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  1. Article ; Online: Dr Ulf Glendor has left us at age 71.

    Andersson, Lars / Andreasen, Jens Ove

    Dental traumatology : official publication of International Association for Dental Traumatology

    2020  Volume 36, Issue 3, Page(s) 217

    Language English
    Publishing date 2020-05-19
    Publishing country Denmark
    Document type Journal Article
    ZDB-ID 2030722-6
    ISSN 1600-9657 ; 1600-4469
    ISSN (online) 1600-9657
    ISSN 1600-4469
    DOI 10.1111/edt.12565
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2038: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Book: RNA-chromatin interactions

    Ørom, Ulf Andersson Vang

    methods and protocols

    (Methods in molecular biology ; 2161 ; Springer protocols)

    2020  

    Author's details edited by Ulf Andersson Vang Ørom
    Series title Methods in molecular biology ; 2161
    Springer protocols
    Collection
    Language English
    Size x, 266 Seiten, Illustrationen
    Publisher Humana Press
    Publishing place New York, NY
    Publishing country United States
    Document type Book
    HBZ-ID HT020551060
    ISBN 978-1-0716-0679-7 ; 9781071606803 ; 1-0716-0679-4 ; 1071606808
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Zs A 7042 -2161- verfügbar in Königswinter Königswinter

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  3. Book: miRNA biogenesis

    Ørom, Ulf Andersson

    methods and protocols

    (Methods in molecular biology ; 1823 ; Springer protocols)

    2018  

    Author's details edited by Ulf Andersson Vang Ørom
    Series title Methods in molecular biology ; 1823
    Springer protocols
    Collection
    Language English
    Size xi, 238 Seiten, Illustrationen, 25.4 cm x 17.8 cm
    Publisher Humana Press
    Publishing place New York, NY
    Publishing country United States
    Document type Book
    HBZ-ID HT019748737
    ISBN 978-1-4939-8623-1 ; 9781493986248 ; 1-4939-8623-6 ; 1493986244
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Zs A 7042 -1823- verfügbar in Königswinter Königswinter

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  4. Book: Enhancer RNAs

    Ørom, Ulf Andersson

    methods and protocols

    (Methods in molecular biology ; 1468 ; Springer protocols)

    2017  

    Author's details edited by Ulf Andersson Ørom
    Series title Methods in molecular biology ; 1468
    Springer protocols
    Collection
    Keywords Non-coding RNA.
    Subject code 572.88
    Language English
    Size xi, 252 Seiten, Illustrationen, Diagramme, 26 cm
    Publisher Humana Press
    Publishing place New York
    Publishing country United States
    Document type Book
    Note Includes bibliographical references
    HBZ-ID HT019126302
    ISBN 978-1-4939-4033-2 ; 9781493940356 ; 1-4939-4033-3 ; 149394035X
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Zs A 7042 -1468- verfügbar in Königswinter Königswinter

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  5. Article ; Online: Hyperinflammation: On the pathogenesis and treatment of macrophage activation syndrome.

    Andersson, Ulf

    Acta paediatrica (Oslo, Norway : 1992)

    2021  Volume 110, Issue 10, Page(s) 2717–2722

    Abstract: Macrophage activation syndrome (MAS) is a subtype of hemophagocytic lymphohistiocytosis (HLH) diseases. The underlying mechanism of these life-threatening disorders is impaired granule-mediated cytotoxicity exerted by natural killer (NK) cells and T ... ...

    Abstract Macrophage activation syndrome (MAS) is a subtype of hemophagocytic lymphohistiocytosis (HLH) diseases. The underlying mechanism of these life-threatening disorders is impaired granule-mediated cytotoxicity exerted by natural killer (NK) cells and T lymphocytes. This function is meant for elimination of virus-infected cells, malignant cells and to prevent exaggerated immune responses. The normal outcome after an attack by NK or cytotoxic T cells is apoptosis of the target cell. This prevents cytotoxic inflammatory responses in adjacent tissues which occur after lytic cell death. Extensive cell lysis can even produce a cytokine storm, as evidenced in MAS. Programmed proinflammatory lytic cell death, pyroptosis, caused by activated inflammasomes is central in the pathogenesis of MAS. Pyroptosis mediates IL-18 cytokine release, which robustly stimulates NK and T cells to produce IFN-γ, the key macrophage-activating signal which initiates a burst of inflammatory cytokines and chemokines. Lytic cell death also mediates a discharge of the prototype alarmin high mobility group box protein 1 (HMGB1), a proinflammatory molecule present in all cells and that mediates the pathogenesis of MAS as outlined here. Therapeutic options to control causal factors operating in the pathogenesis of MAS are also discussed.
    Language English
    Publishing date 2021-05-11
    Publishing country Norway
    Document type Journal Article ; Review
    ZDB-ID 203487-6
    ISSN 1651-2227 ; 0365-1436 ; 0803-5253
    ISSN (online) 1651-2227
    ISSN 0365-1436 ; 0803-5253
    DOI 10.1111/apa.15900
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Um IV Zs.95: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: The cholinergic anti-inflammatory pathway alleviates acute lung injury.

