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  • 1
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    Unknown
    Publication Date: 2017-04-03
    Description: Geophysics Open archive. Free access to worldwide scientists during search and submission process. Earth-Prints is an open archive created and maintained by Istituto Nazionale di Geofisica e Vulcanologia with the collaboration of Programma Nazionale Ricerche in Antartide. It is maintained by CILEA .
    Description: Unpublished
    Description: Rome, Italy
    Description: open
    Keywords: Open Access ; Geophysics ; 05. General::05.03. Educational, History of Science, Public Issues::05.03.99. General or miscellaneous
    Repository Name: Istituto Nazionale di Geofisica e Vulcanologia (INGV)
    Type: Oral presentation
    Format: 4779008 bytes
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  • 2
    Publication Date: 2020-03-02
    Description: The present paper describes a multidisciplinary approach to the evaluation of a seismically triggered landslide that occurred in the Cerda area (Italy) on September 6, 2002, about 1 h after an earthquake took place in the south Tyrrhenian Sea. The study was focused on an analysis of the role of the seismic input in triggering the landslide, in view of the evidence that no other mass movement was recorded in the adjacent areas despite geological and geomorphological spatial homogeneity. The studied area is located on a slope of the western flank of the Fiume Imera Settentrionale (Northern Sicily), which is made up of clayey–arenitic rocks. The slope inclines gently but is not uniform due to fluvial, gravitative, and rainwash processes. Field data dealing with global positioning system (GPS), geology, geomorphology, geophysics (vertical electrical sounding, or VES), and geochemistry (soil gas fluxes and composition) were acquired and analysed in order to investigate the cause–effect relationships between the earthquake and the mass movement. The GPS survey allowed us to map the ground failures that have also been classified on the basis of their kinematical meaning (i.e., compressive, distensive, or transcurrent structures). The geological analysis revealed outcropping rocks and tectonic structures. The geomorphologic survey highlighted the presence of preexisting landslide bodies. The geophysical survey detected a buried surface located at a depth of about 100 m . Finally, the geochemical survey showed that the gas released from the displaced mass came from a shallow depth and was not related to any active fault system. The abovementioned information allowed us to interpret the landslide event as a partial reactivation of a preexisting landslide body that was triggered by the earthquake.
    Description: Ministero dell’Istruzione, dell’Universita` e della Ricerca (MIUR), Cofinanziamento Progetti di Ricerca di Rilevante Interesse Nazionale (COFIN PRIN) 2002 Project "Valutazione dell’Erosione del Suolo in Ambiente Mediterraneo"
    Description: Published
    Description: 101–116
    Description: partially_open
    Keywords: Landslide ; Earthquake ; Geochemistry ; Geophysics ; GPS ; Triggering mechanism ; 04. Solid Earth::04.04. Geology::04.04.03. Geomorphology
    Repository Name: Istituto Nazionale di Geofisica e Vulcanologia (INGV)
    Type: article
    Format: 1773148 bytes
    Format: 539 bytes
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  • 3
    Publication Date: 2005
    Keywords: Subduction zone ; Plate tectonics ; decollement ; Geol. aspects ; Ocean Drilling Program ; GRL ; 0500 ; Computational ; Geophysics ; (3200, ; 3252, ; 7833) ; 0900 ; Exploration ; Geophysics ; 3000 ; Marine ; Geology ; and ; Geophysics ; 8000 ; Structural ; Geology ; 8100 ; Tectonophysics
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  • 4
    Publication Date: 2005-12-03
    Description: Macrophages and dendritic cells (DCs) are crucial for immune and inflammatory responses and belong to a network of cells that has been termed the mononuclear phagocyte system (MPS). However, the origin and lineage of these cells remain poorly understood. Here, we describe the isolation and clonal analysis of a mouse bone marrow progenitor that is specific for monocytes, several macrophage subsets, and resident spleen DCs in vivo. It was also possible to recapitulate this differentiation in vitro by using treatment with the cytokines macrophage colony-stimulating factor and granulocyte-macrophage colony-stimulating factor. Thus, macrophages and DCs appear to renew from a common progenitor, providing a cellular and molecular basis for the concept of the MPS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fogg, Darin K -- Sibon, Claire -- Miled, Chaouki -- Jung, Steffen -- Aucouturier, Pierre -- Littman, Dan R -- Cumano, Ana -- Geissmann, Frederic -- A133856/PHS HHS/ -- G0900867/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Jan 6;311(5757):83-7. Epub 2005 Dec 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM, Laboratory of