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1Latest Papers from Table of Contents or Articles in PressS. Sawcer ; G. Hellenthal ; M. Pirinen ; C. C. Spencer ; N. A. Patsopoulos ; L. Moutsianas ; A. Dilthey ; Z. Su ; C. Freeman ; S. E. Hunt ; S. Edkins ; E. Gray ; D. R. Booth ; S. C. Potter ; A. Goris ; G. Band ; A. B. Oturai ; A. Strange ; J. Saarela ; C. Bellenguez ; B. Fontaine ; M. Gillman ; B. Hemmer ; R. Gwilliam ; F. Zipp ; A. Jayakumar ; R. Martin ; S. Leslie ; S. Hawkins ; E. Giannoulatou ; S. D'Alfonso ; H. Blackburn ; F. Martinelli Boneschi ; J. Liddle ; H. F. Harbo ; M. L. Perez ; A. Spurkland ; M. J. Waller ; M. P. Mycko ; M. Ricketts ; M. Comabella ; N. Hammond ; I. Kockum ; O. T. McCann ; M. Ban ; P. Whittaker ; A. Kemppinen ; P. Weston ; C. Hawkins ; S. Widaa ; J. Zajicek ; S. Dronov ; N. Robertson ; S. J. Bumpstead ; L. F. Barcellos ; R. Ravindrarajah ; R. Abraham ; L. Alfredsson ; K. Ardlie ; C. Aubin ; A. Baker ; K. Baker ; S. E. Baranzini ; L. Bergamaschi ; R. Bergamaschi ; A. Bernstein ; A. Berthele ; M. Boggild ; J. P. Bradfield ; D. Brassat ; S. A. Broadley ; D. Buck ; H. Butzkueven ; R. Capra ; W. M. Carroll ; P. Cavalla ; E. G. Celius ; S. Cepok ; R. Chiavacci ; F. Clerget-Darpoux ; K. Clysters ; G. Comi ; M. Cossburn ; I. Cournu-Rebeix ; M. B. Cox ; W. Cozen ; B. A. Cree ; A. H. Cross ; D. Cusi ; M. J. Daly ; E. Davis ; P. I. de Bakker ; M. Debouverie ; B. D'Hooghe M ; K. Dixon ; R. Dobosi ; B. Dubois ; D. Ellinghaus ; I. Elovaara ; F. Esposito ; C. Fontenille ; S. Foote ; A. Franke ; D. Galimberti ; A. Ghezzi ; J. Glessner ; R. Gomez ; O. Gout ; C. Graham ; S. F. Grant ; F. R. Guerini ; H. Hakonarson ; P. Hall ; A. Hamsten ; H. P. Hartung ; R. N. Heard ; S. Heath ; J. Hobart ; M. Hoshi ; C. Infante-Duarte ; G. Ingram ; W. Ingram ; T. Islam ; M. Jagodic ; M. Kabesch ; A. G. Kermode ; T. J. Kilpatrick ; C. Kim ; N. Klopp ; K. Koivisto ; M. Larsson ; M. Lathrop ; J. S. Lechner-Scott ; M. A. Leone ; V. Leppa ; U. Liljedahl ; I. L. Bomfim ; R. R. Lincoln ; J. Link ; J. Liu ; A. R. Lorentzen ; S. Lupoli ; F. Macciardi ; T. Mack ; M. Marriott ; V. Martinelli ; D. Mason ; J. L. McCauley ; F. Mentch ; I. L. Mero ; T. Mihalova ; X. Montalban ; J. Mottershead ; K. M. Myhr ; P. Naldi ; W. Ollier ; A. Page ; A. Palotie ; J. Pelletier ; L. Piccio ; T. Pickersgill ; F. Piehl ; S. Pobywajlo ; H. L. Quach ; P. P. Ramsay ; M. Reunanen ; R. Reynolds ; J. D. Rioux ; M. Rodegher ; S. Roesner ; J. P. Rubio ; I. M. Ruckert ; M. Salvetti ; E. Salvi ; A. Santaniello ; C. A. Schaefer ; S. Schreiber ; C. Schulze ; R. J. Scott ; F. Sellebjerg ; K. W. Selmaj ; D. Sexton ; L. Shen ; B. Simms-Acuna ; S. Skidmore ; P. M. Sleiman ; C. Smestad ; P. S. Sorensen ; H. B. Sondergaard ; J. Stankovich ; R. C. Strange ; A. M. Sulonen ; E. Sundqvist ; A. C. Syvanen ; F. Taddeo ; B. Taylor ; J. M. Blackwell ; P. Tienari ; E. Bramon ; A. Tourbah ; M. A. Brown ; E. Tronczynska ; J. P. Casas ; N. Tubridy ; A. Corvin ; J. Vickery ; J. Jankowski ; P. Villoslada ; H. S. Markus ; K. Wang ; C. G. Mathew ; J. Wason ; C. N. Palmer ; H. E. Wichmann ; R. Plomin ; E. Willoughby ; A. Rautanen ; J. Winkelmann ; M. Wittig ; R. C. Trembath ; J. Yaouanq ; A. C. Viswanathan ; H. Zhang ; N. W. Wood ; R. Zuvich ; P. Deloukas ; C. Langford ; A. Duncanson ; J. R. Oksenberg ; M. A. Pericak-Vance ; J. L. Haines ; T. Olsson ; J. Hillert ; A. J. Ivinson ; P. L. De Jager ; L. Peltonen ; G. J. Stewart ; D. A. Hafler ; S. L. Hauser ; G. McVean ; P. Donnelly ; A. Compston
