Description: © The Author(s), 2021. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Long, M. D., Wagner, L. S., King, S. D., Evans, R. L., Mazza, S. E., Byrnes, J. S., Johnson, E. A., Kirby, E., Bezada, M. J., Gazel, E., Miller, S. R., Aragon, J. C., & Liu, S. Evaluating models for lithospheric loss and intraplate volcanism beneath the Central Appalachian Mountains. Journal of Geophysical Research: Solid Earth, 126(10), (2021): e2021JB022571, https://doi.org/10.1029/2021JB022571.

Description: The eastern margin of North America has been shaped by a series of tectonic events including the Paleozoic Appalachian Orogeny and the breakup of Pangea during the Mesozoic. For the past ∼200 Ma, eastern North America has been a passive continental margin; however, there is evidence in the Central Appalachian Mountains for post-rifting modification of lithospheric structure. This evidence includes two co-located pulses of magmatism that post-date the rifting event (at 152 and 47 Ma) along with low seismic velocities, high seismic attenuation, and high electrical conductivity in the upper mantle. Here, we synthesize and evaluate constraints on the lithospheric evolution of the Central Appalachian Mountains. These include tomographic imaging of seismic velocities, seismic and electrical conductivity imaging along the Mid-Atlantic Geophysical Integrative Collaboration array, gravity and heat flow measurements, geochemical and petrological examination of Jurassic and Eocene magmatic rocks, and estimates of erosion rates from geomorphological data. We discuss and evaluate a set of possible mechanisms for lithospheric loss and intraplate volcanism beneath the region. Taken together, recent observations provide compelling evidence for lithospheric loss beneath the Central Appalachians; while they cannot uniquely identify the processes associated with this loss, they narrow the range of plausible models, with important implications for our understanding of intraplate volcanism and the evolution of continental lithosphere. Our preferred models invoke a combination of (perhaps episodic) lithospheric loss via Rayleigh-Taylor instabilities and subsequent small-scale mantle flow in combination with shear-driven upwelling that maintains the region of thin lithosphere and causes partial melting in the asthenosphere.

Description: The authors acknowledge support from the U.S. National Science Foundation EarthScope and GeoPRISMS programs via grants EAR-1460257 (R. L. Evans), EAR-1249412 (E. Gazel), EAR-1249438 (E. A. Johnson), EAR-1250988 (S. D. King), EAR-1251538 (E. Kirby), and EAR-1251515 (M. D. Long). The collection and dissemination of most of the geophysical data and models discussed in this study were facilitated by the Incorporated Research Institutions for Seismology (IRIS). The facilities of the IRIS Consortium are supported by the United States National Science Foundation under Cooperative Agreement EAR-1261681.

Description: The secreted anthrax toxin consists of three components: the protective antigen (PA), edema factor (EF) and lethal factor (LF). LF, a zinc metalloproteinase, compromises the host immune system primarily by targeting mitogen-activated protein kinase kinases in macrophages. Peptide substrates and small-molecule inhibitors bind LF in the space between domains 3 and 4 of the hydrolase. Domain 3 is attached on a hinge to domain 2 via residues Ile300 and Pro385, and can move through an angular arc of greater than 35° in response to the binding of different ligands. Here, multiple LF structures including five new complexes with co-crystallized inhibitors are compared and three frequently populated LF conformational states termed `bioactive', `open' and `tight' are identified. The bioactive position is observed with large substrate peptides and leaves all peptide-recognition subsites open and accessible. The tight state is seen in unliganded and small-molecule complex structures. In this state, domain 3 is clamped over certain substrate subsites, blocking access. The open position appears to be an intermediate state between these extremes and is observed owing to steric constraints imposed by specific bound ligands. The tight conformation may be the lowest-energy conformation among the reported structures, as it is the position observed with no bound ligand, while the open and bioactive conformations are likely to be ligand-induced.

