How Cosmic Web Environment Affects Galaxy Quenching Across Cosmic Time

We investigate how cosmic web structures affect galaxy quenching in the IllustrisTNG (TNG-100) cosmological simulations by reconstructing the cosmic web in each snapshot using the DisPerSE framework. We measure the distance from each galaxy with stellar mass log(M*/Msun)>=8 to the nearest node (dnode) and the nearest filament spine (dfil) and study the dependence of both median specific star formation rate () and median gas fraction () on these distances. We find that of galaxies is only dependent on cosmic web environment at z<2, with the dependence increasing with time. At z<=0.5, 8<=log(M*/Msun)<9 galaxies are quenched at dnode<1 Mpc, and significantly star formation-suppressed at dfil<1 Mpc, trends which are driven mostly by satellite galaxies. At z of log(M*/Msun)=10 galaxies actually experience an upturn in at dnode<0.2 Mpc (this is caused by both satellites and centrals). Much of this cosmic web-dependence of star formation activity can be explained by the evolution in . Our results suggest that in the past ~10 Gyr, low-mass satellites are quenched by rapid gas stripping in dense environments near nodes and gradual gas starvation in intermediate-density environments near filaments, while at earlier times cosmic web structures efficiently channeled cold gas into most galaxies. State-of-the-art ongoing spectroscopic surveys such as SDSS and DESI, as well as those planned with JWST and Roman are required to test our predictions against observations.Comment: 5 Figures, 15 pages, submitted to ApJ Letter

Filaments of The Slime Mold Cosmic Web And How They Affect Galaxy Evolution

We present a novel method for identifying cosmic web filaments using the IllustrisTNG (TNG100) cosmological simulations and investigate the impact of filaments on galaxies. We compare the use of cosmic density field estimates from the Delaunay Tessellation Field Estimator (DTFE) and the Monte Carlo Physarum Machine (MCPM), which is inspired by the slime mold organism, in the DisPerSE structure identification framework. The MCPM-based reconstruction identifies filaments with higher fidelity, finding more low-prominence/diffuse filaments and better tracing the true underlying matter distribution than the DTFE-based reconstruction. Using our new filament catalogs, we find that most galaxies are located within 1.5-2.5 Mpc of a filamentary spine, with little change in the median specific star formation rate and the median galactic gas fraction with distance to the nearest filament. Instead, we introduce the filament line density, {\Sigma}fil(MCPM), as the total MCPM overdensity per unit length of a local filament segment, and find that this parameter is a superior predictor of galactic gas supply and quenching. Our results indicate that most galaxies are quenched and gas-poor near high-line density filaments at z10.5 galaxies is mainly driven by mass, while lower-mass galaxies are significantly affected by the filament line density. In high-line density filaments, satellites are strongly quenched, whereas centrals have reduced star formation, but not gas fraction, at z<=0.5. We discuss the prospect of applying our new filament identification method to galaxy surveys with SDSS, DESI, Subaru PFS, etc. to elucidate the effect of large-scale structure on galaxy formation.Comment: Submitted to ApJ, comments welcome. Data available at https://github.com/farhantasy/CosmicWeb-Galaxies

Bulge growth through disk instabilities in high-redshift galaxies

The role of disk instabilities, such as bars and spiral arms, and the associated resonances, in growing bulges in the inner regions of disk galaxies have long been studied in the low-redshift nearby Universe. There it has long been probed observationally, in particular through peanut-shaped bulges. This secular growth of bulges in modern disk galaxies is driven by weak, non-axisymmetric instabilities: it mostly produces pseudo-bulges at slow rates and with long star-formation timescales. Disk instabilities at high redshift (z>1) in moderate-mass to massive galaxies (10^10 to a few 10^11 Msun of stars) are very different from those found in modern spiral galaxies. High-redshift disks are globally unstable and fragment into giant clumps containing 10^8-10^9 Msun of gas and stars each, which results in highly irregular galaxy morphologies. The clumps and other features associated to the violent instability drive disk evolution and bulge growth through various mechanisms, on short timescales. The giant clumps can migrate inward and coalesce into the bulge in a few 10^8 yr. The instability in the very turbulent media drives intense gas inflows toward the bulge and nuclear region. Thick disks and supermassive black holes can grow concurrently as a result of the violent instability. This chapter reviews the properties of high-redshift disk instabilities, the evolution of giant clumps and other features associated to the instability, and the resulting growth of bulges and associated sub-galactic components.Comment: 37 pages, 9 figures. Invited refereed review to appear in "Galactic Bulges", E. Laurikainen, D. Gadotti, R. Peletier (eds.), Springe

