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H J Meyer-Rienecker

Publications and source records attributed to H J Meyer-Rienecker.

30 records · Page 2Linked to original sources
PubMed1977

Anomalous lymphocyte-antigen reaction in relatives of multiple sclerosis patients. A study of a possible genetic factor in the disease.

A combined familial study of multiple sclerosis (MS) in England and in the Rostock area of the GDR using the macrophage electrophoretic mobility (MEM)-LAD test embracing 132 relatives has revealed a closely similar pattern of distribution of "anomalous" LAD (Linoleic Acid Depression) values in relatives (77% type of reaction) to that originally reported in the British study. The anomaly in predominantly associated with females--all mothers of MS patients being affected, whilst daughters and sisters are also represented. In addition unusual full MS type of reaction (90% reduction) has been found in some children related to patients. There is clearly a genetic element in the development of MS probably mainfested in the inborn mishandling of unsaturated fatty acids suggested by Thompson; no recognizable pattern of inheritance is noticeable even within the combined material. There is evidence that the metabolic anomaly alone does not inevitably lead to MS, and the full abnormality may be present at an early age. A survey about the examinations and a selection of characteristic family trees of MS are given, illustrating the manner in which the 77% type anomaly is distributed with occasional omission of a generation.

Adult↗
PubMed1977

[Cytopherometry in neurologic diseases (author's transl)].

Cytopherometry in neurologic diseases is discussed with regard to antigenic reactivity, the formation of cytokines and the direct changes of electrophoretic mobility of immune-competent cells. The Macrophage-Electrophoresis-Mobility (MEM) test, the variants of the method and additional techniques produced some results of diagnostic and immunpathologic value. A general and unspecific sensitization during cellular immune reaction in lesions of the nervous parenchyma was detectable. Using adequate antigens and extended methods of characterisation in the test system, differentiated reactivity, mainly of the inflammatory diseases and in some pathogenetic processes - including a defect of cell-membrane - was found. Typical findings were shown with the MEM-LAD (linoleic acid depression) test in M.S. This technique led to novel pathogenetic, family-genetic and therapeutic aspects. Similar diagnostic progress in various types of brain tumors was shown by using tumorassociated antigens. Analysis of specific factors of cellular immunity was extented by developing a thymosine assay and direct assessment of cytokines, especially fo the MSF (macrophage slowing factor) in the MSF assay. The thymosine assay may prove valuable for the cellular basis of immunologic processes (in particular myasthenia and therapeutic thymectomy). With the direct MSF assay a differentiated high MSF activity in the CSF in chronic neuroimmunologic processes and particularly in M.S. was shown which led to novel aspects of the immunology of the CSF. The characteristics of the MSF, found after column-chromatographic fractionation, showed identical zytokine activity in CSF and the supernatants of lymphocyte-antigen-incubation which lay in the lower range of molecular weight of migration inhibitory lymphokines.

Antibody Formation↗
PubMed1976

[Demonstration of a factor in cerebrospinal fluid with inhibitory activity for electrophoretic cell mobility in multiple sclerosis (author's transl)].

Inhibition of electrophoretic cell migration using cerebrospinal fluid (CSF) directly was investigated by the modified MEM (macrophage electrophoretic mobility) and TEEM (tanned sheep erythrocyte electrophoretic mobility) tests, respectively. An inhibitory activity of macrophage slowing factor (MSF)--one of in vivo lymphokines--in CSF was established in cases of multiple sclerosis (17.5 +/- 3.8%), and neurolues. The value of this MSF assay turned out to be significantly different from the remaining inflammatory ailments of the nervous system (10.1 +/- 6.8%). Results of other neurological diseases were found to be very much lower (5.1 +/- 4.2%). It seems important, for immunopathogenesis and the diagnosis of neuroimmunological diseases with enhanced cellular immunoreaction, to evaluate MSF activity in CSF. To characterize the active factor in CSF (and serum) these fluids were fractionated by gel filtration chromatography as well as supernatants from lymphocyte-antigen incubation in MS patients. The main activity for inhibition of electrophoretic cell mobility was eluated in the same fraction in these fluids. It could be shown that units have a molecular weight of about 15000 Daltons; this value for MSF lies below those for other inhibitory lymphokines.

