Corrosion testing of materials in simulated superheated geothermal environment

Publisher's version (útgefin grein)This paper reports the results of corrosion study for carbon steel, austenitic stainless steel, as well as titanium and nickel-based alloys which were tested in a simulated superheated geothermal environment (SSGE) in flow-through reactors to investigate the corrosion behaviour to aid in the future material selection for high temperature deep geothermal application. The testing fluid was superheated steam (T = 350 °C and P = 10 bars gauge) containing H2S, CO2 and HCl with condensate of pH = 3. The corrosion rate for all samples was negligible but carbon steel was prone to localized damage under a magnetite film with a sulphur rich sublayer.The authors would like to thank the Icelandic Research Fund (RANNÍS, grants no. 163108-051, 163108-052 and 163108-053) and Geothermal Research Group (GEORG) for funding this project. Employees at Innovation Center of Iceland (ICI) and employees at Grein Research for their technical assistance. The authors would also like to give gratitude to Nippon Steel Sumitomo Metals and TIMET for collaboration and providing samples for testing.Peer reviewe

Supercritical Fluid Geochemistry in Geothermal Systems

Publisher's versionSupercritical fluids exist in the roots of many active high-temperature geothermal systems. Utilization of such supercritical resources may multiply energy production from geothermal systems; yet, their occurrence, formation mechanism, and chemical properties are poorly constrained. Flow-through experiments at 260°C and 400-420°C were performed to study the chemical and mineralogical changes associated with supercritical fluid formation near shallow magmatic intrusions by conductive heating and boiling of conventional subcritical geothermal fluids. Supercritical fluids formed by isobaric heating of liquid geothermal water had similar volatile element concentrations (B, C, and S) as the subcritical water. In contrast, mineral-forming element concentrations (Si, Na, K, Ca, Mg, and Cl) in the supercritical fluid were much lower. The results are consistent with the observed mineral deposition of quartz, aluminum silicates, and minor amount of salts during boiling. Similar concentration patterns have been predicted from geochemical modeling and were observed at Krafla, Iceland, for the IDDP-1 supercritical fluid discharge. The experimental results confirm previous findings that supercritical fluids may originate from conductive heating of subcritical geothermal reservoir fluids characterized by similar or lower elemental concentrations with minor input of volcanic gas.We would like to thank Ríkey Kjartansdóttir, Andri Ísak Thórhallsson, and Helgi Arnar Alfreðsson for their valuable help. This work was funded by the Swiss National Science Foundation (CRSII2_1418431/1, Sinergia COTHERM), Georg (11-04-003), and The Energy Research Fund of Landsvirkjun in 2018 and 2019.Peer Reviewe

Impact of fluid-rock interaction on water uptake of the Icelandic crust: Implications for the hydration of the oceanic crust and the subducted water flux