Nature Publishing Group (NPG)
Published 2011Staff ViewPublication Date: 2011-08-13Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Alleles ; Cell Differentiation/immunology ; Europe/ethnology ; Genetic Predisposition to Disease/*genetics ; Genome, Human/genetics ; Genome-Wide Association Study ; HLA-A Antigens/genetics ; HLA-DR Antigens/genetics ; HLA-DRB1 Chains ; Humans ; Immunity, Cellular/genetics/*immunology ; Major Histocompatibility Complex/genetics ; Multiple Sclerosis/*genetics/*immunology ; Polymorphism, Single Nucleotide/genetics ; Sample Size ; T-Lymphocytes, Helper-Inducer/cytology/immunologyPublished by: -
2Latest Papers from Table of Contents or Articles in PressBelikan, P., Bühler, U., Wolf, C., Pramanik, G. K., Gollan, R., Zipp, F., Siffrin, V.
The American Association of Immunologists (AAI)
Published 2018Staff ViewPublication Date: 2018-04-10Publisher: The American Association of Immunologists (AAI)Print ISSN: 0022-1767Electronic ISSN: 1550-6606Topics: MedicinePublished by: -
3Articles: DFG German National LicensesStaff View
ISSN: 1365-3083Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: The T helper-1 (Th-1)/T helper-2 (Th-2) paradigm is relevant for the pathogenesis and therapy of multiple sclerosis. In experimental autoimmune encephalomyelitis, a shift towards a Th-2 immune response serves as treatment of the disease. In the human immune system, the factors which determine and modulate the differentiation of CD4+ T cells into the Th-1 or Th-2 phenotype have yet to be elucidated completely. Here, the split-well approach was used to analyse costimulatory requirements for the generation of myelin basic protein-specific T-cell subsets considered to play a major role in the pathogenesis of multiple sclerosis. Myelin basic protein-specific T-cell lines were isolated from peripheral blood cells of healthy individuals in the presence or absence of a blockade of the costimulatory molecule B7-1, previously reported to be involved in the development of Th-1 cells. T-helper type was determined by the interferon/interleukin ratio. Blockade of B7-1 did not increase the number of Th-2-like myelin basic protein-specific T-cell lines. Thus, these data show no evidence for an influence of B7-1 blockade on the development of human myelin basic protein-specific T-cell subsets. These results have to be taken into account when discussing whether antibody-mediated B7-1 blockade might be a suitable therapy in multiple sclerosis, as demonstrated in experimental autoimmune encephalomyelitis.Type of Medium: Electronic ResourceURL: -
4Articles: DFG German National LicensesStaff View
ISSN: 1435-1463Keywords: Glutamate ; excitatory neurotransmitter ; lamotrigine ; Parkinson's disease ; basal ganglia pathwaysSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary Recent experiments provide evidence that the NMDA-antagonist MK-801 has a locomotor-stimulating effect in monoamine-depleted rodents. These findings are based upon a hypothetical pathway-circuit including the basal ganglia as a model reflecting hypo- and hyperkinetic movement disorders. We have treated 5 patients suffering from Parkinson's disease with the antiepileptic drug “lamotrigine” which does not appear to be an NMDA-antagonist but acts functionally as a glutamate antagonist by inhibition of presynaptic glutamate release.Type of Medium: Electronic ResourceURL: -
5Articles: DFG German National LicensesStaff View
