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  • 1
    Publication Date: 2015-01-30
    Description: A key event in human evolution is the expansion of modern humans of African origin across Eurasia between 60 and 40 thousand years (kyr) before present (bp), replacing all other forms of hominins. Owing to the scarcity of human fossils from this period, these ancestors of all present-day non-African modern populations remain largely enigmatic. Here we describe a partial calvaria, recently discovered at Manot Cave (Western Galilee, Israel) and dated to 54.7 +/- 5.5 kyr bp (arithmetic mean +/- 2 standard deviations) by uranium-thorium dating, that sheds light on this crucial event. The overall shape and discrete morphological features of the Manot 1 calvaria demonstrate that this partial skull is unequivocally modern. It is similar in shape to recent African skulls as well as to European skulls from the Upper Palaeolithic period, but different from most other early anatomically modern humans in the Levant. This suggests that the Manot people could be closely related to the first modern humans who later successfully colonized Europe. Thus, the anatomical features used to support the 'assimilation model' in Europe might not have been inherited from European Neanderthals, but rather from earlier Levantine populations. Moreover, at present, Manot 1 is the only modern human specimen to provide evidence that during the Middle to Upper Palaeolithic interface, both modern humans and Neanderthals contemporaneously inhabited the southern Levant, close in time to the likely interbreeding event with Neanderthals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hershkovitz, Israel -- Marder, Ofer -- Ayalon, Avner -- Bar-Matthews, Miryam -- Yasur, Gal -- Boaretto, Elisabetta -- Caracuta, Valentina -- Alex, Bridget -- Frumkin, Amos -- Goder-Goldberger, Mae -- Gunz, Philipp -- Holloway, Ralph L -- Latimer, Bruce -- Lavi, Ron -- Matthews, Alan -- Slon, Viviane -- Mayer, Daniella Bar-Yosef -- Berna, Francesco -- Bar-Oz, Guy -- Yeshurun, Reuven -- May, Hila -- Hans, Mark G -- Weber, Gerhard W -- Barzilai, Omry -- England -- Nature. 2015 Apr 9;520(7546):216-9. doi: 10.1038/nature14134. Epub 2015 Jan 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] The Dan David Laboratory for the Search and Study of Modern Humans, Sackler Faculty of Medicine, Tel Aviv University, PO Box 39040, Tel Aviv 6997801, Israel [2] The Steinhardt Museum of Natural History and National Research Center, Tel Aviv University, PO Box 39040, Tel Aviv 6997801, Israel. ; Archaeology Division, Ben-Gurion University of the Negev, PO Box 653, Beer-Sheva 8410501, Israel. ; Geological Survey of Israel, 30 Malkhe Israel Street, Jerusalem 95501, Israel. ; Max Planck Society-Weizmann Institute Center for Integrative Archaeology and Anthropology, D-REAMS Radiocarbon Laboratory, Weizmann Institute of Science, Rehovot 76100, Israel. ; 1] Max Planck Society-Weizmann Institute Center for Integrative Archaeology and Anthropology, D-REAMS Radiocarbon Laboratory, Weizmann Institute of Science, Rehovot 76100, Israel [2] Department of Anthropology and Human Evolutionary Biology, Harvard University, 11 Divinity Avenue, Cambridge, Massachusetts 02138, USA. ; Department of Geography, The Hebrew University of Jerusalem, Jerusalem 91905, Israel. ; Institute of Archaeology, The Hebrew University of Jerusalem, Mount Scopus, Jerusalem 91905, Israel. ; Department of Human Evolution, Max-Planck-Institute for Evolutionary Anthropology, Deutscher Platz 6, D-04103, Leipzig, Germany. ; Department of Anthropology, Columbia University, New York 10027, USA. ; 1] Department of Anatomy, Case Western Reserve University, Cleveland, Ohio 44106, USA [2] Department of Orthodontics, Case Western Reserve University School of Dental Medicine, 10900 Euclid Avenue, Cleveland, Ohio 44106, USA. ; 8 Dan Street, Modi'in 7173161, Israel. ; Institute of Earth Sciences, The Hebrew University of Jerusalem, Edmond J. Safra Campus, Givat Ram, Jerusalem 91904, Israel. ; The Dan David Laboratory for the Search and Study of Modern Humans, Sackler Faculty of Medicine, Tel Aviv University, PO Box 39040, Tel Aviv 6997801, Israel. ; The Steinhardt Museum of Natural History and National Research Center, Tel Aviv University, PO Box 39040, Tel Aviv 6997801, Israel. ; Department of Archaeology, Simon Fraser University, 8888 University Drive, Burnaby, British Columbia V5A 1S6, Canada. ; Zinman Institute of Archaeology, University of Haifa, Haifa 3498838, Israel. ; 