Pre-print (óritrýnt handrit)Oceanic crust is a major transport medium of water into the mantle wedge and the convecting mantle. Yet, the water content of the oceanic crust remains uncertain. Active geothermal systems situated at on-land spreading centers provide a unique opportunity to study the hydration of the oceanic crust, with well constrained systems and boreholes reaching depths of >4 km. Here, we present hydrogen isotope data of geothermal fluids and altered basalt for three Icelandic geothermal systems: the meteoric water fed system at Krafla and the seawater fed systems at Reykjanes and Surtsey. The bulk rock δD values of altered and hydrated basalts from these localities, which exhibit significantly higher water contents (up to 8.9 wt.%) than magmatic (non-hydrated) basalts, vary greatly from −125 to −96 at Krafla, from −80 to −46 at Reykjanes and from −78 to −46 at Surtsey. The corresponding fluids have δD values of −84.1 to −81.1 at Krafla, −23.1 to −14.9 at Reykjanes and +2.1 to +4.3 at Surtsey. Comparison of isotope modeling results to the natural data reveals that hydration of the Icelandic crust and corresponding hydrogen isotopic characteristics are controlled by (1) the isotope composition of the source fluid, (2) isotope fractionation between the aqueous geothermal fluids and the alteration minerals formed, and (3) the type and quantity of alteration minerals formed. These factors in turn depend on the extent of fluid-rock interaction and temperature. Using the same modeling approach and expanding it to datasets available for the oceanic crust, we assessed the hydration state and δD values of the oceanic crust as a function of depth. We show that 1400 to 1650 Tg H2O/yr is added to the igneous oceanic crust upon alteration by seawater and that the upper part (<2 km) of oceanic crust hosts almost 50% of the added water. The corresponding hydrogen isotope composition of the hydrated crust was calculated to an average of −55 ±6 . Upon subduction and subsequent dehydration, 80–90% of water with δD values of −35 to −10 will be released to the crustal forearc and mantle wedge. The remaining dehydrated slab with δD values of ∼−160 to −85 is expected to be transported to deeper levels modifying the mantle’s water budget and isotopic composition.This project was financially supported by NordVulk, the International Continental Scientific Drilling Program (ICDP) through a grant to the SUSTAIN project, and the Icelandic Research Fund (project number: 163083-051). SAH acknowledges support from the Icelandic Research Fund (project number: 196139-051). HS Orka and Landsvirkjun kindly provided access to the drill cuttings. J. Cullen, T. Larson, R. Ólafsdóttir and Á.E. Sveinbjörnsdóttir are thanked for assistance during sample preparation and data acquisition. BIK is particularly grateful of being part of this project as without the project-related lab work she would have never met her future husband E.W. Marshall IV. We thank four anonymous reviewers for their constructive comments and suggestions to an earlier version of this manuscript. Louis Derry is thanked for careful editorial handling of this study

Genomic profiling of breast tumours in relation to BRCA abnormalities and phenotypes

To access publisher full text version of this article. Please click on the hyperlink in Additional Links fieldINTRODUCTION: Germline mutations in the BRCA1 and BRCA2 genes account for a considerable fraction of familial predisposition to breast cancer. Somatic mutations in BRCA1 and BRCA2 have not been found and the involvement of these genes in sporadic tumour development therefore remains unclear. METHODS: The study group consisted of 67 primary breast tumours with and without BRCA1 or BRCA2 abnormalities. Genomic alterations were profiled by high-resolution (~7 kbp) comparative genome hybridisation (CGH) microarrays. Tumour phenotypes were analysed by immunohistochemistry on tissue microarrays using selected biomarkers (ER, PR, HER-2, EGFR, CK5/6, CK8, CK18). RESULTS: Classification of genomic profiles through cluster analysis revealed four subgroups, three of which displayed high genomic instability indices (GII). Two of these GII-high subgroups were enriched with either BRCA1- or BRCA2-related tumours whereas the third was not BRCA-related. The BRCA1-related subgroup mostly displayed non-luminal phenotypes, of which basal-like were most prominent, whereas the other two genomic instability subgroups BRCA2- and GII-high-III (non-BRCA), were almost entirely of luminal phenotype. Analysis of genome architecture patterns revealed similarities between the BRCA1- and BRCA2 subgroups, with long deletions being prominent. This contrasts with the third instability subgroup, not BRCA-related, where small gains were more prominent. CONCLUSIONS: The results suggest that BRCA1- and BRCA2-related tumours develop largely through distinct genetic pathways in terms of the regions altered while also displaying distinct phenotypes. Importantly, we show that the development of a subset of sporadic tumours is similar to that of either familial BRCA1- or BRCA2 tumours. Despite their differences, we observed clear similarities between the BRCA1- and BRCA2-related subgroups reflected in the type of genomic alterations acquired with deletions of long DNA segments being prominent. This suggests similarities in the mechanisms promoting genomic instability for BRCA1- and BRCA2-associated tumours, possibly relating to deficiency in DNA repair through homologous recombination. Indeed, this feature characterized both familial and sporadic tumours displaying BRCA1- or BRCA2-like spectrums of genomic alterations. The importance of these findings lies in the potential benefit from targeted therapy, through the use of agents leading to DNA double-strand breaks such as PARP inhibitors (olaparib) and cisplatin, for a much larger group of patients than the few BRCA1 and BRCA2 germline mutation carriers

CpG promoter methylation of the ALKBH3 alkylation repair gene in breast cancer.