    Andersson, Ulf

    Molecular medicine (Cambridge, Mass.)

    2020  Volume 26, Issue 1, Page(s) 64

    Abstract: The ubiquiotous nuclear protein HMGB1 is extracellularly released by dying cells or activated innate immunity cells to promote inflammation. Extracellular HMGB1 plays a prominent role in the pathogenesis of acute lung injury of infectious as well as ... ...

    Abstract The ubiquiotous nuclear protein HMGB1 is extracellularly released by dying cells or activated innate immunity cells to promote inflammation. Extracellular HMGB1 plays a prominent role in the pathogenesis of acute lung injury of infectious as well as sterile origin including hyperoxia. Excessive amounts of systemic HMGB1 and HMGB1-partner molecule complexes can be retained in the pulmonary circulation indicated by a substantial reduction of HMGB1 plasma levels in arterial versus venous blood. The cholinergic antiinflammatory mechanism ameliorates pulmonary inflammation by inhibiting HMGB1 release and HMGB1 receptor expression. This comprehension was recently reinforced by results reported in Molecular Medicine by Sitapara and coworkers demonstrating that administration of an α7 nicotinic acetylcholine receptor agonist attenuated hyperoxia-induced acute inflammatory lung injury by alleviating the accumulation of HMGB1 in the airways and the circulation. Activating the cholinergic antiinflammatory path might be considered to alleviate severe COVID-19 with or without concurrent oxygen-induced lung injury.
    MeSH term(s) Acute Lung Injury/immunology ; Acute Lung Injury/pathology ; Acute Lung Injury/prevention & control ; Animals ; Betacoronavirus/immunology ; COVID-19 ; Coronavirus Infections/immunology ; Coronavirus Infections/pathology ; Coronavirus Infections/prevention & control ; Coronavirus Infections/virology ; HMGB1 Protein/antagonists & inhibitors ; Humans ; Neuroimmunomodulation/drug effects ; Nicotinic Agonists/therapeutic use ; Pandemics/prevention & control ; Pneumonia, Viral/immunology ; Pneumonia, Viral/pathology ; Pneumonia, Viral/prevention & control ; Pneumonia, Viral/virology ; SARS-CoV-2
    Chemical Substances HMGB1 Protein ; Nicotinic Agonists
    Keywords covid19
    Language English
    Publishing date 2020-06-29
    Publishing country England
    Document type Letter
    ZDB-ID 1283676-x
    ISSN 1528-3658 ; 1076-1551
    ISSN (online) 1528-3658
    ISSN 1076-1551
    DOI 10.1186/s10020-020-00184-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4456: 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)

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  7. Article ; Online: Vagus nerve SARS-CoV-2 infection and inflammatory reflex dysfunction: Is there a causal relationship?

    Andersson, Ulf / Tracey, Kevin J

    Journal of internal medicine

    2023  Volume 295, Issue 1, Page(s) 91–102

    Abstract: Autonomic dysfunction is a clinical hallmark of infection caused by SARS-CoV-2, but the underlying mechanisms are unknown. The vagus nerve inflammatory reflex is an important, well-characterized mechanism for the reflexive suppression of cytokine storm, ... ...

    Abstract Autonomic dysfunction is a clinical hallmark of infection caused by SARS-CoV-2, but the underlying mechanisms are unknown. The vagus nerve inflammatory reflex is an important, well-characterized mechanism for the reflexive suppression of cytokine storm, and its experimental or clinical impairment facilitates the onset and progression of hyperinflammation. Recent pathological evidence from COVID-19 victims reveals viral infection and inflammation in the vagus nerve and associated nuclei in the medulla oblongata. Although it has been suggested that vagus nerve inflammation in these patients mediates dysregulated respiration, whether it also contributes to dysfunction of the vagus nerve inflammatory reflex has not been addressed. Because lethality and tissue injury in acute COVID-19 are characterized by cytokine storm, it is plausible to consider evidence that impairment of the inflammatory reflex may contribute to overproduction of cytokines and resultant hyperinflammatory pathogenesis. Accordingly, here the authors discuss the inflammatory reflex, the consequences of its dysfunction in COVID-19, and whether there are opportunities for therapeutic intervention.
    MeSH term(s) Humans ; COVID-19/complications ; SARS-CoV-2 ; Cytokine Release Syndrome/etiology ; Inflammation ; Cytokines ; Reflex/physiology ; Vagus Nerve/physiology
    Chemical Substances Cytokines
    Language English
    Publishing date 2023-11-29
    Publishing country England
    Document type Journal Article
    ZDB-ID 96274-0
    ISSN 1365-2796 ; 0954-6820
    ISSN (online) 1365-2796
    ISSN 0954-6820
    DOI 10.1111/joim.13746
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ua VI Zs.44: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: The cholinergic anti-inflammatory pathway alleviates acute lung injury

    Ulf Andersson

    Molecular Medicine, Vol 26, Iss 1, Pp 1-

    2020  Volume 4

    Abstract: Abstract The ubiquiotous nuclear protein HMGB1 is extracellularly released by dying cells or activated innate immunity cells to promote inflammation. Extracellular HMGB1 plays a prominent role in the pathogenesis of acute lung injury of infectious as ... ...

