ALBERT

Description: Portable X-Ray Fluorescence (pXRF) analysers allow on-site geochemical analysis of rock powders and drill core. The main advantages of pXRF analysis over conventional laboratory analysis are the speed of data collection and the low cost of the analyses, permitting the collection of extensive, spatially representative datasets. However, these factors only become useful if the quality of the data meets the requirements needed for the purposes of the study. Here, we evaluate the possible use of portable XRF to determine element concentrations and ratios used in exploration for komatiite-hosted nickel sulphides. A portable XRF analyser was used to measure a series of chalcophile and lithophile element concentrations (Si, S, K, Ca, Ti, Cr, Fe, Ni, Cu, Zn, As, Sr, and Zr) of 75 samples from three komatiite units associated with nickel sulphide ores in the Yilgarn Craton, Western Australia. Crucial steps in the study were the development of a strict calibration process as well as numerous data quality checks. The 670 analyses collected in this study were compared with conventional laboratory XRF data on discriminant diagrams commonly utilized in exploration for komatiite-hosted nickel sulphides (Cr vs Ni and Ni/Ti vs Ni/Cr). After comparing the results obtained with pXRF during this study with the laboratory values, we can conclude that portable XRF analyses can be used for rapid assessment of the nickel sulphide prospectivity of komatiites provided that strict control protocols are followed. Supplementary Material: is available at http://www.geolsoc.org.uk/SUP18706

Description: The alpha chain of the human histocompatibility antigen HLA-G was identified as an array of five 37- to 39-kilodalton isoforms by the use of two-dimensional gel electrophoresis. Both cell-associated and secreted HLA-G antigens are prominent in first trimester villous cytotrophoblasts and are greatly reduced in third trimester cytotrophoblasts. Allelic variation was not detected, an indication that HLA-G is not obviously polymorphic in cytotrophoblasts. Among the following choriocarcinoma cell lines studied, HLA-G is expressed in JEG but not in Jar or BeWo. Expression of endogenous HLA-G genes has not been found in normal lymphoid cells. Thus, HLA-G is subject to both cell type-specific and developmental regulation and is expressed in early gestation human cytotrophoblasts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kovats, S -- Main, E K -- Librach, C -- Stubblebine, M -- Fisher, S J -- DeMars, R -- AI-15586/AI/NIAID NIH HHS/ -- HD-24495/HD/NICHD NIH HHS/ -- P0I HD-24180/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Apr 13;248(4952):220-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Oncology, University of Wisconsin, Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2326636" target="_blank"〉PubMed〈/a〉

Description: Cytotrophoblasts, specialized placental cells, proliferate early in pregnancy and then differentiate into tumor-like cells that establish blood flow to the placenta by invading the uterus and its vasculature. In this study, cytotrophoblasts cultured under hypoxic conditions (2 percent oxygen), mimicking the environment near the uterine surface before 10 weeks of gestation, continued proliferating and differentiated poorly. When cultured in 20 percent oxygen, mimicking the environment near uterine arterioles, the cells stopped proliferating and differentiated normally. Thus, oxygen tension determines whether cytotrophoblasts proliferate or invade, thereby regulating placental growth and cellular architecture.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Genbacev, O -- Zhou, Y -- Ludlow, J W -- Fisher, S J -- CA 56904/CA/NCI NIH HHS/ -- HD30367/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1669-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Stomatology, University of California, San Francisco, CA 94143-0512, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9287221" target="_blank"〉PubMed〈/a〉

