The Stripe 82 Massive Galaxy Project III: A Lack of Growth Among Massive Galaxies

The average stellar mass (Mstar) of high-mass galaxies (Mstar > 3e11 Msun) is expected to grow by ~30% since z~1, largely through ongoing mergers that are also invoked to explain the observed increase in galaxy sizes. Direct evidence for the corresponding growth in stellar mass has been elusive, however, in part because the volumes sampled by previous redshift surveys have been too small to yield reliable statistics. In this work, we make use of the Stripe 82 Massive Galaxy Catalog to build a mass-limited sample of 41,770 galaxies (Mstar > 1.6e11) with optical to near-IR photometry and a large fraction (>55%) of spectroscopic redshifts. Our sample spans 139 square degrees, significantly larger than most previous efforts. After accounting for a number of potential systematic errors, including the effects of Mstar scatter, we measure galaxy stellar mass functions over 0.3 < z < 0.65 and detect no growth in the typical Mstar of massive galaxies with an uncertainty of 9%. This confidence level is dominated by uncertainties in the star formation history assumed for Mstar estimates, although our inability to characterize low surface-brightness outskirts may be the most important limitation of our study. Even among these high-mass galaxies, we find evidence for differential evolution when splitting the sample by recent star formation (SF) activity. While low-SF systems appear to become completely passive, we find a mostly sub-dominant population of galaxies with residual, but low rates of star formation (~1 Msun/yr) number density does not evolve. Interestingly, these galaxies become more prominent at higher Mstar, representing ~10% of all galaxies at Mstar ~ 1e12 Msun and perhaps dominating at even larger masses.Comment: Accepted in Ap

Capturing Experiential Learning in a Program by Curriculum Mapping

Like many higher education institutions, amplifying experiential learning (EL) is a priority for the University of Calgary. In order to capture the extent and complexity of EL that exists in an institution, it is crucial to have a common understanding of the concept. In 2018, the University of Calgary created the EL Working Group, tasked with creating a definition of EL and framework unique to our institutional context. One way to capture EL across a program of study is through curriculum mapping. By identifying where EL already exists, a group can determine current strengths as well as how to improve EL offerings in future. In the example provided in our paper, we show the results of one such mapping process and provide recommendations for others considering using this process for capturing EL across a program of study

The Stripe 82 Massive Galaxy Project II: Stellar Mass Completeness of Spectroscopic Galaxy Samples from the Baryon Oscillation Spectroscopic Survey

The Baryon Oscillation Spectroscopic Survey (BOSS) has collected spectra for over one million galaxies at $0.15<z<0.7$ over a volume of 15.3 Gpc$^3$ (9,376 deg$^2$) -- providing us an opportunity to study the most massive galaxy populations with vanishing sample variance. However, BOSS samples are selected via complex color cuts that are optimized for cosmology studies, not galaxy science. In this paper, we supplement BOSS samples with photometric redshifts from the Stripe 82 Massive Galaxy Catalog and measure the total galaxy stellar mass function (SMF) at $z\sim0.3$ and $z\sim0.55$. With the total SMF in hand, we characterize the stellar mass completeness of BOSS samples. The high-redshift CMASS ("constant mass") sample is significantly impacted by mass incompleteness and is 80% complete at $\log_{10}(M_*/M_{\odot}) >11.6$ only in the narrow redshift range $z=[0.51,0.61]$. The low redshift LOWZ sample is 80% complete at $\log_{10}(M_*/M_{\odot}) >11.6$ for $z=[0.15,0.43]$. To construct mass complete samples at lower masses, spectroscopic samples need to be significantly supplemented by photometric redshifts. This work will enable future studies to better utilize the BOSS samples for galaxy-formation science.Comment: 18 pages, 17 figures, 5 table

Arabidopsis ETO1 specifically interacts with and negatively regulates type 2 1-aminocyclopropane-1-carboxylate synthases

