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  • 1
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    Rescue of the abnormal skeletal phenotype in Ts65Dn Down syndrome mice using genetic and therapeutic modulation of trisomic Dyrk1a (2015)
    Oxford University Press
    Details
    Publication Date: 2015-09-25
    Description: Trisomy 21 causes skeletal alterations in individuals with Down syndrome (DS), but the causative trisomic gene and a therapeutic approach to rescue these abnormalities are unknown. Individuals with DS display skeletal alterations including reduced bone mineral density, modified bone structure and distinctive facial features. Due to peripheral skeletal anomalies and extended longevity, individuals with DS are increasingly more susceptible to bone fractures. Understanding the genetic and developmental origin of DS skeletal abnormalities would facilitate the development of therapies to rescue these and other deficiencies associated with DS. DYRK1A is found in three copies in individuals with DS and Ts65Dn DS mice and has been hypothesized to be involved in many Trisomy 21 phenotypes including skeletal abnormalities. Return of Dyrk1a copy number to normal levels in Ts65Dn mice rescued the appendicular bone abnormalities, suggesting that appropriate levels of DYRK1A expression are critical for the development and maintenance of the DS appendicular skeleton. Therapy using the DYRK1A inhibitor epigallocatechin-3-gallate improved Ts65Dn skeletal phenotypes. These outcomes suggest that the osteopenic phenotype associated with DS may be rescued postnatally by targeting trisomic Dyrk1a .
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 2
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    Dextral, normal, and sinistral faulting across the eastern California shear zone–Mina deflection transition, California-Nevada, USA (2019)
    Geological Society of America (GSA)
    In: Geosphere
    Details
    Publication Date: 2019
    Description: 〈span〉Strike-slip faults commonly include extensional and contractional bends and stepovers, whereas rotational stepovers are less common. The Volcanic Tableland, Black Mountain, and River Spring areas (California and Nevada, USA) (hereafter referred to as the VBR region) straddle the transition from the dominantly NW-striking dextral faults that define the northwestern part of the eastern California shear zone into a rotational stepover characterized by dominantly NE-striking sinistral faults that define the southwestern Mina deflection. New detailed geologic mapping, structural studies, and 〈sup〉40〈/sup〉Ar/〈sup〉39〈/sup〉Ar geochronology across the VBR region allow us to calculate Pliocene to Pleistocene fault slip rates and test predictions for the kinematics of fault slip transfer into this rotational stepover. In the VBR, Mesozoic basement is nonconformably overlain by a Miocene sequence of rhyolite, dacite, and andesite volcanic rocks that yield 〈sup〉40〈/sup〉Ar/〈sup〉39〈/sup〉Ar ages between 22.878 ± 0.051 Ma and 11.399 ± 0.041 Ma. Miocene rocks are unconformably overlain by an extensive sequence of Pliocene basalt and andesite lava flows and cinder cones that yield 〈sup〉40〈/sup〉Ar/〈sup〉39〈/sup〉Ar ages between 3.606 ± 0.060 Ma and 2.996 ± 0.027 Ma. The Pliocene sequence is, in turn, unconformably overlain by Quaternary tuffs and sedimentary rocks. This sequence of rocks is cut by NS- to NW-striking normal faults across the Volcanic Tableland that transition northward into NS-striking normal faults across the Black Mountain area and that, in turn, transition northward into NW-striking dextral and NE-striking sinistral faults in the River Spring area. A range of geologic markers were used to measure offset across the faults in the VBR, and combined with the age of the markers, yield minimum ~EW-extension rates of ~0.5 mm/yr across the Volcanic Tableland and Black Mountain regions, and minimum NW-dextral slip and NE-sinistral slip rates of ~0.7 and ~0.3 mm/yr, respectively, across the River Spring region. In the River Spring area, our preferred minimum dextral slip and sinistral slip rates are 0.8–0.9 mm/yr and 0.7–0.9 mm/yr, respectively. We propose three kinematic fault slip models, two irrotational and one rotational, whereby the VBR region transfers a portion of dextral