Description: Trophoblast adhesion to the uterine wall is the requisite first step of implantation and, subsequently, placentation. At the maternal-fetal interface, we investigated the expression of selectin adhesion systems that enable leukocyte capture from the bloodstream. On the maternal side, human uterine epithelial cells up-regulated selectin oligosaccharide-based ligands during the window of receptivity. On the fetal side, human trophoblasts expressed L-selectin. This ligand-receptor system was functional, because beads coated with the selectin ligand 6-sulfo sLe(x) bound to trophoblasts, and trophoblasts bound to ligand-expressing uterine luminal epithelium in tissue sections. These results suggest that trophoblast L-selectin mediates interactions with the uterus and that this adhesion mechanism may be critical to establishing human pregnancy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Genbacev, Olga D -- Prakobphol, Akraporn -- Foulk, Russell A -- Krtolica, Ana R -- Ilic, Dusko -- Singer, Mark S -- Yang, Zhi-Qiang -- Kiessling, Laura L -- Rosen, Steven D -- Fisher, Susan J -- DE 07244/DE/NIDCR NIH HHS/ -- HL 64597/HL/NHLBI NIH HHS/ -- R37GM23547/GM/NIGMS NIH HHS/ -- U01 HD 42283/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 17;299(5605):405-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Stomatology, Anatomy, and Pharmaceutical Chemistry, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532021" target="_blank"〉PubMed〈/a〉

Description: Preterm birth is associated with 5 to 18% of pregnancies and is a leading cause of infant morbidity and mortality. Spontaneous preterm labor, a syndrome caused by multiple pathologic processes, leads to 70% of preterm births. The prevention and the treatment of preterm labor have been long-standing challenges. We summarize the current understanding of the mechanisms of disease implicated in this condition and review advances relevant to intra-amniotic infection, decidual senescence, and breakdown of maternal-fetal tolerance. The success of progestogen treatment to prevent preterm birth in a subset of patients at risk is a cause for optimism. Solving the mystery of preterm labor, which compromises the health of future generations, is a formidable scientific challenge worthy of investment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4191866/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4191866/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Romero, Roberto -- Dey, Sudhansu K -- Fisher, Susan J -- DA06668/DA/NIDA NIH HHS/ -- HD068524/HD/NICHD NIH HHS/ -- P50 HD055764/HD/NICHD NIH HHS/ -- R01 HD068524/HD/NICHD NIH HHS/ -- R37 HD076253/HD/NICHD NIH HHS/ -- U54 HD055764/HD/NICHD NIH HHS/ -- ZIA HD002400-23/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):760-5. doi: 10.1126/science.1251816. Epub 2014 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Perinatology Research Branch, Program for Perinatal Research and Obstetrics, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Bethesda, MD, Wayne State University/the Detroit Medical Center, Detroit, MI, USA. Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, MI, USA. Department of Epidemiology and Biostatistics, Michigan State University, East Lansing, MI, USA. romeror@mail.nih.gov. ; Division of Reproductive Sciences, Perinatal Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA. ; Department of Obstetrics, Gynecology and Reproductive Sciences, Department of Anatomy, and Center for Reproductive Sciences, University of California San Francisco, San Francisco, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25124429" target="_blank"〉PubMed〈/a〉

