ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Myelomonocytic cell recruitment causes fatal CNS vascular injury during acute viral meningitis (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-11-18
    Description: Lymphocytic choriomeningitis virus infection of the mouse central nervous system (CNS) elicits fatal immunopathology through blood-brain barrier breakdown and convulsive seizures. Although lymphocytic-choriomeningitis-virus-specific cytotoxic T lymphocytes (CTLs) are essential for disease, their mechanism of action is not known. To gain insights into disease pathogenesis, we observed the dynamics of immune cells in the meninges by two-photon microscopy. Here we report visualization of motile CTLs and massive secondary recruitment of pathogenic monocytes and neutrophils that were required for vascular leakage and acute lethality. CTLs expressed multiple chemoattractants capable of recruiting myelomonocytic cells. We conclude that a CD8(+) T-cell-dependent disorder can proceed in the absence of direct T-cell effector mechanisms and rely instead on CTL-recruited myelomonocytic cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2702264/" 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/PMC2702264/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jiyun V -- Kang, Silvia S -- Dustin, Michael L -- McGavern, Dorian B -- AI055037/AI/NIAID NIH HHS/ -- AI070967-01/AI/NIAID NIH HHS/ -- NS041219-06/NS/NINDS NIH HHS/ -- NS061447-01/NS/NINDS NIH HHS/ -- R01 AI055037/AI/NIAID NIH HHS/ -- R01 AI055037-05/AI/NIAID NIH HHS/ -- England -- Nature. 2009 Jan 8;457(7226):191-5. doi: 10.1038/nature07591. Epub 2008 Nov 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular Pathogenesis, Helen L. and Martin S. Kimmel Center for Biology and Medicine, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19011611" target="_blank"〉PubMed〈/a〉
    Keywords: Acute Disease ; Animals ; Blood-Brain Barrier/physiopathology ; Central Nervous System/*blood supply/immunology/*pathology/virology ; Lymphocytic choriomeningitis virus/immunology/*pathogenicity ; Meninges/blood supply/immunology/pathology/virology ; Meningitis, Viral/*immunology/*pathology/physiopathology ; Mice ; Mice, Inbred C57BL ; Monocytes/cytology/*immunology ; Neutrophil Infiltration ; Neutrophils/cytology/*immunology ; Seizures/immunology/pathology/physiopathology ; Stromal Cells/virology ; T-Lymphocytes, Cytotoxic/cytology/immunology
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Cross-linking cellular prion protein triggers neuronal apoptosis in vivo (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-31
    Description: Neuronal death is a prominent, but poorly understood, pathological hallmark of prion disease. Notably, in the absence of the cellular prion protein (PrPC), the disease-associated isoform, PrPSc, appears not to be intrinsically neurotoxic, suggesting that PrPC itself may participate directly in the prion neurodegenerative cascade. Here, cross-linking PrPC in vivo with specific monoclonal antibodies was found to trigger rapid and extensive apoptosis in hippocampal and cerebellar neurons. These findings suggest that PrPC functions in the control of neuronal survival and provides a model to explore whether cross-linking of PrPC by oligomeric PrPSc can promote neuronal loss during prion infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Solforosi, Laura -- Criado, Jose R -- McGavern, Dorian B -- Wirz, Sebastian -- Sanchez-Alavez, Manuel -- Sugama, Shuei -- DeGiorgio, Lorraine A -- Volpe, Bruce T -- Wiseman, Erika -- Abalos, Gil -- Masliah, Eliezer -- Gilden, Donald -- Oldstone, Michael B -- Conti, Bruno -- Williamson, R Anthony -- AG00080/AG/NIA NIH HHS/ -- AG04342/AG/NIA NIH HHS/ -- AI09484/AI/NIAID NIH HHS/ -- HL63817/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2004 Mar 5;303(5663):1514-6. Epub 2004 Jan 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14752167" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology/*metabolism ; *Apoptosis ; Cell Survival ; Cerebellum/*cytology ; Complement Activation ; Dimerization ; Hippocampus/*cytology ; Immunoglobulin Fab Fragments/immunology/metabolism ; Immunoglobulin G/immunology/metabolism ; In Situ Nick-End Labeling ; Mice ; Mice, Inbred C57BL ; Neural Cell Adhesion Molecules/immunology/metabolism ; Neurons/*physiology ; PrPC Proteins/chemistry/immunology/*metabolism ; Recombinant Proteins/metabolism ; Signal Transduction
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Transcranial amelioration of inflammation and cell death after brain injury (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-12-10
    Description: Traumatic brain injury (TBI) is increasingly appreciated to be highly prevalent and deleterious to neurological function. At present, no effective treatment options are available, and little is known about the complex cellular response to TBI during its acute phase. To gain insights into TBI pathogenesis, we developed a novel murine closed-skull brain injury model that mirrors some pathological features associated with mild TBI in humans and used long-term intravital microscopy to study the dynamics of the injury response from its inception. Here we demonstrate that acute brain injury induces vascular damage, meningeal cell death, and the generation of reactive oxygen species (ROS) that ultimately breach the glial limitans and promote spread of the injury into the parenchyma. In response, the brain elicits a neuroprotective, purinergic-receptor-dependent inflammatory response characterized by meningeal neutrophil swarming and microglial reconstitution of the damaged glial limitans. We also show that the skull bone is permeable to small-molecular-weight compounds, and use this delivery route to modulate inflammation and therapeutically ameliorate brain injury through transcranial administration of the ROS scavenger, glutathione. Our results shed light on the acute cellular response to TBI and provide a means to locally deliver therapeutic compounds to the site of injury.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3930079/" 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/PMC3930079/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roth, Theodore L -- Nayak, Debasis -- Atanasijevic, Tatjana -- Koretsky, Alan P -- Latour, Lawrence L -- McGavern, Dorian B -- ZIA NS003112-05/Intramural NIH HHS/ -- England -- Nature. 2014 Jan 9;505(7482):223-8. doi: 10.1038/nature12808. Epub 2013 Dec 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24317693" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Topical ; Animals ; Antioxidants/administration & dosage/therapeutic use ; Astrocytes/pathology ; Brain/drug effects/pathology ; Brain Injuries/*complications/diagnosis/drug therapy/*pathology ; Cell Death/drug effects ; Disease Models, Animal ; Encephalitis/complications/drug therapy/*pathology/*prevention & control ; Glasgow Coma Scale ; Glutathione/administration & dosage/therapeutic use ; Humans ; Intracranial Hemorrhages/complications/diagnosis ; Male ; Meninges/drug effects/pathology ; Mice ; Microglia/cytology/drug effects/physiology ; Neuroprotective Agents/administration & dosage/therapeutic use ; Neutrophils/drug effects/physiology ; Purinergic P2 Receptor Antagonists/administration & ; dosage/pharmacology/therapeutic use ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species/metabolism ; Receptors, Purinergic P2/metabolism ; Receptors, Purinergic P2X7/metabolism ; Skull/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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Generation of recombinant lymphocytic choriomeningitis viruses with trisegmented genomes stably expressing two additional genes of interest (2009)
    National Academy of Sciences
    Details
    Publication Date: 2009-02-10
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Opposing STAT1 and STAT3 roles in IL-21 function [Immunology and Inflammation] (2015)
    National Academy of Sciences
    Details
    Publication Date: 2015-07-29
    Description: IL-21 is a type I cytokine essential for immune cell differentiation and function. Although IL-21 can activate several STAT family transcription factors, previous studies focused mainly on the role of STAT3 in IL-21 signaling. Here, we investigated the role of STAT1 and show that STAT1 and STAT3 have at least...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...