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  1. Book: Erdwärmesonden und Erdwärmekollektoren in Mecklenburg-Vorpommern

    Obst, Karsten / Iffland, Joachim / Schwerdtfeger, Beate / Brandes, Juliane

    Leitfaden zur geothermischen Nutzung des oberflächennahen Untergrundes

    2015  

    Author's details Herausgeber: Landesamt für Umwelt, Naturschutz und Geologie Mecklenburg-Vorpommern (LUNG) ; Bearbeitung: Dipl.-Geol. Dr. Karsten Obst, Dipl.-Geophys. Joachim Iffland ; unter Mitwirkung von Dipl.-Geoln. Dr. Beate Schwerdtfeger, Dipl.-Geoln. Juliane Brandes
    Language German
    Size 32 Seiten, 20 Seiten in verschiedener Zählung, Illustrationen, Diagramme
    Edition 2. überarbeitete und erweiterte Auflage
    Publisher Landesamt für Umwelt, Naturschutz und Geologie Mecklenburg-Vorpommern (LUNG)
    Publishing place Güstrow
    Publishing country Germany
    Document type Book
    HBZ-ID HT019202976
    ISBN 978-3-9808263-5-8 ; 3-9808263-5-X
    Database Catalogue ZB MED Nutrition, Environment, Agriculture

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    In stock of ZB MED Bonn / Germany

    Shelf markLoan statusLocation
    164/429 available for loan (reading room) Freihandmagazin (U1)

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  2. Book ; Online ; Thesis: Influence of IL-12

    Obst, Juliane [Verfasser]

    2017  

    Author's details IL-23 signaling on Alzheimer’s disease β-amyloid pathology / Juliane Obst
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language English
    Publisher Medizinische Fakultät Charité - Universitätsmedizin Berlin
    Publishing place Berlin
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

    Full text online

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  3. Article ; Online: Spermine and spermidine modulate T-cell function in older adults with and without cognitive decline ex vivo.

    Fischer, Maximilian / Ruhnau, Johanna / Schulze, Juliane / Obst, Daniela / Flöel, Agnes / Vogelgesang, Antje

    Aging

    2020  Volume 12, Issue 13, Page(s) 13716–13739

    Abstract: The global increase in neurodegenerative disorders is one of the most crucial public health issues. Oral polyamine intake was shown to improve memory performance which is thought to be mediated at least in part via increased autophagy induced in brain ... ...

    Abstract The global increase in neurodegenerative disorders is one of the most crucial public health issues. Oral polyamine intake was shown to improve memory performance which is thought to be mediated at least in part via increased autophagy induced in brain cells. In Alzheimer's Disease, T-cells were identified as important mediators of disease pathology. Since autophagy is a central regulator of cell activation and cytokine production, we investigated the influence of polyamines on T-cell activation, autophagy, and the release of Th1/Th2 cytokines from blood samples of patients (n=22) with cognitive impairment or dementia in comparison to healthy controls (n=12)
    MeSH term(s) Aged ; Aged, 80 and over ; Aging/physiology ; Autophagy/drug effects ; Autophagy/immunology ; Case-Control Studies ; Cognitive Dysfunction/blood ; Cognitive Dysfunction/immunology ; Cognitive Dysfunction/physiopathology ; Cognitive Dysfunction/prevention & control ; Cytokines/analysis ; Cytokines/immunology ; Cytokines/metabolism ; Dementia/blood ; Dementia/immunology ; Dementia/physiopathology ; Dementia/prevention & control ; Dietary Supplements ; Down-Regulation ; Female ; Healthy Volunteers ; Humans ; Lymphocyte Activation/drug effects ; Male ; Spermidine/administration & dosage ; Spermine/administration & dosage ; T-Lymphocytes/drug effects ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
    Chemical Substances Cytokines ; Spermine (2FZ7Y3VOQX) ; Spermidine (U87FK77H25)
    Language English
    Publishing date 2020-06-30
    Publishing country United States
    Document type Journal Article ; Observational Study ; Research Support, Non-U.S. Gov't
    ISSN 1945-4589
    ISSN (online) 1945-4589
    DOI 10.18632/aging.103527
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: PLCγ2 regulates TREM2 signalling and integrin-mediated adhesion and migration of human iPSC-derived macrophages.

    Obst, Juliane / Hall-Roberts, Hazel L / Smith, Thomas B / Kreuzer, Mira / Magno, Lorenza / Di Daniel, Elena / Davis, John B / Mead, Emma

    Scientific reports

    2021  Volume 11, Issue 1, Page(s) 19842

    Abstract: Human genetic studies have linked rare coding variants in microglial genes, such as TREM2, and more recently PLCG2 to Alzheimer's disease (AD) pathology. The P522R variant in PLCG2 has been shown to confer protection for AD and to result in a subtle ... ...