Description: The mammalian embryo cannot develop without the placenta. Its specialized cells (trophoblast, endoderm, and extraembryonic mesoderm) form early in development. They attach the embryo to the uterus (implantation) and form vascular connections necessary for nutrient transport. In addition, the placenta redirects maternal endocrine, immune, and metabolic functions to the embryo's advantage. These complex activities are sensitive to disruption, as shown by the high incidence of early embryonic mortality and pregnancy diseases in humans, as well as the numerous peri-implantation lethal mutations in mice. Integration of molecular and developmental approaches has recently produced insights into the molecules that control these processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cross, J C -- Werb, Z -- Fisher, S J -- HD 22210/HD/NICHD NIH HHS/ -- HD 26732/HD/NICHD NIH HHS/ -- HD 30367/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1508-18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985020" target="_blank"〉PubMed〈/a〉

Description: The reference human genome sequence set the stage for studies of genetic variation and its association with human disease, but epigenomic studies lack a similar reference. To address this need, the NIH Roadmap Epigenomics Consortium generated the largest collection so far of human epigenomes for primary cells and tissues. Here we describe the integrative analysis of 111 reference human epigenomes generated as part of the programme, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression. We establish global maps of regulatory elements, define regulatory modules of coordinated activity, and their likely activators and repressors. We show that disease- and trait-associated genetic variants are enriched in tissue-specific epigenomic marks, revealing biologically relevant cell types for diverse human traits, and providing a resource for interpreting the molecular basis of human disease. Our results demonstrate the central role of epigenomic information for understanding gene regulation, cellular differentiation and human disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4530010/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4530010/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roadmap Epigenomics Consortium -- Kundaje, Anshul -- Meuleman, Wouter -- Ernst, Jason -- Bilenky, Misha -- Yen, Angela -- Heravi-Moussavi, Alireza -- Kheradpour, Pouya -- Zhang, Zhizhuo -- Wang, Jianrong -- Ziller, Michael J -- Amin, Viren -- Whitaker, John W -- Schultz, Matthew D -- Ward, Lucas D -- Sarkar, Abhishek -- Quon, Gerald -- Sandstrom, Richard S -- Eaton, Matthew L -- Wu, Yi-Chieh -- Pfenning, Andreas R -- Wang, Xinchen -- Claussnitzer, Melina -- Liu, Yaping -- Coarfa, Cristian -- Harris, R Alan -- Shoresh, Noam -- Epstein, Charles B -- Gjoneska, Elizabeta -- Leung, Danny -- Xie, Wei -- Hawkins, R David -- Lister, Ryan -- Hong, Chibo -- Gascard, Philippe -- Mungall, Andrew J -- Moore, Richard -- Chuah, Eric -- Tam, Angela -- Canfield, Theresa K -- Hansen, R Scott -- Kaul, Rajinder -- Sabo, Peter J -- Bansal, Mukul S -- Carles, Annaick -- Dixon, Jesse R -- Farh, Kai-How -- Feizi, Soheil -- Karlic, Rosa -- Kim, Ah-Ram -- Kulkarni, Ashwinikumar -- Li, Daofeng -- Lowdon, Rebecca -- Elliott, GiNell -- Mercer, Tim R -- Neph, Shane J -- Onuchic, Vitor -- Polak, Paz -- Rajagopal, Nisha -- Ray, Pradipta -- Sallari, Richard C -- Siebenthall, Kyle T -- Sinnott-Armstrong, Nicholas A -- Stevens, Michael -- Thurman, Robert E -- Wu, Jie -- Zhang, Bo -- Zhou, Xin -- Beaudet, Arthur E -- Boyer, Laurie A -- De Jager, Philip L -- Farnham, Peggy J -- Fisher, Susan J -- Haussler, David -- Jones, Steven J M -- Li, Wei -- Marra, Marco A -- McManus, Michael T -- Sunyaev, Shamil -- Thomson, James A -- Tlsty, Thea D -- Tsai, Li-Huei -- Wang, Wei -- Waterland, Robert A -- Zhang, Michael Q -- Chadwick, Lisa H -- Bernstein, Bradley