Mononuclear Phagocyte Biology, Avenir Team, Necker Enfants Malades Institute, 75015 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16322423" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Cell Separation ; Clone Cells ; Colony-Stimulating Factors/pharmacology ; Dendritic Cells/*cytology ; Flow Cytometry ; Granulocyte Colony-Stimulating Factor/pharmacology ; Hematopoietic Stem Cell Transplantation ; Macrophage Colony-Stimulating Factor/pharmacology ; Macrophages/*cytology ; Mice ; Mice, Inbred C57BL ; Myeloid Progenitor Cells/*cytology/immunology ; Proto-Oncogene Proteins c-kit/analysis ; Receptors, Cytokine/analysis ; Receptors, HIV/analysis ; Recombinant Proteins ; Spleen/cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):43-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy ; Brain-Derived Neurotrophic Factor/metabolism ; Cells, Cultured ; Clinical Trials as Topic ; Corpus Striatum/pathology ; Disease Models, Animal ; Gene Expression Regulation ; Humans ; Huntington Disease/*drug therapy/genetics/pathology/*physiopathology ; Mice ; Mitochondria/metabolism ; Mutation ; Nerve Tissue Proteins/chemistry/*genetics/metabolism/*physiology ; Neurons/*physiology ; Nuclear Proteins/chemistry/*genetics/metabolism/*physiology ; Peptides ; Transcription Factors/metabolism ; Trinucleotide Repeat Expansion
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-09-06
    Description: Large numbers of noncoding RNA transcripts (ncRNAs) are being revealed by complementary DNA cloning and genome tiling array studies in animals. The big and as yet largely unanswered question is whether these transcripts are relevant. A paper by Willingham et al. shows the way forward by developing a strategy for large-scale functional screening of ncRNAs, involving small interfering RNA knockdowns in cell-based screens, which identified a previously unidentified ncRNA repressor of the transcription factor NFAT. It appears likely that ncRNAs constitute a critical hidden layer of gene regulation in complex organisms, the understanding of which requires new approaches in functional genomics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mattick, John S -- New York, N.Y. -- Science. 2005 Sep 2;309(5740):1527-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Australian Research Council Special Research Centre for Functional and Applied Genomics, Institute for Molecular Bioscience, University of Queensland, Brisbane, QLD 4072, Australia. j.mattick@imb.uq.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16141063" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Conserved Sequence ; DNA-Binding Proteins/antagonists & inhibitors ; *Genomics ; Humans ; Mice ; NFATC Transcription Factors ; Nuclear Proteins/antagonists & inhibitors ; *RNA Interference ; RNA, Untranslated/antagonists & inhibitors/genetics/*physiology ; Transcription Factors/antagonists & inhibitors ; beta Karyopherins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2005-04-23
    Description: The CLOCK transcription factor is a key component of the molecular circadian clock within pacemaker neurons of the hypothalamic suprachiasmatic nucleus. We found that homozygous Clock mutant mice have a greatly attenuated diurnal feeding rhythm, are hyperphagic and obese, and develop a metabolic syndrome of hyperleptinemia, hyperlipidemia, hepatic steatosis, hyperglycemia, and hypoinsulinemia. Expression of transcripts encoding selected hypothalamic peptides associated with energy balance was attenuated in the Clock mutant mice. These results suggest that the circadian clock gene network plays an important role in mammalian energy balance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3764501/" 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/PMC3764501/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turek, Fred W -- Joshu, Corinne -- Kohsaka, Akira -- Lin, Emily -- Ivanova, Ganka -- McDearmon, Erin -- Laposky, Aaron -- Losee-Olson, Sue -- Easton, Amy -- Jensen, Dalan R -- Eckel, Robert H -- Takahashi, Joseph S -- Bass, Joseph -- AG11412/AG/NIA NIH HHS/ -- AG18200/AG/NIA NIH HHS/ -- DK02675/DK/NIDDK NIH HHS/ -- DK26356/DK/NIDDK NIH HHS/ -- HL59598/HL/NHLBI NIH HHS/ -- HL75029/HL/NHLBI NIH HHS/ -- K08 DK002675/DK/NIDDK NIH HHS/ -- P01 AG011412/AG/NIA NIH HHS/ -- R01 AG018200/AG/NIA NIH HHS/ -- R01 DK026356/DK/NIDDK NIH HHS/ -- R01 HL059598/HL/NHLBI NIH HHS/ -- R01 HL075029/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2005 May 13;308(5724):1043-5. Epub 2005 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Northwestern University, Evanston, IL 60208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15845877" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/pathology ; Animals ; Body Weight ; Brain/metabolism ; CLOCK Proteins ; *Circadian Rhythm ; Dietary Fats/administration & dosage ; Energy Intake ; *Energy Metabolism ; *Feeding Behavior ; Hepatocytes/pathology ; Hyperglycemia ; Hyperlipidemias ; Insulin/blood ; Leptin/blood ; Metabolic Syndrome X/genetics/*physiopathology ; Mice ; Mice, Inbred C57BL ; Motor Activity ; Mutation ; Neuropeptides/genetics/metabolism ; Obesity/genetics/*physiopathology ; Trans-Activators/*genetics/*physiology ; Weight Gain
