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Biomedical subjects

S Eriksson

Publications and source records attributed to S Eriksson.

At least 397 records · Page 22Linked to original sources
PubMed1986

Familial alpha 1-antichymotrypsin deficiency.

We studied patients and their relatives with partial deficiency, approximately 50% of normal plasma levels, of alpha 1-antichymotrypsin (ACT), an acute phase reactant with anti-cathepsin G activity. Six of eight ACT deficient individuals, over 25 years of age, had liver and three of eight lung manifestations, varying from severe disease to subtle laboratory abnormalities. The ACT of deficient individuals (who are heterozygotes for a rare gene, q = 0.003) had normal crossed immunoelectrophoretic properties. The abnormal gene is inherited in an autosomal, dominant way. The results suggest that deficiency of this antiprotease, which also has immune response modulating properties, may predispose to liver and lung disease.

Adolescent↗
PubMed1986

PMN migration measured by bottom filter counts in modified Boyden chambers. Chemokinetic deactivation and vinblastine inhibition of chemotaxis.

Polymorphonuclear leukocyte (PMN) migration and chemotaxis were studied by a modified Boyden chamber technique in 100% autologous serum with casein as attractant. PMN chemotaxis was induced by increasing the top gradient concentration of casein to 20 mg/ml. Under non-gradient condition, casein 20 mg/ml inhibited PMN migration, which was thought to be due to chemotactic deactivation. Vinblastine 0.01 microgram/ml partially inhibited PMN migration in a casein gradient with a top gradient concentration of 20 mg casein/ml. It is suggested that PMN migration in the casein gradient was composed of both vinblastine-sensitive chemotaxis and vinblastine-resistant chemotaxis.

Caseins↗
PubMed1985

Biosynthesis of abnormally glycosylated hepatoma secretory proteins in cell cultures.

We studied, by electrophoretic techniques, the physiochemical properties of 4 glycoproteins, alpha 1-antitrypsin, alpha 1-antichymotrypsin, alpha 1-acid glycoprotein and transferrin synthesized by three different human hepatoma cell lines. A common feature was the export of glycoproteins with retarded electrophoretic mobility, indicating incomplete sialylation, and a predominance of atypical, highly branched carbohydrate chains. The abnormal glycosylation pattern may be specific for malignant transformation of hepatocytes and possibly related to the intracellular accumulation of some of these proteins in malignant cells.

Carcinoma, Hepatocellular↗
PubMed1985

The N-terminal amino acid sequence from alpha 1-antitrypsin isolated from liver inclusion bodies.

The alpha 1-antitrypsin from the liver of a subject with alpha i-antitrypsin deficiency was purified and subjected to automated Edman degradation. The N-terminal amino acid sequence from position 1 to 12 was identical to that in plasma alpha 1-antitrypsin, type Z. This result precludes that the intrahepatic accumulation of Z alpha 1-antitrypsin is due to a defective removal of a signal peptide.

Amino Acid Sequence↗
PubMed1985

Cell cycle-dependent expression of mammalian ribonucleotide reductase. Differential regulation of the two subunits.

Consistent with its specialized role in DNA synthesis, the activity of ribonucleotide reductase is cell cycle-dependent, reaching its maximum during S-phase. This paper demonstrates, however, the levels of the two protein subunits, M1 and M2, of this enzyme vary independently of one another. The level of protein M1 was determined by use of a two-site monoclonal antibody-enzyme immunoassay and found to be constant throughout the cell cycle in bovine kidney MDBK cells. Pulse-chase experiments showed that the half-life of protein M1 was 15 h. This contrasts with our previous results demonstrating an S-phase-correlated increase in the concentration of protein M2 and a half-life of this subunit of 3 h. Therefore, ribonucleotide reductase is controlled during the cell cycle by the level of protein M2.

Animals↗
PubMed1985

Protein B1 of ribonucleotide reductase. Direct analytical data and comparisons with data indirectly deduced from the nucleotide sequence of the Escherichia coli nrdA gene.

The total composition, the N-terminal amino acid sequence, and the amino acid sequences of four internal regions have been determined for the ribonucleotide reductase large subunit, protein B1, prepared from a recombinant lambda-lysogenic Escherichia coli K strain, which overproduces the enzyme 30-50-fold. The data have been compared with those previously reported for B1 prepared from a thymine-starved E. coli B strain and with the indirectly derived primary structure of B1 recently reported from the nucleotide sequence of the E. coli K nrdA gene. Two major differences to these results were found. First, the B1 polypeptides started with initiator Met-1 (45%), Asn-2 (30%) or Gln-3 (15%), demonstrating a different type of N-terminal heterogeneity than that found earlier. Secondly, the total amino acid composition as derived from hydrolyzed protein B1 differed substantially from the amino acid composition derived from the nucleotide data. This has the consequence that Cys, Arg, Thr and possibly Val and Ser appear more frequently whereas Asx, Glx, Tyr and possibly Gly appear less frequently in the nucleotide-derived data as compared to direct protein hydrolysates. We suggest usage of other reading frames in the approximate area of residues 630-700 of the primary structure of the nrdA gene to compensate for these discrepancies and for the relatively high incidence of uncommon codons in the reading frame proposed for this area of the gene. Such changes have implications on the previously assigned putative active-site region of protein B1.

