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312 results on '"Storch, M."'

51. Die Handlungskrise

Author

Storch, Maja, Krause, Frank, Storch, M ( Maja ), Krause, F ( Frank ), Brandstätter, Veronika; https://orcid.org/0000-0002-6824-1754, Herrmann, Marcel, Storch, Maja, Krause, Frank, Storch, M ( Maja ), Krause, F ( Frank ), Brandstätter, Veronika; https://orcid.org/0000-0002-6824-1754, and Herrmann, Marcel

Published
2014

53. Validation of the German version of the patient activation measure 13 (PAM13-D) in an international multicentre study of primary care patients

Author

Brenk-Franz, K., Hibbard, J.H., Herrmann, W.J., Freund, T., Szecsenyi, J., Djalali, S., Steurer-Stey, C., Sonnichsen, A., Tiesler, F., Storch, M., Schneider, N., Gensichen, J., Brenk-Franz, K., Hibbard, J.H., Herrmann, W.J., Freund, T., Szecsenyi, J., Djalali, S., Steurer-Stey, C., Sonnichsen, A., Tiesler, F., Storch, M., Schneider, N., and Gensichen, J.

Abstract

Contains fulltext : 126177.pdf (publisher's version ) (Open Access), The patients' active participation in their medical care is important for patients with chronic diseases. Measurements of patient activation are needed for studies and in clinical practice. This study aims to validate the Patient Activation Measure 13 (PAM13-D) in German-speaking primary care patients. This international cross-sectional multicentre study enrolled consecutively patients from primary care practices in three German-speaking countries: Germany, Austria, and Switzerland. Patients completed the PAM13-D questionnaire. General Self-Efficacy scale (GSE) was used to assess convergent validity. Furthermore Cronbach's alpha was performed to assess internal consistency. Exploratory factor analysis was used to evaluate the underlying factor structure of the items. We included 508 patients from 16 primary care practices in the final analysis. Results were internally consistent, with a Cronbach's alpha of 0.84. Factor analysis revealed one major underlying factor. The mean values of the PAM13-D correlated significantly (r = 0.43) with those of the GSE. The German PAM13 is a reliable and valid measure of patient activation. Thus, it may be useful in primary care clinical practice and research.

Published
2013

54. Myelin oligodendrocyte glycoprotein induces experimental autoimmune encephalomyelitis in the 'resistant' Brown Norway rat: disease susceptibility is determined by MHC and MHC-linked effects on the B cell response

Author

Stefferl A, Brehm U, Storch M, Lambracht-Washington D, Bourquin C, Wonigeit K, Hans Lassmann, and Linington C

Subjects
B-Lymphocytes, Encephalomyelitis, Autoimmune, Experimental, T-Lymphocytes, Immunology, Adoptive Transfer, Immunity, Innate, Rats, Major Histocompatibility Complex, Myelin-Associated Glycoprotein, Oligodendroglia, Haplotypes, Species Specificity, Animals, Congenic, Rats, Inbred Lew, Rats, Inbred BN, Antigens, Surface, Immunology and Allergy, Animals, Myelin-Oligodendrocyte Glycoprotein, Disease Susceptibility, Myelin Proteins, Autoantibodies
Abstract

Experimental autoimmune encephalomyelitis (EAE) induced by active immunization with the myelin oligodendrocyte glycoprotein (MOG) is an Ab-mediated, T cell-dependent autoimmune disease that replicates the inflammatory demyelinating pathology of multiple sclerosis. We report that disease susceptibility and severity are determined by MHC and MHC-linked effects on the MOG-specific B cell response that mediate severe clinical EAE in the EAE-resistant Brown Norway (BN) rat. Immunization with the extracellular domain of MOG in CFA induced fulminant clinical disease associated with widespread demyelination and with an inflammatory infiltrate containing large numbers of polymorphonuclear cells and eosinophils within 10 days of immunization. To analyze the effects of the MHC (RT1 system) we compared BN (RT1 n) rats with Lewis (LEW) (RT1 l) and two reciprocal MHC congenic strains, LEW.1N (RT1n) and BN.1L (RT1 l). This comparison revealed that disease severity and clinical course were strongly influenced by the MHC haplotype that modulated the pathogenic MOG-specific autoantibody response. The intra-MHC recombinant congenic strain LEW.1R38 demonstrated that gene loci located both within the centromeric segment of the MHC containing classical class I and class II genes and within the telomeric RT1.M region containing the MOG gene are involved in determining Ab production and disease susceptibility. This study indicates that the current T cell-centered interpretation of MHC-mediated effects on disease susceptibility must be reassessed in multiple sclerosis and other autoimmune diseases in which autoantibody is involved in disease pathogenesis.

Published
1999

60. Protracted, relapsing and demyelinating experimental autoimmune encephalomyelitis in DA rats immunized with syngeneic spinal cord and incomplete Freund's adjuvant.

