Search PubMed⌕ Search

Biomedical subjects

U Johnson

Publications and source records attributed to U Johnson.

At least 19 recordsLinked to original sources
PubMed1992

HLA antigens and recurrent acute otitis media.

The frequencies of a number of HLA antigens were investigated in 45 individuals with clinical recurrent acute otitis media (rAOM), defined as six or more episodes of AOM during a 12-month period, and were compared to those in a control group from the same district. HLA-A2 was found to occur in 80% of the rAOM group, as compared to 55.9% of controls (p less than 0.01). HLA-A3 antigen occurred in only 11.1% of the rAOM group in contrast to 27.5% of controls (p less than 0.05). Among 22 prospectively followed children without any AOM during their first 3 years of life, the frequencies of HLA-A2 and HLA-A3 antigens were comparable with those among controls.

Acute Disease↗
PubMed1991

HLA frequency in patients with recurrent acute otitis media.

Clinical data suggest the involvement of hereditary factors in children susceptible to recurrent acute otitis media. That relationships of varying degree exist between the frequencies of certain HLA antigens and various disease entities is well established. In the present study, we investigated the frequencies of a number of HLA antigens in 45 patients with clinical recurrent acute otitis media and compared these frequencies with those in a control group from the same district. The HLA-A2 antigen occurred in 80% (36/45) of the group with recurrent acute otitis media, as compared with 56% of controls. Of a subgroup of 11 children with recurrent acute otitis media who were prospectively followed up, 10 (91%) were HLA-A2 positive. The HLA-A3 antigen occurred in only 11% (5/45) of the group with recurrent acute otitis media as a whole (n = 45) in comparison with 28% of controls. Among 22 prospectively followed up children without any episode of acute otitis media during the first 3 years of life, the frequency of HLA-A2 was 45% (10/22) and that of HLA-A3, 32% (7/22). The results indicate the existence of a relationship between recurrent acute otitis media and the HLA-A locus, suggesting the involvement of genetic factors in the disease.

Acute Disease↗
PubMed1991

Human leukocyte antigens in relation to colonization by mutans streptococci in the oral cavity.

Mutans streptococci are well established as caries-inducing microorganisms in man. Most humans carry the bacteria, but in highly different numbers. This cannot be explained by environmental factors only. The aim of this study was to investigate a possible association between levels of colonization by mutans streptococci and the presence of certain B and DR human leukocyte antigens (HLA). Altogether, 170 subjects who had their HLA antigens determined (76 renal transplant patients and 94 healthy blood donors) were selected for the investigation. Paraffin-stimulated saliva samples were taken using the wooden spatula method with subsequent cultivation of mutans streptococci on mitis salivarius bacitracin agar plates. An association between the absence of HLA-DR 4 antigens and low, or undetectable, levels of mutans streptococci was found. This was statistically significant for the immunosuppressed renal transplant subjects. The same trend was observed among the healthy blood donors.

Adult↗
PubMed1991

Alloimmunization to human immunoglobulin genetic markers is frequent in early rheumatoid arthritis.

HLA and Gm allotypes of 99 consecutive Swedish patients with rheumatoid arthritis were determined. Ninety-two of the 198 haplotypes contained DR4, a significant increase. The patients' sera from 3 different occasions were studied for anti-immunoglobulin profile as judged by 6 selected anti-Rh coats, 4 of them being monoclonal anti-Ds restricted as to allotype. Ninety-two of the patients were reactive with a polyclonal anti-Rh Ri as against 10 with the monoclonal carrying the G1m(f) allotype. Antibodies to Ig coats carrying defined allotypes were more frequently observed in patients not carrying the allotype in question than in those individuals possessing it. The difference was significant or highly significant as regards presence/absence of G1m(a), G3m(b) and G3m(g), respectively. Anti-G1m(a) and anti-G3m(g) cooccurred in 17 of the patients. Results consistent with presence/absence of particular anti-immunoglobulins at the 3 examinations were observed in 74 of the patients. Gm allotypes or antiallotypes were not statistically related with DR4 status. In conclusion, alloimmunization to Gm markers frequently occurs in early rheumatoid arthritis.

Adult↗
PubMed1989

HLA-typing in a family with six intracranial aneurysms.

The pedigree of a family where three of nine siblings had suffered from aneurysmal subarachnoid haemorrhage (SAH) was explored, by means of interviews and revisions of population and medical records. We thus found two nephews with previously ruptured intracranial aneurysms. Subsequently high resolution computerised tomography (CT) scans were performed in the remaining six siblings, one of which was shown to harbor an intracranial aneurysm. This individual was subjected to uncomplicated clipping of the aneurysm. Typing of human leukocyte antigen (HLA) was performed in 15 individuals of the pedigree. Three of the six HLA-antigens recently reported to occur in increased frequently in a series of (non-familial) patients with ruptured aneurysm were found, namely B7, DR2 and Cw2. Most noteable was the expression of the antigen B7 in five of the six individuals with aneurysm in the investigated family. At present HLA-typing is not a useful screening tool to identify individuals in the general population with an increased risk of developing intracranial aneurysms. The present study shows that HLA-typing could neither be used to predict the occurrence of intracranial aneurysms in the siblings in the investigated family. HLA-typing may provide further clues to our understanding of the etiology of intracranial aneurysms, especially concerning possible genetic factors. The authors thus would like to encourage HLA-typing in previously known and newly detected families with accumulation of intracranial aneurysms.