Owens Valley fault slip northwestward into the Mina deflection. In irrotational model 1, Owens Valley fault slip is partitioned into two components, one northeastward onto the White Mountain fault zone and one northwestward into the Volcanic Tableland. Slip from the two zones is then transferred northward into the southwestern Mina deflection. In irrotational model 2, Owens Valley fault slip is partitioned into three components, with the third component partitioned west-northwest onto the Sierra Nevada frontal fault zone. In the rotational model, predicted sinistral slip rates across the southwestern Mina deflection are at least 115% greater than our observed minimum slip rates, implying our minimum observed rates underestimate true sinistral slip rates. A comparison of summed geologic fault slip rates, parallel to motion of the Sierra Nevada block relative to the central Great Basin, from the Sierra Nevada northeastward across the VBR region and into western Nevada are the same as geodetic rates, if our assumptions about the geologic slip rate across the dextral White Mountain fault zone is correct.〈/span〉
    Electronic ISSN: 1553-040X
    Topics: Geosciences
    Published by Geological Society of America (GSA)
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  • 3
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    Vitamin C selectively kills KRAS and BRAF mutant colorectal cancer cells by targeting GAPDH (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-11-07
    Description: More than half of human colorectal cancers (CRCs) carry either KRAS or BRAF mutations and are often refractory to approved targeted therapies. We found that cultured human CRC cells harboring KRAS or BRAF mutations are selectively killed when exposed to high levels of vitamin C. This effect is due to increased uptake of the oxidized form of vitamin C, dehydroascorbate (DHA), via the GLUT1 glucose transporter. Increased DHA uptake causes oxidative stress as intracellular DHA is reduced to vitamin C, depleting glutathione. Thus, reactive oxygen species accumulate and inactivate glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Inhibition of GAPDH in highly glycolytic KRAS or BRAF mutant cells leads to an energetic crisis and cell death not seen in KRAS and BRAF wild-type cells. High-dose vitamin C impairs tumor growth in Apc/Kras(G12D) mutant mice. These results provide a mechanistic rationale for exploring the therapeutic use of vitamin C for CRCs with KRAS or BRAF mutations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4778961/" 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/PMC4778961/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yun, Jihye -- Mullarky, Edouard -- Lu, Changyuan -- Bosch, Kaitlyn N -- Kavalier, Adam -- Rivera, Keith -- Roper, Jatin -- Chio, Iok In Christine -- Giannopoulou, Eugenia G -- Rago, Carlo -- Muley, Ashlesha -- Asara, John M -- Paik, Jihye -- Elemento, Olivier -- Chen, Zhengming -- Pappin, Darryl J -- Dow, Lukas E -- Papadopoulos, Nickolas -- Gross, Steven S -- Cantley, Lewis C -- KL2 TR000458/TR/NCATS NIH HHS/ -- P01 CA117969/CA/NCI NIH HHS/ -- P01 CA117969-09/CA/NCI NIH HHS/ -- P01 CA120964/CA/NCI NIH HHS/ -- P01 CA120964-07/CA/NCI NIH HHS/ -- S10 RR022615/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Dec 11;350(6266):1391-6. doi: 10.1126/science.aaa5004. Epub 2015 Nov 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Meyer Cancer Center, Department of Medicine, Weill Cornell Medical College, New York, NY 10065, USA. ; Meyer Cancer Center, Department of Medicine, Weill Cornell Medical College, New York, NY 10065, USA. Biological and Biomedical Sciences Graduate Program, Harvard Medical School, Boston, MA 02115, USA. ; Department of Pharmacology, Weill Cornell Medical College, New York, NY 10065, USA. ; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA. ; Molecular Oncology Research Institute and Division of Gastroenterology, Tufts Medical Center, Boston, MA 02111, USA. ; Department of Physiology and Biophysics, Weill Cornell Medical College, New York, NY 10065, USA. ; Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute, Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA. ; Division of Signal Transduction, Beth Israel Deaconess Medical Center and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA. ; Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY 10065, USA. ; Department of Biostatistics and Epidemiology, Weill Cornell Medical College, New York, NY 10065, USA. ; Meyer Cancer Center, Department of Medicine, Weill Cornell Medical College, New York, NY 10065, USA. lcantley@med.cornell.