Erythrocytes↗
PubMed1976

The linoleic acid depression (LAD) test for multiple sclerosis using the macrophage electrophoretic mobility (MEM) test.

With the macrophage electrophoretic mobility (MEM) test of Field & Caspary, lymphocyte sensitization to thyroid antigen (F1-fraction) is demonstrable in all subjects--multiple sclerosis (MS) patients, those with other (destructive) neurological diseases (OND) and normals. The MEM-LAD test enables a further differentiation to be made in neurological patients compared ot normals: Linoleic acid inhibits the positive result by about 95 per cent in the case of MS, 58 per cent in normals and 45 per cent in OND. The high reduction appears to be a characteristic of MS. It is seen at all stages and in all forms of the disease and is not materially influenced by moderate immunosuppressive therapy. The mothers of MS patients show an intermediate result of about 78 per cent, suggesting a familial (genetic) background to the metabolic phenomenon described here; there is, however, evidence of an added exogenic factor for the development of the disease. The theoretical basis of the LAD test suggests further therapeutic trials of linoleic acid in treatment of MS.

Adolescent↗
PubMed1975

[Aspects of the value of humoral antibodies in encephalomyelitis of neuroallergic origin].

The importance of humoral antibodies formed in the course of neuroallergic diseases characterized by a cytergic type of reaction and especially in the course of experimental allergic encephalomyelitis (EAEM) is discussed, special attention being given to the importance of pathogenetic, immunodynamic, diagnostic, and therapeutic factors. The circulating antibodies of EAEM induced by cellular and humoral immunoprocesses are assumed to produce either intensifying or mitigating effects. Among the most important functions are the influence of immune globulins on the blood/brain boundary lesion, the gliotoxic and myelinotoxic effects, and the detection of a blockade of the intraneural transmission. The therapeutical effect to be discussed in the light of the protective effects of humoral antibodies is a mere conception in view of incompletely understood mechanisms including those governing the chronology and dynamics of immunoprocesses associated with multiple sclerosis, especially since the antigen-specific induction of tolerance appears to be far more essential.

Animals↗
PubMed1975

[Experimental allergic encephalomyelitis as a model for the study of therapeutic concepts for encephalomyelitis disseminata].

The induction of immunological tolerance with, and for, the caused organotypical antigen is a conception for a specific therapy for neuroimmunological diseases with at least a partial autoallergic pathogenesis. Appropriate to a set step-by-step programme for the development of antigen-specific therapy preventive tolerance experiments were carried out at the model of experimental allergic encephalomyelitis (EAEM) with allogenic myelin basic protein (BP) prepared from rabbits. The result is: 100 ug BP given intravenously simultaneously with 100 ug BP in incomplete Freud's adjuvant given intracutanously twice a week and 40 mg Cyclophosphamid given daily during the minor clinical incidence rate and no signs of EAEM pathomorphologically. A longlasting tolerance for the BP could be obtained as a test proved after 100 days. Hints are given for further potential therapeutic treatments, such as the use of antigen bound chemically to the immunosuppressive drug or the use of chemically modified BP for the induction of a specific tolerance.

Animals↗
PubMed1975

[Experimental prevention and suppression of neuroallergic diseases].

For concepts of therapy for neuro-allergic diseases, especially of the encephalomyelitis disseminata type the experimental allergic encephalomyelitis (EAEM)--as a neuro-immunological disease of the first order and a classic pattern for the specification of immunological processes--can be used for more and more extensive testing. After an exposition of the different forms of treatment (prevention, suppression and therapy) and their value the possibility of inducing tolerance a versus the encephalitogenic protein is discussed following the EAEM example--taking the view that all measures taken up to now in the case of neuro-allergic diseases have been unspecific and consequently not set down. In addition emphasis was laid on the assumption of tolerance induction after sensitization which is important to the formation of a therapy for encephalomyelitis disseminata.

Animals↗