BACKGROUND: In Arabidopsis, ETO1 (ETHYLENE-OVERPRODUCER1) is a negative regulator of ethylene evolution by interacting with AtACS5, an isoform of the rate-limiting enzyme, 1-aminocyclopropane-1-carboxylate synthases (ACC synthase or ACS), in ethylene biosynthetic pathway. ETO1 directly inhibits the enzymatic activity of AtACS5. In addition, a specific interaction between ETO1 and AtCUL3, a constituent of a new type of E3 ubiquitin ligase complex, suggests the molecular mechanism in promoting AtACS5 degradation by the proteasome-dependent pathway. Because orthologous sequences to ETO1 are found in many plant species including tomato, we transformed tomato with Arabidopsis ETO1 to evaluate its ability to suppress ethylene production in tomato fruits. RESULTS: Transgenic tomato lines that overexpress Arabidopsis ETO1 (ETO1-OE) did not show a significant delay of fruit ripening. So, we performed yeast two-hybrid assays to investigate potential heterologous interaction between ETO1 and three isozymes of ACC synthases from tomato. In the yeast two-hybrid system, ETO1 interacts with LE-ACS3 as well as AtACS5 but not with LE-ACS2 or LE-ACS4, two major isozymes whose gene expression is induced markedly in ripening fruits. According to the classification of ACC synthases, which is based on the C-terminal amino acid sequences, both LE-ACS3 and AtACS5 are categorized as type 2 isozymes and possess a consensus C-terminal sequence. In contrast, LE-ACS2 and LE-ACS4 are type 1 and type 3 isozymes, respectively, both of which do not possess this specific C-terminal sequence. Yeast two-hybrid analysis using chimeric constructs between LE-ACS2 and LE-ACS3 revealed that the type-2-ACS-specific C-terminal tail is required for interaction with ETO1. When treated with auxin to induce LE-ACS3, seedlings of ETO1-OE produced less ethylene than the wild type, despite comparable expression of the LE-ACS3 gene in the wild type. CONCLUSION: These results suggest that ETO1 family proteins specifically interact with and negatively regulate type 2 ACC synthases. Our data also show that Arabidopsis ETO1 can regulate type 2 ACS in a heterologous plant, tomato

Evolution of the Automotive Body Coating Process—A Review

Automotive coatings and the processes used to coat automobile surfaces exemplify the avant-garde of technologies that are capable of producing durable surfaces, exceeding customers’ expectations of appearance, maximizing efficiency, and meeting environmental regulations. These accomplishments are rooted in 100 years of experience, trial-and-error approaches, technique and technology advancements, and theoretical assessments. Because of advancements directed at understanding the how, why, when, and where of automobile coatings, the progress in controlling droplets and their deposition attributes, and the development of new technologies and paint chemistries, a comprehensive and up-to-date review of automobile coatings and coating technologies was considered to be of value to industrial practitioners and researchers. Overall, the critical performance factors driving the development and use of advanced automotive coatings and coating technologies are (a) aesthetic characteristics; (b) corrosion protection; (c) mass production; (d) cost and environmental requirements; and (e) appearance and durability. Although the relative importance of each of these factors is debatable, the perfection of any one at the expense of another would be unacceptable. Hence, new developments in automotive coatings are described and discussed in the following review, and then related to improvements in production technologies and paints. Modern automotive coating procedures are also discussed in detail. Finally, an extrapolation into the future of automotive coating is offered with a view of the developments and technologies needed for an increasingly efficient and more sustainable coatings industry

The Stripe 82 Massive Galaxy Project. I. Catalog Construction

The Stripe 82 Massive Galaxy Catalog (S82-MGC) is the largest-volume stellar mass-limited sample of galaxies beyond z ≈ 0.1 constructed to date. Spanning 139.4 deg2, the S82-MGC includes a mass-limited sample of 41,770 galaxies with log M*/M⊙ ≳ 11.2 to z ≈ 0.7, sampling a volume of 0.3 Gpc3, roughly equivalent to the volume of the Sloan Digital Sky Survey-I/II (SDSS-I/II) z \u3c 0.15 main sample. The catalog is built on three pillars of survey data: the SDSS Stripe 82 Coadd photometry which reaches r-band magnitudes of ∼23.5 AB, Y JHK photometry at depths of 20th magnitude (AB) from the UK Infrared Deep Sky Survey Large Area Survey, and over 70,000 spectroscopic galaxy redshifts from the SDSS-I/II and the Baryon Oscillation Spectroscopic Survey. We describe the catalog construction and verification, the production of 9-band matched aperture photometry, tests of existing and newly estimated photometric redshifts required to supplement spectroscopic redshifts for 55% of the log M*/M⊙ ≳ 11.2 sample, and geometric masking. We provide near-IR based stellar mass estimates and compare these to previous estimates. All catalog products are made publicly available. The S82-MGC not only addresses previous statistical limitations in high-mass galaxy evolution studies, but also begins tackling inherent data challenges in the coming era of wide-field imaging surveys

Thioredoxin-1 maintains mechanistic target of rapamycin (mTOR) function during oxidative stress in cardiomyocytes