Description: The solubility of OH in pure synthetic rutile was experimentally constrained at 0.5-2.0 GPa and 500-900 {degrees}C, in equilibrium with four oxygen fugacity (fO2) buffering mineral assemblages: hematite-magnetite (HM), nickel-nickel oxide (NNO), cobalt-cobalt oxide (CCO), and iron-wustite (IW). The hydroxyl concentration ([OH], in parts per million H2O by weight) of equilibrated rutile crystals was characterized by FTIR spectroscopy. Measurements at 1 GPa at individual fO2 buffers demonstrate that [OH] in rutile depends strongly on temperature: at HM, [OH] increases from 48 to 267 ppm as temperature rises from 500 to 900 {degrees}C, whereas at NNO, [OH] increases from 108 to 956 ppm over the same temperature range. The [OH] in rutile also increases strongly with decreasing fO2 at any pressure and temperature, and exhibits a slight, linear, positive dependence on pressure at a given temperature and fO2. The observed systematic dependences on pressure, temperature, and fO2 indicate that hydrogen substitutes into rutile as hydroxyl, (OH), via forward progress of the reaction Ti4+O2 + [1/2]H2O = Ti3+O(OH) + [1/4]O2. Our measured [OH] values are significantly greater than those determined in previous studies on finer-grained, polycrystalline rutile, which likely suffered diffusive loss of H during quenching. This is supported by our observation of narrow, OH-depleted rims on otherwise high-OH run products, pointing to minor but important diffusive H loss from crystal rims during quenching. Fitting of isothermal variations in composition with fO2 at 1 GPa and temperature indicates nearly ideal, multi-site mixing of the TiO2-TiOOH solid solution. A fit to the entire data set suggests standard volume, enthalpy, and entropy of the hydration reaction of, respectively, 1.90 {+/-} 0.48 cm3/mol, 219.3 {+/-} 1.3 kJ/mol, and 19.9 {+/-} 1.4 J/(mol{middle dot}K) (1{sigma} uncertainty). These constraints form the basis for use of [OH] in rutile as a thermobarometer and oxybarometer in experimental and natural systems. The moderate to high [OH] in nominally anhydrous rutile at all investigated temperatures, pressures, and fO2 values imply that Ti3+ may be higher than previously suspected in some terrestrial geologic settings.

Description: IJERPH, Vol. 15, Pages 632: Burden and Risk Factors for Cold-Related Illness and Death in New York City International Journal of Environmental Research and Public Health doi: 10.3390/ijerph15040632 Authors: Kathryn Lane Kazuhiko Ito Sarah Johnson Elizabeth A. Gibson Andrew Tang Thomas Matte Exposure to cold weather can cause cold-related illness and death, which are preventable. To understand the current burden, risk factors, and circumstances of exposure for illness and death directly attributed to cold, we examined hospital discharge, death certificate, and medical examiner data during the cold season from 2005 to 2014 in New York City (NYC), the largest city in the United States. On average each year, there were 180 treat-and-release emergency department visits (average annual rate of 21.6 per million) and 240 hospital admissions (29.6 per million) for cold-related illness, and 15 cold-related deaths (1.8 per million). Seventy-five percent of decedents were exposed outdoors. About half of those exposed outdoors were homeless or suspected to be homeless. Of the 25% of decedents exposed indoors, none had home heat and nearly all were living in single-family or row homes. The majority of deaths and illnesses occurred outside of periods of extreme cold. Unsheltered homeless individuals, people who use substances and become incapacitated outdoors, and older adults with medical and psychiatric conditions without home heat are most at risk. This information can inform public health prevention strategies and interventions.

Description: BACKGROUND There is conflicting evidence regarding the benefit of postmastectomy radiation therapy (PMRT) for pathologic stage T3N0M0 breast cancers. We analyzed data from the Surveillance, Epidemiology, and End Results (SEER) database to investigate the benefit of PMRT in this patient population. METHODS We queried the SEER database for T3N0M0 breast cancer patients diagnosed from 2000 to 2010 who underwent modified radical mastectomy. We excluded males, patients with unknown radiation timing/type, other primary tumors, and survival 〈6 months. A total of 2525 patients were included in the analysis. We performed univariate and multivariate statistical analysis using chi-square tests, log-rank tests, and Cox proportional hazards regression. The primary endpoints were overall survival (OS) and cancer-specific survival (CSS). RESULTS Of the 2525 patients identified, 1063 received PMRT. The median follow-up was 56 months (range, 6-131 months). On univariate analysis, PMRT improved OS (76.5% vs 61.8%, P 〈.01) and CSS (85.0% vs 82.4%, P 〈.01) at 8 years. The use of PMRT remained significant on multivariate analysis: PMRT improved OS (hazard ratio 0.63, P 〈.001) and CSS (hazard ratio 0.77, P  = .045). Low tumor grade ( P 〈.01) and marital status of “married” ( P  = .01) also was a predictor of improved CSS on multivariate analysis. CONCLUSIONS PMRT was associated with significant improvements in both CSS and OS in patients with T3N0M0 breast cancers treated with modified radical mastectomy from 2000 to 2010. PMRT should be strongly considered in T3N0M0 patients. Postmastectomy radiation therapy is associated with significant improvements in overall and cause-specific survival in patients with T3N0M0 breast cancers treated with modified radical mastectomy from 2000 to 2010 in the SEER database. Postmastectomy radiation therapy should be strongly considered for patients who have T3N0M0 tumors. Cancer 2014. © 2014 American Cancer Society .