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  1. Article ; Online: Behandeling van spasticiteit in verpleeghuizen: botulinetoxine A als onderdeel van de therapie.

    Wolswijk, Adrie H M / Dirkx, Anita E M

    Nederlands tijdschrift voor geneeskunde

    2015  Volume 159, Page(s) A7833

    Abstract: Complications of spasticity can severely limit daily activities and care-giving. For those who treat or provide care to patients with spasticity in nursing homes, it is important to recognise complaints in order to prevent serious complications such as ... ...

    Title translation Treatment of spasticity in nursing homes: botulinum toxin type A as part of therapy.
    Abstract Complications of spasticity can severely limit daily activities and care-giving. For those who treat or provide care to patients with spasticity in nursing homes, it is important to recognise complaints in order to prevent serious complications such as care-related pain, contractures and pressure sores. The involvement of a rehabilitation physician is essential to provide a high standard of care. We present two nursing home patients, a 95-year-old woman and a 63-year-old man, with severe upper limb complications following spasticity. Both patients received botulinum toxin injections in the affected muscles, combined with an appropriate splint. A treatment team consisting of a specialist in geriatric medicine, a rehabilitation physician, a physical and an occupational therapist provided consistent daily care in the institution. These efforts substantially reduced care-related pain and improved social behaviour and care options. If spasticity prohibits treatment or care, consultation of a rehabilitation physician at an early stage is indicated.
    MeSH term(s) Aged, 80 and over ; Botulinum Toxins, Type A/therapeutic use ; Female ; Humans ; Male ; Middle Aged ; Muscle Spasticity/complications ; Muscle Spasticity/drug therapy ; Neuromuscular Agents/administration & dosage ; Neuromuscular Agents/therapeutic use ; Nursing Homes ; Pain/etiology ; Pain/prevention & control
    Chemical Substances Neuromuscular Agents ; Botulinum Toxins, Type A (EC 3.4.24.69)
    Language Dutch
    Publishing date 2015
    Publishing country Netherlands
    Document type Case Reports ; English Abstract ; Journal Article ; Review
    ZDB-ID 82073-8
    ISSN 1876-8784 ; 0028-2162
    ISSN (online) 1876-8784
    ISSN 0028-2162
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.18: Show issues Location:
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  2. Article: Monocyte/macrophage infiltration in tumors: modulators of angiogenesis.

    Dirkx, Anita E M / Oude Egbrink, Mirjam G A / Wagstaff, John / Griffioen, Arjan W

    Journal of leukocyte biology

    2006  Volume 80, Issue 6, Page(s) 1183–1196

    Abstract: The role of a tumor immune infiltrate in cancer progression and metastasis has been debated frequently. Although often considered to be associated with improved prognosis and leading to the enhanced survival of cancer patients, inflammatory cells have ... ...

    Abstract The role of a tumor immune infiltrate in cancer progression and metastasis has been debated frequently. Although often considered to be associated with improved prognosis and leading to the enhanced survival of cancer patients, inflammatory cells have also been described to assist the tumor's capabilities to progress, proliferate, and metastasize. Tumor-associated macrophages (TAMs), for example, have been shown to be symbiotically related to tumor cells: Tumor cells recruit TAMs and provide them with survival factors, and TAMs in turn produce a variety of angiogenic factors in response to the tumor microenvironment. This review will describe the composition of an immune infiltrate in tumors and the angiogenic and angiostatic properties of the cells present. Special emphasis will be on the angiogenesis-associated activities of TAMs. The development of immunotherapy and gene therapy using TAMs to mediate tumor cytotoxicity or to deliver gene constructs will be discussed as well. As immunotherapy has so far not been as effective as anticipated, a combination therapy in which angiostatic agents are used as well is put forward as a novel strategy to treat cancer.
    MeSH term(s) Angiogenesis Inhibitors/therapeutic use ; Animals ; Cell Proliferation ; Combined Modality Therapy ; Humans ; Immunity, Cellular/drug effects ; Intercellular Signaling Peptides and Proteins/immunology ; Macrophages/immunology ; Macrophages/pathology ; Neoplasm Metastasis ; Neoplasms/blood supply ; Neoplasms/immunology ; Neoplasms/mortality ; Neoplasms/pathology ; Neoplasms/therapy ; Neovascularization, Pathologic/immunology ; Neovascularization, Pathologic/mortality ; Neovascularization, Pathologic/pathology ; Neovascularization, Pathologic/therapy ; Tumor Escape/drug effects ; Tumor Escape/immunology
    Chemical Substances Angiogenesis Inhibitors ; Intercellular Signaling Peptides and Proteins
    Language English
    Publishing date 2006-12
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1189/jlb.0905495
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 603: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  3. Article: HIV-1 Tat increases the adhesion of monocytes and T-cells to the endothelium in vitro and in vivo: implications for AIDS-associated vasculopathy.