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26541605" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein/genetics ; Animals ; Ascorbic Acid/administration & dosage/pharmacology/*therapeutic use ; Cell Line, Tumor ; Colorectal Neoplasms/*drug therapy/*genetics ; Dehydroascorbic Acid/metabolism ; Female ; Glucose Transporter Type 1/metabolism ; Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)/metabolism ; Glycolysis/drug effects ; Humans ; Mice ; Mice, Mutant Strains ; Mice, Nude ; Proto-Oncogene Proteins/*genetics ; Proto-Oncogene Proteins B-raf/*genetics ; Proto-Oncogene Proteins p21(ras)/genetics ; Reactive Oxygen Species/metabolism ; Xenograft Model Antitumor Assays ; ras Proteins/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    High-fat diet enhances stemness and tumorigenicity of intestinal progenitors (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-03-05
    Description: Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we show that high-fat diet (HFD)-induced obesity augments the numbers and function of Lgr5(+) intestinal stem cells of the mammalian intestine. Mechanistically, a HFD induces a robust peroxisome proliferator-activated receptor delta (PPAR-delta) signature in intestinal stem cells and progenitor cells (non-intestinal stem cells), and pharmacological activation of PPAR-delta recapitulates the effects of a HFD on these cells. Like a HFD, ex vivo treatment of intestinal organoid cultures with fatty acid constituents of the HFD enhances the self-renewal potential of these organoid bodies in a PPAR-delta-dependent manner. Notably, HFD- and agonist-activated PPAR-delta signalling endow organoid-initiating capacity to progenitors, and enforced PPAR-delta signalling permits these progenitors to form in vivo tumours after loss of the tumour suppressor Apc. These findings highlight how diet-modulated PPAR-delta activation alters not only the function of intestinal stem and progenitor cells, but also their capacity to initiate tumours.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4846772/" 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/PMC4846772/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beyaz, Semir -- Mana, Miyeko D -- Roper, Jatin -- Kedrin, Dmitriy -- Saadatpour, Assieh -- Hong, Sue-Jean -- Bauer-Rowe, Khristian E -- Xifaras, Michael E -- Akkad, Adam -- Arias, Erika -- Pinello, Luca -- Katz, Yarden -- Shinagare, Shweta -- Abu-Remaileh, Monther -- Mihaylova, Maria M -- Lamming, Dudley W -- Dogum, Rizkullah -- Guo, Guoji -- Bell, George W -- Selig, Martin -- Nielsen, G Petur -- Gupta, Nitin -- Ferrone, Cristina R -- Deshpande, Vikram -- Yuan, Guo-Cheng -- Orkin, Stuart H -- Sabatini, David M -- Yilmaz, Omer H -- AI47389/AI/NIAID NIH HHS/ -- DK043351/DK/NIDDK NIH HHS/ -- K08 CA198002/CA/NCI NIH HHS/ -- K99 AG041765/AG/NIA NIH HHS/ -- K99 AG045144/AG/NIA NIH HHS/ -- P30 CA014051/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- R00 AG041765/AG/NIA NIH HHS/ -- R00 AG045144/AG/NIA NIH HHS/ -- R01 AI047389/AI/NIAID NIH HHS/ -- R01 CA103866/CA/NCI NIH HHS/ -- R01 CA129105/CA/NCI NIH HHS/ -- R37 AI047389/AI/NIAID NIH HHS/ -- T32DK007191/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Mar 3;531(7592):53-8. doi: 10.1038/nature17173.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The David H. Koch Institute for Integrative Cancer Research at MIT, Department of Biology, MIT, Cambridge, Massachusetts 02139, USA. ; Division of Hematology/Oncology, Boston Children's Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Howard Hughes Medical Institute, Harvard Stem Cell Institute, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Division of Gastroenterology and Molecular Oncology Research Institute, Tufts Medical Center, Boston, Massachusetts 02111, USA. ; Departments of Pathology, Gastroenterology, and Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA. ; Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute and Harvard T. H. Chan School of Public