E -- Costello, Joseph F -- Ecker, Joseph R -- Hirst, Martin -- Meissner, Alexander -- Milosavljevic, Aleksandar -- Ren, Bing -- Stamatoyannopoulos, John A -- Wang, Ting -- Kellis, Manolis -- 5R24HD000836/HD/NICHD NIH HHS/ -- ES017166/ES/NIEHS NIH HHS/ -- F32 HL110473/HL/NHLBI NIH HHS/ -- F32HL110473/HL/NHLBI NIH HHS/ -- K99 HL119617/HL/NHLBI NIH HHS/ -- K99HL119617/HL/NHLBI NIH HHS/ -- P01 DA008227/DA/NIDA NIH HHS/ -- P30AG10161/AG/NIA NIH HHS/ -- P50 MH096890/MH/NIMH NIH HHS/ -- R01 AG015819/AG/NIA NIH HHS/ -- R01 AG017917/AG/NIA NIH HHS/ -- R01 ES024984/ES/NIEHS NIH HHS/ -- R01 ES024992/ES/NIEHS NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01 HG007175/HG/NHGRI NIH HHS/ -- R01 HG007354/HG/NHGRI NIH HHS/ -- R01AG15819/AG/NIA NIH HHS/ -- R01AG17917/AG/NIA NIH HHS/ -- R01HG004037/HG/NHGRI NIH HHS/ -- R01HG004037-S1/HG/NHGRI NIH HHS/ -- R01NS078839/NS/NINDS NIH HHS/ -- RC1HG005334/HG/NHGRI NIH HHS/ -- RF1 AG015819/AG/NIA NIH HHS/ -- T32 ES007032/ES/NIEHS NIH HHS/ -- T32 GM007198/GM/NIGMS NIH HHS/ -- T32 GM007266/GM/NIGMS NIH HHS/ -- T32 GM081739/GM/NIGMS NIH HHS/ -- U01 ES017154/ES/NIEHS NIH HHS/ -- U01AG46152/AG/NIA NIH HHS/ -- U01DA025956/DA/NIDA NIH HHS/ -- U01ES017154/ES/NIEHS NIH HHS/ -- U01ES017155/ES/NIEHS NIH HHS/ -- U01ES017156/ES/NIEHS NIH HHS/ -- U01ES017166/ES/NIEHS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Feb 19;518(7539):317-30. doi: 10.1038/nature14248.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Computer Science and Artificial Intelligence Lab, Massachusetts Institute of Technology, 32 Vassar St, Cambridge, Massachusetts 02139, USA. [2] The Broad Institute of Harvard and MIT, 415 Main Street, Cambridge, Massachusetts 02142, USA. [3] Department of Genetics, Department of Computer Science, 300 Pasteur Dr., Lane Building, L301, Stanford, California 94305-5120, USA. ; 1] Computer Science and Artificial Intelligence Lab, Massachusetts Institute of Technology, 32 Vassar St, Cambridge, Massachusetts 02139, USA. [2] The Broad Institute of Harvard and MIT, 415 Main Street, Cambridge, Massachusetts 02142, USA. ; 1] Computer Science and Artificial Intelligence Lab, Massachusetts Institute of Technology, 32 Vassar St, Cambridge, Massachusetts 02139, USA. [2] The Broad Institute of Harvard and MIT, 415 Main Street, Cambridge, Massachusetts 02142, USA. [3] Department of Biological Chemistry, University of California, Los Angeles, 615 Charles E Young Dr South, Los Angeles, California 90095, USA. ; Canada's Michael Smith Genome Sciences Centre, BC Cancer Agency, 675 West 10th Avenue, Vancouver, British Columbia V5Z 1L3, Canada. ; 1] The Broad Institute of Harvard and MIT, 415 Main Street, Cambridge, Massachusetts 02142, USA. [2] Department of Stem Cell and Regenerative Biology, 7 Divinity Ave, Cambridge, Massachusetts 02138, USA. ; Epigenome Center, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. ; Department of Cellular and Molecular Medicine, Institute of Genomic Medicine, Moores Cancer Center, Department of Chemistry and Biochemistry, University of California San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA. ; Genomic Analysis Laboratory, Howard Hughes Medical Institute &The Salk Institute for Biological Studies, 10010 N. Torrey Pines Road, La Jolla, California 92037, USA. ; Department of Genome Sciences, University of Washington, 3720 15th Ave. NE, Seattle, Washington 98195, USA. ; 1] Computer Science and Artificial Intelligence Lab, Massachusetts Institute of Technology, 32 Vassar St, Cambridge, Massachusetts 02139, USA. [2] The Broad Institute of Harvard and MIT, 415 Main Street, Cambridge, Massachusetts 02142, USA. [3] Biology Department, Massachusetts Institute of Technology, 31 Ames St, Cambridge, Massachusetts 02142, USA. ; The Broad Institute of Harvard and MIT, 415 Main Street, Cambridge, Massachusetts 02142, USA. ; 1] The Broad