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Biomedical subjects

B Lang

Publications and source records attributed to B Lang.

At least 199 records · Page 11Linked to original sources
PubMed1987

Antibody heterogeneity and specificity in myasthenia gravis.

Anti-AChR is heterogeneous within individuals and between individuals. Anti-AChR idiotypes are not shared to any large extent. Ten monoclonal antibodies raised against human AChR: (a) bind to five partially overlapping regions; (b) are not idiotypically identical even within a region; (c) do not all bind to the main immunogenic region; (d) four distinguish between normal and denervated human AChR; (e) can be used to define the antigenic determinants in MG. Antigenic specificities vary in different clinical groups. Antigenic specificities can change during the course of the disease, but some remain relatively constant. Thymus cultures make antibodies with the same specificity as those present in the serum of the individual. All monoclonal antibodies bind to myoid cells of normal and MG thymus. We find no convincing evidence of naturally occurring antiidiotype antibodies in MG sera.

Antibodies, Monoclonal↗
PubMed1987

The effect of myasthenic syndrome antibody on presynaptic calcium channels in the mouse.

1. The action of immunoglobulin G obtained from patients with Lambert-Eaton myasthenic syndrome (LEMS IgG) was investigated by injecting mice, followed by intracellular recordings from the mouse diaphragm. 2. End-plate potential quantal content was studied over a range of Ca2+ concentrations. Curves of log quantal content versus log Ca2+ concentration were shifted to the right by LEMS IgG. For low Ca2+ concentrations, release continued to follow Poisson statistics after LEMS IgG treatment. 3. Miniature end-plate potential (m.e.p.p.) frequency was measured in solutions containing high K+ concentrations. LEMS IgG significantly reduced m.e.p.p. frequency at each K+ concentration studied. 4. M.e.p.p. frequency was measured at fixed high-K+ concentration (15.9 mM) for a range of Ca2+ concentrations. The log-log plot of m.e.p.p. frequency versus Ca2+ concentration was shifted downwards throughout by LEMS IgG. 5. M.e.p.p. frequency was not affected by LEMS IgG in Ca2+-free solutions (K+ concentration 15.9 mM) or in solutions of low Ca2+ concentration (K+ concentration 5.9 mM). 6. At each Ca2+ concentration studied, m.e.p.p. amplitudes were not affected by LEMS IgG. 7. The data suggest that LEMS IgG acts on presynaptic voltage-dependent Ca2+ channels to cause their loss of function, probably by down-regulation.

Action Potentials↗
PubMed1987

[Infection of the CNS caused by Listeria monocytogenes].

This report examines two cases of infection of the central nervous system by Listeria monocytogenes (L.m.). Both cases show that listeriosis is not only a differential diagnosis of purulent meningitis, but can also be the cause of an isolated brain stem syndrome with normal cerebrospinal fluid cell count. The prognosis depends crucially on the early antibiotic therapy (ampicillin). The first patient was a chronic alcoholic. He died of fulminant septic shock and meningitis with brain stem encephalitis (cell count of cerebrospinal fluid: 10500/microliters). L.m. was isolated from blood cultures and from cerebrospinal fluid. The second patient had no indications of preexisting immunological disorder. Two days after perianal injections for haemorrhoids, symptoms of a progredient brain stem syndrome developed. The cell count of cerebrospinal fluid was only 10/mu, but L.m. was isolated from blood cultures. The patient died of circulatory failure. At autopsy, a brain stem encephalitis and cerebellitis with inflammation of the surrounding leptomeninx was identified.

Cerebral Ventricles↗
PubMed1986

Lipid peroxidation dependent aldrin epoxidation in liver microsomes, hepatocytes and granulation tissue cells.

Lipid peroxidation activity was determined in liver microsomes, hepatocytes and cultured granuloma cells by measuring ethane and pentane production with an improved capillary gas chromatographic method. Lipid peroxidation initiated by ferrous ions and NADPH produced significantly more hydrocarbons at 4% O2 than under atmospheric (21% O2), hyperoxic or hypoxic conditions. In liver microsomes ferrous ions and ascorbic acid stimulated the non-enzymatic lipid peroxidation and concomitantly the epoxidation of aldrin. The results demonstrate that epoxidation of aldrin can be triggered by the iron initiated lipid peroxidation.