Observational Diagnostics of Gas Flows: Insights from Cosmological Simulations

Galactic accretion interacts in complex ways with gaseous halos, including galactic winds. As a result, observational diagnostics typically probe a range of intertwined physical phenomena. Because of this complexity, cosmological hydrodynamic simulations have played a key role in developing observational diagnostics of galactic accretion. In this chapter, we review the status of different observational diagnostics of circumgalactic gas flows, in both absorption (galaxy pair and down-the-barrel observations in neutral hydrogen and metals; kinematic and azimuthal angle diagnostics; the cosmological column density distribution; and metallicity) and emission (Lya; UV metal lines; and diffuse X-rays). We conclude that there is no simple and robust way to identify galactic accretion in individual measurements. Rather, progress in testing galactic accretion models is likely to come from systematic, statistical comparisons of simulation predictions with observations. We discuss specific areas where progress is likely to be particularly fruitful over the next few years.Comment: Invited review to appear in Gas Accretion onto Galaxies, Astrophysics and Space Science Library, eds. A. J. Fox & R. Dave, to be published by Springer. Typos correcte

Determinants of Restaurant Systematic Risk: A Reexamination

This study reexamines determinants of the systematic risk or beta of restaurant firms based on the financial data of 75 U.S. restaurant firms from 1996 through 1999. Our weighted least-squares regression analysis found that restaurant systematic risk correlated negatively with assets turnover but positively with quick ratio. The findings suggest that high efficiency in generating sales revenue helps lower the systematic risk, while excess liquidity tends to increase the risk

Gas Accretion and Star Formation Rates

Cosmological numerical simulations of galaxy evolution show that accretion of metal-poor gas from the cosmic web drives the star formation in galaxy disks. Unfortunately, the observational support for this theoretical prediction is still indirect, and modeling and analysis are required to identify hints as actual signs of star-formation feeding from metal-poor gas accretion. Thus, a meticulous interpretation of the observations is crucial, and this observational review begins with a simple theoretical description of the physical process and the key ingredients it involves, including the properties of the accreted gas and of the star-formation that it induces. A number of observations pointing out the connection between metal-poor gas accretion and star-formation are analyzed, specifically, the short gas consumption time-scale compared to the age of the stellar populations, the fundamental metallicity relationship, the relationship between disk morphology and gas metallicity, the existence of metallicity drops in starbursts of star-forming galaxies, the so-called G dwarf problem, the existence of a minimum metallicity for the star-forming gas in the local universe, the origin of the alpha-enhanced gas forming stars in the local universe, the metallicity of the quiescent BCDs, and the direct measurements of gas accretion onto galaxies. A final section discusses intrinsic difficulties to obtain direct observational evidence, and points out alternative observational pathways to further consolidate the current ideas.Comment: Invited review to appear in Gas Accretion onto Galaxies, Astrophysics and Space Science Library, eds. A. J. Fox & R. Dav\'e, to be published by Springe

The Ubiquitin Peptidase UCHL1 Induces G0/G1 Cell Cycle Arrest and Apoptosis Through Stabilizing p53 and Is Frequently Silenced in Breast Cancer

Background: Breast cancer (BrCa) is a complex disease driven by aberrant gene alterations and environmental factors. Recent studies reveal that abnormal epigenetic gene regulation also plays an important role in its pathogenesis. Ubiquitin carboxyl- terminal esterase L1 (UCHL1) is a tumor suppressor silenced by promoter methylation in multiple cancers, but its role and alterations in breast tumorigenesis remain unclear. Methodology/Principal Findings: We found that UCHL1 was frequently downregulated or silenced in breast cancer cell lines and tumor tissues, but readily expressed in normal breast tissues and mammary epithelial cells. Promoter methylation of UCHL1 was detected in 9 of 10 breast cancer cell lines (90%) and 53 of 66 (80%) primary tumors, but rarely in normal breast tissues, which was statistically correlated with advanced clinical stage and progesterone receptor status. Pharmacologic demethylation reactivated UCHL1 expression along with concomitant promoter demethylation. Ectopic expression of UCHL1 significantly suppressed the colony formation and proliferation of breast tumor cells, through inducing G0/G1 cell cycle arrest and apoptosis. Subcellular localization study showed that UCHL1 increased cytoplasmic abundance of p53. We further found that UCHL1 induced p53 accumulation and reduced MDM2 protein level, and subsequently upregulated the expression of p21, as well as cleavage of caspase3 and PARP, but not in catalytic mutant UCHL1 C90Sexpressed cells

