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  1. Book ; Thesis: Regulation von tissue factor (Gewebsthromboplastin) in vaskulärem Endothel

    Bierhaus, Angelika

    1995  

    Author's details vorgelegt von Angelika Bierhaus
    Language German
    Size 131 Bl. : Ill., graph. Darst.
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Heidelberg, Univ., Diss., 1996
    HBZ-ID HT007219192
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    96 E 1427 order for loan Magazin

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  2. Article ; Online: Critical evaluation of mouse models used to study pain and loss of pain perception in diabetic neuropathy.

    Bierhaus, A / Nawroth, P P

    Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association

    2012  Volume 120, Issue 4, Page(s) 188–190

    Abstract: A number of studies have addressed diabetic neuropathy (DN) in transgenic and knock out mouse models to unravel the molecular mechanisms underlying metabolic pain and loss of pain perception. However, it is difficult to compare these studies with each ... ...

    Abstract A number of studies have addressed diabetic neuropathy (DN) in transgenic and knock out mouse models to unravel the molecular mechanisms underlying metabolic pain and loss of pain perception. However, it is difficult to compare these studies with each other or even with human DN due to experimental differences including the type of diabetes, the background strain of the respective mouse model, the methods of diabetes induction and the duration of diabetes, animal age and gender. To receive useful information for DN from genetically modified mice, it is therefore mandatory to first define the appropriate model and - if necessary - to backcross transgenic strains into the respective background to allow a reliable (and at least in part translatable to human DN) interpretation of the results.
    MeSH term(s) Agnosia/etiology ; Agnosia/genetics ; Animals ; Diabetic Neuropathies/complications ; Diabetic Neuropathies/etiology ; Diabetic Neuropathies/genetics ; Diabetic Neuropathies/pathology ; Disease Models, Animal ; Evaluation Studies as Topic ; Humans ; Mice/genetics ; Mice/metabolism ; Mice/physiology ; Mice, Transgenic ; Pain/etiology ; Pain/genetics ; Pain/pathology ; Pain Perception/physiology
    Language English
    Publishing date 2012-04
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1225416-2
    ISSN 1439-3646 ; 0947-7349
    ISSN (online) 1439-3646
    ISSN 0947-7349
    DOI 10.1055/s-0032-1304567
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Entzündung und Verlust des Schmerzempfindens bei diabetischer Neuropathie

    Bierhaus, Angelika

    Symposium medical

    2006  Volume 17, Issue 8, Page(s) 22

    Language German
    Document type Article
    ZDB-ID 1161444-4
    ISSN 0943-9250
    Database Current Contents Medicine

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  4. Article ; Online: Multiple levels of regulation determine the role of the receptor for AGE (RAGE) as common soil in inflammation, immune responses and diabetes mellitus and its complications.

    Bierhaus, A / Nawroth, P P

    Diabetologia

    2009  Volume 52, Issue 11, Page(s) 2251–2263

    Abstract: The pattern recognition receptor or receptor for AGE (RAGE) is constitutionally expressed in a few cell types only. However in almost all cells studied so far it is induced by reactions known to initiate inflammation. Its biological activity seems to be ... ...

    Abstract The pattern recognition receptor or receptor for AGE (RAGE) is constitutionally expressed in a few cell types only. However in almost all cells studied so far it is induced by reactions known to initiate inflammation. Its biological activity seems to be mainly dependent on the presence of its various ligands, including AGE, S100-calcium binding protein/calgranulins, high-mobility group protein 1, amyloid-beta-peptides and the family of beta-sheet fibrils, all known to be elevated in chronic metabolic, malignant and inflammatory diseases. The RAGE pathway interacts with cytokine-, lipopolysaccharide-, oxidised LDL- and glucose-triggered cellular reactions by turning a short-lasting inflammatory response into a sustained change of cellular function driven by perpetuated activation of the proinflammatory transcription factor, nuclear factor kappa-B. RAGE-mediated persistent cell activation is of pivotal importance in various experimental and clinical settings, including diabetes and its complications, neurodegeneration, ageing, tumour growth, and autoimmune and infectious inflammatory disease. Due to RAGE's central role in maintaining perpetuated cell activation, various therapeutic attempts to block RAGE or its ligands are currently under investigation. Despite broad experimental evidence for the role of RAGE in chronic disease, knowledge of its physiological function is still missing, limiting predictions about safety of long-term inhibition of RAGE x ligand interaction in chronic diseases.
    MeSH term(s) Animals ; Cell Physiological Phenomena ; Diabetes Complications/immunology ; Diabetes Complications/physiopathology ; Diabetes Mellitus/immunology ; Diabetes Mellitus/physiopathology ; Glycation End Products, Advanced/metabolism ; Homeostasis ; Humans ; Inflammation/immunology ; Inflammation/physiopathology ; Leukocyte L1 Antigen Complex/metabolism ; Mice ; Models, Animal ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic/immunology ; Receptors, Immunologic/physiology
    Chemical Substances Glycation End Products, Advanced ; Leukocyte L1 Antigen Complex ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic
    Language English
    Publishing date 2009-07-28
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1694-9
    ISSN 1432-0428 ; 0012-186X
    ISSN (online) 1432-0428
    ISSN 0012-186X
    DOI 10.1007/s00125-009-1458-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 279: Show issues Location:
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  5. Article: The Alzheimer's disease-diabetes angle: inevitable fate of aging or metabolic imbalance limiting successful aging. Preface.