Aldrin↗
PubMed1985

[Autoimmune hemolytic anemia in ulcerative colitis. Report on 7 cases, possible treatment and review of the literature].

Warm-antibody autoimmune hemolytic anemia (AIHA) is a rare but typical extraintestinal complication of ulcerative colitis. Seven cases with this condition are reported here and 24 further cases from the literature are reviewed. There were no essential differences between the two groups of patients with respect to clinical and immuno-hematological findings. However, the introduction of immunosuppressive drugs has led to a change in therapy and prognosis in recent years. Our observations suggest that treatment with steroids and azathioprine is to be recommended, with accompanying therapy of the underlying disease. In patients failing to respond to this immunosuppressive regimen, splenectomy or surgical treatment of the affected intestines must be considered. For every patient with ulcerative colitis and hyperregenerative anemia the possibility of warm autoantibody formation must be ruled out by performing the direct antiglobulin test.

Adult↗
PubMed1985

Action of Lambert-Eaton myasthenic syndrome IgG at mouse motor nerve terminals.

We have studied the electrophysiological effects of IgG obtained from four patients with Lambert-Eaton myasthenic syndrome (LEMS) (two with small cell carcinoma), using the mouse passive transfer model. Mice received LEMS or control IgG or plasma, 10 to 60 mg daily. Microelectrode intracellular recordings were made from diaphragm muscle. LEMS IgG and plasma decreased end-plate potential quantal content similarly, confirming IgG as the active factor. LEMS IgG was equally effective in C5-deficient mice, indicating that late complement components are not required. The time course of decline and recovery of quantal content closely followed that of the human IgG in the mouse serum, with time to half-maximal effect of about 1.5 days in each case. Binding/dissociation of IgG or down/up regulation of the antigenic determinants, possibly Ca2+ channels, has a half-life of between 2 and 36 hours. The results confirm our concept that IgG antibody to nerve terminal determinants underlies the disorder of transmitter release in LEMS.

Adult↗
PubMed1985

[In vitro and in vivo studies with interleukin 2 (IL-2) and various immunostimulants in a patient with AIDS].

We report on a lethal course of an acquired immunodeficiency syndrome (AIDS) in a young female patient. She had spent her vacancies six years before diagnosis in Haiti, where a sexual intercourse with a Haitian man had occurred. Leading clinical symptoms consisted of recurrent Herpes simplex infections of the genital and perianal region as well as unexplained high temperatures. There were some typical laboratory and immunologic features of this disease with leukopenia, hypergammaglobulinemia, cutaneous anergy, a reduction of peripheral T-lymphocytes (OKT 3) and an almost complete loss of OKT 4 (helper cells) positive lymphocytes. The mitogenic response upon stimulation with allogeneic cells (MLC) or with the mitogens PHA, Con A and PWM was significantly reduced. There was no measurable interleukin-2 (IL-2) secretion of peripheral blood lymphocytes. Several immunostimulators (thymopentin, inosiplex, bestatin) were tested in lymphocyte proliferation assays in vitro. The mitogenic response could not be enhanced by neither of these substances. A clinical trial with Delimmun (inosiplex) for 14 days did not show any clinical or immunologic improvement in this patient. The intravenous application of high dose immunoglobulin G was without any observable effect. The proliferation inducing capacity of a highly purified IL-2 preparation on the AIDS cells in vitro led us to a clinical trial with this substance. We applied 100 Bödeker units of IL-2 per kg body weight and day subcutaneously for 16 days. A therapeutical effect, however, could not be observed. Cell marker analyses did not show significant changes in lymphocyte subpopulation composition under IL-2 therapy. There was an increase in the spontaneous cell proliferation 14 days after start of IL-2 therapy. The PHA- and IL-2 response of the AIDS cells, however, was unchanged. It cannot be excluded that an administration of IL-2 in earlier stages of AIDS may have beneficial effects.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Anti-acetylcholine receptor idiotypes in myasthenia gravis analysed by rabbit anti-sera.