Author

Lorentzen, J C, Issazadeh-Navikas, Shohreh, Storch, M, Mustafa, M I, Lassman, H, Linington, C, Klareskog, L, Olsson, T, Lorentzen, J C, Issazadeh-Navikas, Shohreh, Storch, M, Mustafa, M I, Lassman, H, Linington, C, Klareskog, L, and Olsson, T

Abstract

Udgivelsesdato: 1995-Dec-31, Experimental autoimmune encephalomyelitis (EAE) is a model for multiple sclerosis (MS). However, MS is a chronic, relapsing and demyelinating disease, whereas EAE in rats is typically a brief and monophasic disorder showing little demyelination. We demonstrate here that DA rats develop severe, protracted and relapsing EAE (SPR-EAE) after a subcutaneous immunization at the tail base with syngeneic spinal cord and incomplete Freund's adjuvant (IFA). The neurological deficits were accompanied by demyelinating inflammatory lesions in the spinal cord, with infiltrating T lymphocytes and perivascular deposition of immunoglobulins and complement. The induction of SPR-EAE was associated with humoral autoreactivity to myelin oligodendrocyte glycoprotein (MOG) and cellular autoreactivity to the rat myelin basic protein (MBP) peptides 69-87 and 87-101. These two peptides, as well as whole rat MBP, were encephalitogenic. In conclusion, we believe that the presently described demyelinating SPR-EAE represents a useful model for MS.

Published
1995

73. High power ICRH and NB heating results in TEXTOR

Author

Messiaen, A M, primary, Conrads, H, additional, Gaigneaux, M, additional, Ongena, J, additional, Weynants, R R, additional, Bertschinger, G, additional, Beuken, J M, additional, Cornelissen, P, additional, Delvigne, T, additional, Durodie, F, additional, Esser, H G, additional, Euringer, H, additional, Fuchs, G, additional, Giesen, B, additional, Gorg, B, additional, Hillis, D L, additional, Hoenen, F, additional, Hutteman, P, additional, Jadoul, M, additional, Koch, R, additional, Kever, H, additional, Korten, M, additional, Kohlhaas, W, additional, Lebeau, D, additional, Lochter, M, additional, Reiter, D, additional, Rusbuldt, D, additional, Sauer, M, additional, Schlueter, J, additional, Soltwisch, H, additional, Storch, M, additional, Telesca, G, additional, Uhlemann, R, additional, Vandenplas, P E, additional, Nieuwenhove, R Van, additional, Oost, G Van, additional, Wassenhove, G Van, additional, Waidmann, G, additional, Wang, J G, additional, Winter, J, additional, Wolf, G H, additional, and Yang, J W, additional

Published
1990
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83. Optimal Tradeoffs Between Size and Slowdown for Universal Parallel Networks.

Author

der Heide, F. Meyer auf, Storch, M., and Wanka, R.

Subjects
PARALLEL processing, COMPUTER science
Abstract

A parallel processor network is called n-universal with slowdown s if it can simulate each computation of each constant-degree processor network with n processors with slowdown s. We prove the following lower bound tradeoff: for each constant-degree n-universal network of size m with slowdown s, m·s = Ω (n log m) holds. Our tradeoff holds for a very general model of simulations. It covers all previously considered models and all known techniques for simulations among networks. For m ≥ n, this improves a previous lower bound by a factor of log log n, proved for a weaker simulation model. For m < n, this is the first nontrivial lower bound for this problem. In this case this lower bound is asymptotically tight. [ABSTRACT FROM AUTHOR]

Published
1997
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95. Soluble recombinant complement receptor 1 inhibits inflammation and demyelination in antibody-mediated demyelinating experimental allergic encephalomyelitis

Author

Piddlesden, S. J., Storch, M. K., Hibbs, M., Freeman, A. M., Lassmann, H., and Paul Morgan

Subjects
Immunology, Immunology and Allergy
Abstract

Activation of complement may contribute to tissue damage in many inflammatory diseases, including those that are clearly T cell driven. We have previously provided evidence that C is involved in tissue damage in multiple sclerosis and in the animal models of this disease, experimental allergic encephalomyelitis and Ab-mediated demyelinating experimental allergic encephalomyelitis, the latter being a model more closely resembling multiple sclerosis. The development of a soluble recombinant form of human complement receptor 1 (sCR1) with potent C-inhibiting activity both in vitro and in vivo provides a potential means of preventing C-mediated tissue damage in animal models and in human disease. Here, we describe the effects of this agent on clinical disease and pathology in Ab-mediated demyelinating experimental allergic encephalomyelitis in the rat. Daily i.p. injection of sCR1 (20 mg/kg) over 6 days completely suppressed serum C activity, reduced the severity of clinical disease (clinical score 1.33 vs 2.79 in untreated animals), inhibited central nervous system inflammation (inflammatory index 2.76 vs 6.55), and almost completely blocked demyelination (average 2.43% cord cross-section vs 8.81%). Deposition of C components C1, C3, and C9 was also markedly inhibited in sCR1-treated animals. This dramatic effect on a demyelinating disease, achieved using a well-tolerated biologic reagent, offers an exciting new prospect for therapy in multiple sclerosis.

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