Biomedical subjects

B Ryberg

Publications and source records attributed to B Ryberg.

51 records · Page 3Linked to original sources

PubMed1983

The ontogenetic mouse brain model employed in the characterization of antibrain antibodies in multiple sclerosis.

The complement-fixing antibrain antibodies which may be found in patients with multiple sclerosis (MS) belong to several specificities, of which only two are as yet identified. In order to study three of the incompletely characterized specificities, the ontogenetic evolution of the corresponding antigens in mouse brain was followed. MS serum containing antibodies to sulfatide, a relatively myelin-specific glycolipid, served as a control. The studied antigens were virtually absent at birth and accumulated at different rates during the postnatal period. The results give valuable clues for the further study of the antibrain antibodies in MS.

Animals↗

PubMed1983

Differentiation among inhibitory actions of omeprazole, cimetidine, and SCN- on gastric acid secretion.

The action of the substituted benzimidazole omeprazole (H 168/68) was studied in three different in vitro preparations: the isolated guinea pig gastric mucosa, isolated intact and permeable rabbit gastric glands, and hog fundic microsomal membrane vesicles containing H+-K+-ATPase. The effects of omeprazole were compared with those of cimetidine and thiocyanate (SCN-). Under all the conditions studied, cimetidine only counteracted histamine-induced acid secretion, consonant with its H2-receptor antagonism. In contrast, omeprazole and SCN- were found not only to inhibit histamine-induced secretion but also basal acid formation and acid formation induced by dibutyryl cAMP and a high cell medium concentration of K+. Moreover, acid production induced by ATP in permeable gastric glands was antagonized by omeprazole and SCN-, whereas cimetidine was without effect. The interaction pattern of omeprazole and SCN- was differentiated by studies using the weak base antipyrine in the isolated mucosal preparation, where it was found that antipyrine could reverse the inhibition induced by SCN- but not that of omeprazole. Furthermore, omeprazole was found to inhibit the isolated H+-K+-ATPase, whereas cimetidine or SCN- was without effect. In the isolated mucosal preparation omeprazole caused an increase in K+ secretion rates in parallel with the inhibition of acid formation. This was in contrast to what was observed for cimetidine and SCN-, which exhibited no such increased K+ secretion. The results obtained from intact mucosa and isolated glands are in agreement with the ability of omeprazole to inhibit the isolated H+-K+-ATPase and thus provide evidence of a novel mechanism of action for this inhibitor.

Adenosine Triphosphatases↗

PubMed1982

Antibrain antibodies in multiple sclerosis. Relation to clinical variables.

IgG antibrain antibodies (ABA) of several specificities can be demonstrated in multiple sclerosis (MS) with the complement fixation technique. This technique seems to discriminate between IgG specifically and non-specifically bound to CNS preparations. Complement-fixing ABA were titrated in paired serum and CSF samples from 87 patients with clinically definite MS, 15 patients with probable MS, 29 patients with other neurological diseases, and 13 "healthy" controls. In addition, sera from 55 non-MS patients were tested. In 40% of the sera and 88% of the CSF samples from patients with clinically definite MS, ABA reacting with human brain homogenate were demonstrated. The corresponding figures for probable MS were 21% and 73%, and for the controls 11% and 6%. Two of 9 sera from patients with the Guillain-Barré syndrome were strongly positive. There was a tendency for higher CSF ABA titres in younger MS patients and in those with an earlier onset of disease. ABA titres in serum and CSF were both correlated with a more malignant course. Irrespective of the mechanism of induction of ABA in MS--an excessive immunogenic stimulation and/or a defective immunoregulation--they are potentially pathogenic in several ways, e.g. (1) by direct antibody action. (2) by interaction with complement, (3) by antibody-dependent K-cell-mediated cytotoxicity, and (4) by interaction with phagocytic cells. Of several correlations among the routine CSF variables in MS, the finding of more pronounced abnormalities in male patients was notable.