1] The Steinhardt Museum of Natural History and National Research Center, Tel Aviv University, PO Box 39040, Tel Aviv 6997801, Israel [2] Department of Anatomy and Anthropology, Sackler Faculty of Medicine, Tel Aviv University, PO Box 39040, Tel Aviv 6997801, Israel. ; Department of Orthodontics, Case Western Reserve University School of Dental Medicine, 10900 Euclid Avenue, Cleveland, Ohio 44106, USA. ; 1] Department of Anthropology, University of Vienna, Althanstrasse 12-14, A-1090 Vienna, Austria [2] The Core Facility for Micro-Computed Tomography, University of Vienna, Althanstrasse 12-14, A-1090, Vienna, Austria. ; Israel Antiquities Authority, PO Box 586, Jerusalem 91004, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25629628" target="_blank"〉PubMed〈/a〉
    Keywords: Africa/ethnology ; Animals ; *Caves ; Europe/ethnology ; *Fossils ; Humans ; Israel ; Neanderthals/anatomy & histology/physiology ; *Phylogeny ; Skull/*anatomy & histology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2015-03-15
    Description: Sepsis is a frequently fatal condition characterized by an uncontrolled and harmful host reaction to microbial infection. Despite the prevalence and severity of sepsis, we lack a fundamental grasp of its pathophysiology. Here we report that the cytokine interleukin-3 (IL-3) potentiates inflammation in sepsis. Using a mouse model of abdominal sepsis, we showed that innate response activator B cells produce IL-3, which induces myelopoiesis of Ly-6C(high) monocytes and neutrophils and fuels a cytokine storm. IL-3 deficiency protects mice against sepsis. In humans with sepsis, high plasma IL-3 levels are associated with high mortality even after adjusting for prognostic indicators. This study deepens our understanding of immune activation, identifies IL-3 as an orchestrator of emergency myelopoiesis, and reveals a new therapeutic target for treating sepsis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4376966/" 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/PMC4376966/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weber, Georg F -- Chousterman, Benjamin G -- He, Shun -- Fenn, Ashley M -- Nairz, Manfred -- Anzai, Atsushi -- Brenner, Thorsten -- Uhle, Florian -- Iwamoto, Yoshiko -- Robbins, Clinton S -- Noiret, Lorette -- Maier, Sarah L -- Zonnchen, Tina -- Rahbari, Nuh N -- Scholch, Sebastian -- Klotzsche-von Ameln, Anne -- Chavakis, Triantafyllos -- Weitz, Jurgen -- Hofer, Stefan -- Weigand, Markus A -- Nahrendorf, Matthias -- Weissleder, Ralph -- Swirski, Filip K -- 5R01HL095612/HL/NHLBI NIH HHS/ -- R01 HL095612/HL/NHLBI NIH HHS/ -- R56 AI104695/AI/NIAID NIH HHS/ -- R56-AI104695/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2015 Mar 13;347(6227):1260-5. doi: 10.1126/science.aaa4268.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Department of Visceral, Thoracic and Vascular Surgery, Technische Universitat Dresden, Dresden, Germany. fswirski@mgh.harvard.edu georg.weber@uniklinikum-dresden.de. ; Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. ; Department of Anesthesiology, University of Heidelberg, Heidelberg, Germany. ; Department of Visceral, Thoracic and Vascular Surgery, Technische Universitat Dresden, Dresden, Germany. ; Department of Clinical Pathobiochemistry and Institute for Clinical Chemistry and Laboratory Medicine, Technische Universitat Dresden, Dresden, Germany. ; Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA. ; Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. fswirski@mgh.harvard.edu georg.weber@uniklinikum-dresden.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25766237" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocyte Subsets/immunology ; Cytokines/immunology/metabolism ; Disease Models, Animal ; Humans ; Inflammation ; Interleukin-3/blood/*immunology/metabolism ; Lipopolysaccharides/immunology ; Lymphoid Tissue/immunology ; Mice ; Mice, Inbred BALB C ; Monocytes/immunology ; Myelopoiesis ; Neutrophils/immunology ; Peritonitis/immunology/pathology ; Prognosis ; Sepsis/*immunology/mortality/pathology/therapy
    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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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ball, Steven G -- Bhattacharya, Debashish -- Weber, Andreas P M -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):659-60. doi: 10.1126/science.aad8864.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Universite de Lille CNRS, UMR 8576-UGSF-Unite de Glycobiologie Structurale et Fonctionnelle, F 59000 Lille, France. ; Department of Ecology, Evolution and Natural Resources, Rutgers University, New Brunswick, NJ 08901, USA. debash.bhattacharya@gmail.com. ; Institute for Plant Biochemistry, Center of Excellence on Plant Sciences, Heinrich-Heine-University, Universitatsstrasse 1, D-40225 Dusseldorf, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912842" target="_blank"〉PubMed〈/a〉
