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Biomedical subjects

L Hammarström

Publications and source records attributed to L Hammarström.

At least 253 records · Page 14Linked to original sources
PubMed1987

C2 deficiency, moderately low IgG2 concentrations and lack of the G2m(23) allotype marker in a child with repeated bacterial infections.

C2 deficiency was demonstrated in an 11-year-old boy with a past history of recurrent purulent otitis media, pneumonia, H. influenzae meningitis and S. pneumoniae septicaemia. The major histocompatibility complex haplotypes present, A10, B18, DR2, BF*S, C2*QO, C4*A4, C4*B2 and A28, B18, DR2, BF*S, C2*Q0, C4*A4, C4*B2, were in accord with previous observations in C2 deficiency. The concentrations of C1q, C5, factor B and factor D were in the low normal range and the hemolytic activity of the alternative pathway was slightly decreased. In addition, the patient showed moderately low IgG2 concentrations and lacked the IgG2 subclass marker G2m(23). The findings indicate that the patient's susceptibility to bacterial infections may be due to C2 deficiency in combination with the presence of an IgG allotype associated with impaired antibody responses to carbohydrate antigens.

Bacterial Infections↗
PubMed1987

IgG subclasses of specific antibodies in Ixodes ricinus-borne borreliosis.

Ixodes ricinus-borne borreliosis may run a protracted course. In this study we investigated the different IgG subclasses of antibodies to borreliae at different stages of the disease. In addition to the dominant subclass IgG1 and IgG3 response was found in most cases. This antibody subclass pattern with contributions of IgG2 often persists into the late stage of the disease and may last for decades. The IgG subclass response elicited by this spirochaetosis does not conform to the expected IgG4 restricted response after chronic antigenic stimulation.

Adult↗
PubMed1986

Cloning of cDNA for human T-cell replacing factor (interleukin-5) and comparison with the murine homologue.

We have cloned cDNA for T-cell replacing factor (interleukin-5), which replaces T-cell helper function for normal B cells which secrete immunoglobulin, from human T cell leukemia line, ATL-2, using mouse interleukin-5 cDNA as probe. Total nucleotide sequence of the cDNA (816 base pairs) was determined and compared with that of mouse interleukin-5 cDNA. The cloned cDNA encoded the interleukin-5 precursor of 134 amino acids containing an N-terminal signal sequence. Although the human interleukin-5 precursor is one amino acid longer than the murine homologue, the sizes of the mature proteins appear similar. The nucleotide and amino acid sequence homologies of the coding regions of human and murine interleukin-5 are 77% and 70%, respectively. Human interleukin-5 synthesized by the direction of the cloned cDNA induced immunoglobulin synthesis in human B cells stimulated by Staphylococcus aureus mitogen.

Amino Acid Sequence↗
PubMed1986

Specific chromosome markers involved with chronic T lymphocyte tumors.

In a series of 12 patients with chronic T cell tumors, 9 showed abnormalities of the long arm of chromosome #14. The most common aberration was an inversion with breakpoints in q11 and q32, which was seen in 7 patients. One patient had a translocation between chromosomes #9 and #14, with breaks in 9q34 and 14q11, and in another patient, the two long arms of chromosome #14 were fused together in q32, forming a dicentric chromosome. The results confirm earlier suggestions that rearrangements of band 14q11 are involved with T cell tumors and may be of importance for the development of the disease. Chromosome #8 aberrations were seen in seven patients, six of whom had an extra 8q in common. Abnormalities of chromosome #7 occurred in five patients, but the breaks were localized in different bands. The significance of the karyotypic changes in our present and previous series of patients is discussed, together with data from other laboratories.

Chromosome Aberrations↗
PubMed1986

DNA rearrangements in human B- and T-cell malignancies.

During normal differentiation lymphocytes rearrange immunoglobulin and T-lymphocyte receptor genes. The identification of a rearrangement pattern may serve as a unique clonotypic marker of a lymphoid tumor and can also be used to identify the cellular origin of the neoplasia. The cloning of abnormal breakpoints has resulted in detailed information on the inter-chromosomal translocation process and has also provided probes, which specifically identify abnormal translocations. The use of inter-chromosomal translocation-specific probes in conjunction with immunoglobulin and T-cell receptor gene probes makes it possible not only to prove monoclonality but also to provide strong evidence for neoplasia.

B-Lymphocytes↗
PubMed1986

Fluoride-induced cystic changes in the enamel organ of the rat molar.

