Polymorphism of the osteopontin gene and clinical course of multiple sclerosis in the Polish population.

Osteopontin (OPN) is a key cytokine involved in T-cell activation in multiple sclerosis (MS). We investigated whether polymorphism of the osteopontin gene affects MS occurrence and clinical course in a Polish population. Disability in 100 MS patients was evaluated using the Expanded Disability Status Scale (EDSS).

On the lack of a clear-cut association between alpha-2-macroglobulin deletion and the risk of Alzheimer disease in Poland.

Alzheimer disease (AD) is a complex, multi-factorial disease with the potential involvement of several genes. Alpha-2- macroglobulin (A2M) has been implicated in AD on the basis of its ability to mediate the clearance and degradation of -amyloid peptide. Nevertheless, it is not clear whether there are racial differences in frequency of polymorphisms of A2M in AD.

TNFα gene G-308A polymorphism and the risk of ischemic stroke.

TNFα, a significant immune mediator, may contribute to the initiation and progression of the ischemic stroke. Genetics of TNFα molecule may have an important role in the risk of ischemic stroke. The most interesting aspects of the G-308A polymorphism remain unexplained; there are many discrepancies between the results.

Erythrocyte transketolase activity in patients with diabetic and alcoholic neuropathies.

Introduction: The activity of erythrocyte transketolase induced by thiamine pyrophosphate and normalized to age of the patient is a marker of thiamine metabolism disturbances with pathological consequences in the central and peripheral nervous system. The measurement of erythrocyte transketolase activity enables evaluation of the thiamine status and therapeutic decisions in the disorders of the nervous system related to its deficiency. The aim of the study was to compare different modes of expression of transketolase activity in the most frequent acquired neuropathies.

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

Until now, the question as to the role of immunological mechanisms in neuronal death of extrapyramidal cell systems in Parkinson's disease (PD) has not been fully resolved. One of the approaches includes examination of circulating blood cells. In our studies on 24 PD patients, peripheral blood was studied before and after medication with L-DOPA compounds.

Interleukin 17 receptor in multiple sclerosis patients treated with interferon β-1a.

Interleukin 17 (IL-17) and its receptor IL-17R1 produced by T-helper cells named Th17 are involved in the pathology of autoimmune diseases. In contrast to the at least partially explained role of IL-17 in pathology of multiple sclerosis, the significance of IL-17R in MS is unclear. Therefore we have studied the expression of IL-17R in the stable phase of multiple sclerosis treated by interferon β-1a.

Clinical trials in relapsing-remitting multiple sclerosis /a new proposal for dealing with basic problems and restrictions.

The natural course of multiple sclerosis is characterized by a high variability of pattern, relapse rate and different progression indices. They also present a dramatic impact on the interpretation of treatment trials. Reports, based on uncontrolled observations are therefore of little value.

Acute disseminated encephalomyelitis (ADEM).

ADEM is a disease that is characterized by an inflammatory reaction and demyelination in the central nervous system, with a distinct tendency to a peripheral localization of pathological changes. ADEM happens to occur with a temporal, and probably also with a causative relationship to viral, exanthematous diseases, as well as to preventive vaccinations. However, there are still many unresolved problems with respect to the relationship of ADEM to multiple sclerosis (MS), especially in instances with a multiphasic course of the disease.

Blood-brain barrier breakdown and cerebellar degeneration in the course of experimental neoplastic disease. Are circulating Cytokine-Induced Neutrophil Chemoattractant-1 (CINC-1) and -2alpha(CINC-2alpha) the involved mediators?

Cerebellar degeneration belongs to indirect effects of malignancy on the nervous system. Although the involvement of immune system is accepted as a hypothesis of its pathology, the clinical observations of ineffective immunomodulatory therapy suggest complex pathomechanisms, which await elucidation. The aim of this study was to prove the blood-brain barrier integrity, its relation to cerebellar degeneration and the role of circulating Cytokine-Induced Neutrophil Chemoattractant-1 (CINC-1) and Cytokine-Induced Neutrophil Chemoattractant-2alpha (CINC-alpha) in indirect effects of experimental malignancy.