    Abstract Human genetic studies have linked rare coding variants in microglial genes, such as TREM2, and more recently PLCG2 to Alzheimer's disease (AD) pathology. The P522R variant in PLCG2 has been shown to confer protection for AD and to result in a subtle increase in enzymatic activity. PLCγ2 is a key component of intracellular signal transduction networks and induces Ca
    MeSH term(s) Biomarkers ; Calcium/metabolism ; Cell Adhesion/genetics ; Cell Movement/genetics ; Cytokines/metabolism ; Extracellular Matrix ; Gene Knockdown Techniques ; Humans ; Induced Pluripotent Stem Cells/cytology ; Induced Pluripotent Stem Cells/metabolism ; Inflammation Mediators/metabolism ; Integrins/metabolism ; Macrophages/cytology ; Macrophages/metabolism ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Phagocytosis ; Phospholipase C gamma/genetics ; Phospholipase C gamma/metabolism ; Receptors, Immunologic/genetics ; Receptors, Immunologic/metabolism ; Signal Transduction
    Chemical Substances Biomarkers ; Cytokines ; Inflammation Mediators ; Integrins ; Membrane Glycoproteins ; Receptors, Immunologic ; TREM2 protein, human ; PLCG2 protein, human (EC 3.1.4.3) ; Phospholipase C gamma (EC 3.1.4.3) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2021-10-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-021-96144-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: The Role of Microglia in Prion Diseases: A Paradigm of Functional Diversity.

    Obst, Juliane / Simon, Emilie / Mancuso, Renzo / Gomez-Nicola, Diego

    Frontiers in aging neuroscience

    2017  Volume 9, Page(s) 207

    Abstract: Inflammation is a major component of neurodegenerative diseases. Microglia are the innate immune cells in the central nervous system (CNS). In the healthy brain, microglia contribute to tissue homeostasis and regulation of synaptic plasticity. Under ... ...

    Abstract Inflammation is a major component of neurodegenerative diseases. Microglia are the innate immune cells in the central nervous system (CNS). In the healthy brain, microglia contribute to tissue homeostasis and regulation of synaptic plasticity. Under disease conditions, they play a key role in the development and maintenance of the neuroinflammatory response, by showing enhanced proliferation and activation. Prion diseases are progressive chronic neurodegenerative disorders associated with the accumulation of the scrapie prion protein PrP
    Language English
    Publishing date 2017-06-23
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2558898-9
    ISSN 1663-4365
    ISSN 1663-4365
    DOI 10.3389/fnagi.2017.00207
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Replicative senescence dictates the emergence of disease-associated microglia and contributes to Aβ pathology.

    Hu, Yanling / Fryatt, Gemma L / Ghorbani, Mohammadmersad / Obst, Juliane / Menassa, David A / Martin-Estebane, Maria / Muntslag, Tim A O / Olmos-Alonso, Adrian / Guerrero-Carrasco, Monica / Thomas, Daniel / Cragg, Mark S / Gomez-Nicola, Diego

    Cell reports

    2021  Volume 35, Issue 10, Page(s) 109228

    Abstract: The sustained proliferation of microglia is a key hallmark of Alzheimer's disease (AD), accelerating its progression. Here, we aim to understand the long-term impact of the early and prolonged microglial proliferation observed in AD, hypothesizing that ... ...

    Abstract The sustained proliferation of microglia is a key hallmark of Alzheimer's disease (AD), accelerating its progression. Here, we aim to understand the long-term impact of the early and prolonged microglial proliferation observed in AD, hypothesizing that extensive and repeated cycling would engender a distinct transcriptional and phenotypic trajectory. We show that the early and sustained microglial proliferation seen in an AD-like model promotes replicative senescence, characterized by increased βgal activity, a senescence-associated transcriptional signature, and telomere shortening, correlating with the appearance of disease-associated microglia (DAM) and senescent microglial profiles in human post-mortem AD cases. The prevention of early microglial proliferation hinders the development of senescence and DAM, impairing the accumulation of Aβ, as well as associated neuritic and synaptic damage. Overall, our results indicate that excessive microglial proliferation leads to the generation of senescent DAM, which contributes to early Aβ pathology in AD.
    MeSH term(s) Amyloid beta-Peptides/genetics ; Animals ; Cellular Senescence/genetics ; Disease Models, Animal ; Humans ; Mice ; Mice, Transgenic ; Microglia/metabolism
    Chemical Substances Amyloid beta-Peptides
    Language English
    Publishing date 2021-06-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2021.109228
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: PLCγ2 regulates TREM2 signalling and integrin-mediated adhesion and migration of human iPSC-derived macrophages