Many substances have been found to cause enamel disturbances in toxic doses, and it has been postulated that these disturbances are linked to the formation of sub-ameloblastic cysts. In the present investigation, fluoride-induced sub-ameloblastic cysts in developing rat molars were related to fluoride dose, age of the animals, and the plasma fluoride level. The sub-ameloblastic cysts, which developed predominantly towards the end of the secretory stage of amelogenesis, appeared shortly after fluoride administration and regressed within 3 days. Hypoplasias and internal defects were found in the enamel under the disturbed ameloblast layer. The highest plasma fluoride levels were found in the youngest animals 24 h after injection. The frequency and size of the sub-ameloblastic cysts were clearly related to the fluoride-dose and age of the animal and, subsequently, to the plasma fluoride level.

Ameloblasts↗
PubMed1986

Ultrastructure of fluoride-induced cysts in the rat molar enamel organ.

Earlier studies have shown that a single high dose of fluoride induces subameloblastic cysts separated by morphologically unaltered ameloblasts in the developing rat molar. In the present investigation, the ultrastructure of both the ameloblasts forming the cystic wall, and the cells within the cystic lumina were studied by means of transmission electron microscopy. It was shown that 24 h after fluoride injection the ameloblasts of the cystic wall showed various degrees of cytoplasmic and nuclear alterations. Some cells displayed signs of necrosis as indicated by condensation of the chromatin. The cytoplasmic changes varied from altered organelle morphology to fragmentation and almost complete shedding of the whole cytoplasm. In the ameloblasts of the cystic wall secretory products accumulated intracellularly, in distended rough endoplasmatic reticulum, in vesicles of the Golgi region and extracellularly between ameloblasts as well as between cells in the stratum intermedium, indicating an altered matrix secretion. Electron lucent material, cell and cell fragments were found in the cystic lumina, the two latter apparently originating from the ameloblastic layer. The degenerative changes seemed to follow the normal pattern of cell degeneration.

Ameloblasts↗
PubMed1986

Correlation between deficiency of immunoglobulin subclass G3 and Gm allotype.

Gm allotypes were investigated in 63 Swedes: 46 females and 17 males, in whom serum IgG3 was below 0.35 g/l. Both monoclonal antibodies and polyclonal antisera were used for the quantification. Concentrations of the other IgG subclasses were within the age-related normal ranges. The distribution of the IgG1 genetic markers G1m(a,x,f) differed markedly from that observed in normal Swedes (p less than 0.001). Thus G1m(a) was present in 60 subjects as compared to an expected 36, and phenotype G1m(-f) in 34 subjects as against an expected 8. The mean IgG3 concentration was numerically lower in the G1m(-f) group than in the G1m(+f) cohort, and individuals with IgG3 levels 0.10 g/l were more frequent in the G1m(-f) group. Among Caucasians, G3mg is in linkage disequilibrium with G1ma and our interpretations is that the haplotype G1ma;ax G2m-n G3mg is markedly increased in individuals with IgG3 deficiency.

Dysgammaglobulinemia↗
PubMed1986

Immunoglobulin G (IgG) and IgA subclass pattern of human antibodies to Shigella flexneri and Salmonella serogroup B and D lipopolysaccharide O antigens.

The subclass distribution of human serum antibodies to the O-antigenic lipopolysaccharides of Salmonella serogroups B and D and to Shigella flexneri serotypes 1b, 2a, and 4a lipopolysaccharide antigens were analyzed in an enzyme-linked immunosorbent assay with monoclonal antibodies to the immunoglobulin subclasses. The patients had culture-verified Salmonella (17 Swedes) or Shigella flexneri (23 Vietnamese; 11 children and 12 adults) infections. Consecutive samples drawn during 1 year postinfection were investigated. Antibodies to the Salmonella antigens were mainly of the immunoglobulin G1 (IgG1), IgA1, and IgA2 subclasses. For the Salmonella serogroup B O polysaccharide, the IgA1 and IgA2 subclasses had peak values earlier than (6/9) or coinciding with the IgG1 (3/9) peak value. Furthermore, the IgA2 response to Salmonella serogroup B was positively correlated to the duration of the carrier state (P less than 0.001); the corresponding IgA1 response was less well correlated but was still significant (P less than 0.02). In the case of the Shigella flexneri O polysaccharide, specific antibodies appeared mainly in the IgG1 and IgA1 subclasses. Some IgG2 was also found, surprisingly even in very young patients. No subclass shift with time within the immunoglobulin classes was noted in any of the groups.

Antibodies, Bacterial↗
PubMed1986

Viral etiology in myasthenia gravis? Analysis of thymic tissue.

Thymic cells from 26 myasthenia gravis patients were investigated by viral isolation using inoculation of supernatants obtained from thymic tissue homogenates into human and monkey cells. Living cells from 14 thymuses were also cocultivated with monkey cell lines and with human embryonic lung fibroblasts. None of the thymic biopsies showed any cytopathic effect in these cell cultures sensitive to a broad spectrum of viruses. Cytomegalovirus antigen was not detected in any of 25 biopsies investigated in an imprint immunofluorescence assay.

Antigens, Viral↗