    Keywords: Alphaproteobacteria/*genetics/pathogenicity ; Animals ; Archaea/metabolism ; *Biological Evolution ; Endocytosis ; Energy Metabolism/genetics ; Eukaryota/genetics ; *Host-Pathogen Interactions ; Humans ; Mitochondria/*genetics ; Plastids/*genetics ; Rickettsia/genetics/pathogenicity ; Symbiosis/*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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  • 4
    Publication Date: 2016-03-05
    Description: Hepatocellular carcinoma (HCC) is the second most common cause of cancer-related death. Non-alcoholic fatty liver disease (NAFLD) affects a large proportion of the US population and is considered to be a metabolic predisposition to liver cancer. However, the role of adaptive immune responses in NAFLD-promoted HCC is largely unknown. Here we show, in mouse models and human samples, that dysregulation of lipid metabolism in NAFLD causes a selective loss of intrahepatic CD4(+) but not CD8(+) T lymphocytes, leading to accelerated hepatocarcinogenesis. We also demonstrate that CD4(+) T lymphocytes have greater mitochondrial mass than CD8(+) T lymphocytes and generate higher levels of mitochondrially derived reactive oxygen species (ROS). Disruption of mitochondrial function by linoleic acid, a fatty acid accumulated in NAFLD, causes more oxidative damage than other free fatty acids such as palmitic acid, and mediates selective loss of intrahepatic CD4(+) T lymphocytes. In vivo blockade of ROS reversed NAFLD-induced hepatic CD4(+) T lymphocyte decrease and delayed NAFLD-promoted HCC. Our results provide an unexpected link between lipid dysregulation and impaired anti-tumour surveillance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4786464/" 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/PMC4786464/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ma, Chi -- Kesarwala, Aparna H -- Eggert, Tobias -- Medina-Echeverz, Jose -- Kleiner, David E -- Jin, Ping -- Stroncek, David F -- Terabe, Masaki -- Kapoor, Veena -- ElGindi, Mei -- Han, Miaojun -- Thornton, Angela M -- Zhang, Haibo -- Egger, Michele -- Luo, Ji -- Felsher, Dean W -- McVicar, Daniel W -- Weber, Achim -- Heikenwalder, Mathias -- Greten, Tim F -- ZIA BC011345-06/Intramural NIH HHS/ -- ZIABC011303/PHS HHS/ -- England -- Nature. 2016 Mar 10;531(7593):253-7. doi: 10.1038/nature16969. Epub 2016 Mar 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gastrointestinal Malignancy Section, Thoracic and Gastrointestinal Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Cell Processing Section, Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Vaccine Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Experimental Transplantation and Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Institute of Surgical Pathology, University and University Hospital Zurich, Zurich 8091, Switzerland. ; Division of Oncology, Department of Medicine and Pathology, Stanford University, California 94305, USA. ; Cancer and Inflammation Program, National Cancer Institute, Frederick, Maryland 21702, USA. ; Institute of Virology, Technische Universitat Munchen/Helmholtz Zentrum Munchen, Munich 81675, Germany. ; Division of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Heidelberg 69120, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26934227" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/immunology/metabolism/*pathology ; CD8-Positive T-Lymphocytes/immunology/pathology ; *Carcinogenesis/immunology/pathology ; Carcinoma, Hepatocellular/*immunology/metabolism/*pathology ; Case-Control Studies ; Choline/metabolism ; Diet ; Disease Models, Animal ; Genes, myc ; Hepatocytes/metabolism/pathology ; Humans ; Linoleic Acid/metabolism ; Lipid Metabolism ; Liver/immunology/pathology ; Liver Neoplasms/*immunology/metabolism/*pathology ; Male ; Methionine/deficiency ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism/pathology ; Non-alcoholic Fatty Liver Disease/*immunology/metabolism/pathology ; Oxidative Stress ; Reactive Oxygen Species/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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