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  • 1
    Online Resource
    Online Resource
    Neutralizing Antibodies Against Botulinum Toxin A After a Wasp Sting
    American Medical Association (AMA) ; 2006
    In:  Archives of Neurology Vol. 63, No. 12 ( 2006-12-01), p. 1808-
    Details
    In: Archives of Neurology, American Medical Association (AMA), Vol. 63, No. 12 ( 2006-12-01), p. 1808-
    Type of Medium: Online Resource
    ISSN: 0003-9942
    URL: Article
    DOI: 10.1001/archneur.63.12.1808
    RVK:
    XA 10000
    Language: English
    Publisher: American Medical Association (AMA)
    Publication Date: 2006
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  • 2
    Online Resource
    Online Resource
    Medical aspects of toxin weapons
    Elsevier BV ; 2005
    In:  Toxicology Vol. 214, No. 3 ( 2005-10), p. 210-220
    Details
    In: Toxicology, Elsevier BV, Vol. 214, No. 3 ( 2005-10), p. 210-220
    Type of Medium: Online Resource
    ISSN: 0300-483X
    URL: Article
    DOI: 10.1016/j.tox.2005.06.015
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2005
    detail.hit.zdb_id: 1500781-9
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  • 3
    Online Resource
    Online Resource
    The synaptic vesicle protein 2C mediates the uptake of botulinum neurotoxin A into phrenic nerves
    Wiley ; 2006
    In:  FEBS Letters Vol. 580, No. 8 ( 2006-04-03), p. 2011-2014
    Details
    In: FEBS Letters, Wiley, Vol. 580, No. 8 ( 2006-04-03), p. 2011-2014
    Type of Medium: Online Resource
    ISSN: 0014-5793
    URL: Article
    DOI: 10.1016/j.febslet.2006.02.074
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2006
    detail.hit.zdb_id: 1460391-3
    SSG: 12
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  • 4
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    Online Resource
    Botulinum toxin A does not alter capsaicin-induced pain perception in human skin
    Elsevier BV ; 2007
    In:  Journal of the Neurological Sciences Vol. 260, No. 1-2 ( 2007-09), p. 38-42
    Details
    In: Journal of the Neurological Sciences, Elsevier BV, Vol. 260, No. 1-2 ( 2007-09), p. 38-42
    Type of Medium: Online Resource
    ISSN: 0022-510X
    URL: Article
    DOI: 10.1016/j.jns.2007.03.023
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2007
    detail.hit.zdb_id: 1500645-1
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  • 5
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    Online Resource
    Identification of the protein receptor binding site of botulinum neurotoxins B and G proves the double-receptor concept
    Proceedings of the National Academy of Sciences ; 2007
    In:  Proceedings of the National Academy of Sciences Vol. 104, No. 1 ( 2007-01-02), p. 359-364
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 104, No. 1 ( 2007-01-02), p. 359-364
    Abstract: Botulinum neurotoxins (BoNTs) cause muscle paralysis by selectively cleaving core components of the vesicular fusion machinery within motoneurons. Complex gangliosides initially bind into a pocket that is conserved among the seven BoNTs and tetanus neurotoxin. Productive neurotoxin uptake also requires protein receptors. The interaction site of the protein receptor within the neurotoxin is currently unknown. We report the identification and characterization of the protein receptor binding site of BoNT/B and BoNT/G. Their protein receptors, synaptotagmins I and II, bind to a pocket at the tip of their H CC (C-terminal domain of the C-terminal fragment of the heavy chain) that corresponds to the unique second carbohydrate binding site of tetanus neurotoxin, the sialic acid binding site. Substitution of amino acids in this region impaired binding to synaptotagmins and drastically decreased toxicity at mouse phrenic nerve preparations; CD-spectroscopic analyses evidenced that the secondary structure of the mutated neurotoxins was unaltered. Deactivation of the synaptotagmin binding site by single mutations led to virtually inactive BoNT/B and BoNT/G when assayed at phrenic nerve preparations of complex-ganglioside-deficient mice. Analogously, a BoNT B mutant with deactivated ganglioside and synaptotagmin binding sites lacked appreciable activity at wild-type mouse phrenic nerve preparations. Thus, these data exclude relevant contributions of any cell surface molecule other than one ganglioside and one protein receptor to the entry process of BoNTs, which substantiates the double-receptor concept. The molecular characterization of the synaptotagmin binding site provides the basis for designing a novel class of potent binding inhibitors.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0609713104
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2007
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 6
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    Botulinum neurotoxins C, E and F bind gangliosides via a conserved binding site prior to stimulation‐dependent uptake with botulinum neurotoxin F utilising the three isoforms of SV2 as second receptor