To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked FilesDNA repair of alkylation damage is defective in various cancers. This occurs through somatically acquired inactivation of the MGMT gene in various cancer types, including breast cancers. In addition to MGMT, the two E. coli AlkB homologs ALKBH2 and ALKBH3 have also been linked to direct reversal of alkylation damage. However, it is currently unknown whether ALKBH2 or ALKBH3 are found inactivated in cancer.Methylome datasets (GSE52865, GSE20713, GSE69914), available through Omnibus, were used to determine whether ALKBH2 or ALKBH3 are found inactivated by CpG promoter methylation. TCGA dataset enabled us to then assess the impact of CpG promoter methylation on mRNA expression for both ALKBH2 and ALKBH3. DNA methylation analysis for the ALKBH3 promoter region was carried out by pyrosequencing (PyroMark Q24) in 265 primary breast tumours and 30 proximal normal breast tissue samples along with 8 breast-derived cell lines. ALKBH3 mRNA and protein expression were analysed in cell lines using RT-PCR and Western blotting, respectively. DNA alkylation damage assay was carried out in cell lines based on immunofluorescence and confocal imaging. Data on clinical parameters and survival outcomes in patients were obtained and assessed in relation to ALKBH3 promoter methylation.The ALKBH3 gene, but not ALKBH2, undergoes CpG promoter methylation and transcriptional silencing in breast cancer. We developed a quantitative alkylation DNA damage assay based on immunofluorescence and confocal imaging revealing higher levels of alkylation damage in association with epigenetic inactivation of the ALKBH3 gene (P = 0.029). In our cohort of 265 primary breast cancer, we found 72 cases showing aberrantly high CpG promoter methylation over the ALKBH3 promoter (27%; 72 out of 265). We further show that increasingly higher degree of ALKBH3 promoter methylation is associated with reduced breast-cancer specific survival times in patients. In this analysis, ALKBH3 promoter methylation at >20% CpG methylation was found to be statistically significantly associated with reduced survival (HR = 2.3; P = 0.012). By thresholding at the clinically relevant CpG methylation level (>20%), we find the incidence of ALKBH3 promoter methylation to be 5% (13 out of 265).ALKBH3 is a novel addition to the catalogue of DNA repair genes found inactivated in breast cancer. Our results underscore a link between defective alkylation repair and breast cancer which, additionally, is found in association with poor disease outcome.Icelandic Centre for Researc

The Surtsey volcano geothermal system: An analogue for seawater-oceanic crust interaction with implications for the elemental budget of the oceanic crust

