[Recurrent purulent meningitis in a patient with Behcet's syndrome].
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Biomedical subjects
Publications and source records attributed to B Johansson.
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The cytoxicity in vitro fo peripheral blood lymphocytes from patients with carcinoma of the urinary bladder (TCC-bladder) against allogeneic target cells from established cell lines was studied by the 51Cr-release assay. Lymphocytes from both untreated and treated TCC-bladder patients have a significantly elevated mean cytotoxicity to TCC-bladder target cells. Tumour cell destruction by lymphocytes from TCC-bladder patients shows a clear disease related specificity. In TCC-bladder patients a superimposed cytotoxicity exists, probably reflecting reactions against one or several tumour - associated antigens. In treated patients this cytotoxicity may be masked by higher incidence of cross reaction.
In 1969 a clinical trial was started where patients with bladder carcinoma stage T2 and grade 3 were subjected to preoperative radiotherapy followed by cystectomy. The survival rate in this series was higher than in a previous series of comparable patients who were given full irradiation without cystectomy.
Patients with poorly differentiated prostatic carcinoma and skeletal metastases were randomized to treatment with 2.6-cis-diphenylhexamethylcyclotetrasiloxane (2.6-cis) and estramustine-17-phosphate (estramustine). Parallel with the clinical study a group of non-randomized patients were treated with 2.6-cis. Cytological regression of the tumor could be registered in half of the estramustine group but not in the 2.6-cis group. There were no drug-related changes in blood chemistry, kidney function tests, hematology or liver enzymes. There was in increase in acid and alkaline phosphatase in both groups but more pronounced in the 2.6-cis group. In both groups follicle-stimulating and luteinizing hormone values were depressed. Testicular and penis atrophy was observed in the 2.6-cis group. Relief of pain and marked improvement of conditions occurred in the majority of the cases in both groups. In general, no tumor regression was observed during administration of 300 mg. 2.6-cis daily for at least 3 months. Some tumor regression was noted during 600 mg. estramustine therapy daily.
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Amphetamine productes protein leakage in the brain when given to rats under nitrous oxide anesthesia. The blood-brain barrier dysfunction is caused by the combined effect of blood pressure increase and vasodilatation. In the present experiments pretreatment with dexamethasone, 2 mg.kg-1, diminished the amphetamine-induced extravasation of Evans blue albumin and 125IHSA in the rats' brain. Possible explanations to the effect of dexamethasone on cerebrovascular permeability are discussed.
Differences between feeding practices in earlier investigations prompted the present study of iron and vitamin E supplementation in breast milk fed preterm infants. A new and highly sensitive technique for quantitation of alpha-tocopherol in serum was used. Studies on 34 infants with a birth weight below 2000 g or gestational age less than or equal to 35 weeks showed that supplementation with 16.5 mg tocopheryl acetate/day from 10 days of age resulted in a significantly higher haemoglobin concentration and lower reticulocyte count at 8-10 weeks than supplementation with 1.5 mg/day (p is less than 0.05). Studies on 23 infants with a birth weight of 2000-2499 g revealed subnormal alpha-tocopherol levels in 2 of the infants given 1.5 mg tocopheryl acetate/day but there was no effect on the haemoglobin concentration at 8-10 weeks. There were no untoward effects of an early iron supplementation with 2-3 mg Fe++ (as ferrous succinate)/kg/day. It is concluded that extra supplementation with vitamin E is advisable also in breast milk fed preterm infants. A low dosage iron supplementation from 3 weeks of age is safe.
Quick-release and quick-stretch experiments have been performed on preparations of smooth muscle from rat portal vein and rabbit urinary bladder. The low equivalent mass of the isotonic lever (8 mg) implied that inertial oscillations were limited to the first 5-10 msec after the load step. The high time resolution achieved in this way enabled us to separate three components in the length response to a step change in force: (1) an immediate passive elastic recoil, (2) an isotonic velocity transient lasting 50-75 msec and (3) shortening of the contractile element after its full adjustment to the new load. The maximal series elastic recoil was about 10% of the total muscle length in portal vein but only some 3% in urinary bladder. Stiffness of series elasticity increased in proportion to force and was about 3 times higher in bladder than in portal vein at any force level. Force-velocity relations for loads less than Po could be fitted to Hill's equation; Vmax in 4 AC-stimulated portal veins was 0.53 +/- 0.03 muscle lengths/sec and in 8 K+-activated bladder preparations 0.18 +/- 0.01 muscle lengths/sec. Application of loads greater than Po produced rates of lengthening greater than expected from an extrapolation of Hill's hyperbola. The nature of the transient component is discussed in the light of recent studies of force and velocity transients in skeletal muscle.
