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1

Recombinant forms of myelin antigens expressed on CHO cells as a tool for identiÞ cation of autoantibodies in serum of MS patients

100%
Jaskiewicz E., Michalowska-Wender G., Wender M.
Acta Neurobiologiae Experimentalis
|
2009
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tom 69
|
nr 1
A contribution of B cells and autoantibodies has been demonstrated in MS leading to interest in the use of such autoantibodies as diagnostic or prognostic markers and as a basis for immunomodulatory therapy. ELISA and Western blotting fail to detect reactivity against epitopes displayed by native antigens expressed on myelin sheats. We describe a cell-based assay that specifi cally identifi es serum antibodies directed against myelin autoantigens: MBP, PLP and MOG. The method detects antibody binding to recombinant antigens in their native conformation on MBP, PLP or MOG transfected mammalian (hamster ovary) cells. 36 patients with relapsing-remitting MS diagnosed according to criteria of Mc Donald were recruited. Age 38.2 and duration of the disease 7.1. Serum anti-MBP, anti-PLP and anti MOG IgG autoantibodies were detected in MS patients and 35 healthy donors by FACS analysis. Compared with healthy controls the titers of IgG autoantibodies directed against membrane-bound recombinant myelin antigens were most signifi cantly increased for PLP, no quite signifi cant for MBP and not signifi cant for MOG. The titers of anti-MBP antibodies were low in contrast to high titers of anti-MOG antibodies in both groups suggesting a nonspecifi c binding. The cell-based assay detection of autoantibodies directed against recombinant myelin antigens could be a useful tool providing the serological markers in diagnosis and progression of MS. Indeed, it could allow to obtain molecular characteristics of disease in each patient in term of an antibody response against certain myelin and non-myelin antigens. We have shown that in RRMS patients elevated level of serum antibodies against PLP is signifi cant, what should be considered in search for specific immunomodulatory therapy in MS.
2

Pattern of delta gamma 16 TCR genes in multiple sclerosis versus myasthenia gravis

100%
Michalowska-Wender G., Nowak J., Wender M.
Acta Neurobiologiae Experimentalis
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1997
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tom 57
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nr 5
3

Extent of the oxidative damage to DNA (8-oxo-2dG) in multiple sclerosis

100%
Dorszewska J., Michalowska-Wender G., Wender M.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
|
nr 1
There are some hypotheses that oxidative damage to DNA secondary to infl ammation may contribute to irreversible alterations in MS plaques. To test this assumption, we have estimated the level of a DNA oxidative marker, the level of a purine oxidation product, the 8-oxo-2-deoxyguanosine (8-oxo-2dG) in lymphocytes of MS patients. Material and methods: Peripheral blood was collected from 28 patients with clinically defi nite MS aged from 19 to 46 years. The duration of MS was 4.2 ± 3.1 years. The mean of EDSS was 2.0 ± 0.8. In MRI study 14 cases were gadolinium positive and 14 negative. Thirty healthy volunteers make up the control group. DNA was isolated from peripheral blood lymphocytes and then hydrolyzed to nucleosides using P1 nuclease. In order to determine 8-oxo-2dG level, the nucleoside mixture was applied to the HPLC/ UV system, coupled to an electrochemical detector. Results and discussion: The mean level of 8-oxo 2dG in MS patients was 19.6 ± 35.1 and, compared to that established for control subjects (12.3 ± 7.2), showed no statistically signifi cant differences. The comparison of 8-oxo-2dG in subgroups of patients divided according to duration of the disease showed the higher number of cases with DNA damage in patients of the subgroup with shorter duration of the disease. The mean level of 8-oxo-2dG in gadolinium positive MS cases was 17.3 ± 13.1 and in gadolinium negative ones it was 9.6 ± 4.0. The difference was signifi cant. Conclusions: (1) Oxidative damage to DNA is not a general feature in MS patients but it may frequently appear in the early period of the disease; (2) The higher level of oxidative marker of DNA damage in MS, noted in active period of the disease, testifi es to the relationship between the studied variable and MS process.
4

Cachexia - induced cerebellar degeneration: Involvement of serum TNF and MCP-1 in the course of experimental neoplastic disease

100%
Michalak S., Wender M., Michalowska-Wender G.
Acta Neurobiologiae Experimentalis
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2006
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tom 66
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nr 2
5

Impact of cytokines on pathomechanism of diabetic and alcoholic neuropathies

100%
Michalowska-Wender G., Adamcewicz G., Wender M.
Acta Neurobiologiae Experimentalis
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2006
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tom 66
|
nr 4
6

Impact of L-DOPA treatment of patients with Parkinson`s disease on mononuclear subsets and phagocytosis in the peripheral blood

100%
Hurny A., Michalowska-Wender G., Wender M.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
The question as to the role of immunological mechanisms in neuronal death of extrapyramidal cell systems in Parkinson`s disease is till now not fully resolved. One of the approaches includes an examination of circulating blood cells. In our studies consisting of 24 patients the peripheral blood was studied before and after medication with L-DOPA compounds. Patients with Parkinson`s disease demonstrated an increase of lymphocyte Cd95/CD3 as well as a considerable number of cells dead by apoptotic processes. After treatment with L-DOPA both the percentage of CD95/CD3, acknowledged as an antigen marker characteristic for apoptotic cells as well as the number of cells dead by apoptotic processes were decreased. These findings thus indicate that levodopa treatment in Parkinson`s disease has an impact on apoptotic processes in this instance, and this should be taken into consideration as a positive event in the pathomechanism effected by this treatment.
7

The effect of azathioprine treatment on IgG and its subclasses in multiple sclerosis

100%
Losy J., Michalowska-Wender G., Wender M.
Acta Neurobiologiae Experimentalis
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1992
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tom 52
|
nr 3
8
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Metabolic syndrome in type 1 diabetes mellitus. Does it have any impact on the course of pregnancy?

76%
Wender-Ozegowska E., Zawiejska A., Michalowska-Wender G., Iciek R., Wender M., Brazert J.
Journal of Physiology and Pharmacology
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2011
|
tom 62
|
nr 5
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