Biomedical subjects
Publications and source records attributed to V Neumann.
In our opinion there is no specific germ for multiple sclerosis. The pathogenic process is developed after a clinically "silent" period and results in a demyelinization process. Partially genetical aspects have to take into account for certain disease processes. Up to now both, the theory of infection as well as the neuroallergetic theory are of importance.
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In pregnancy, an increase in serum calcitriol and parathyroid hormone concentrations has been reported in several studies, though the increase in parathyroid hormone remains controversial. In magnesium deficiency states, parathyroid hormone and calcitriol secretion may be decreased. Because magnesium deficiency may occur in insulin-dependent diabetic patients, mainly because of urinary magnesium losses, we hypothesized that serum parathyroid hormone and calcitriol do not increase in the diabetic pregnancy. We studied, in a prospective longitudinal manner, 35 nondiabetic and 199 insulin-dependent diabetic pregnancies. In diabetic women, the goals of glycemic control were fasting blood glucose below 100 mg/dL and postprandial blood glucose less than 140 mg/dL. Serum magnesium, calcium, parathyroid hormone (whole molecule; ie, 1-84 fragment), and calcitriol were measured three times: 1) 8-12 weeks, 2) 22-28 weeks, and 3) 32-38 weeks' gestation. In normal women, serum parathyroid hormone did not change significantly over pregnancy, and a wide scatter of values was observed. Serum calcitriol increased significantly with advancing gestation. In diabetic women, serum parathyroid hormone had a narrow scatter, but values were within the low-normal range. During the third trimester there was no increase, and even a decrease, in serum calcitriol concentrations. Diabetics had, throughout pregnancy, significantly reduced serum magnesium concentrations when compared with controls. Their serum calcium and ionized calcium concentrations were similar to those of controls, except in the third trimester, when diabetic women had significantly lower serum calcium and ionized calcium concentrations than controls. We speculate that mineral metabolism abnormalities in diabetic pregnancies might be due to relative magnesium and/or insulin deficiency.
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The concept of seronegative polyarthritis is reviewed in relation to its clinical, immunogenetic, pathological and therapeutic features.
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The diagnostic value of CSF oligoclonal IgG bands, intrathecal IgG synthesis, cytology and markers of myelin breakdown in the cerebro-spinal fluid were evaluated in multiple sclerosis. None of the various immunological alterations were unique to MS. The diagnosis depends therefore mainly on course and clinical symptoms, but can be supported by CSF analysis.
The paper describes scanning electron microscopic observations of electric field induced fusions of human lymphocytes. The cells were fused by application of short-time (20 microseconds) field pulses of 5 kV/cm after dielectrophoretic collection at about 1.2 MHz and 750 V/cm. Electron microscopy clearly demonstrates membrane fusion and the stability of initial stages of fusion.
There are neither specific cell investigations nor immunological tests for the diagnosis of MS. Various immunological alterations occur in the course of the disease, but none is unique to MS. Accurate diagnosis remains confined to the clinical field. The diagnosis can be supported by CSF analysis. Laboratory examinations can help to determine the particular stage of the disease and provide clues to the etiology and pathogenesis. The appearance of abnormal CSF levels increases the certainty of the diagnosis.
The available defensive mechanisms are generally sufficient to protect the central nervous system (CNS) against the penetration of infectious particles. The blood-brain-barrier plays a decisive role in this process. The present paper represents the most important circumstances realizing that: 1. The macrophage-lymphocyte-system, 2. the "oligoclonal-CSF-IgG-reaction", and 3. the influence of psychological and physiological burdens on clinical-chemical or immunological parameters. It seems to be important to overcome the instability of the immunosystem and to reestablish the base-line.
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The fusion of human cells of the cerebrospinal fluid and of the peripheral blood is reported, as well as the fusion of these cells with tomato protoplasts. The cells were fused by applying short-time electric pulses after dielectrophoretic collection. The importance of this method for diagnosis and therapy is discussed and possible applications are mentioned.