Adult↗
PubMed1987

Complement components in normal pregnancy.

Sixteen complement components were analysed at three different occasions during a normal pregnancy. Samples were also obtained at delivery and six weeks post partum. All factors but C1 IA and D increased during the pregnancy. Six weeks after the delivery, the levels of all components but C1s, C4 and C6 showed a beginning normalisation. In 15 per cent of the women, C1 IA was functionally inactive at delivery.

Complement System Proteins↗
PubMed1987

Age at onset, sex distribution and HLA antigen frequency in patients with primary glomerulonephritis progressing to terminal uraemia. An epidemiological survey.

In a retrospective study of 138 HLA-typed patients with primary glomerulonephritis progressing to terminal uraemia, a bimodal curve of age at onset of disease was observed among males. An initial peak occurred between 16 and 25 years of age, and a second peak between the ages of 46 and 55. The prevalence of HLA B40 was found to be high among males in the first group, and a relationship was found to exist between the presence of HLA B40 and increased titres of ASO (antistreptolysin O). No such findings were made either in the second group of males or in the female group. Among females, a single peak for age of onset occurred between 6 and 15 years. The frequency of HLA B40 did not differ significantly from that of the controls. The results of this study suggest a relationship to exist, predominantly in younger males, between primary glomerulonephritis with fatal outcome and HLA B40-related alterations in the immunological response to beta-streptococcal infection.

Adolescent↗
PubMed1986

C1 activation, with C1q in excess of functional C1 in synovial fluid from patients with rheumatoid arthritis.

Free Clq, in functionally active form was present in increased amounts in the synovial fluid of patients with rheumatoid arthritis. The presence of free Clq was associated with low concentrations of hemolytic C1, low C4 and raised amounts of C3dg/d fragments in the synovial fluid. The findings suggested intra-articular C1 activation with dissociation of C1 into free C1q and complexes containing C1r, C1s, and C1 inactivator. However, the immunochemical properties of synovial fluid C1r-C1s-C1 inactivator complexes appeared to differ from those of the complexes formed in serum, which hampered quantification with the assay used. Control patients with osteoarthritis or spondylarthritic syndromes did not show evidence of intra-articular complement activation, even though 1 patient with Reiter's disease had unexplained low concentrations of synovial fluid C4 and C3. The concentrations of circulating complement components were largely normal in the patients. Slightly increased concentrations of free C1q and C1r-C1s-C1 inactivator complexes in serum and C3dg/d fragments in EDTA plasma were observed, particularly in the patients with rheumatoid arthritis.

Adult↗
PubMed1985

Sequential studies of complement activation in systemic lupus erythematosus.

C1 and C3 activation, measured as C1r-C1s-C1 inactivator C1s-C1r-C1IA complexes in serum and circulating C3d were studied in serial samples from 33 patients with SLE. All patients demonstrated exacerbations during observation periods of 10-30 months and were divided into groups according to principal clincal features (mild SLE, severe extra-renal SLE, and lupus glomerulonephritis). Increased C1 activation was consistently found during exacerbation. C3d in plasma was a feature associated with severe disease flares. Activation of C1, but not of C3, was documented before flare-ups of disease activity, but such predictive information was mostly restricted to patients with extra-renal disease. C2 cleavage in plasma, studied serially in a few patients, appeared to be closely associated with C1 activation. Circulating immune complexes, measured with solid-phase C1q assay, did not always increase before development of clinical manifestations. Remission of symptoms was paralleled by decreasing concentrations of C1r-C1s-C1IA and of, when present, C3d. Similar findings were made for immune complexes but only in severe disease. Persisting C3d was observed in 3 patients, who subsequently developed renal failure. C1q levels were transiently low during flare-ups of lupus glomerulonephritis, but otherwise the concentrations of C1q, C4 and C3 did not show consistent patterns of variation in relation to disease activity.

Adolescent↗
PubMed1985

Complement activation in primary biliary cirrhosis: an in vitro model.

Increased concentrations of C3dg were demonstrated in plasma from patients with primary biliary cirrhosis (PBC), indicating in vivo activation of C3. Rapid spontaneous C3 cleavage by the classical pathway was observed in vitro in serum and in EDTA plasma reconstituted with Ca++ and Mg++, suggesting the presence of complement-activating substances. On incubation with fresh normal serum, purified polyclonal IgM from patients with PBC induced C1 activation, C4 cleavage, and C3dg formation. No C3 cleavage was observed when PBC-IgM was incubated with a C2-deficient serum. We suggest that the complement activation in vivo in PBC, which occurs predominantly by the classical pathway and is characterized by increased concentrations of C1 activation complexes, decreased C4 concentrations, and hypercatabolism of C3, is attributable to an abnormal IgM population.

