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13. Natural history of multiple sclerosis

Author

Ebers, G. C.

Subjects
Multiple sclerosis -- History, Health, Psychology and mental health, History
Abstract

The natural history of multiple sclerosis (MS) should be considered in the context of better understood disorders where the problems of definition, ascertainment, and outcomes can be more easily appreciated. [...]

Published
2001

36. Sitzung vom 15. December 1888

Author

Virchow, Ritter, v. Luschan, Zintgraff, Ehrenreich, Gross, V., Rütimeyer, L., Olshausen, Handtmann, Altrichter, Schumann, Jentsch, Treichel, v. Prollius, Tewes, Lotz, Ebers, G., Grossi, V., Langen, A., Bässler, Taubner, v. Kaufmann, Friedel, Bastian, Mönch, Schwartz, W., and v. Binzer

Published
1888

37. Sitzung vom 13. April 1889

Author

Kollmann, Reverdin, v. Schulenburg, W., Ornstein, Ascherson, Brugsch, H., Ebers, G., Ernst, A., Lent, Tewes, Weigel, Jentsch, Treichel, A., Guttmann, S., Stübel, Reiss, Koppel, Jagor, Pander, Bastian, ten Kate, Bartels, Finn, Grempler, Nehring, Wankel, Magdalena, Olshausen, Ascherson, P., Virchow, R., Hollmann, Fritsch, G., Jagor, F., Lecoq, and Seehars

Published
1889

38. Sitzung vom 21. Juli 1894

Author

Ebers, G., Ermann, Ad., Philippi, R. A., Bobrinskoy, Krause, E., Studer, Th., Bannwarth, Hörnes, M., Virchow, Rud., Solger, Pigorini, Schumann, H., Forrer, R., Dieseldorff, E. P., Schellhas, Bartels, M., Beyfuss, Bastian, Möbius, K., Waldeyer, Grünwedel, Seler, E., and Treichel, A.

Published
1894

39. Sitzung vom 15. December 1894

Author

Virchow, Rud., Ritter, W., Ebers, G., Boas, F., Schmeltz, J. D. E., Belck, W., Pisko, J., Höft, Grabowsky, Förstemann, E., Dieseldorff, E. P., Seler, E., Schütz, Karl, Möller, A., Voss, A., Nötling, F., Bastian, Lehmann-Nitsche, Ohnefalsch-Richter, Schumann, H., Buchholz, Helm, Rademacher, Solger, B., Ehrenreich, P., Much, Bartels, v. Heyden, A., and Hahn, Ed.

Published
1894

40. The relationship of age with the clinical phenotype in multiple sclerosis.

Author

Scalfari, A., Lederer, C., Daumer, M., Nicholas, R., Ebers, G. C., and Muraro, P. A.

Subjects
MULTIPLE sclerosis, DISEASE progression, DISEASE relapse, MEDICAL history taking, RANDOMIZED controlled trials, PATIENTS
Abstract

Background: The multiple sclerosis (MS) clinical course and relapses frequency before progression vary widely. Objective: To investigate the influence of age on the MS phenotype. Methods: Among 751 primary progressive (PP = 217) and secondary progressive (SP = 534) MS patients from the London Ontario database, we assessed the relationship of age on the relapse frequency and on the progressive phase evolution, and the impact of relapses on the age at onset of progression. Results: Age at onset did not influence the early attacks frequency, but patients younger at onset had larger number of total attacks before progression (age = 27.4, 31.0 and 32.8 mean years; ⩾4, 2–3 and 1 relapses, respectively) and longer latency to SP. Although frequent early relapses predicted younger age at SP onset, patients with no attacks (primary progressive multiple sclerosis (PPMS)), or 1, 2–3 and ⩾4 relapses during the relapsing-remitting phase started progressing at similar age (38.6, 41.3, 41.4 and 39.2 mean years, respectively). The age at onset of progressive phase did not affect its evolution. Conclusions: Age strongly influences the phenotype before progression. Relapsing-remitting patients younger at onset are more likely to display a predominantly inflammatory course, yet relapses number does not affect the age at onset of progression. [ABSTRACT FROM AUTHOR]

Published
2016
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42. Survival in MS.