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2005-10-01
    Description: Monocular deprivation normally alters ocular dominance in the visual cortex only during a postnatal critical period (20 to 32 days postnatal in mice). We find that mutations in the Nogo-66 receptor (NgR) affect cessation of ocular dominance plasticity. In NgR-/- mice, plasticity during the critical period is normal, but it continues abnormally such that ocular dominance at 45 or 120 days postnatal is subject to the same plasticity as at juvenile ages. Thus, physiological NgR signaling from myelin-derived Nogo, MAG, and OMgp consolidates the neural circuitry established during experience-dependent plasticity. After pathological trauma, similar NgR signaling limits functional recovery and axonal regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2856689/" 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/PMC2856689/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGee, Aaron W -- Yang, Yupeng -- Fischer, Quentin S -- Daw, Nigel W -- Strittmatter, Stephen M -- R01 NS039962/NS/NINDS NIH HHS/ -- R01 NS039962-10/NS/NINDS NIH HHS/ -- R01 NS042304/NS/NINDS NIH HHS/ -- R01 NS042304-08/NS/NINDS NIH HHS/ -- R01 NS056485/NS/NINDS NIH HHS/ -- R01 NS056485-04/NS/NINDS NIH HHS/ -- R37 NS033020/NS/NINDS NIH HHS/ -- R37 NS033020-15/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 30;309(5744):2222-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16195464" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chondroitin Sulfate Proteoglycans/metabolism ; Darkness ; Dominance, Ocular/*physiology ; Electrophysiology ; GPI-Linked Proteins ; Gene Targeting ; Mice ; Mice, Inbred C57BL ; Mutation ; Myelin Basic Protein/metabolism ; Myelin Proteins/genetics/metabolism/*physiology ; Myelin Sheath/*physiology ; Myelin-Associated Glycoprotein/metabolism ; Neurites/physiology ; Neuronal Plasticity/*physiology ; Neurons/*physiology ; Photic Stimulation ; Receptors, Cell Surface/genetics/*physiology ; Signal Transduction ; Visual Cortex/cytology/growth & development/*physiology ; gamma-Aminobutyric Acid/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2005-02-05
    Description: The gene encoding the Nod2 protein is frequently mutated in Crohn's disease (CD) patients, although the physiological function of Nod2 in the intestine remains elusive. Here we show that protective immunity mediated by Nod2 recognition of bacterial muramyl dipeptide is abolished in Nod2-deficient mice. These animals are susceptible to bacterial infection via the oral route but not through intravenous or peritoneal delivery. Nod2 is required for the expression of a subgroup of intestinal anti-microbial peptides, known as cryptdins. The Nod2 protein is thus a critical regulator of bacterial immunity within the intestine, providing a possible mechanism for Nod2 mutations in CD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kobayashi, Koichi S -- Chamaillard, Mathias -- Ogura, Yasunori -- Henegariu, Octavian -- Inohara, Naohiro -- Nunez, Gabriel -- Flavell, Richard A -- New York, N.Y. -- Science. 2005 Feb 4;307(5710):731-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15692051" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylmuramyl-Alanyl-Isoglutamine/*immunology ; Animals ; *Antibody Formation ; Female ; Gene Expression ; Gene Targeting ; Ileum/*immunology/microbiology ; *Immunity, Innate ; Immunity, Mucosal ; Immunoglobulins/biosynthesis ; Interleukins/biosynthesis ; Intestinal Diseases/immunology/microbiology ; Intestinal Mucosa/immunology/microbiology ; Intracellular Signaling Peptides and Proteins/*physiology ; Ligands ; Lipopolysaccharides/toxicity ; Listeria monocytogenes/growth & development/immunology/isolation & purification ; Listeriosis/*immunology/microbiology ; Liver/microbiology ; Macrophages/immunology ; Male ; Membrane Glycoproteins/physiology ; Mice ; Nod2 Signaling Adaptor Protein ; Oligonucleotide Array Sequence Analysis ; Protein Precursors/biosynthesis/genetics ; Receptors, Cell Surface/physiology ; Serum Albumin/immunology ; Signal Transduction ; Spleen/microbiology ; Toll-Like Receptors ; Tumor Necrosis Factor-alpha/biosynthesis ; alpha-Defensins/*biosynthesis/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-08-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2005 Aug 26;309(5739):1310-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16123271" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics ; Animals ; Blood Glucose/analysis ; Female ; Glucuronidase ; Insulin/blood/metabolism ; Insulin Resistance ; Insulin-Like Growth Factor I/metabolism ; Longevity/*genetics ; Male ; Membrane Proteins/blood/*genetics/*physiology ; Mice ; Mutation ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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