Recombinant forms of myelin antigens expressed on Chinese hamster ovary (CHO) cells as a tool for identification of autoantibodies in serum of multiple sclerosis patients.

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 fail to detect reactivity against epitopes displayed by native antigens expressed on myelin sheats. We describe a cell-based assay that specifically identifies serum antibodies directed against three major myelin autoantigens: MBP, PLP and MOG.

Impact of methylprednisolone treatment on the expression of macrophage inflammatory protein 3alpha and B lymphocyte chemoattractant in serum of multiple sclerosis patients.

In order to extend our studies designed to elucidate the mechanism of action of intravenous methylprednisolone (ivMP) in symptomatic therapy of relapses in multiple sclerosis (MS) victims, we have evaluated the expression of chemokines: macrophage inflammatory protein 3alpha (MIP-3alpha) and B-lymphocyte chemoattractant (CXCL13) before and after treatment. The data from further exploration of the MP mechanism of action in MS relapses may be helpful in establishing the treatment design, that would be specific both for individuals, and for the disease phase. The mean levels of MIP-3alpha in sera of MS patients showed no statistically significant differences compared to control subjects.

Peripheral blood cell immunomarkers in the course of methylprednisolone treatment of multiple sclerosis relapses.

Intravenous methylprednisolone (MP) is the standard method in the treatment of acute relapses in multiple sclerosis (MS) and is believed to affect various immunological processes involved in the pathology of MS, including apoptosis and phagocytosis. Peripheral blood was obtained from 50 patients, with clinically definite MS, fulfilling the revised criteria of McDonald, a day before, after 5 days of MP treatment, and two weeks after conclusion of the treatment. Intravenous administration of 1.

Impact of cytokines on the pathomechanism of diabetic and alcoholic neuropathies.

Diabetic and alcoholic neuropathies are heterogeneous groups with variable lesions of axons or myelin. Their pathogenesis is complex and involves multiple pathways. To elucidate the impact of immunological factors in development of these neuropathies the expression of some cytokines in serum was studied: tumour necrosis factor a (TNF-a), monocyte chemotactic protein-1 (MCP-1) and growth-regulated oncogene alpha (GRO-alpha; CXCL1).

Value of Pelli-Robson contrast sensitivity chart for evaluation of visual system in multiple sclerosis patients.

Background And Purpose: The Multiple Sclerosis Functional Composite (MSFC) score, in addition to the commonly used EDSS scale, is one of the standard procedures used for a quantitative evaluation of the clinical state of patients with multiple sclerosis (MS). These methods, however, do not include an evaluation of the visual system. Hence, a search for sensitive tests evaluating the state of the visual system is important.

Effect of methylprednisolone treatment on expression of sPECAM-1 and CXCL10 chemokine in serum of MS patients.

In order to elucidate the mechanism of intravenous methylprednisolone (IVMP) therapy of relapses in multiple sclerosis (MS) patients, we have undertaken a study on the expression of the chemokines: soluble platelet endothelial cell adhesion molecule (sPECAM-1) and interferon gamma-inducible protein (CXCL10), before and after treatment. As more becomes known about the mechanism of methylprednisolone (MP) action, it may be possible to find a more specific treatment as well for the individual patients as the phase of the disease. The mean level of sPECAM-1 in our material was almost identical in either the MS and control subjects.

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

Cerebellar degeneration may be recognized as a remote effect of a growing tumor. We have analysed serum concentrations of tumor necrosis factor-alpha (TNF-alpha), macrophage chemoattractant protein-1 (MCP-1), thyroxine and insulin to elucidate the pathomechanism which may be of importance for the development of central degeneration in cachectic Morris hepatoma bearing rats. Serum TNF-alpha and MCP-1 levels were evaluated by means of the ELISA system, while thyroxine and insulin were estimated by radioimmunoassay.

[Evaluation of soluble platelet cell adhesion molecule sPECAM-1 and chemokine MCP-1 (CCL2) concentration in CSF of patients with tick-borne encephalitis].