    Wiley ; 2009
    In:  Journal of Neurochemistry Vol. 110, No. 6 ( 2009-09), p. 1942-1954
    Details
    In: Journal of Neurochemistry, Wiley, Vol. 110, No. 6 ( 2009-09), p. 1942-1954
    Abstract: The high toxicity of clostridial neurotoxins primarily results from their specific binding and uptake into neurons. At motor neurons, the seven botulinum neurotoxin serotypes A–G (BoNT/A–G) inhibit acetylcholine release, leading to flaccid paralysis, while tetanus neurotoxin blocks neurotransmitter release in inhibitory neurons, resulting in spastic paralysis. Uptake of BoNT/A, B, E and G requires a dual interaction with gangliosides and the synaptic vesicle (SV) proteins synaptotagmin or SV2, whereas little is known about the entry mechanisms of the remaining serotypes. Here, we demonstrate that BoNT/F as wells depends on the presence of gangliosides, by employing phrenic nerve hemidiaphragm preparations derived from mice expressing GM3, GM2, GM1 and GD1a or only GM3. Subsequent site‐directed mutagenesis based on homology models identified the ganglioside binding site at a conserved location in BoNT/E and F. Using the mice phrenic nerve hemidiaphragm assay as a physiological model system, cross‐competition of full‐length neurotoxin binding by recombinant binding fragments, plus accelerated neurotoxin uptake upon increased electrical stimulation, indicate that BoNT/F employs SV2 as protein receptor, whereas BoNT/C and D utilise different SV receptor structures. The co‐precipitation of SV2A, B and C from Triton‐solubilised SVs by BoNT/F underlines this conclusion.
    Type of Medium: Online Resource
    ISSN: 0022-3042 , 1471-4159
    URL: Issue
    URL: Article
    DOI: 10.1111/jnc.2009.110.issue-6
    DOI: 10.1111/j.1471-4159.2009.06298.x
    Language: English
    Publisher: Wiley
    Publication Date: 2009
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    SSG: 12
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  • 7
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    Online Resource
    Characterization of CD6-Negative Suppressor Cells Facilitating HLA-Haploidentical Stem Cell Transplantation.
    American Society of Hematology ; 2005
    In:  Blood Vol. 106, No. 11 ( 2005-11-16), p. 2909-2909
    Details
    In: Blood, American Society of Hematology, Vol. 106, No. 11 ( 2005-11-16), p. 2909-2909
    Abstract: HLA- haploidentical stem cell transplantation (SCT) has been shown to be a suitable alternative for treatment of hematopoietic malignancies if no matched donor is available. Haploidentical family members sharing one HLA-haplotype may differ in one or more HLA-antigens of the second haplotype. The risks are rejection of the graft and severe graft-versus-host disease (GVHD). In particular unmodified grafts may cause severe GVHD, and T-cell depleted grafts may be rejected. We have designed a protocol of unmodified marrow transplantation supplemented by G-CSF mobilized blood cells (MBC) 6 days after marrow transplantation from which CD6-positive cells are depleted. These cells facilitate engraftment and modify GVHD. Patients were conditioned with 12 Gy total body irradiation (TBI), donor leukocytes, antithymocyte globulin and cyclophosphamide, unmodified marrow was given on day 0 and CD6-depleted MBC on day 6. In a first series of 53 patients CD6 cells were depleted by indirect loading and depletion with goat-anti-mouse antibody coupled to Dynabeads. The second series comprised 22 patients whose MBC were depleted using the CliniMacs system with CD6-antibody directly bound to immunomagnetic beads. Table I shows the median and the range () of the cell numbers transplanted after CD6 depletion comparing the two methods. Table II shows the number of patients with acute GVHD in relation to the median of all given transplants. Rejection of the transplant was not observed in 71 evaluable patients. GVHD & gt;= 2 occurred in 47 %, GVHD & gt;= 3 in 21% of 70 evaluable patients. The incidence of acute GVHD was lower in patients given less CD4 cells (p=0.06), it was significantly lower in patients given MBC separated by immunomagnetic beads charged with the specific antibody (p & lt; 0.02). The content of CD8-positive, NK-, B- and CD34-positive cells had no effect on the incidence of GVHD. We conclude from these results that transfusion of CD6-depleted MBC on day 6 facilitates engraftment of marrow from HLA-haploidentical donors without T cell depletion without jeopardizing engraftment and without severe GVHD, if CD4 cells are depleted. A particular advantage is the content of NK cells and CD8 T cells maintaining a potential GVL-effect. Tab.I CD34 x 10e6/kg CD56 x 10e6/kg CD19 x 10e6/kg CD8 x 10e6/kg CD4 x 10e6/kg Indirect labelling (N=53) 7.3 (0.4–35.8) 19.8 (4.8–65.4) 36.1(5.6–117.3) 5.8 (0.75–55) 3.9 (0.12–65.4) Direct labelling (N=22) 13.4(2.5–29.1) 17.1 (1.7–57.3) 48.7 (5.1–175) 2.0 (0.12–13.2) 0.47 (0.05–2.5) Table II aGVHD 0 aGVHD I–II aGVHD III–IV total CD4 & lt;2.29 x 10e6/kg 16 10 4 30 CD4 & gt;2.28 x 10e6/kg 11 16 11 38 CD8 & lt;4.62 x 10e6/kg 11 13 7 31 CD8 & gt;4.61 x 10e6/kg 16 13 8 37