    Matzen, Kathrin / Dirkx, Anita E M / oude Egbrink, Mirjam G A / Speth, Cornelia / Götte, Matthias / Ascherl, Gudrun / Grimm, Thomas / Griffioen, Arjan W / Stürzl, Michael

    Virus research

    2004  Volume 104, Issue 2, Page(s) 145–155

    Abstract: HIV-1-infected patients exhibit severe damages of the aortic endothelium, develop angioproliferative lesions such as Kaposi's sarcoma (KS), and have an increased risk of cardiovascular diseases and atherosclerosis. An increased adhesion of leukocytes to ... ...

    Abstract HIV-1-infected patients exhibit severe damages of the aortic endothelium, develop angioproliferative lesions such as Kaposi's sarcoma (KS), and have an increased risk of cardiovascular diseases and atherosclerosis. An increased adhesion of leukocytes to the endothelium is a common pathogenic parameter of AIDS-associated vascular diseases. Here we show that the HIV-1 Tat protein, a regulatory protein of HIV-1 released by infected cells, and TNF-alpha, a cytokine increased in sera and tissues of HIV-1-infected patients, activate synergistically the adhesion of leukocytes to endothelial cells both in vitro and in vivo. This effect is selectively mediated by HIV-1 Tat, since HIV-1 Nef, another HIV-1 regulatory protein, and the HIV-1 envelope protein gp41, had no effect. In vitro adhesion assays with PBMC and quantitative cell type analysis of adherent cells by FACS demonstrated that HIV-1 Tat selectively activates the adhesion of T-cells and monocytes but not of B-cells. Intravital microscopic studies in mice confirmed the synergistic activity of HIV-1 Tat and TNF-alpha on leukocyte adhesion to the endothelium in vivo. These data indicate that HIV-1 Tat in cooperation with TNF-alpha may contribute to the vascular damage and cardiovascular diseases observed in AIDS patients but also to the prominent extravasation of T-cells and monocytes which is a key process in the formation and progression of KS lesions.
    MeSH term(s) Cell Adhesion/drug effects ; Cell Adhesion/physiology ; Cell Aggregation ; Cells, Cultured ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/immunology ; Gene Products, tat/immunology ; Gene Products, tat/pharmacology ; HIV-1/chemistry ; Humans ; In Vitro Techniques ; Monocytes/drug effects ; Monocytes/immunology ; RNA, Messenger ; Receptors, Cytoadhesin/metabolism ; T-Lymphocytes/drug effects ; T-Lymphocytes/immunology ; Tumor Necrosis Factor-alpha/immunology ; tat Gene Products, Human Immunodeficiency Virus
    Chemical Substances Gene Products, tat ; RNA, Messenger ; Receptors, Cytoadhesin ; Tumor Necrosis Factor-alpha ; tat Gene Products, Human Immunodeficiency Virus
    Language English
    Publishing date 2004-09-01
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 605780-9
    ISSN 1872-7492 ; 0168-1702
    ISSN (online) 1872-7492
    ISSN 0168-1702
    DOI 10.1016/j.virusres.2004.04.001
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1965: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  4. Article ; Online: Anti-angiogenesis therapy can overcome endothelial cell anergy and promote leukocyte-endothelium interactions and infiltration in tumors.

    Dirkx, Anita E M / oude Egbrink, Mirjam G A / Castermans, Karolien / van der Schaft, Daisy W J / Thijssen, Victor L J L / Dings, Ruud P M / Kwee, Lucy / Mayo, Kevin H / Wagstaff, John / Bouma-ter Steege, Jessica C A / Griffioen, Arjan W

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2006  Volume 20, Issue 6, Page(s) 621–630

    Abstract: ... leukocyte-vessel wall interactions by circumvention of EC anergy in vivo, i.e., by the up-regulation ...