Cross-Platform Array Screening Identifies COL1A2, THBS1, TNFRSF10D and UCHL1 as Genes Frequently Silenced by Methylation in Melanoma

Epigenetic regulation of tumor suppressor genes (TSGs) has been shown to play a central role in melanomagenesis. By integrating gene expression and methylation array analysis we identified novel candidate genes frequently methylated in melanoma. We validated the methylation status of the most promising genes using highly sensitive Sequenom Epityper assays in a large panel of melanoma cell lines and resected melanomas, and compared the findings with those from cultured melanocytes. We found transcript levels of UCHL1, COL1A2, THBS1 and TNFRSF10D were inversely correlated with promoter methylation. For THBS1 and UCHL1 the effect of this methylation on expression was confirmed at the protein level. Identification of these candidate TSGs and future research designed to understand how their silencing is related to melanoma development will increase our understanding of the etiology of this cancer and may provide tools for its early diagnosis

Epigenetic control of the ubiquitin carboxyl terminal hydrolase 1 in renal cell carcinoma

<p>Abstract</p> <p>Background</p> <p>The ubiquitin carboxyl-terminal hydrolase 1 (UCHL1) gene involved in the regulation of cellular ubiquitin levels plays an important role in different cellular processes including cell growth and differentiation. Aberrant expression of UCHL1 has been found in a number of human solid tumors including renal cell carcinoma (RCC). In RCC, UCHL1 overexpression is associated with tumor progression and an altered von Hippel Lindau gene expression.</p> <p>Methods</p> <p>To determine the underlying mechanisms for the heterogeneous UCHL1 expression pattern in RCC the UCHL1 promoter DNA methylation status was determined in 17 RCC cell lines as well as in 32 RCC lesions and corresponding tumor adjacent kidney epithelium using combined bisulfite restriction analysis as well as bisulfite DNA sequencing.</p> <p>Results</p> <p>UCHL1 expression was found in all 32 tumor adjacent kidney epithelium samples. However, the lack of or reduced UCHL1 mRNA and/or protein expression was detected in 13/32 RCC biopsies and 7/17 RCC cell lines and due to either a total or partial methylation of the UCHL1 promoter DNA. Upon 2'-deoxy-5-azacytidine treatment an induction of UCHL1 mRNA and protein expression was found in 9/17 RCC cell lines, which was linked to the demethylation degree of the UCHL1 promoter DNA.</p> <p>Conclusion</p> <p>Promoter hypermethylation represents a mechanism for the silencing of the UCHL1 gene expression in RCC and supports the concept of an epigenetic control for the expression of UCHL1 during disease progression.</p

Quantitative Methylation Profiles for Multiple Tumor Suppressor Gene Promoters in Salivary Gland Tumors

Methylation profiling of tumor suppressor gene (TSGs) promoters is quickly becoming a powerful diagnostic tool for the early detection, prognosis, and even prediction of clinical response to treatment. Few studies address this in salivary gland tumors (SGTs); hence the promoter methylation profile of various TSGs was quantitatively assessed in primary SGT tissue to determine if tumor-specific alterations could be detected.DNA isolated from 78 tumor and 17 normal parotid gland specimens was assayed for promoter methylation status of 19 TSGs by fluorescence-based, quantitative methylation-specific PCR (qMSP). The data were utilized in a binary fashion as well as quantitatively (using a methylation quotient) allowing for better profiling and interpretation of results..Screening promoter methylation profiles in SGTs showed considerable heterogeneity. The methylation status of certain markers was surprisingly high in even normal salivary tissue, confirming the need for such controls. Several TSGs were found to be associated with malignant SGTs, especially SDC. Further study is needed to evaluate the potential use of these associations in the detection, prognosis, and therapeutic outcome of these rare tumors