Author

Goodin, D. S., Reder, A. T., Ebers, G. C., Cutter, G., Kremenchutzky, M., Oger, J., Langdon, D., Rametta, M., Beckmann, K., DeSimone, T. M., and Knappertz, V.

Published
2012
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48. Influence of HLA-DRB1 alleles on the susceptibility and resistance to multiple sclerosis in Japanese patients with respect.

Author

Isobe, N., Matsushita, T., Yamasaki, R., Ramagopalan, S. V., Kawano, Y., Nishimura, Y., Ebers, G. C., and Kira, J.

Subjects
HLA histocompatibility antigens, MULTIPLE sclerosis, JAPANESE people, CONTROL groups, AQUAPORINS, LOCUS (Genetics), PATIENTS, DISEASES
Abstract

Background: Epistatic interactions between human leukocyte antigen (HLA)-DRB1 alleles alter multiple sclerosis (MS) risk in Caucasians. Such interactions have never been studied in Asian MS patients. Objective: To investigate the influence of HLA-DRB1 alleles, including epistatic interactions at this locus, in Japanese MS patients with and without the anti-aquaporin 4 (AQP4) antibody. Methods: The HLA-DRB1 locus was genotyped in 108 MS patients and 127 healthy controls. MS patients were further classified into two groups according to anti-AQP4 antibody status (27 positive and 81 negative). Results: HLA-DRB1*09 (adjusted odds ratio (OR) = 0.243, 95% confidence interval (CI) 0.099-0.533) and HLA-DRB1*01 (adjusted OR= 0.327, 95% CI 0.103-0.873) decreased the incidence of anti-AQP4 antibody-negative MS. By contrast, HLA-DRB1*12 increased the risk of anti-AQP4 antibody-positive MS (adjusted OR= 3.691, 95% CI 1.233-10.565). Individuals with HLA-DRB1*09/15 decreased the risk of anti-AQP4 antibody-negative MS (adjusted OR= 0.164, 95% CI 0.026-0.593), while those with HLA-DRB1*12/15 increased the risk of anti-AQP4 antibody-positive MS (adjusted OR= 10.870, 95% CI 2.004-81.752). Conclusions: The ability of HLA-DRB1*09 to reduce the risk of anti-AQP4 antibody-negative MS may arise from an interaction with HLA-DRB1*15. By contrast, HLA-DRB1*12 increases susceptibility to anti-AQP4 antibody-positive MS, possibly via an interaction with HLA-DRB1*15. [ABSTRACT FROM AUTHOR]

Published
2010
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49. Genetic loading in familial migraine with aura.

Author

Noble-Topham S E, Cader M Z, Dyment D A, Rice G P A, Brown J D, Ebers G C, Noble-Topham, S E, Cader, M Z, Dyment, D A, Rice, G P A, Brown, J D, and Ebers, G C

Subjects
MIGRAINE, GENETICS, NEUROLOGY
Abstract

Migraine with aura (MA) arises from a combination of genetic and environmental factors. The sibling risk, age at onset, and aura type were compared in 54 MA probands categorised by family history of MA. Three family types were ascertained each having an MA proband and: (1) an MA parent and MA offspring (three generation; n=15), (2) either an MA parent or an MA offspring (two generation; n=20), and (3) neither an MA parent nor an MA offspring (one generation; n=19). The crude recurrence risk to siblings of probands was 2.7-fold higher in three generation compared with two generation MA families (chi(2)=6.24, p=0.0125) and 4.8-fold higher in three generation compared with one generation MA families (chi(2)=9.95, p<0.002). The mean age at onset decreased with an increase in genetic load. The MA probands from three generation families were significantly younger than probands from the one generation families (F=5.14, p=0.030). MA probands from three generation families were more likely to report more than one type of aura than MA probands from two generation families (chi(2)=4.44, p=0.035). The significant difference in genetic loading and the earlier age at onset in the three generation families add further evidence for a genetic basis for MA and the difference in sibling risks demonstrates that the MA population is heterogeneous. [ABSTRACT FROM AUTHOR]

Published
2003
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