Adolescent↗

PubMed1982

A longitudinal study of antibrain antibodies in multiple sclerosis.

The presence of complement-fixing antibrain antibodies is a distinctive feature of multiple sclerosis (MS). In a longitudinal study of 35 MS patients antibrain antibody titres in serum were followed for up to 5 years; in 18 of them also CSF titres were determined. No consistent correlations between antibrain antibody titres and clinical events were found. Thus, MS relapses are not caused by a general increase in antibrain antibody titres, and conversely the relapses did not cause a boosting of antibrain antibodies. Significant variations in the local plaque environment are, however, not ruled out by the present results.

Adolescent↗

PubMed1982

Clinical and cerebrospinal fluid findings in lymphocytic meningo-radiculitis (Bannwarth's syndrome).

11 patients with lymphocytic meningo-radiculitis (Bannwarth's syndrome) are described. The disease is characterized by intensive pain, often radiating and migrating, and neurological deficits, i.e. peripheral facial palsies, as well as disseminated radiculopathies. In 4 patients the onset was preceded by an arthropod bite, close to which 3 patients exhibited an erythema chronicum migrans. In the cerebrospinal fluid there was a mononuclear pleocytosis, predominantely by lymphocytes. In the early stages, a plasma cell reaction was frequently encountered. Protein analysis indicated a defect in the blood brain barrier and an intrathecal synthesis of IgG. All patients recovered almost completely from their neurological symptoms within 1-2 months, irrespective of treatment.

Adult↗

PubMed1981

Immunoglobulin characterization by bacterial absorption of antibrain antibodies in multiple sclerosis.

Complement-fixing (CF) antibrain antibodies are frequently found in serum and CSF in multiple sclerosis (MS). They represent several specificities and appear to be synthesized on both sides of the blood-brain barrier. Five sera and six CSF samples from 11 MS patients, representing 6 different specificities of antibodies, were absorbed with a series of bacterial strains with affinity for various immunoglobulins. Reactivity with brain preparations was eliminated by absorption with the following IgG absorbents: Staphylococcus aureus strain Cowan I, group A streptococcus strain A R1, and group G streptococcus strain G 148, but not by absorption with strains with low or no affinity for IgG. The results indicate in all tested samples the IgG1 and/or IgG2 nature of the antibrain antibodies.

Absorption↗

PubMed1980

Intrathecal and extrathecal production of antibrain antibodies in multiple sclerosis.

Complement-fixing antibrain antibodies of several specificities were titrated in paired serum and CSF samples from 27 MS patients. The results indicated that the antibodies were synthesized on both sides of the blood-brain barrier in proportions that showed a great interindividual variation. It is suggested that this variation applies also to other MS-associated immunoglobulins.

Antibody Formation↗

PubMed1980

Multiple sclerosis: search for a serologic inhibitor.

Complement-fixing (CF) antibrain antibodies are frequently found in serum and CSF in multiple sclerosis (MS). A negative result in the test for these antibodies might depend not only on a lack of antibodies, but also on serologic inhibiting factors. To test this possibility, serum and concentrated CSF samples without demonstrable CF antibrain antibodies were allowed to interact with two standardized positive complement fixation reactions; one for antibrain antibodies and the other a Wasserman reaction. No evidence of inhibiting activity was found in 11 CSF and 15 serum samples from 20 MS patients. On the other hand, inhibiting activity was seen in serum from four of 12 patients with neoplasms and from three of 11 patients with rheumatoid arthritis.

Brain↗

PubMed1979

Acute measles infection in a case of multiple sclerosis.

A young woman with firm evidence of early multiple sclerosis (MS), who had never had measles, developed a clinically and serologically evident measles infection. Follow-up 1 year later confirmed the MS diagnosis. Thus, if measles can have a causal role in MS, it is probably not the only agent with this ability.

Adult↗

PubMed1978

Multiple specificities of antibrain antibodies in multiple sclerosis and chronic myelopathy.