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V106.11.2909.2909
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2005
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 8
    Online Resource
    Online Resource
    Botulinum neurotoxin — from laboratory to bedside
    Springer Science and Business Media LLC ; 2006
    In:  Neurotoxicity Research Vol. 9, No. 2-3 ( 2006-6), p. 133-140
    Details
    In: Neurotoxicity Research, Springer Science and Business Media LLC, Vol. 9, No. 2-3 ( 2006-6), p. 133-140
    Type of Medium: Online Resource
    ISSN: 1029-8428 , 1476-3524
    URL: Article
    DOI: 10.1007/BF03033931
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2006
    detail.hit.zdb_id: 2074876-0
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  • 9
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    Online Resource
    Graft-Vs-Leukemia Effects of Allogeneic Stem Cell Transplantation from HLA-Haploidentical Family Members as Compared to HLA-Identical Sibling Donors
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 3009-3009
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 3009-3009
    Abstract: Allogeneic stem cell transplantation produces a strong graft-versus-leukemia effect which may be enhanced by HLA-mismatches and immune recognition as a result of pregnancy. Therefore we compared the results of HLA-haploidentical transplantation (N=113) to those of HLA-identical sibling (N=195) transplantation performed in the same time. Cases were matched by disease category (acute myeloid leukemia-myelodysplastic syndromes, AML/MDS, acute lymphoid leukemia ALL and lymphoma-chronic lymphocytic leukemia NHL/CLL) and stage of the disease (early, intermediate and advanced). HLA-haploidentical transplants were performed with unmodified bone marrow followed by CD6-depleted mobilized blood stem cells on day 6.; patients with leukemia were in more advanced disease in leukemia, they were younger and more often male. In multivariate analysis survival was influenced by HLA-mismatch, stage of the disease and age of the patient, but conditioning treatment and CMV-seropositivity had no significant effect. Transplant related mortality was influenced by the age of the patient and HLA-match, to a lesser extent by the disease category and the stage, whereas CMV-seropositivity and conditioning had no influence. Remission duration was dependent on the stage of the disease, the donor recipient gender combination and the conditioning treatment in univariate analysis; in multivariate analysis only CMV-seropositivity had a poor prognostic impact. In comparable disease stages the relapse rate was not different in HLA-haploidentical from HLA-identical transplantation as was the rate of acute GVHD. In contrast the rate of chronic GVHD was lower in HLA-haploidentical transplantation. In ALL, relapse rate and remission duration was inferior with non-myeloablative conditioning as compared to myeloablative total body irradiation. In HLA-haploidentical transplantation the response rate of leukemia was better in patients homozygous for the cross reactive HLA-C group given a transplant from a heterozygous donor suggestive of NK activity. This GVL activity was not associated with GVH activity. Similarly maternal donors were superior to paternal donors and female donors in male recipients better than other gender combinations for the control of leukemia without increased GVHD. Non-inherited maternal antigen (NIMA) and inherited paternal antigen (IPA) in the graft-vs-host direction had a weak influence on the relapse rate, but no influence on GVHD. On an observational basis several sons and daughters transplanted with stem cells from the mother had a strong GVL effect without any signs of GVHD. However two have been lost due to untreatable pulmonary complications. Donors with cytotoxic antibodies have been excluded from donation, but cellular reactivity will have to be assessed in more detail. Recent progress in controlling EBV-associated disease by selection of donor T cells without expansion will improve HLA-haploidentical transplantation and show the way to selecting donor with the appropriate immune repertoire including reactivity to leukemia.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.3009.3009
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 10
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    Online Resource
    Foreword
    Elsevier BV ; 2009
    In:  Toxicon Vol. 54, No. 5 ( 2009-10), p. 549-
    Details
    In: Toxicon, Elsevier BV, Vol. 54, No. 5 ( 2009-10), p. 549-
    Type of Medium: Online Resource
    ISSN: 0041-0101
    URL: Article
    DOI: 10.1016/j.toxicon.2009.02.004
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2009
    detail.hit.zdb_id: 1498784-3
    SSG: 12
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