    Juliane Obst / Hazel L. Hall-Roberts / Thomas B. Smith / Mira Kreuzer / Lorenza Magno / Elena Di Daniel / John B. Davis / Emma Mead

    Scientific Reports, Vol 11, Iss 1, Pp 1-

    2021  Volume 17

    Abstract: Abstract Human genetic studies have linked rare coding variants in microglial genes, such as TREM2, and more recently PLCG2 to Alzheimer’s disease (AD) pathology. The P522R variant in PLCG2 has been shown to confer protection for AD and to result in a ... ...

    Abstract Abstract Human genetic studies have linked rare coding variants in microglial genes, such as TREM2, and more recently PLCG2 to Alzheimer’s disease (AD) pathology. The P522R variant in PLCG2 has been shown to confer protection for AD and to result in a subtle increase in enzymatic activity. PLCγ2 is a key component of intracellular signal transduction networks and induces Ca2+ signals downstream of many myeloid cell surface receptors, including TREM2. To explore the relationship between PLCγ2 and TREM2 and the role of PLCγ2 in regulating immune cell function, we generated human induced pluripotent stem cell (iPSC)- derived macrophages from isogenic lines with homozygous PLCG2 knockout (Ko). Stimulating TREM2 signalling using a polyclonal antibody revealed a complete lack of calcium flux and IP1 accumulation in PLCγ2 Ko cells, demonstrating a non-redundant role of PLCγ2 in calcium release downstream of TREM2. Loss of PLCγ2 led to broad changes in expression of several macrophage surface markers and phenotype, including reduced phagocytic activity and survival, while LPS-induced secretion of the inflammatory cytokines TNFα and IL-6 was unaffected. We identified additional deficits in PLCγ2- deficient cells that compromised cellular adhesion and migration. Thus, PLCγ2 is key in enabling divergent cellular functions and might be a promising target to increase beneficial microglial functions.
    Keywords Medicine ; R ; Science ; Q
    Subject code 572
    Language English
    Publishing date 2021-10-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Interleukin-12/23 deficiency differentially affects pathology in male and female Alzheimer's disease-like mice.

    Eede, Pascale / Obst, Juliane / Benke, Eileen / Yvon-Durocher, Genevieve / Richard, Bernhard C / Gimber, Niclas / Schmoranzer, Jan / Böddrich, Annett / Wanker, Erich E / Prokop, Stefan / Heppner, Frank L

    EMBO reports

    2020  Volume 21, Issue 3, Page(s) e48530

    Abstract: Pathological aggregation of amyloid-β (Aβ) is a main hallmark of Alzheimer's disease (AD). Recent genetic association studies have linked innate immune system actions to AD development, and current evidence suggests profound gender differences in AD ... ...

    Abstract Pathological aggregation of amyloid-β (Aβ) is a main hallmark of Alzheimer's disease (AD). Recent genetic association studies have linked innate immune system actions to AD development, and current evidence suggests profound gender differences in AD pathogenesis. Here, we characterise gender-specific pathologies in the APP23 AD-like mouse model and find that female mice show stronger amyloidosis and astrogliosis compared with male mice. We tested the gender-specific effect of lack of IL12p40, the shared subunit of interleukin (IL)-12 and IL-23, that we previously reported to ameliorate pathology in APPPS1 mice. IL12p40 deficiency gender specifically reduces Aβ plaque burden in male APP23 mice, while in female mice, a significant reduction in soluble Aβ
    MeSH term(s) Alzheimer Disease/genetics ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Brain/metabolism ; Disease Models, Animal ; Female ; Interleukin-12/deficiency ; Interleukin-12/genetics ; Interleukin-12 Subunit p40/deficiency ; Interleukin-12 Subunit p40/genetics ; Interleukin-23 Subunit p19/deficiency ; Interleukin-23 Subunit p19/genetics ; Male ; Mice ; Mice, Transgenic ; Plaque, Amyloid
    Chemical Substances Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Il12b protein, mouse ; Il23a protein, mouse ; Interleukin-12 Subunit p40 ; Interleukin-23 Subunit p19 ; Interleukin-12 (187348-17-0)
    Language English
    Publishing date 2020-01-30
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.15252/embr.201948530
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5433: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 41: Show issues