Institute of Harvard and MIT, 415 Main Street, Cambridge, Massachusetts 02142, USA. [2] The Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, 43 Vassar St, Cambridge, Massachusetts 02139, USA. ; 1] Department of Cellular and Molecular Medicine, Institute of Genomic Medicine, Moores Cancer Center, Department of Chemistry and Biochemistry, University of California San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA. [2] Ludwig Institute for Cancer Research, 9500 Gilman Drive, La Jolla, California 92093, USA. ; Department of Neurosurgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, 1450 3rd Street, San Francisco, California 94158, USA. ; Department of Pathology, University of California San Francisco, 513 Parnassus Avenue, San Francisco, California 94143-0511, USA. ; Department of Medicine, Division of Medical Genetics, University of Washington, 2211 Elliot Avenue, Seattle, Washington 98121, USA. ; 1] Computer Science and Artificial Intelligence Lab, Massachusetts Institute of Technology, 32 Vassar St, Cambridge, Massachusetts 02139, USA. [2] The Broad Institute of Harvard and MIT, 415 Main Street, Cambridge, Massachusetts 02142, USA. [3] Department of Computer Science &Engineering, University of Connecticut, 371 Fairfield Way, Storrs, Connecticut 06269, USA. ; Department of Microbiology and Immunology and Centre for High-Throughput Biology, University of British Columbia, 2125 East Mall, Vancouver, British Columbia V6T 1Z4, Canada. ; Bioinformatics Group, Department of Molecular Biology, Division of Biology, Faculty of Science, University of Zagreb, Horvatovac 102a, 10000 Zagreb, Croatia. ; Department of Molecular and Cell Biology, Center for Systems Biology, The University of Texas, Dallas, NSERL, RL10, 800 W Campbell Road, Richardson, Texas 75080, USA. ; Department of Genetics, Center for Genome Sciences and Systems Biology, Washington University in St Louis, 4444 Forest Park Ave, St Louis, Missouri 63108, USA. ; Institute for Molecular Bioscience, University of Queensland, St Lucia, Queensland 4072, Australia. ; 1] The Broad Institute of Harvard and MIT, 415 Main Street, Cambridge, Massachusetts 02142, USA. [2] Brigham &Women's Hospital, 75 Francis Street, Boston, Massachusetts 02115, USA. ; 1] Department of Genetics, Center for Genome Sciences and Systems Biology, Washington University in St Louis, 4444 Forest Park Ave, St Louis, Missouri 63108, USA. [2] Department of Computer Science and Engineeering, Washington University in St. Louis, St. Louis, Missouri 63130, USA. ; 1] Department of Applied Mathematics and Statistics, Stony Brook University, Stony Brook, New York 11794-3600, USA. [2] Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA. ; Molecular and Human Genetics Department, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. ; Biology Department, Massachusetts Institute of Technology, 31 Ames St, Cambridge, Massachusetts 02142, USA. ; 1] The Broad Institute of Harvard and MIT, 415 Main Street, Cambridge, Massachusetts 02142, USA. [2] Brigham &Women's Hospital, 75 Francis Street, Boston, Massachusetts 02115, USA. [3] Harvard Medical School, 25 Shattuck St, Boston, Massachusetts 02115, USA. ; Department of Biochemistry, Keck School of Medicine, University of Southern California, 1450 Biggy Street, Los Angeles, California 90089-9601, USA. ; ObGyn, Reproductive Sciences, University of California San Francisco, 35 Medical Center Way, San Francisco, California 94143, USA. ; Center for Biomolecular Sciences and Engineering, University of Santa Cruz, 1156 High Street, Santa Cruz, California 95064, USA. ; 1] Canada's Michael Smith Genome Sciences Centre, BC Cancer Agency, 675 West 10th Avenue, Vancouver, British Columbia V5Z 1L3, Canada. [2] Department of Molecular Biology and Biochemistry, Simon Fraser University, 8888 University Drive, Burnaby, British Columbia V5A 