Pre-print (óritrýnt handrit)Surtsey is a young volcanic island in the offshore extension of Iceland's southeast rift zone that grew from the seafloor during explosive and effusive eruptions in 1963–1967. In 1979, a cored borehole (SE-1) was drilled to 181 m depth and in 2017 three cored boreholes (SE-2a, SE-2b and SE-3) were drilled to successively greater depths. The basaltic deposits host a low-temperature (40–141 °C) seawater-dominated geothermal system. Surtsey provides an ideal environment to study water-rock interaction processes in a young seawater geothermal system. Elemental concentrations (SiO2, B, Na, Ca, Mg, F, dissolved inorganic carbon, SO4, Cl) and isotope contents (δD, δ18O) in borehole fluids indicate that associated geothermal waters in submarine deposits originated from seawater modified by reactions with the surrounding basalt. These processes produce authigenic minerals in the basaltic lapilli tuff and a corresponding depletion of certain elements in the residual waters. Coupling of measured and modelled concentrations investigates the effect of temperature and associated abundance of authigenic minerals on chemical fluxes from and to the igneous oceanic crust during low-temperature alteration. The annual chemical fluxes calculated at 50–150 °C range from −0.01 to +0.1×1012 mol yr−1 for SiO2, +0.2 to +129×1012 mol yr−1 for Ca, −129 to −0.8×1012 mol yr−1 for Mg and −21 to +0.4 × 1012 mol yr−1 for SO4 where negative values indicate chemical fluxes from the ocean into the oceanic crust and positive values indicate fluxes from the oceanic crust to the oceans. These flux calculations reveal that water-rock interaction at varying water-rock ratios and temperatures produces authigenic minerals that serve as important sinks of seawater-derived SiO2, Mg and SO4. In contrast, water rock interaction accompanied by dissolution of basaltic glass and primary crystal fragments provides a significant source of Ca. Such low-temperature alteration could effectively influence the elemental budget of the oceanic igneous crust and ocean waters. The modeling provides insights into water chemistries and chemical fluxes in low temperature MOR recharge zones. Surtsey also provides a valuable young analogue for assessing the chemical evolution of fluid discharge over the life cycles of seamounts in ridge flank systems.Funding for this project was provided by the University of Iceland Recruitment fund, the International Continental Scientific Drilling Program (ICDP) through a grant to the SUSTAIN project, the Icelandic Science Fund, ICF-RANNÍS, the Bergen Research Foundation and K.G. Jebsen Centre for Deep Sea Research at University of Bergen, Norway, the German Research Foundation (DFG), and DiSTAR, Federico II, University of Naples, Federico II, Italy. The University of Utah, USA and the two Icelandic power companies Reykjavík Energy and Landsvirkjun, contributed additional funds. The authors would like to thank P. Bergsten, A.M. di Stefano, C.F. Gorny, J. Gunnarsson-Robin, G.H. Guðfinsson, Þ. Högnadóttir, E.W. Marshall, R. Ólafssdóttir, D.B. Ragnarsson and Þ.M. Þorbjarnardóttir for their contribution and assistance during sampling, sample preparation, analyses and data evaluation. The authors would like to thank M. E. Böttcher for careful editorial handling. Two anonymous reviewers and J. Alt are thanked for their thoughtful and valuable reviews

EZH2-mediated epigenetic repression of DNA repair in promoting breast tumor initiating cells

Members of the Polycomb-group (PcG) family of proteins, including EZH2 (enhancer of zeste homolog 2), are involved in establishing epigenetic silencing of developmental genes in adult and embryonic stem cells, and their deregulation has been implicated in cancer. In a recent report, EZH2-mediated epigenetic repression of DNA damage repair in breast tumor initiating cells (BTICs) was identified as a mechanism that could promote expansion of BTICs, and may contribute to cancer progression

CpG island hypermethylation of BRCA1 and loss of pRb as co-occurring events in basal/triple-negative breast cancer

Triple-negative breast cancer (TNBC) occurs in approximately 15% of all breast cancer patients, and the incidence of TNBC is greatly increased in BRCA1 mutation carriers. This study aimed to assess the impact of BRCA1 promoter methylation with respect to breast cancer subtypes in sporadic disease. Tissue microarrays (TMAs) were constructed representing tumors from 303 patients previously screened for BRCA1 germline mutations, of which a subset of 111 sporadic tumors had previously been analyzed with respect to BRCA1 methylation. Additionally, a set of eight tumors from BRCA1 mutation carriers were included on the TMAs. Expression analysis was performed on TMAs by immunohistochemistry (IHC) for BRCA1, pRb, p16, p53, PTEN, ER, PR, HER2, CK5/6, CK8, CK18, EGFR, MUC1, and Ki-67. Data on BRCA1 aberrations and IHC expression was examined with respect to breast cancer-specific survival. The results demonstrate that CpG island hypermethylation of BRCA1 significantly associates with the basal/triple-negative subtype. Low expression of pRb, and high/intense p16, were associated with BRCA1 promoter hypermethylation, and the same effects were seen in BRCA1 mutated tumors. The expression patterns of BRCA1, pRb, p16 and PTEN were highly correlated, and define a subgroup of TNBCs characterized by BRCA1 aberrations, high Ki-67 (≥ 40%) and favorable disease outcome. In conclusion, our findings demonstrate that epigenetic inactivation of the BRCA1 gene associates with RB/p16 dysfunction in promoting TNBCs. The clinical implications relate to the potential use of targeted treatment based on PARP inhibitors in sporadic TNBCs, wherein CpG island hypermethylation of BRCA1 represents a potential marker of therapeutic response