To test the hypothesis that chronic furosemide treatment in otherwise healthy newborn animals may lead to lowered bone mineral [calcium (Ca) and magnesium (Mg)] content, healthy littermates within each litter of Sprague-Dawley rat pups were randomly assigned to three groups: control, low dose furosemide (5 mg/kg/day), and high dose furosemide (15 mg/kg/day). The pups were treated between days 4 and 28 postnatally. The wet and dry weights of kidneys and tibiae significantly correlated with body weights at sacrifice. Furosemide-treated pups demonstrated a dose-dependent growth delay, decreased total bone (tibiae) Ca and Mg, increased urine Ca and Mg concentration, and a significant inverse correlation between bone Ca and urine Ca concentration. There was no significant difference among the groups when bone Ca and Mg were normalized to per gram of bone dry weight. There were no significant differences among the groups with respect to bone phosphorus or urinary phosphorus concentration; kidney and serum Ca and Mg; or serum sodium, potassium, alkaline phosphatase and immunoreactive parathyroid hormone concentration. We conclude that chronic furosemide therapy leads to growth failure and to increased urinary losses of Ca and Mg. Total bone Ca and Mg in the furosemide-treated pups were diminished in proportion to growth retardation but the bone mineral content per unit of dry weight remained similar to control pups.
An epidemiological study of multiple sclerosis (MS) in the district of Halle, Halle-Neustadt and the area near the river Saale was carried out. We found 178 patients with a definite diagnosis in a total population of 396,529, corresponding to a prevalence of 44.9/100,000. The annual incidence rate was 2/100,000. When probable but not definitely diagnosed cases are included in the count, the estimated prevalence rises to 53.7/100,000 population.
Pulsed methylprednisolone (PMP) has been shown to produce clinical improvement and reduction in the ESR and acute phase protein concentrations in patients with active rheumatoid arthritis and has been advocated for use either as an alternative to slow-acting antirheumatoid drugs (SAARDs) or in conjunction with SAARDs to accelerate the response to treatment. To test these potential roles for PMP 45 patients with active RA were randomly allocated to treatment with PMP alone, PMP + sulphasalazine (SAS - at a maintenance dose of 2.0 g/day), or PMP + D-penicillamine (DPA - at a maintenance dose of 500 mg/day). In each case three 1 g intravenous infusions were given on alternate days during the first week of the trial. Patients were monitored for 24 weeks by standard clinical and laboratory measurements. All three treatment groups showed significant clinical and laboratory improvements at two weeks. With PMP + DPA and PMP + SAS these improvements were sustained and were not significantly different in these two treatment groups. However, in the 'PMP only' group ESR and CRP rose to pretreatment values by eight weeks. Twelve patients withdrew from the study owing to a relapse of the RA. No serious adverse effects were seen in the 'PMP only' group. Both combination regimens were well tolerated; adverse effects seen were attributable to either DPA or SAS. We conclude that PMP alone is insufficient for treatment of RA but can be used successfully in combination with either DPA or SAS. A comparison between these results obtained from two previous groups of 15 patients treated with DPA alone and SAS alone (using the same study design) shows that PMP accelerated the response to therapy by at least six weeks.
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Patients with ankylosing spondylitis were asked to follow a 'klebsiella exclusion diet' for 5 months of a 10-month study. The same percentage of faecal samples were positive for klebsiella whether the patients were on or off the experimental diet. The diet also failed to influence variability of klebsiella serotypes. We found no correlation between acquisition of klebsiella and deterioration of disease symptoms, as recorded by the patients. Furthermore, carriage of klebsiella did not correlate with any of the following parameters of disease activity measured in the outpatient clinic: morning stiffness, pain measured on a visual analogue scale, analgesic consumption, ESR, total serum IgA. We found no evidence, therefore, that faecal klebsiella is involved in disease exacerbations of ankylosing spondylitis.
The concept of seronegative spondarthritis, linking several diseases around ankylosing spondylitis, has received considerable clinical and genetic support, especially through the discovery of a high frequency of HLA-B27 in these disorders. Exogenous factors would appear to be responsible for some manifestations of the disease, but the role of Klebsiella micro-organisms is equivocal, and dietary control does not affect clinical manifestations. Increased serum and salivary IgA antibodies in active ankylosing spondylitis patients tend to suggest that IgA may act as an acute-phase reactant.