Health, Boston, Massachusetts 02115, USA. ; Whitehead Institute for Biomedical Research, Howard Hughes Medical Institute, Department of Biology, MIT, Cambridge, Massachusetts 02142, USA. ; Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA. ; Department of Medicine, University of Wisconsin-Madison, Madison, Wisconsin 53705, USA. ; Division of Digestive Diseases, University of Mississippi Medical Center, Jackson, Missisippi 39216, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26935695" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; Cell Self Renewal/drug effects ; Cell Transformation, Neoplastic/*drug effects ; Colonic Neoplasms/*pathology ; Diet, High-Fat/*adverse effects ; Female ; Genes, APC ; Humans ; Intestines/*pathology ; Male ; Mice ; Obesity/chemically induced/pathology ; Organoids/drug effects/metabolism/pathology ; PPAR delta/metabolism ; Signal Transduction/drug effects ; Stem Cell Niche/drug effects ; Stem Cells/*drug effects/metabolism/*pathology ; beta Catenin/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Characterization and transcription of arsenic respiration and resistance genes during in situ uranium bioremediation (2013)
    Springer Nature
    Details
    Publication Date: 2013-01-23
    Description: Characterization and transcription of arsenic respiration and resistance genes during in situ uranium bioremediation The ISME Journal 7, 370 (February 2013). doi:10.1038/ismej.2012.109 Authors: Ludovic Giloteaux, Dawn E Holmes, Kenneth H Williams, Kelly C Wrighton, Michael J Wilkins, Alison P Montgomery, Jessica A Smith, Roberto Orellana, Courtney A Thompson, Thomas J Roper, Philip E Long & Derek R Lovley
    Keywords: Geobacterarsenic respirationarsenic resistancegene transcriptionuranium bioremediation
    Print ISSN: 1751-7362
    Electronic ISSN: 1751-7370
    Topics: Biology
    Published by Springer Nature on behalf of The International Society for Microbial Ecology (ISME).
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  • 6
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    Enrichment of specific protozoan populations during in situ bioremediation of uranium-contaminated groundwater (2013)
    Springer Nature
    Details
    Publication Date: 2013-06-26
    Description: Enrichment of specific protozoan populations during in situ bioremediation of uranium-contaminated groundwater The ISME Journal 7, 1286 (July 2013). doi:10.1038/ismej.2013.20 Authors: Dawn E Holmes, Ludovic Giloteaux, Kenneth H Williams, Kelly C Wrighton, Michael J Wilkins, Courtney A Thompson, Thomas J Roper, Philip E Long & Derek R Lovley
    Keywords: GeobacterBreviataPeptococcaceaeHexamitidaeuranium bioremediationprotozoan predation
    Print ISSN: 1751-7362
    Electronic ISSN: 1751-7370
    Topics: Biology
    Published by Springer Nature on behalf of The International Society for Microbial Ecology (ISME).
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  • 7
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    Evidence for Post-Jurassic Tectonism in Eastern North America: ABSTRACT (1979)
    American Association of Petroleum Geologists
    Details
    Publication Date: 1979-01-01
    Print ISSN: 0149-1423
    Electronic ISSN: 1943-2674
    Topics: Geosciences
    Published by American Association of Petroleum Geologists
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  • 8
    Electronic Resource
    Electronic Resource
    Heater for Gas Chromatographic Columns (1960)
    s.l. : American Chemical Society
    Analytical chemistry 32 (1960), S. 447-448 
    Details
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ac60159a048
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  • 9
    Electronic Resource
    Electronic Resource
    Determination of volatile materials in polymers (1970)
    s.l. : American Chemical Society
    Analytical chemistry 42 (1970), S. 688-688 
    Details
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ac60288a006
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  • 10
    Electronic Resource
    Electronic Resource
    Molecular Still for Small Volumes (1949)
    s.l. : American Chemical Society
    Analytical chemistry 21 (1949), S. 1575-1575 
    Details
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ac60036a046
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