The presence of complement-fixing antibodies against brain antigens was tested in paired serum and cerebrospinal fluid (CSF) samples from 60 multiple sclerosis (MS) patients, 15 patients with chronic myelopathy of undetermined cause (CM) and 60 control patients. Six MS sera, 34 MS CSF, 4 CM sera, 3 CM CSF, 4 control sera and 1 control CSF gave positive reactions either with a lipid extract or a saline extract of normal human brain. The proportion of anticomplementary CSF was significantly higher in the MS group than in the control group (15% vs 0%, P less than 0.01). The reactivity of a large number of individual positive samples was further investigated. Seven antibody specificities were discerned in the MS samples. Most samples reacted with non-lipid antigens, the dominating being a heat-labile, nonlipid component associated with CNS myelin. Antibodies to cerebroside and sulfatide were detected in a few patients. A number of samples reacted with cholesterol in combination with a variety of lipids. Positive samples from the CM patients exhibited a similar heterogeneity. In the control group positive reactions were seen in one patient with systemic lupus erythematosus (SLE), two patients with rheumatoid arthritis (RA), and one with a spinal meningioma. The reaction patterns of these patients were different from those commonly seen in MS patients. The complement-fixing antibrain antibodies in MS CSF are usually of IgG class (Ryberg 1976). This applies also to the positive MS sera in this study. The distribution of the antibodies between serum and CSF indicated, in several cases, an intrathecal synthesis. All of a number of human brains, including one MS brain, contained all 6 antigens (haptens) reactive in saline extracts. Antibodies to tissues outside the CNS were rarely detected in MS patients. The varied humoral autoimmune response in MS might reflect a heterogeneity in the MS patients, the disease itself or its causative agent.

Adolescent↗

PubMed1977

Analysis of the actions of cimetidine and metiamide on gastric acid secretion in the isolated guinea pig gastric mucosa.

Cumulative dose-response curves for histamine were determined on acid secretion from the isolated guinea pig gastric mucosa. Two H2-receptor antagonists-metiamide and cimetidine-behaved like competitive antagonists to histamine on gastric acid secretion in vitro. The isolated guinea pig gastric mucosa seems to be a suitable in vitro model for analysing the action of compounds on receptors involved in acid secretion.

Animals↗

PubMed1976

Complement-fixing antibrain antibodies in multiple sclerosis. Comparison of their occurrence in cerebrospinal fluid and serum.

Cerebrospinal fluid (CSF) and serum samples from 40 multiple sclerosis (MS) patients and 48 control patients were examined by a microcomplement fixation test for the presence of antibodies against saline extracts of human brain. When tested with an IgG content standardized in 100 mg per 100 ml, 13 of the MS CSF and one of the corresponding MS sera were positive, whereas none of the control specimens were positive. The antibody was shown to be highly organ specific when tested against extracts of myocard, spleen, kidney and peripheral nerve. Chromatographic experiments showed the antibody to belong to the IgG class. It was concluded that the antibody was probably synthesized intrathecally in 12 and extrathecally in one MS patient.

Adolescent↗

PubMedDate not supplied

The biology and pathobiology of the ECL cells.