    Bierhaus, Angelika / Nawroth, Peter P

    Journal of Alzheimer's disease : JAD

    2009  Volume 16, Issue 4, Page(s) 673–675

    MeSH term(s) Aging ; Alzheimer Disease/metabolism ; Diabetes Mellitus/metabolism ; Humans
    Language English
    Publishing date 2009
    Publishing country Netherlands
    Document type Introductory Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1440127-7
    ISSN 1875-8908 ; 1387-2877
    ISSN (online) 1875-8908
    ISSN 1387-2877
    DOI 10.3233/JAD-2009-1023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Multiple levels of regulation determine the role of the receptor for AGE (RAGE) as common soil in inflammation, immune responses and diabetes mellitus and its complications

    Bierhaus, A / Nawroth, P. P

    Diabetologia. 2009 Nov., v. 52, no. 11

    2009  

    Abstract: The pattern recognition receptor or receptor for AGE (RAGE) is constitutionally expressed in a few cell types only. However in almost all cells studied so far it is induced by reactions known to initiate inflammation. Its biological activity seems to be ... ...

    Abstract The pattern recognition receptor or receptor for AGE (RAGE) is constitutionally expressed in a few cell types only. However in almost all cells studied so far it is induced by reactions known to initiate inflammation. Its biological activity seems to be mainly dependent on the presence of its various ligands, including AGE, S100-calcium binding protein/calgranulins, high-mobility group protein 1, amyloid-β-peptides and the family of β-sheet fibrils, all known to be elevated in chronic metabolic, malignant and inflammatory diseases. The RAGE pathway interacts with cytokine-, lipopolysaccharide-, oxidised LDL- and glucose-triggered cellular reactions by turning a short-lasting inflammatory response into a sustained change of cellular function driven by perpetuated activation of the proinflammatory transcription factor, nuclear factor kappa-B. RAGE-mediated persistent cell activation is of pivotal importance in various experimental and clinical settings, including diabetes and its complications, neurodegeneration, ageing, tumour growth, and autoimmune and infectious inflammatory disease. Due to RAGE's central role in maintaining perpetuated cell activation, various therapeutic attempts to block RAGE or its ligands are currently under investigation. Despite broad experimental evidence for the role of RAGE in chronic disease, knowledge of its physiological function is still missing, limiting predictions about safety of long-term inhibition of RAGE × ligand interaction in chronic diseases.
    Language English
    Dates of publication 2009-11
    Size p. 2251-2263.
    Publisher Springer-Verlag
    Publishing place Berlin/Heidelberg
    Document type Article
    ZDB-ID 1694-9
    ISSN 1432-0428 ; 0012-186X
    ISSN (online) 1432-0428
    ISSN 0012-186X
    DOI 10.1007/s00125-009-1458-9
    Database NAL-Catalogue (AGRICOLA)

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    Zs.A 279: Show issues Location:
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  7. Article: Critical Evaluation of Mouse Models Used to Study Pain and Loss of Pain Perception in Diabetic Neuropathy

    Bierhaus, A. / Nawroth, P. P.

    Experimental and Clinical Endocrinology & Diabetes

    2012  Volume 120, Issue 04, Page(s) 188–190

    Abstract: A number of studies have addressed diabetic neuropathy (DN) in transgenic and knock out mouse models to unravel the molecular mechanisms underlying metabolic pain and loss of pain perception. However, it is difficult to compare these studies with each ... ...

    Abstract A number of studies have addressed diabetic neuropathy (DN) in transgenic and knock out mouse models to unravel the molecular mechanisms underlying metabolic pain and loss of pain perception. However, it is difficult to compare these studies with each other or even with human DN due to experimental differences including the type of diabetes, the background strain of the respective mouse model, the methods of diabetes induction and the duration of diabetes, animal age and gender. To receive useful information for DN from genetically modified mice, it is therefore mandatory to first define the appropriate model and – if necessary – to backcross transgenic strains into the respective background to allow a reliable (and at least in part translatable to human DN) interpretation of the results.
    Keywords diabetes ; neuropathy ; animal models
    Language English
    Publishing date 2012-03-08
    Publisher © J. A. Barth Verlag in Georg Thieme Verlag KG
    Publishing place Stuttgart ; New York
    Document type Article
    ZDB-ID 1225416-2
    ISSN 1439-3646 ; 0947-7349
    ISSN (online) 1439-3646
    ISSN 0947-7349
    DOI 10.1055/s-0032-1304567
    Database Thieme publisher's database

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  8. Article: Therapie der diabetischen Neuropathie.