1S6, Canada. [3] Department of Medical Genetics, University of British Columbia, 2329 West Mall, Vancouver, BC, Canada, V6T 1Z4. ; Dan L. Duncan Cancer Center, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. ; 1] Canada's Michael Smith Genome Sciences Centre, BC Cancer Agency, 675 West 10th Avenue, Vancouver, British Columbia V5Z 1L3, Canada. [2] Department of Medical Genetics, University of British Columbia, 2329 West Mall, Vancouver, BC, Canada, V6T 1Z4. ; Department of Microbiology and Immunology, Diabetes Center, University of California, San Francisco, 513 Parnassus Ave, San Francisco, California 94143-0534, USA. ; 1] University of Wisconsin, Madison, Wisconsin 53715, USA. [2] Morgridge Institute for Research, 330 N. Orchard Street, Madison, Wisconsin 53707, USA. ; USDA/ARS Children's Nutrition Research Center, Baylor College of Medicine, 1100 Bates Street, Houston, Texas 77030, USA. ; 1] Department of Molecular and Cell Biology, Center for Systems Biology, The University of Texas, Dallas, NSERL, RL10, 800 W Campbell Road, Richardson, Texas 75080, USA. [2] Bioinformatics Division, Center for Synthetic and Systems Biology, TNLIST, Tsinghua University, Beijing 100084, China. ; National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, Research Triangle Park, North Carolina 27709, USA. ; 1] The Broad Institute of Harvard and MIT, 415 Main Street, Cambridge, Massachusetts 02142, USA. [2] Massachusetts General Hospital, 55 Fruit St, Boston, Massachusetts 02114, USA. [3] Howard Hughes Medical Institute, 4000 Jones Bridge Road, Chevy Chase, Maryland 20815-6789, USA. ; 1] Canada's Michael Smith Genome Sciences Centre, BC Cancer Agency, 675 West 10th Avenue, Vancouver, British Columbia V5Z 1L3, Canada. [2] Department of Microbiology and Immunology and Centre for High-Throughput Biology, University of British Columbia, 2125 East Mall, Vancouver, British Columbia V6T 1Z4, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25693563" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fisher, Susan J -- Giudice, Linda C -- New York, N.Y. -- Science. 2013 May 17;340(6134):825. doi: 10.1126/science.1239644.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Obstetrics, Gynecology and Reproductive Sciences, University of California San Francisco, CA 94143, USA. sfisher@cgl.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23687039" target="_blank"〉PubMed〈/a〉

Description: The Monts de Cristal Complex of Gabon consists of several igneous bodies interpreted to be remnants of a tectonically dismembered, 〉100 km long and 1–3 km wide, ultramafic–mafic intrusion emplaced at 2765–2775 Ma. It is the most significant mafic–ultramafic layered complex yet identified on the Congo Craton. The complex consists largely of orthopyroxenite cumulates, with less abundant olivine-orthopyroxenite and norite, and rare harzburgite and dunite. Mineral compositions (Fo ol 84, Mg# Opx 85, An plag 60–68, Cr/Fe chromite 1–1·45) and whole-rock data suggest that the parent magma was a low-Ti basalt containing approximately 10% MgO and 0·5% TiO 2 . Trace element and Rb–Sr and Sm–Nd isotope data indicate the presence of an enriched component, possibly derived from crustal contamination of a magma generated in the sub-lithospheric mantle. Most rocks show a highly unusual pattern of strong Pt enrichment (10–150 ppb) at low concentrations of Pd (1–15 ppb), Au (1–2 ppb), Cu (1–20 ppm), and S (〈500 ppm), suggesting that unlike in most other PGE-rich intrusions globally, platinum in the Monts de Cristal Complex is not hosted in magmatic sulfides. Synchrotron X-ray fluorescence mapping has revealed the location of buried small Pt particles, most of which are associated with As. We propose that this constitutes some of the strongest evidence yet in support of magmatic crystallization of a Pt–As phase from S-undersaturated magma.