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  9. Conference proceedings: IL-12/IL-23 signalling in Alzheimer’s disease

    Eede, Pascale / Obst, Juliane / Becher, Burkhard / Prokop, Stefan / Heppner, Frank

    2015  , Page(s) 15dgnnP15

    Event/congress 60th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN); Berlin; Deutsche Gesellschaft für Neuropathologie und Neuroanatomie; 2015
    Keywords Medizin, Gesundheit
    Publishing date 2015-08-25
    Publisher German Medical Science GMS Publishing House; Düsseldorf
    Document type Conference proceedings
    DOI 10.3205/15dgnn39
    Database German Medical Science

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  10. Article ; Online: TREM2 Alzheimer's variant R47H causes similar transcriptional dysregulation to knockout, yet only subtle functional phenotypes in human iPSC-derived macrophages.

    Hall-Roberts, Hazel / Agarwal, Devika / Obst, Juliane / Smith, Thomas B / Monzón-Sandoval, Jimena / Di Daniel, Elena / Webber, Caleb / James, William S / Mead, Emma / Davis, John B / Cowley, Sally A

    Alzheimer's research & therapy

    2020  Volume 12, Issue 1, Page(s) 151

    Abstract: Background: TREM2 is a microglial cell surface receptor, with risk mutations linked to Alzheimer's disease (AD), including R47H. TREM2 signalling via SYK aids phagocytosis, chemotaxis, survival, and changes to microglial activation state. In AD mouse ... ...

    Abstract Background: TREM2 is a microglial cell surface receptor, with risk mutations linked to Alzheimer's disease (AD), including R47H. TREM2 signalling via SYK aids phagocytosis, chemotaxis, survival, and changes to microglial activation state. In AD mouse models, knockout (KO) of TREM2 impairs microglial clustering around amyloid and prevents microglial activation. The R47H mutation is proposed to reduce TREM2 ligand binding. We investigated cell phenotypes of the R47H mutant and TREM2 KO in a model of human microglia, and compared their transcriptional signatures, to determine the mechanism by which R47H TREM2 disrupts function.
    Methods: We generated human microglia-like iPSC-macrophages (pMac) from isogenic induced pluripotent stem cell (iPSC) lines, with homozygous R47H mutation or TREM2 knockout (KO). We firstly validated the effect of the R47H mutant on TREM2 surface and subcellular localization in pMac. To assess microglial phenotypic function, we measured phagocytosis of dead neurons, cell morphology, directed migration, survival, and LPS-induced inflammation. We performed bulk RNA-seq, comparing significant differentially expressed genes (DEGs; p < 0.05) between the R47H and KO versus WT, and bioinformatically predicted potential upstream regulators of TREM2-mediated gene expression.
    Results: R47H modified surface expression and shedding of TREM2, but did not impair TREM2-mediated signalling, or gross phenotypes that were dysregulated in the TREM2 KO (phagocytosis, motility, survival). However, altered gene expression in the R47H TREM2 pMac overlapped by 90% with the TREM2 KO and was characterised by dysregulation of genes involved with immunity, proliferation, activation, chemotaxis, and adhesion. Downregulated mediators of ECM adhesion included the vitronectin receptor αVβ3, and consequently, R47H TREM2 pMac adhered weakly to vitronectin compared with WT pMac. To counteract these transcriptional defects, we investigated TGFβ1, as a candidate upstream regulator. TGFβ1 failed to rescue vitronectin adhesion of pMac, although it improved αVβ3 expression.
    Conclusions: The R47H mutation is not sufficient to cause gross phenotypic defects of human pMac under standard culture conditions. However, overlapping transcriptional defects with TREM2 KO supports the hypothesised partial loss-of-function effects of the R47H mutation. Furthermore, transcriptomics can guide us to more subtle phenotypic defects in the R47H cells, such as reduced cell adhesion, and can be used to predict targets for therapeutic intervention.
    MeSH term(s) Alzheimer Disease/genetics ; Brain ; Humans ; Induced Pluripotent Stem Cells ; Macrophages ; Membrane Glycoproteins/genetics ; Microglia ; Phenotype ; Receptors, Immunologic/genetics
    Chemical Substances Membrane Glycoproteins ; Receptors, Immunologic ; TREM2 protein, human
    Language English
    Publishing date 2020-11-16
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2506521-X
    ISSN 1758-9193 ; 1758-9193
    ISSN (online) 1758-9193
    ISSN 1758-9193
    DOI 10.1186/s13195-020-00709-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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