The enterochromaffin-like (ECL) cells represent the predominant endocrine cell population in the acid-producing part of the stomach of both experimental animals and man. These cells actively produce and store histamine in addition to an anticipated but as yet unidentified peptide hormone and are under the control of gastrin. An acute gastrin stimulus causes exocytosis of the cytoplasmic granules/vesicles (and release of histamine and activation of the histamine-forming enzyme, histidine decarboxylase), while a more sustained gastrin stimulus causes first hypertrophy and then hyperplasia of the ECL cells in the rat (at most, a fivefold increase in the cell number). These effects can be demonstrated following infusion of gastrin or following an increase in the concentration of circulating gastrin of endogenous origin. The growth of the ECL cells reflects an accelerated self-replication rate. As studied in the rat, the self-replication rate is accelerated quite soon after induction of hypergastrinemia (blockade of acid secretion), the rate is maximally elevated within two weeks and then declines to control values at ten and 20 weeks despite the sustained hypergastrinemia. Lifelong hypergastrinemia in rats is associated not only with ECL-cell hyperplasia but also with an increased incidence of ECL-cell carcinoids. Recently, we could show that alpha-fluoromethylhistidine, which is a suicide inhibitor of histidine decarboxylase, effectively depletes the ECL cells of histamine and that the histamine-depleted ECL cells respond to gastrin with hyperplasia in a manner identical to normal ECL cells. Other factors beside gastrin seem to participate in the control of ECL-cell function and proliferation. Although exogenous somatostatin is known to suppress the activity of the ECL cells, we have failed to obtain evidence that the somatostatin cells in the oxyntic mucosa play a role in the physiological control of the ECL cells. The vagus, however, is important for the ability of the ECL cells to respond to gastrin. This conclusion is based on the observation that vagal denervation suppresses the hyperplastic response of the ECL cells to gastrin. Porta-cava shunting, on the other hand, greatly enhances the responsiveness of the ECL cells to gastrin. The mechanism behind this effect is unknown.

Animals↗

PubMedDate not supplied

Bannwarth's syndrome (lymphocytic meningoradiculitis) in Sweden.

Lymphocytic meningoradiculitis of Bannwarth is often associated with a tick bite and erythema chronicum migrans, and therefore may be a European counterpart of Lyme disease in North America. Of nine patients with lymphocytic meningoradiculitis studied at the Neurologic Clinic in Lund, Sweden, six were found to have elevated antibody titers to the Lyme spirochete. These studies support the conclusion that the two diseases are related and may be overlapping sectors of a larger clinical spectrum caused by one infectious agent.

Bites and Stings↗

PubMedDate not supplied

The biology and physiology of the ECL cell.

The enterochromaffin-like (ECL) cells, which are the predominant endocrine cell type in the acid-producing part of the vertebrate stomach, are characterized by numerous, electron-lucent vesicles and few electron-dense granules in the cytoplasm. The biological and physiological significance of the ECL cells remains poorly understood. They produce and store histamine and pancreastatin and are thought to produce an as yet unidentified peptide hormone. The most important clue to their function is their willingness to respond to changes in circulating gastrin. The present review presents current knowledge of the biology and physiology of the rat stomach ECL cells. Examination of serially sectioned ECL cells has revealed that the cytoplasmic vesicles almost invariably contain an electron-dense core, suggesting that perhaps the distinction between granules and vesicles is artificial. We propose a life cycle of the secretory organelles in the ECL cells with a progressive development from granules to vesicles. The results showed that the gastrin-evoked release of histamine and pancreastatin was accompanied by loss of vesicles, and that synthesis of histamine and pancreastatin was accelerated by sustained infusion of gastrin, a treatment that was associated with renewal of vesicles. The events described are instrumental in bringing about a change in the "steady state" or "equilibrium" of the ECL cells, from a non-stimulated, resting state to a gastrin-stimulated, active state. This change is attained within six to eight hr. The next "steady state" change is that from "normal-sized" but active ECL cells to "hypertrophic" ECL cells. The increase in cell size is complete after about one week. The gastrin-evoked increase in the ECL cell self-replication rate is maximal after about 10 days, after which time there is a gradual return back to pre-stimulation values. The ECL cell density increases fairly slowly and does not reach maximum (four-fold increase) until after 20 weeks hypergastrinemia. The activity of the histamine-forming enzyme, histidine decarboxylase, is elevated by gastrin and remains elevated for as long as the gastrin stimulus is maintained (the longest time studied was 20 weeks). The physiological significance of the ECL cells is probably related to their capacity to produce and store histamine and an as yet unidentified peptide hormone. The ECL cells are thought to be the source of histamine necessary for the gastrin-evoked acid response. In addition, preliminary evidence suggests that the ECL cells and the anticipated ECL cell hormone play a role in bone formation.

Animals↗