Quantitative analyses of plasma concentrations of retinol binding protein (RBP), prealbumin and total proteins were performed in normal subjects and in forty-two patients suffering from diseases of the intestine and liver. The visual dark adaptation ability (DAA) was also assessed. Reduction of DAA and of RBP and prealbumin levels was noted in patients with chronic liver disease and fat malabsorption. In sixty-eight patients with intestinal diseases the RBP concentration seemed to be reduced in relation to the degree and duration of steatorrhoea. Furthermore, inflammatory activity, as revealed by laborabory tests, markedly reduced the RBP level. Treatment with vitamin A increased the RBP and prealbumin concentrations and restored the DAA to normal in patients with malabsorption but normal liver function. In patients with liver disease reduced DAA and serum RBP values were not affected by vitamin A therapy. Only at RBP concentrations below half the normal was impairment of the dark adaptation observed, suggesting that serum RBP is a more sensitive indicator of vitamin A deficiency than measurement of dark adaptation.
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Purified blood lymphocytes from 81 consecutive and previously untreated patients with Hodgkin's disease were studied in vitro. The patients were evaluated 23 to 52 months after institution of therapy and were divided into two prognostic groups: 1. Complete remission with or without previous relapse/relapses. 2. Uncontrolled relapse or decreased from Hodgkin's disease. Lymphocyte activation by concanavalin A, pokeweed mitogen or phytohaemagglutinin was impaired and spontaneous DNA synthesis was high in patients with poor prognosis as compared to the good prognosis group. The prognostic information increased if the four lymphocyte tests were combined in a score (range 0-8). All 8 patients with pronounced lymphocyte defects (score 7-8), died, while all patients with score 0 and 1 were in complete remission. In contrast, total lymphocyte and T-lymphocyte counts and lymphocyte stimulation by PPD were of no prognostic value. The ability of certain lymphocyte functions to predict prognosis was equal or better than that of age and better than clinical staging, histopathology and symptoms.
4-Aminopyridine (4-AP) increased the spontaneous mechanical activity of the isolated rat portal vein. Since denervation and adrenergic receptor blockade failed to prevent this effect of 4-AP it is suggested that the drug enhances the electrical excitability of the muscle membrane. 4-AP significantly increased the response of the muscle to electrical nerve stimulation in most experiments but had little effect on the response to applied noradrenaline (NA). Both spontaneous and evoked release of 3H-activity, following preincubation in 3H-noradrenaline, were increased in the presence of 4-AP (10(-3) M). The present results with 4-AP can be explained by its known ability to block the transient potassium conductance which accompanies the action potential in excitable tissues.
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A protein, ASCA, is isolated from amyloid fibrils extracted from heart tissue of five different patients with senile cardiac amyloidosis (SCA). The proteins of all five patients showed immunological identity when reacted with an antiserum raised against one of the proteins. In contrast, no reaction was obtained with antisera against a variety of other amyloid proteins. The antiserum against the subunit protein of senile cardiac amyloid did not react with any other amyloid preparations tested, nor with extracts of normal heart tissue. Thus, the subunit protein appeared to be unique to senile heart amyloid. The protein could form fibrils in vitro, had a mol wt of about 6,000 daltons and the amino acid compositions investigated in two cases showed extensive similarities but were clearly different from that of protein AA of secondary amyloid fibrils.
Control and ethanol-intoxicated rats were given a small air embolus in the right common carotid artery after ligation of the external carotid branch. The extravasation of Evans blue-labelled albumin (EBA) was studied. Control rats dispalyed a slight extravasation of EBA through arteries and arterioles at the surface of the right hemisphere with a slight spread into adjacent brain parenchyma. Additionally, ethanol-intoxicated rats showed a great leakage through small blood vessels even deep in the right hemisphere and a blue-staining of most of the embolized hemisphere. Thus it was shown that during embolization, ethanol increases the vascular permeability to macromolecules. It is proposed that this phenomenon mainly is due to injury to the endothelial cells.
The cerebrovascular permeability to protein was studied in hypercapnic rats and in rats with epileptic seizures induced by bicuculline and homocysteine. Despite the differences of the basic pathophysiological mechanisms involved in these models, the blood-brain barrier (BBB) dysfunction was clearly related to the combined effects of high blood pressure and cerebral vasodilatation, thus indicating mechanical factors to be predominantly involved. The BBB changes were most frequent in central and basal regions in contrast to those induced by acute hypertension, which are most common in cortical areas.