Unlabelled: Platelet-endothelial cell adhesion molecule-1 (PECAM-1) is a glycoprotein involved in the transendothelial migration of leukocytes and MCP-1 is a proinflammatory protein, member of the 1 subfamily of chemokines, acting as activator of specific leukocytes. The expression of PECAM-1 and MCP-1 was studied in various pathological processes, but very little is known about the significance of these molecules during inflammatory reaction in viral diseases of the nervous system, including tick-borne encephalitis.

Material And Methods: Cerebrospinal fluid was obtained from 17 patients with TBE, treated at the Department of Infection Diseases in Białystok.

Two novel presenilin 1 gene mutations connected with frontotemporal dementia-like clinical phenotype: genetic and bioinformatic assessment.

Mutations in the amyloid precursor protein (APP), presenilin 1 (PSEN1) and presenilin 2 (PSEN2) genes are associated with early-onset familial Alzheimer's disease (EOAD). There are several reports describing mutations in PSEN1 in cases with frontotemporal dementia (FTD). We identified two novel mutations in the PSEN1 gene: L226F and L424H.

CCL2 (MCP-1) and CCL5 (RANTES) levels in the peripheral blood of multiple sclerosis patients treated with Glatiramer Acetate (Copaxone).

The MCP-1 and RANTES levels were measured in 20 multiple sclerosis patients before and after 1 year daily treatment with 20 mg of subcutaneously applied glatiramer acetate. The level of MCP-1 in serum from multiple sclerosis patients was lower than in control subjects. After one year of therapy with glatiramer acetate, the level of MCP-1 was almost identical with that at the starting point.

Minimal changes of TNF-alpha and MCP-1 expression in blood serum of rats subjected to experimental cardiac arrest.

Unlabelled: The elucidation of various aspects of the pathomechanism of experimental cardiac arrest may contribute valuable information for the treatment of cardiac arrests in humans. The model of clinical death in rats introduced by Korpatchev et al. was used.

[Heterogeneity of demyelination in multiple sclerosis and clinical differences].

Recent studies of demyelination in multiple sclerosis revealed four different patterns, which led to the assumption of disease heterogeneity, but without evident correlation with clinical and neuroimaging picture. Therefore at present it seems too early to conclude that multiple sclerosis is not a uniform entity, but a group of different diseases.

Association of influenza incidence with multiple sclerosis onset.

The aim of this study was to investigate the environmental factors influencing the tangible changes in the incidence of multiple sclerosis (MS) over a period of the past 30 years in the town Gniezno, Poland. We analysed many environmental factors to which the whole population was exposed in the respective period. The following factors were considered: viral infections (influenza, measles, varicella, rubella, mumps), atmospheric air pollution and climate conditions.

Presenilin 1 mutations in Polish families with early-onset Alzheimer's disease.

Mutations in Presenilin 1 (PS1) and Presenilin 2 (PS2) genes account for up to 50% of familial early-onset Alzheimer's disease (EOAD). In order to assess the genetic contribution of the PS genes in a series of Polish patients, we performed a mutational analysis in 6 autosomal dominant (ADEOAD), 8 familial and 41 sporadic EOAD cases from Poznan region. Three missense mutations in the PS1 gene (Ala246Glu in exon 7, Pro267Leu in exon 8, and Leu424Arg in exon 12) were found in patients from families with ADEOAD.

Amyloid precursor protein gene analysis in familial Alzheimer's disease cases: a lack of mutations in exons 16 and 17.

The beta-amyloid precursor protein (APP) gene (on chromosome 21), Presenilin 1 (PS1) gene (on chromosome 14) and Presenilin 2 (PS2) gene (on chromosome 1) are responsible for autosomal dominant early-onset Alzheimer's disease (EOAD). Missense mutations in these genes cause abnormal APP processing with subsequent overproduction of amyloidogenic and toxic A beta (42 peptide. A mutational analysis of APP, PS1, and PS2 genes can be used for both symptomatic and presymptomatic genetic testing and counselling in familial Alzheimer's disease (FAD).