Complement Activation↗
PubMed1978

The role of C1s, C1r and properdin in the initiation of the C3b-dependent feedback mechanism of the complement system.

The influence of activated C1s, C1r and properdin in the fluid phase initiation of the C3b-dependent feedback mechanism of the human complement was studied. It was found that C1s caused conversion of C3 and factor B in a normal serum, but not in a serum genetically deficient in C4 or in a serum to which Na2EDTA had been added. When a normal serum was incubated with C1r before incubation with C1s, only C3 was converted, whereas factor B remained in the unaltered native state. Properdin did not influence the C1s mediated conversion of C3 and factor B. When activated properdin was added to a properdin-depleted serum, both C3 and factor B were converted. Activated properdin was also incubated with purified C3 and purified C3b. It was shown that C3 was converted to C3b, but C3b was not degraded despite prolonged incubation.

Chromatography, Affinity↗
PubMed1977

Purification of C-reactive protein on DEAE-cellulose by a simple two-step procedure utilizing the calcium-dependency of the protein.

A simple procedure for isolating C-reactive protein is presented. The method consists of two chromatographic separations on diethylaminoethyl (DEAE)-cellulose columns and utilized the difference between the binding of C-reactive protein to DEAE in the presence and absence of calcium. Electrophoretically pure C-reactive protein can be recovered from serum or ascitic fluid with a yield of approx. 50--60% within one day.

C-Reactive Protein↗
PubMed1977

C1 subcomponents in acute pneumococcal otitis media in children.

Twenty children with acute pneumococcal otitis media were studied. In 6 children the infection ran a normal course and healed after the first episode and in 14 it relapsed. The serum levels of the immunoglobulins IgG, IgA and IgM were normal in all 20 children. Specific antibodies to pneumococcal polysaccharide were found in all cases, with no differences in the titers between the relapsed cases and those that healed. The complement components were quantitated with electroimmuno assay. G1q proved depressed in 60 per cent of the relapsed cases and in 16 per cent of the healed cases. C1r and C1s were disproportionally high compared with the C1q levels. Furthermore, crossed immunoelectrophoresis revealed abnormal complexes composed of C1r and C1s, and complexes composed of C1r, C1s and C1 IA. These complexes were more pronounced in sera from the children with relapsing otitis media.

Acute Disease↗
PubMed1976

Force velocity relations in vascular smooth muscle: the influence of pH, pCa, and noradrenaline.

The kinetics of vascular smooth musclw activity was studied by means of afterloaded isotonic contractions of the tetanized rat portal vein at varied pH (8.0-5.9), pCa (3.4-2.1), and during noradrenaline incubation (0.4 mug/ml). Under control conditions (pH 7.3, pCa 2.6) the following parameters of the force velocity relation were calculated: a of Hill's equation (relating to the isometric peak tension) = 0.36; b (relating to the actual muscle length) = 0.19 ML/s; VM Trelating to the actual muscle length) = 0.56 ML/s. Within the range of pCa between 2.0 and 3.2 the amount of force generation (= delta P) depended on the extracellular calcium level whereas the extrapolated velocity of shortening of the unloaded preparation (= VM) did not. Also pH changes between 8.0 and 6.8 as well as noradrenaline incubation at a pH of 5.9 affected delta P quite considerably, but VM only scarcely. At a pH of 6.3, however, VM was distinctly diminished, and a reduced calcium sensitivity of the ATPase was inferred from the shift of ED50 of extracellular calcium from 0.66 mM Ca at a pH of 7.3 to 1.56 mM Ca at a pH of 6.3 (P less than 0.0005). It is concluded from these results that the experimental conditions-pCa between 2.0 and 3.2, pH between 8.0 and 6.8, and noradrenaline added at a pH of 5.9-obviously change the intracellular calcium concentration which influences the number of activated interaction sites rather than the velocity of crossbridge movement.

Animals↗
PubMed1976

Effects of granulocyte neutral proteases on complement components.

The proteolytic effects of collagenase and elastase from human granulocytes were investigated on the human complement components C3 and C5 in serum and with purified components. The conversion of C3 was analyzed with crossed immunoelectrophoresis as described by Ganrot, and the conversion of C5 was detected with immunoelectrophoresis according to Scheidegger's method. Collagenase converted C3 to C3b but had no detectable effect on C5. Elastase converted C3 to C3b and converted C5 to a C5b-like fragment. The proteolysis by collagenase and elastase in serum was not detectable until the molar ratio for enzyme to the protease inhibitors alpha1-antitrypsin and alpha2-macroglobulin was greater than 1.

Complement C3↗