs sorted out from ITD+ AML samples contained the ITD insert revealing their leukemic origin and, upon ex vivo culture with cytokines, they acquired DC morphology. Notably, mDC/pDCs were detectable concurrently with single lineage mDCs and pDCs in all ITD+ AML (n = 11) and ITD− AML (n = 12) samples analyzed for mixed lineage DCs (Lin−, HLA-DR+, CD11c+, CD123+). ITD+ AML mDCs/pDCs could be only partially activated with CD40L and CpG for production of IFN-α, TNF-α, and IL-1α, which may affect the anti-leukemia immune surveillance in the course of disease progression

Cancer Stem Cells and Side Population Cells in Breast Cancer and Metastasis

In breast cancer it is never the primary tumour that is fatal; instead it is the development of metastatic disease which is the major cause of cancer related mortality. There is accumulating evidence that suggests that Cancer Stem Cells (CSC) may play a role in breast cancer development and progression. Breast cancer stem cell populations, including side population cells (SP), have been shown to be primitive stem cell-like populations, being long-lived, self-renewing and highly proliferative. SP cells are identified using dual wavelength flow cytometry combined with Hoechst 33342 dye efflux, this ability is due to expression of one or more members of the ABC transporter family. They have increased resistance to chemotherapeutic agents and apoptotic stimuli and have increased migratory potential above that of the bulk tumour cells making them strong candidates for the metastatic spread of breast cancer. Treatment of nearly all cancers usually involves one first-line agent known to be a substrate of an ABC transporter thereby increasing the risk of developing drug resistant tumours. At present there is no marker available to identify SP cells using immunohistochemistry on breast cancer patient samples. If SP cells do play a role in breast cancer progression/Metastatic Breast Cancer (MBC), combining chemotherapy with ABC inhibitors may be able to destroy both the cells making up the bulk tumour and the cancer stem cell population thus preventing the risk of drug resistant disease, recurrence or metastasis

Histology of the Pharyngeal Constrictor Muscle in 22q11.2 Deletion Syndrome and Non-Syndromic Children with Velopharyngeal Insufficiency

Plastic surgeons aim to correct velopharyngeal insufficiency manifest by hypernasal speech with a velopharyngoplasty. The functional outcome has been reported to be worse in patients with 22q11.2 deletion syndrome than in patients without the syndrome. A possible explanation is the hypotonia that is often present as part of the syndrome. To confirm a myogenic component of the etiology of velopharyngeal insufficiency in children with 22q11.2 deletion syndrome, specimens of the pharyngeal constrictor muscle were taken from children with and without the syndrome. Histologic properties were compared between the groups. Specimens from the two groups did not differ regarding the presence of increased perimysial or endomysial space, fiber grouping by size or type, internalized nuclei, the percentage type I fibers, or the diameters of type I and type II fibers. In conclusion, a myogenic component of the etiology of velopharyngeal insufficiency in children with 22q11.2 deletion syndrome could not be confirmed

Histone Deacetylase Inhibitor Romidepsin Induces HIV Expression in CD4 T Cells from Patients on Suppressive Antiretroviral Therapy at Concentrations Achieved by Clinical Dosing

Persistent latent reservoir of replication-competent proviruses in memory CD4 T cells is a major obstacle to curing HIV infection. Pharmacological activation of HIV expression in latently infected cells is being explored as one of the strategies to deplete the latent HIV reservoir. In this study, we characterized the ability of romidepsin (RMD), a histone deacetylase inhibitor approved for the treatment of T-cell lymphomas, to activate the expression of latent HIV. In an in vitro T-cell model of HIV latency, RMD was the most potent inducer of HIV (EC50 = 4.5 nM) compared with vorinostat (VOR; EC50 = 3,950 nM) and other histone deacetylase (HDAC) inhibitors in clinical development including panobinostat (PNB; EC50 = 10 nM). The HIV induction potencies of RMD, VOR, and PNB paralleled their inhibitory activities against multiple human HDAC isoenzymes. In both resting and memory CD4 T cells isolated from HIV-infected patients on suppressive combination antiretroviral therapy (cART), a 4-hour exposure to 40 nM RMD induced a mean 6-fold increase in intracellular HIV RNA levels, whereas a 24-hour treatment with 1 μM VOR resulted in 2- to 3-fold increases. RMD-induced intracellular HIV RNA expression persisted for 48 hours and correlated with sustained inhibition of cell-associated HDAC activity. By comparison, the induction of HIV RNA by VOR and PNB was transient and diminished after 24 hours. RMD also increased levels of extracellular HIV RNA and virions from both memory and resting CD4 T-cell cultures. The activation of HIV expression was observed at RMD concentrations below the drug plasma levels achieved by doses used in patients treated for T-cell lymphomas. In conclusion, RMD induces HIV expression ex vivo at concentrations that can be achieved clinically, indicating that the drug may reactivate latent HIV in patients on suppressive cART