ISSN: 1433-0407Keywords: Schlüsselwörter Nebenwirkungen ; Kortikoide ; Key words Side effects ; SteroidsSource: Springer Online Journal Archives 1860-2000Topics: MedicineDescription / Table of Contents: Summary Many side effects of steroid treatment have been reported. Even experienced neurologists may not know all important side effects to the nervous system. Autonomic nervous system dysfunction, psychosis and myopathy are more frequently encountered than dependency, reversible dementia, brain atrophy and benign intracranial hypertension. This review describes symptomatology, pathogenesis and treatment of these steroid-induced side effects.Notes: Zusammenfassung Über eine Vielzahl von Nebenwirkungen der Therapie mit Kortikoiden ist berichtet worden. Wichtige Nebenwirkungen auf das Nervensystem sind auch erfahrenen Neurologen nicht immer bekannt. Neben den häufig auftretenden unerwünschten Wirkungen wie vegetativen Störungen, Psychosen und Myopathien finden sich seltene wie Abhängigkeit, dementielle Entwicklung, Hirnatrophie und Pseudotumor cerebri. Diese Übersicht beschreibt Symptomatologie, Pathogenese und Behandlung dieser kortikoidinduzierten Nebenwirkungen.Type of Medium: Electronic ResourceURL: -
6Articles: DFG German National LicensesStaff View
ISSN: 1433-0407Keywords: Schlüsselwörter Multiple Sklerose ; Apoptose ; Immunpathogenese ; CD95 ; TNF ; Keywords Multiple sclerosis ; Apoptosis ; ImmunopathogenesisSource: Springer Online Journal Archives 1860-2000Topics: MedicineDescription / Table of Contents: Abstract Apoptosis, or programmed cell death, is a physiological cell suicide program mainly leading to selective elimination of useless cells. This mechanism is important for the homeostasis of the immune system and presumably plays a two-sided role in the pathogenesis of multiple sclerosis (MS). On the one hand, evidence has been provided that impaired apoptosis might result in increased numbers or persistence of activated myelin-specific T cells, thus inducing the pathophysiologic processes in MS. On the other hand, local tissue damage might involve apoptosis of glial and neuronal cells and lead to the clinical symptoms. Here, an overview is presented on the current knowledge of the role of apoptosis in the pathogenesis of MS, and implications for related therapeutic strategies are discussed.Notes: Zusammenfassung Apoptose, auch programmierter Zelltod genannt, stellt einen physiologischen Prozess zur selektiven Eliminierung vor allem von unerwünschten körpereigenen Zellen dar. Dieser für die Homöostase des Immunsystems wichtige Mechanismus nimmt wahrscheinlich eine ambivalente Schlüsselrolle in der Ätiopathogenese der multiplen Sklerose (MS) ein. So existieren Hinweise dafür, dass bei der MS eine eingeschränkte Apoptose zur pathologischen Existenz und Persistenz aktivierter myelinspezifischer T-Zellen führt, die wiederum für die charakteristische intrazerebrale Entzündung verantwortlich gemacht werden. Gleichzeitig deuten aktuelle Arbeiten aber darauf hin, dass auf der Endstrecke der entzündlichen Reaktion der apoptotische Untergang von Glia- und evtl. auch Nervenzellen zur Gewebeschädigung und somit entscheidend zur klinischen Symptomatik beitragen. Ziel dieser Übersicht ist die Zusammenstellung der bislang gewonnenen Erkenntnisse zur Bedeutung von Apoptose für die Pathogenese der MS und eines Ausblicks auf mögliche apoptoseorientierte Therapiestrategien.Type of Medium: Electronic ResourceURL: -
7Articles: DFG German National LicensesStaff View