    Abstract Tumor escape from immunity, as well as the failure of several anti-cancer vaccination and cellular immunotherapy approaches, is suggested to be due to the angiogenesis-mediated suppression of endothelial cell (EC) adhesion molecules involved in leukocyte-vessel wall interactions. We hypothesized that inhibition of angiogenesis would overcome this escape from immunity. We investigated this in vivo by means of intravital microscopy and ex vivo by immunohistochemistry in two mouse tumor models. Angiogenesis inhibitors anginex, endostatin, and angiostatin, and the chemotherapeutic agent paclitaxel were found to significantly stimulate leukocyte-vessel wall interactions by circumvention of EC anergy in vivo, i.e., by the up-regulation of endothelial adhesion molecules in tumor vessels. This was confirmed by in vitro studies of cultured EC at the protein and mRNA levels. The new angiostatic designer peptide anginex was most potent at overcoming EC anergy; the enhanced leukocyte-vessel interactions led to an increase in the numbers of tumor infiltrating leukocytes. While anginex inhibited tumor growth and microvessel density significantly, the amount of infiltrated leukocytes (CD45), as well as the number of CD8+ cytotoxic T lymphocytes, was enhanced markedly. The current results suggest that immunotherapy strategies can be improved by combination with anti-angiogenesis.
    MeSH term(s) Angiostatins/pharmacology ; Animals ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Clonal Anergy ; Cyclohexanes ; Cyclophosphamide/pharmacology ; Down-Regulation ; Endostatins/pharmacology ; Endothelial Cells ; Endothelium/cytology ; Endothelium/metabolism ; Humans ; Intercellular Adhesion Molecule-1/metabolism ; Leukocytes/cytology ; Leukocytes/metabolism ; Mice ; Neoplasms/blood supply ; Neoplasms/pathology ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/pathology ; Paclitaxel/pharmacology ; Proteins/pharmacology ; Sesquiterpenes/pharmacology ; Tumor Necrosis Factor-alpha ; Vascular Cell Adhesion Molecule-1/metabolism
    Chemical Substances Antineoplastic Agents ; Cyclohexanes ; Endostatins ; Proteins ; Sesquiterpenes ; Tumor Necrosis Factor-alpha ; Vascular Cell Adhesion Molecule-1 ; betapep-25 protein, synthetic ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Angiostatins (86090-08-6) ; Cyclophosphamide (8N3DW7272P) ; Paclitaxel (P88XT4IS4D) ; O-(chloroacetylcarbamoyl)fumagillol (X47GR46481)
    Language English
    Publishing date 2006-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.05-4493com
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2266: Show issues Location:
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    Zs.MO 296: Show issues

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  5. Article: Tumor angiogenesis modulates leukocyte-vessel wall interactions in vivo by reducing endothelial adhesion molecule expression.

    Dirkx, Anita E M / Oude Egbrink, Mirjam G A / Kuijpers, Marijke J E / van der Niet, Sandra T / Heijnen, Viviane V T / Bouma-ter Steege, Jessica C A / Wagstaff, John / Griffioen, Arjan W

    Cancer research

    2003  Volume 63, Issue 9, Page(s) 2322–2329

    Abstract: ... with a large flank tumor was also reduced significantly. Leukocyte rolling, i.e., the step preceding adhesion ...

