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Biomedical subjects

R Hohlfeld

Publications and source records attributed to R Hohlfeld.

169 records · Page 10Linked to original sources

[Alternating ECG changes in dystrophia myotonica (Curschmann-Steinert)].

It is reported on a 39-year-old patient who revealed pathological ECG-findings of the most different kind during several years. Since there were no clues to a myocarditis, later on, however, pareses of atrophical skeletal muscles developed and a distropia myotonica could be diagnosed, the cardiological disturbances are to be regarded as a symptom of this disease. When also a participation of the myocardium in the distrophia myotonica is not unknown, so even in our case the frequently changing disturbances of the nervous impulses of the heart, of the ventricular stimulus conduction and of the replolarisation of different expression as well as the pronounced hypersensitivity to heart glycosides are remarkable individual findings. The interpretation of these findings is problematic. Morphologic and dystrophic changes of the myocardium as well as functional myotonic disturbances on the membraneous system may influence the process of stimulation and may cause the clinical appearances.

Adult↗

Autoimmune human T lymphocytes specific for acetylcholine receptor.

Myasthenia gravis is one of the best characterized human autoimmune disorders. Circulating autoantibodies to the nicotinic acetylcholine receptor (AChR) at the neuromuscular junction play a prominent part in the effector phase, that is, the immunoregulation. Indirect evidence, such as thymic abnormalities and the association with certain histocompatibility antigens (for example HLA-B8,-DR3) suggests a defect of immunoregulation at the level of thymus-dependent (T) lymphocytes. We report here on the isolation of autoreactive T cells from six patients with myasthenia gravis. From one of these patients, who is homozygous for HLA-DR3, we established a long-term T-cell line. The line cells are specific for purified fish and human AChR, display the surface phenotype of inducer/helper T cells and are genetically restricted to HLA-DR3. AChR-induced proliferation could be inhibited with two monoclonal antibodies against monomorphic DR determinants and also with DR3-specific alloantiserum.

Autoimmune Diseases↗