ISSN: 1433-0407Keywords: Schlüsselwörter Multiple Sklerose ; Immunpathogenese ; Therapie ; Key words Multiple sclerosis ; Immunopathogenesis ; TherapySource: Springer Online Journal Archives 1860-2000Topics: MedicineDescription / Table of Contents: Summary Extensive research in the field of multiple sclerosis (MS) has lead to a preliminary pathogenetic concept without solving the etiopathogenesis. According to animal experiments and human in vitro studies MS is a T cell-mediated autoimmune disease. Experimental therapeutical strategies are aiming at the inhibition of T cell activation, transmigration through the blood brain barrier and local inflammation and demyelination. Several substances are already being tested in clinical studies with magnetic resonance imaging as a tool to quantify inflammatory lesions and to shorten the study course. This review will give a summary about actual experimental therapies resulting from the current pathogenetic concept.Notes: Zusammenfassung Eingehende Forschung auf dem Gebiet der multiplen Sklerose (MS) konnte die Ätiopathogenese der Erkrankung nicht aufklären, hat jedoch zu der Erstellung eines vorläufigen pathogenetischen Konzepts geführt. Tierexperimentelle Daten und Ergebnisse aus humanen In-vitro-Untersuchungen sprechen dafür, daß die MS eine T-Zell-vermittelte Autoimmunerkrankung ist. Es gibt eine Reihe von experimentellen Therapiestrategien, die in die T-Zellaktivierung eingreifen, im Bereich der Blut-Hirn-Schranke intervenieren oder lokale Entzündungs- und Entmarkungsprozesse hemmen. Die Therapien, die sich auf den Menschen übertragen lassen, befinden sich teilweise bereits in der klinischen Erprobung. Dabei wird die Prüfung durch die Möglichkeit, Entzündungsaktivität im ZNS kernspintomographisch sichtbar zu machen und zu quantifizieren, deutlich verkürzt und vereinfacht. Ziel dieser Übersicht ist eine Zusammenstellung der spezifischen immuntherapeutischen Ansätze, die sich aus den bisherigen pathogenetischen Erkenntnissen ergeben.Type of Medium: Electronic ResourceURL: -
8Articles: DFG German National LicensesStaff View
ISSN: 1435-1463Keywords: Glutamate ; glutamate release ; antiglutamatergic activity ; excitatory neurotransmitter ; Lamotrigine ; Parkinson's disease ; basal ganglia ; neurotransmission ; therapySource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary Antiglutamatergic acting substances are considered to be useful tools for the treatment of hypokinesia in animal models for Parkinson's disease (PD). Moreover, most known antiglutamatergic compounds act postsynaptically and are either toxic or weak with regard to their clinical potency. The antiepileptic drug “Lamotrigine (LTG)” inhibits presynaptic glutamate release and may therefore provide a novel approach for PD therapy. Encouraging results from a pilot project led us to establish a placebo controlled trial including 20 patients with PD. The substance was generally well tolerated. There was a significant difference in the investigator's overall assessment of efficacy (6/10 vs. 2/10 improvement; p〈0.05) and a tendency for LTG to exhibit a beneficial effect in some registration parameters, but no significant differences in motor response were found between the two groups. We failed to confirm that LTG mediates a strong antiparkinsonian effect in this small study, but to clearly demonstrate slight or moderate beneficial effects larger groups are required.Type of Medium: Electronic ResourceURL: