Past and future sea-level change from the surface mass balance of glaciers

We present estimates of sea-level change caused by the global surface mass balance of glaciers, based on the reconstruction and projection of the surface mass balance of all the individual glaciers of the world, excluding the ice sheets in Greenland and Antarctica. The model is validated using a leave-one-glacier-out cross-validation scheme against 3997 observed surface mass balances of 255 glaciers, and against 756 geodetically observed, temporally integrated volume and surface area changes of 341 glaciers. When forced with observed monthly precipitation and temperature data, the glaciers of the world are reconstructed to have lost mass corresponding to 114 ± 5 mm sea-level equivalent (SLE) between 1902 and 2009. Using projected temperature and precipitation anomalies from 15 coupled general circulation models from the Coupled Model Intercomparison Project phase 5 (CMIP5) ensemble, they are projected to lose an additional 148 ± 35 mm SLE (scenario RCP26), 166 ± 42 mm SLE (scenario RCP45), 175 ± 40 mm SLE (scenario RCP60), or 217 ± 47 mm SLE (scenario RCP85) during the 21st century. Based on the extended RCP scenarios, glaciers are projected to approach a new equilibrium towards the end of the 23rd century, after having lost either 248 ± 66 mm SLE (scenario RCP26), 313 ± 50 mm SLE (scenario RCP45), or 424 ± 46 mm SLE (scenario RCP85). Up until approximately 2100, ensemble uncertainty within each scenario is the biggest source of uncertainty for the future glacier mass loss; after that, the difference between the scenarios takes over as the biggest source of uncertainty. Ice mass loss rates are projected to peak 2040 ∼ 2050 (RCP26), 2050 ∼ 2060 (RCP45), 2070 ∼ 2090 (RCP60), or 2070 ∼ 2100 (RCP85)

Folding-competent and folding-defective forms of Ricin A chain have different fates following retrotranslocation from the endoplasmic reticulum

We report that a toxic polypeptide retaining the potential to refold upon dislocation from the endoplasmic reticulum (ER) to the cytosol (ricin A chain; RTA) and a misfolded version that cannot (termed RTAΔ), follow ER-associated degradation (ERAD) pathways in Saccharomyces cerevisiae that substantially diverge in the cytosol. Both polypeptides are dislocated in a step mediated by the transmembrane Hrd1p ubiquitin ligase complex and subsequently degraded. Canonical polyubiquitylation is not a prerequisite for this interaction because a catalytically inactive Hrd1p E3 ubiquitin ligase retains the ability to retrotranslocate RTA, and variants lacking one or both endogenous lysyl residues also require the Hrd1p complex. In the case of native RTA, we established that dislocation also depends on other components of the classical ERAD-L pathway as well as an ongoing ER–Golgi transport. However, the dislocation pathways deviate strikingly upon entry into the cytosol. Here, the CDC48 complex is required only for RTAΔ, although the involvement of individual ATPases (Rpt proteins) in the 19S regulatory particle (RP) of the proteasome, and the 20S catalytic chamber itself, is very different for the two RTA variants. We conclude that cytosolic ERAD components, particularly the proteasome RP, can discriminate between structural features of the same substrate

BAT3 Guides Misfolded Glycoproteins Out of the Endoplasmic Reticulum

Secretory and membrane proteins that fail to acquire their native conformation within the lumen of the Endoplasmic Reticulum (ER) are usually targeted for ubiquitin-dependent degradation by the proteasome. How partially folded polypeptides are kept from aggregation once ejected from the ER into the cytosol is not known. We show that BAT3, a cytosolic chaperone, is recruited to the site of dislocation through its interaction with Derlin2. Furthermore, we observe cytoplasmic BAT3 in a complex with a polypeptide that originates in the ER as a glycoprotein, an interaction that depends on the cytosolic disposition of both, visualized even in the absence of proteasomal inhibition. Cells depleted of BAT3 fail to degrade an established dislocation substrate. We thus implicate a cytosolic chaperone as an active participant in the dislocation of ER glycoproteins.United States. National Institutes of HealthBoehringer Ingelheim Fond

Gradual caldera collapse at Bárdarbunga volcano, Iceland, regulated by lateral magma outflow

Large volcanic eruptions on Earth commonly occur with a collapse of the roof of a crustal magma reservoir, forming a caldera. Only a few such collapses occur per century, and the lack of detailed observations has obscured insight into the mechanical interplay between collapse and eruption.We usemultiparameter geophysical and geochemical data to show that the 110-squarekilometer and 65-meter-deep collapse of Bárdarbunga caldera in 2014-2015 was initiated through withdrawal of magma, and lateral migration through a 48-kilometers-long dike, from a 12-kilometers deep reservoir. Interaction between the pressure exerted by the subsiding reservoir roof and the physical properties of the subsurface flow path explain the gradual, nearexponential decline of both collapse rate and the intensity of the 180-day-long eruption

Phosphorus (P) availability and P transformation rates in Amazonian Dark Earth determined by 33P isotopic dilution.

Amazonian Dark Earth (ADE) often shows increased soil fertility compared to surrounding soils, likely linked to its increased concentration of soil organic matter and macronutrients such as phosphorus (P). For P, there is little knowledge whether the higher P availability is a result of increased biological processes (such as organic P mineralization) or physico-chemical processes (such as sorption/desorption), or both

Biogenesis and functions of bacterial S-layers.

The outer surface of many archaea and bacteria is coated with a proteinaceous surface layer (known as an S-layer), which is formed by the self-assembly of monomeric proteins into a regularly spaced, two-dimensional array. Bacteria possess dedicated pathways for the secretion and anchoring of the S-layer to the cell wall, and some Gram-positive species have large S-layer-associated gene families. S-layers have important roles in growth and survival, and their many functions include the maintenance of cell integrity, enzyme display and, in pathogens and commensals, interaction with the host and its immune system. In this Review, we discuss our current knowledge of S-layer and related proteins, including their structures, mechanisms of secretion and anchoring and their diverse functions

Determining Contaminant Distribution and Migration by Integrating Data from Multiple Cone Penetrometer-Based Tools

The cone penetrometer has been used for geologic characterization at the U.S. Department of Energy-owned Savannah River Site for the past seven years

ZnO-based spinels grown by electrodeposition

We report on the synthesis of thin films of ZnCo 2O 4 and ZnMn 2O 4 spinels, as well as pure Co 3O 4 and Mn 3O 4 spinels, by means of electrodeposition. Spinel thin films have been analyzed by energy dispersive spectroscopy, X-ray diffraction, and Raman spectroscopy. We show that under determined deposition conditions the initial wurtzite structure of Co- and Mn-doped ZnO develops into spinel structures when the Co and Mn concentration in the films is above the solubility limit of these ions in the typical ZnO-wurtzite structure. © 2012 Elsevier Ltd. All rights reserved.This work was supported by Spanish Government through MICINN grants MAT2009-14625-C03-03, MAT2010-21270-C04-04 and MALTA CSD2007-0045. Financial support by the European Commission through NanoCIS project (PIRSES-GA-2010-269279) is gratefully acknowledged. Finally, we also want to acknowledge the support of Vicerrectorado de Investigacion y Desarrollo de la Universitat Politecnica de Valencia through projects UPV2011-0914 PAID-05-11 and UPV2011-0966 PAID-06-11.Tortosa Jorques, MD.; Manjón Herrera, FJ.; Mollar García, MA.; Marí Soucase, B. (2012). ZnO-based spinels grown by electrodeposition. Journal of Physics and Chemistry of Solids. 73(9):1111-1115. https://doi.org/10.1016/j.jpcs.2012.04.002S1111111573

Microbial competition for phosphorus limits the CO2 response of a mature forest

The capacity for terrestrial ecosystems to sequester additional carbon (C) with rising CO2 concentrations depends on soil nutrient availability1,2. Previous evidence suggested that mature forests growing on phosphorus (P)-deprived soils had limited capacity to sequester extra biomass under elevated CO2 (refs. 3–6), but uncertainty about ecosystem P cycling and its CO2 response represents a crucial bottleneck for mechanistic prediction of the land C sink under climate change7. Here, by compiling the first comprehensive P budget for a P-limited mature forest exposed to elevated CO2, we show a high likelihood that P captured by soil microorganisms constrains ecosystem P recycling and availability for plant uptake. Trees used P efficiently, but microbial pre-emption of mineralized soil P seemed to limit the capacity of trees for increased P uptake and assimilation under elevated CO2 and, therefore, their capacity to sequester extra C. Plant strategies to stimulate microbial P cycling and plant P uptake, such as increasing rhizosphere C release to soil, will probably be necessary for P-limited forests to increase C capture into new biomass. Our results identify the key mechanisms by which P availability limits CO2 fertilization of tree growth and will guide the development of Earth system models to predict future long-term C storage

The Utility of Iron Chelators in the Management of Inflammatory Disorders

Since iron can contribute to detrimental radical generating processes through the Fenton and Haber-Weiss reactions, it seems to be a reasonable approach to modulate iron-related pathways in inflammation. In the human organism a counterregulatory reduction in iron availability is observed during inflammatory diseases. Under pathological conditions with reduced or increased baseline iron levels different consequences regarding protection or susceptibility to inflammation have to be considered. Given the role of iron in development of inflammatory diseases, pharmaceutical agents targeting this pathway promise to improve the clinical outcome. The objective of this review is to highlight the mechanisms of iron regulation and iron chelation, and to demonstrate the potential impact of this strategy in the management of several acute and chronic inflammatory diseases, including cancer