    Abstract The expression of endothelial cell (EC) adhesion molecules involved in leukocyte-vessel wall interactions is suppressed in malignancies. In the present study, we investigated in vivo the regulation of leukocyte-vessel wall interactions by the presence of a tumor. By means of intravital microscopy, tumor necrosis factor alpha-stimulated leukocyte-vessel wall interactions were studied in ear skin microvessels of nude mice bearing small human LS174T colon carcinomas and in C57Bl/6 mice bearing murine B16F10 melanomas. Leukocyte-vessel wall interactions were studied both within and outside small tumors growing in the ear, and in ear microvessels of mice with a large tumor growing on their flank. Tumor-free mice were used as controls. Compared with values measured at the edge of the ear and in the contralateral ear, leukocyte adhesion was found to be diminished significantly in vessels inside the ear tumor in both mouse models. This reduction disappeared with increasing distance from the tumor. Surprisingly, the level of leukocyte adhesion in ear venules of mice with a large flank tumor was also reduced significantly. Leukocyte rolling, i.e., the step preceding adhesion, was not influenced by the presence of a tumor in nude mice, but was down-regulated in immune-competent C57Bl/6 mice. Treatment of mice bearing a small ear tumor with a humanized antivascular endothelial growth factor antibody prevented the down-regulation of leukocyte-vessel wall interactions inside the tumor vessels compared with the nontreated group. Fluorescence-activated cell sorter analysis showed that isolated tumor ECs have suppressed levels of intercellular adhesion molecule 1 as compared with ECs from normal mouse tissues. In cultured b.END5 cells the tumor necrosis factor alpha-induced up-regulation of intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 was reduced in ECs that were preincubated with basic fibroblast growth factor or vascular endothelial growth factor. The current results may have an impact on the effectiveness of clinical immunotherapeutic treatment protocols, because immune effector cells may not be able to enter tumor tissue.
    MeSH term(s) Animals ; Cell Communication/physiology ; Colonic Neoplasms/blood supply ; Endothelium, Vascular/cytology ; Humans ; Intercellular Adhesion Molecule-1/biosynthesis ; Leukocytes/pathology ; Melanoma, Experimental/blood supply ; Mice ; Mice, Inbred C57BL ; Mice, Nude ; Neoplasm Transplantation ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/pathology ; Transplantation, Heterologous ; Tumor Cells, Cultured ; Vascular Cell Adhesion Molecule-1/biosynthesis
    Chemical Substances Vascular Cell Adhesion Molecule-1 ; Intercellular Adhesion Molecule-1 (126547-89-5)
    Language English
    Publishing date 2003-05-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
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    Uh III Zs.135/5: Show issues Location:
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  6. Article: Anti-angiogenesis therapy can overcome endothelial cell anergy and promote leukocyte-endothelium interactions and infiltration in tumors

    Dirkx, Anita E. M / Egbrink, Mirjam G. A. oude / Castermans, Karolien / Schaft, Daisy W. J. van der / Thijssen, Victor L. J. L / Dings, Ruud P. M / Kwee, Lucy / Mayo, Kevin H / Wagstaff, John / ter Steege, Jessica C. A. Bouma- / Griffioen, Arjan W

    FASEB journal. 2006 Apr., v. 20, no. 6

    2006  

    Abstract: ... angiogenesis.--Dirkx, A. E. M., oude Egbrink, M. G. A., Castermans, K., van der Schaft, D. W. J., Thijssen, V ... leukocyte-vessel wall interactions by circumvention of EC anergy in vivo, i.e., by the up-regulation ... L. J. L., Dings, R. P. M., Kwee, L., Mayo, K. H., Wagstaff, J., Bouma-ter Steege, J. C ...

    Abstract Tumor escape from immunity, as well as the failure of several anti-cancer vaccination and cellular immunotherapy approaches, is suggested to be due to the angiogenesis-mediated suppression of endothelial cell (EC) adhesion molecules involved in leukocyte-vessel wall interactions. We hypothesized that inhibition of angiogenesis would overcome this escape from immunity. We investigated this in vivo by means of intravital microscopy and ex vivo by immunohistochemistry in two mouse tumor models. Angiogenesis inhibitors anginex, endostatin, and angiostatin, and the chemotherapeutic agent paclitaxel were found to significantly stimulate leukocyte-vessel wall interactions by circumvention of EC anergy in vivo, i.e., by the up-regulation of endothelial adhesion molecules in tumor vessels. This was confirmed by in vitro studies of cultured EC at the protein and mRNA levels. The new angiostatic designer peptide anginex was most potent at overcoming EC anergy; the enhanced leukocyte-vessel interactions led to an increase in the numbers of tumor infiltrating leukocytes. While anginex inhibited tumor growth and microvessel density significantly, the amount of infiltrated leukocytes (CD45), as well as the number of CD8⁺ cytotoxic T lymphocytes, was enhanced markedly. The current results suggest that immunotherapy strategies can be improved by combination with anti-angiogenesis.--Dirkx, A. E. M., oude Egbrink, M. G. A., Castermans, K., van der Schaft, D. W. J., Thijssen, V. L. J. L., Dings, R. P. M., Kwee, L., Mayo, K. H., Wagstaff, J., Bouma-ter Steege, J. C. A., Griffioen, A. W. Anti-angiogenesis therapy can overcome endothelial cell anergy and promote leukocyte-endothelium interactions and infiltration in tumors.
    Language English
    Dates of publication 2006-04
    Size p. 621-630.
    Publishing place The Federation of American Societies for Experimental Biology
    Document type Article
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    Database NAL-Catalogue (AGRICOLA)

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