    Abstract Abstract The ubiquiotous nuclear protein HMGB1 is extracellularly released by dying cells or activated innate immunity cells to promote inflammation. Extracellular HMGB1 plays a prominent role in the pathogenesis of acute lung injury of infectious as well as sterile origin including hyperoxia. Excessive amounts of systemic HMGB1 and HMGB1-partner molecule complexes can be retained in the pulmonary circulation indicated by a substantial reduction of HMGB1 plasma levels in arterial versus venous blood. The cholinergic antiinflammatory mechanism ameliorates pulmonary inflammation by inhibiting HMGB1 release and HMGB1 receptor expression. This comprehension was recently reinforced by results reported in Molecular Medicine by Sitapara and coworkers demonstrating that administration of an α7 nicotinic acetylcholine receptor agonist attenuated hyperoxia-induced acute inflammatory lung injury by alleviating the accumulation of HMGB1 in the airways and the circulation. Activating the cholinergic antiinflammatory path might be considered to alleviate severe COVID-19 with or without concurrent oxygen-induced lung injury.
    Keywords Pneumonia ; ARDS ; ALI ; HMGB1 ; RAGE ; TLR4 ; Therapeutics. Pharmacology ; RM1-950 ; Biochemistry ; QD415-436 ; covid19
    Subject code 610
    Language English
    Publishing date 2020-06-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article: In Silico

    Andersson, Martin / Norinder, Ulf / Chavan, Swapnil / Cotgreave, Ian

    Alternatives to laboratory animals : ATLA

    2023  Volume 51, Issue 3, Page(s) 204–209

    Abstract: ... ...

    Abstract An
    MeSH term(s) Animals ; Eye ; Toxicity Tests ; Solubility ; Irritants/toxicity ; Animal Testing Alternatives
    Chemical Substances Irritants
    Language English
    Publishing date 2023-05-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 605800-0
    ISSN 0261-1929
    ISSN 0261-1929
    DOI 10.1177/02611929231175676
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3391: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  10. Article ; Online: HMGB1 is a critical molecule in the pathogenesis of Gram-negative sepsis.

    Andersson, Ulf / Yang, Huan

    Journal of intensive medicine

    2022  Volume 2, Issue 3, Page(s) 156–166

    Abstract: Gram-negative sepsis is a severe clinical syndrome associated with significant morbidity and mortality. Lipopolysaccharide (LPS), expressed on Gram-negative bacteria, is a potent pro-inflammatory toxin that induces inflammation and coagulation via two ... ...

    Abstract Gram-negative sepsis is a severe clinical syndrome associated with significant morbidity and mortality. Lipopolysaccharide (LPS), expressed on Gram-negative bacteria, is a potent pro-inflammatory toxin that induces inflammation and coagulation via two separate receptor systems. One is Toll-like receptor 4 (TLR4), expressed on cell surfaces and in endosomes, and the other is the cytosolic receptor caspase-11 (caspases-4 and -5 in humans). Extracellular LPS binds to high mobility group box 1 (HMGB1) protein, a cytokine-like molecule. The HMGB1-LPS complex is transported via receptor for advanced glycated end products (RAGE)-endocytosis to the endolysosomal system to reach the cytosolic LPS receptor caspase-11 to induce HMGB1 release, inflammation, and coagulation that may cause multi-organ failure. The insight that LPS needs HMGB1 assistance to generate severe inflammation has led to successful therapeutic results in preclinical Gram-negative sepsis studies targeting HMGB1. However, to date, no clinical studies have been performed based on this strategy. HMGB1 is also actively released by peripheral sensory nerves and this mechanism is fundamental for the initiation and propagation of inflammation during tissue injury. Homeostasis is achieved when other neurons actively restrict the inflammatory response via monitoring by the central nervous system and the vagus nerve through the cholinergic anti-inflammatory pathway. The neuronal control in Gram-negative sepsis needs further studies since a deeper understanding of the interplay between HMGB1 and acetylcholine may have beneficial therapeutic implications. Herein, we review the synergistic overlapping mechanisms of LPS and HMGB1 and discuss future treatment opportunities in Gram-negative sepsis.
    Language English
    Publishing date 2022-03-09
    Publishing country China
    Document type Journal Article ; Review
    ISSN 2667-100X
    ISSN (online) 2667-100X
    DOI 10.1016/j.jointm.2022.02.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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