Description: Chromitites found in layered intrusions and ophiolite complexes are generally enriched in platinum-group elements (PGE), especially IPGE ( i.e ., Ir, Os, Ru)-bearing platinum-group minerals (PGM), and the chromitites are usually poor in base metal sulfide (BMS) minerals. The most common PGM observed is laurite [Ru(Os,Ir)S 2 ], but how the laurite formed is not clearly understood. To address this problem we compare the differences in the composition and shape of PGM in the nine chromite layers (A to K) in the Stillwater Complex, Montana and then extend the study to examine laurites from the Bushveld Complex and ophiolites. The most common PGM in the Stillwater chromitites is laurite, predominantly enclosed in chromite grains. In a few cases the laurite is accompanied by rarer and smaller PGM, including malanite [CuPtRh(±Ir)S] and Pt-Pd-sulfides. Interstitial to the chromite grains the PGM assemblage is quite different, dominantly PPGE ( i.e ., Pt, Pd, and Rh)-bearing, including Pd-Pb, Pt-Pd tellurides, sperrylite, platarsite, minor laurite, and one grain of Pd-Ge. The PGM grains enclosed in chromite formed by a different mechanism to the PGM grains outside chromite. During the crystallization of the chromite the magma was sulfide undersaturated and Ru, Os, Ir, and Rh partitioned into chromite thereby enriching the chromitite layers in IPGE. As the cumulate pile cooled, the fractionated silicate liquid became saturated in a BMS liquid and this migrated among the chromite grains. With further cooling the chromite grains sintered to form larger grains and in some case incorporated small grains of the BMS, which was converted to laurite by the exchange of IPGE and Fe plus Ni between the chromite and the BMS. In contrast, the BMS that was not included in chromite exsolved to form pentlandite, pyrrhotite, and PGM. The shape and composition of the PGM within the chromite grains in the Stillwater chromitite layers is not uniform. Upper and lower layers contain laurites with rounded shapes and an Os content of 7–8%. In the sulfide inclusion-poor middle G layer, the laurites have 5% Os and a predominantly euhedral shape. It is likely that both rounded and euhedral laurites formed by subsolidus ejection of PGE from the chromite as it cooled and recrystallized. The rounded laurite formed in a more BMS and S-rich environment, whereas the euhedral laurite formed in an S-poor environment. Traces of Rh in laurite, PPGM, and BMS inclusions associated with laurite are most abundant in the uppermost layer K, suggesting that the upper-layer chromitites contained more PPGE in solid solution on crystallization. The average size of the laurite grains increases upwards from an average area of 6 μm 2 in layer A to 21 μm 2 in layer K. The larger size of the laurites from higher layers in the intrusion may be the result of them having had a longer period to cool, further from the basal contact. Rutile inclusions are most abundant in chromitite layer B and could be the result of a greater degree of contamination of the magma in the lower layers. Comparison of the shape of Stillwater laurites with those in the Bushveld Complex chromitites reveals similarities with the Bushveld chromitites, as they also contain both euhedral and rounded laurites that are commonly associated with smaller PPGM. Ophiolitic laurites entirely enclosed in chromite are predominantly euhedral and sometimes zoned. Chromitites from ophiolites are generally PPGE-poor and although ophiolitic laurites also form composite PGM with other smaller PGM, these are usually Os- and Ir-rich rather than PPGE-rich. These laurites have a more variable and greater range of Os concentrations than those from the Stillwater and Bushveld Complexes. Most ophiolitic laurites probably formed by crystallizing directly from magma, but it is possible that some formed by diffusing from the chromite in a low f S 2 environment.