    Ziegler, D / Bierhaus, A

    Deutsche medizinische Wochenschrift (1946)

    2007  Volume 132, Issue 19, Page(s) 1043–1047

    Title translation Treatment of diabetic neuropathy.
    MeSH term(s) Analgesics, Opioid/therapeutic use ; Animals ; Anticonvulsants/therapeutic use ; Antidepressive Agents/therapeutic use ; Antioxidants/therapeutic use ; Diabetes Mellitus, Experimental/complications ; Diabetic Neuropathies/therapy ; Humans ; Hyperglycemia/complications ; Hyperglycemia/metabolism ; Nerve Growth Factors/therapeutic use ; Neuralgia/etiology ; Neuralgia/therapy ; Polyneuropathies/therapy ; Protein Kinase Inhibitors/therapeutic use ; Quality of Life ; Reactive Oxygen Species/metabolism ; Transcutaneous Electric Nerve Stimulation ; Vasodilator Agents/therapeutic use
    Chemical Substances Analgesics, Opioid ; Anticonvulsants ; Antidepressive Agents ; Antioxidants ; Nerve Growth Factors ; Protein Kinase Inhibitors ; Reactive Oxygen Species ; Vasodilator Agents
    Language German
    Publishing date 2007-05-11
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 200446-x
    ISSN 1439-4413 ; 0012-0472
    ISSN (online) 1439-4413
    ISSN 0012-0472
    DOI 10.1055/s-2007-979379
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ua VI Zs.60: Show issues Location:
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  9. Article ; Online: Endothelial progenitor cells in regeneration after acute lung injury: do they play a role?

    Rafat, Neysan / Tönshoff, Burkhard / Bierhaus, Angelika / Beck, Grietje C

    American journal of respiratory cell and molecular biology

    2013  Volume 48, Issue 4, Page(s) 399–405

    Abstract: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common disorders in patients requiring critical care. The clinical management of these disorders is difficult and unrewarding, and thus they are among the most common causes of ... ...

    Abstract Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common disorders in patients requiring critical care. The clinical management of these disorders is difficult and unrewarding, and thus they are among the most common causes of death in intensive care units. The activation and damage of pulmonary endothelium comprise the hallmark of ALI/ARDS. Therefore, the recruitment of circulating endothelial progenitor cells (EPCs) to these lesions may exert a beneficial effect on the clinical course of ALI/ARDS. Consequently, cell-based therapies using stem cells to regenerate lung tissue have emerged as potential novel treatment strategies. Although initial studies suggested implantations of exogenously administered bone marrow-derived progenitor cells into damaged vessel walls, recent evidence indicates that this is rather a rare occurrence with uncertain physiologic significance. In the past few years, different populations of progenitor cells were identified, with different functional capacities. This review (1) highlights the different populations of EPCs identified or administered in different models of ALI/ARDS, (2) reports on whether beneficial effects of EPCs could be demonstrated, and (3) puts the conflicting results of different studies into perspective.
    MeSH term(s) Acute Lung Injury/metabolism ; Acute Lung Injury/pathology ; Acute Lung Injury/therapy ; Animals ; Bone Marrow Cells ; Cell- and Tissue-Based Therapy ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Endothelial Cells/transplantation ; Humans ; Regeneration ; Respiratory Distress Syndrome, Adult/metabolism ; Respiratory Distress Syndrome, Adult/pathology ; Respiratory Distress Syndrome, Adult/therapy ; Stem Cell Transplantation ; Stem Cells/metabolism ; Stem Cells/pathology
    Language English
    Publishing date 2013-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2011-0132TR
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Posttranslational modification of lipoproteins--a fatal attraction in metabolic disease?

    Bierhaus, A / Nawroth, P P

    Journal of Alzheimer's disease : JAD

    2005  Volume 7, Issue 4, Page(s) 315–317

    MeSH term(s) Alleles ; Alzheimer Disease/metabolism ; Alzheimer Disease/physiopathology ; Apolipoproteins E/metabolism ; Cholesterol, LDL/metabolism ; Humans
    Chemical Substances Apolipoproteins E ; Cholesterol, LDL
    Language English
    Publishing date 2005-08-24
    Publishing country Netherlands
    Document type Comment ; Journal Article
    ZDB-ID 1440127-7
    ISSN 1875-8908 ; 1387-2877
    ISSN (online) 1875-8908
    ISSN 1387-2877
    DOI 10.3233/jad-2005-7407
    Database MEDical Literature Analysis and Retrieval System OnLINE

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