Anti-idiotype sera, raised in rabbits against anti-acetylcholine receptor (AChR) (idiotype) purified from the serum of three myasthenia gravis patients, inhibited binding of homologous idiotype to the AChR by up to 80%. The expression of idiotype in the three individuals changed very little over a period of several years, during which they showed a declining trend in overall anti-AChR antibody. Only one of the four anti-idiotype sera inhibited the binding of anti-AChR from a number of other patients. Our results indicate a consistency of idiotype expression within an individual, and fail to show substantial idiotype sharing between individuals.

Animals↗
PubMed1984

[HLA typing in patients of German origin with recurrent benign aphthosis and Behçet's disease].

HLA-pattern was analysed in 60 patients with recurrent benign aphthosis (RBA), in another 14 suffering from Behçet's disease (BD) and in 200 healthy individuals, all of German origin. High prevalence rates of HLA-A2, HLA-B5 and HLA-Cw3 haplotypes were found in patients with RBA, yet significant only for HLA-Cw3 (p = 0.01). HLA-B5 was shown in none but two German patients with BD. These results are discussed with particular regard to reports on racial differences of HLA-patterns in the populations of several continents including patients with aphthous disorders.

Adolescent↗
PubMed1984

Passive transfer of Lambert-Eaton myasthenic syndrome in mice: decreased rates of resting and evoked release of acetylcholine from skeletal muscle.

Mice were injected for 1-2 months daily with 10 mg immunoglobulin G (IgG) from four patients with Lambert-Eaton myasthenic syndrome (LEMS); control mice were injected with pooled human IgG from normal donors. Gastrocnemius muscles were homogenised for the assay of acetylcholine (ACh), choline acetyltransferase (ChAT), and cholinesterase (ChE). The ACh, ChAT, and ChE contents of gastrocnemius muscles from "LEMS mice" were about the same as the control values, which were 180 pmol, 40 nmol X h-1 (37 degrees C), and 15 mumol X h-1 (37 degrees C), respectively. Hemidiaphragms were treated with an irreversible ChE inhibitor (Soman) and incubated at 20 degrees C for estimation of ACh release. Resting ACh release from experimental muscles was reduced by about 25% (P2 less than 0.05) and the release evoked by 3 s-1 nervous stimulation by 50% (P2 less than 0.05). On the other hand, 50 mM KCl-induced transmitter release was not abnormal in LEMS mice. The findings indicate that IgG antibody from patients with LEMS may bind to nerve terminal determinants that are involved in quantal and nonquantal ACh release.

Acetylcholine↗
PubMed1983

Passive transfer of Lambert-Eaton myasthenic syndrome with IgG from man to mouse depletes the presynaptic membrane active zones.

In the Lambert-Eaton myasthenic syndrome (LEMS), there is a decreased release of acetylcholine quanta from the nerve terminal by nerve impulse. Recently, an autoimmune origin of LEMS was documented by passive transfer of its electrophysiologic features from man to mouse with IgG. Freeze-fracture electron microscopy of LEMS neuromuscular junctions has revealed a paucity of presynaptic membrane active zones. Thus, the active zones might be the targets of the pathogenic autoantibodies in LEMS. To test this assumption, freeze-fracture electron microscopic studies were done in mice injected with 10 mg of IgG daily from each of three LEMS patients and in control mice treated with normal human IgG or no IgG. IgG from patients 1 and 2 impaired neuromuscular transmission in mice, but IgG from patient 3 failed to do so. After 52-69 days of treatment, diaphragm or anterior tibial muscles were removed and coded. Paired muscles from control mice and mice receiving LEMS IgG were studied "blindly." Satisfactory freeze-fracture replicas of 185 presynaptic membrane P-faces were analyzed by stereometric methods. In mice treated with LEMS IgG that was pathogenic by electrophysiologic criteria, there was a selective depletion of active zones and active-zone particles but not of other membrane particles and there was a concomitant increase of large membrane particles aggregated into clusters. These findings provide additional evidence that the active zones facilitate quantal transmitter release by nerve impulse, lend further support to the assumption that the active-zone particles are Ca2+ channels, and establish mediation of the membrane lesions in LEMS by IgG.

Action Potentials↗