Thioredoxin 1 (Trx1) is a 12-kDa oxidoreductase that catalyzes thiol-disulfide exchange reactions to reduce proteins with disulfide bonds. As such, Trx1 helps protect the heart against stresses, such as ischemia and pressure overload. Mechanistic target of rapamycin (mTOR) is a serine/threonine kinase that regulates cell growth, metabolism, and survival. We have shown previously that mTOR activity is increased in response to myocardial ischemia-reperfusion injury. However, whether Trx1 interacts with mTOR to preserve heart function remains unknown. Using a substrate-trapping mutant of Trx1 (Trx1C35S), we show here that mTOR is a direct interacting partner of Trx1 in the heart. In response to H2O2 treatment in cardiomyocytes, mTOR exhibited a high molecular weight shift in non-reducing SDS-PAGE in a 2-mercaptoethanol-sensitive manner, suggesting that mTOR is oxidized and forms disulfide bonds with itself or other proteins. The mTOR oxidation was accompanied by reduced phosphorylation of endogenous substrates, such as S6 kinase (S6K) and 4E-binding protein 1 (4E-BP1) in cardiomyocytes. Immune complex kinase assays disclosed that H2O2 treatment diminished mTOR kinase activity, indicating that mTOR is inhibited by oxidation. Of note, Trx1 overexpression attenuated both H2O2-mediated mTOR oxidation and inhibition, whereas Trx1 knockdown increased mTOR oxidation and inhibition. Moreover, Trx1 normalized H2O2-induced down-regulation of metabolic genes and stimulation of cell death, and an mTOR inhibitor abolished Trx1-mediated rescue of gene expression. H2O2-induced oxidation and inhibition of mTOR were attenuated when Cys-1483 of mTOR was mutated to phenylalanine. These results suggest that Trx1 protects cardiomyocytes against stress by reducing mTOR at Cys-1483, thereby preserving the activity of mTOR and inhibiting cell death

A stoichiometric complex of neurexins and dystroglycan in brain

In nonneuronal cells, the cell surface protein dystroglycan links the intracellular cytoskeleton (via dystrophin or utrophin) to the extracellular matrix (via laminin, agrin, or perlecan). Impairment of this linkage is instrumental in the pathogenesis of muscular dystrophies. In brain, dystroglycan and dystrophin are expressed on neurons and astrocytes, and some muscular dystrophies cause cognitive dysfunction; however, no extracellular binding partner for neuronal dystroglycan is known. Regular components of the extracellular matrix, such as laminin, agrin, and perlecan, are not abundant in brain except in the perivascular space that is contacted by astrocytes but not by neurons, suggesting that other ligands for neuronal dystroglycan must exist. We have now identified α- and β-neurexins, polymorphic neuron-specific cell surface proteins, as neuronal dystroglycan receptors. The extracellular sequences of α- and β-neurexins are largely composed of laminin-neurexin–sex hormone–binding globulin (LNS)/laminin G domains, which are also found in laminin, agrin, and perlecan, that are dystroglycan ligands. Dystroglycan binds specifically to a subset of the LNS domains of neurexins in a tight interaction that requires glycosylation of dystroglycan and is regulated by alternative splicing of neurexins. Neurexins are receptors for the excitatory neurotoxin α-latrotoxin; this toxin competes with dystroglycan for binding, suggesting overlapping binding sites on neurexins for dystroglycan and α-latrotoxin. Our data indicate that dystroglycan is a physiological ligand for neurexins and that neurexins' tightly regulated interaction could mediate cell adhesion between brain cells

Assessing Sex-Specific Circadian, Metabolic, and Cognitive Phenotypes in the AβPP/PS1 and APPNL-F/NL-F Models of Alzheimer\u27s Disease.

BACKGROUND: Circadian disruption has long been recognized as a symptom of Alzheimer\u27s disease (AD); however, emerging data suggests that circadian dysfunction occurs early on in disease development, potentially preceding any noticeable cognitive deficits. OBJECTIVE: This study compares the onset of AD in male and female wild type (C57BL6/J), transgenic (AβPP/PS1), and knock-in (APPNL-F/NL-F) AD mouse models from the period of plaque initiation (6 months) through 12 months. METHODS: Rhythmic daily activity patterns, glucose sensitivity, cognitive function (Morris water maze, MWM), and AD pathology (plaques formation) were assessed. A comparison was made across sexes. RESULTS: Sex-dependent hyperactivity in AβPP/PS1 mice was observed. In comparison to C57BL/6J animals, 6-month-old male AβPP/PS1 demonstrated nighttime hyperactivity, as did 12-month-old females. Female AβPP/PS1 animals performed significantly worse on a MWM task than AβPP/PS1 males at 12 months and trended toward increased plaque pathology. APPNL-F/NL-F 12-month-old males performed significantly worse on the MWM task compared to 12-month-old females. Significantly greater plaque pathology occurred in AβPP/PS1 animals as compared to APPNL-F/NL-F animals. Female AβPP/PS1 animals performed significantly worse than APPNL-F/NL-F animals in spatial learning and memory tasks, though this was reversed in males. CONCLUSION: Taken together, this study provides novel insights into baseline sex differences, as well as characterizes baseline diurnal activity variations, in the AβPP/PS1 and APPNL-F/NL-F AD mouse models