Amino Acid Sequence↗
PubMed1985

On the mechanism of deoxyribonucleoside toxicity in human T-lymphoblastoid cells. Reversal of growth inhibition by addition of cytidine.

High levels of deoxyadenosine and deoxyguanosine in patients with inherited deficiency of either adenosine deaminase or purine-nucleoside phosphorylase, respectively, are considered to be responsible for the associated immunological disorder. The mechanism involves phosphorylation to the corresponding deoxyribonucleoside triphosphates which subsequently inhibit the CDP-reducing activity of ribonucleotide reductase. Addition of deoxycytidine protects cells from the cytotoxic effects of deoxyadenosine and deoxyguanosine by competition for phosphorylation and by replenishing dCTP, the apparent limiting DNA precursor. Addition of cytidine, but not uridine, led to a reversal of deoxyguanosine and thymidine growth inhibition, comparable to that obtained with deoxycytidine. Analysis of the intracellular nucleotide pools showed that increased levels of cytidine ribonucleotides were sufficient to overcome the inhibitory effects of dGTP and dTTP on CDP reduction, thereby circumventing a depletion of the dCTP pool. A partial reversal of deoxyadenosine toxicity was also obtained with addition of cytidine. In this case little change in the dCTP level was observed, but a decreased dGTP pool appeared to be correlated with growth inhibition. High cytidine ribonucleotide levels partially prevented this effect. The present results may encourage the use of cytidine in combination with deoxycytidine as a pharmacological regime in treatment of immunodeficiency disease associated with increased deoxyribonucleotide levels.

Cell Division↗
PubMed1985

Echocardiographic findings in a patient with left ventricular pseudoaneurysm.

A 57-year-old woman, treated for a large anterior transmural myocardial infarction, was readmitted after 8 weeks because of progressive cardiac failure. Chest X-ray showed cardiomegaly with an atypical cardiac silhouette. Two-dimensional echocardiography disclosed a large left ventricular pseudoaneurysm. The patient underwent resection of the false aneurysm with repair of the left ventricular wall and recovered gradually. Different methods for diagnosing pseudoaneurysm are discussed.

Echocardiography↗
PubMed1985

Regional differences in the idiopathic hemochromatosis gene frequency in Sweden.

Screening for idiopathic hemochromatosis (IH) in 941 men, 55 years of age, did not reveal any individual with both biochemical abnormalities and liver iron content compatible with homozygosity for the IH gene. In a large autopsy series of 8 834 males representative of southern Sweden, we found classical hemochromatosis in 0.1%. The results are in contrast with the high frequency of homozygous IH found in the county of Jämtland in central Sweden. We suggest that the difference in gene frequency is a result of enrichment of the recessive IH gene in the Jämtland population by the mechanisms of sampling and drift. We conclude that population screening for early IH in southern Sweden is not worthwhile.

Autopsy↗
PubMed1985

Alterations in intracellular deoxyribonucleotide levels of mutationally altered ribonucleotide reductases in Escherichia coli.

Four recombinant plasmid clones (pPS305, pPS308, pPS317, and pPS319) coding for Escherichia coli ribonucleotide reductase have been characterized in vivo and in vitro. Each clone carried a different missense mutation affecting the B1 subunit. Measurements were made of deoxyribonucleoside triphosphate pools. Cells carrying the wild-type plasmid, pPS2, overproduced ribonucleotide reductase 10 to 20 times. As a consequence of this elevated enzyme level, the deoxyribonucleotide pools were approximately three times higher. All four mutant clones showed disturbed deoxyribonucleotide pools. The in vitro studies involved chromatography on affinity media, measurements of enzyme activity and allosteric regulation with a variety of substrates and effector molecules, and direct photoaffinity labeling in the presence of dTTP. Clones pPS305 and pPS308 were shown to code for catalytically defective enzymes, whereas clones pPS317 and pPS319 were shown to code for allosterically altered enzymes. The characterized missense mutations can thus be localized to areas involved in regulation of the substrate specificity or to the active site of protein B1. The alteration of the deoxyribonucleotide pools found in cells containing the allosterically defective clones pPS317 and pPS319 clearly demonstrated in vivo significance for the allosteric control of protein B1 in E. coli cells.

Affinity Labels↗
PubMed1985

Chronic 'cryptogenic' liver disease and malignant hepatoma in intermediate alpha 1-antitrypsin deficiency identified by a Pi Z-specific monoclonal antibody.

Using a monoclonal antibody against the Pi Z genetic variant of alpha 1-antitrypsin in an enzyme-linked immunosorbent assay, we have screened plasma samples from 857 consecutive patients with liver disease for the presence of Pi Z alpha 1-antitrypsin. Intermediate alpha 1-antitrypsin deficiency (Pi MZ and SZ) was found in 64 cases, or 7.6%, compared with an expected 4.8% (p less than 0.001). The plasma alpha 1-antitrypsin level was subnormal in only 50% of them. Forty-three of the 64 heterozygotes were men, compared with 494 of 857 (58%) in the total study population (p less than 0.001). At least 14 heterozygotes had cryptogenic liver disease, compared with 3 of 128 sex- and age-matched controls from the same study population (p less than 0.001). Malignant hepatoma occurred in 6 heterozygotes compared with 1 control (p less than 0.01), and in 13 of all 793 non-Pi Z patients (p less than 0.001).

Antibodies, Monoclonal↗
PubMed1985

Ulcer healing and relapse prevention by ranitidine in peptic ulcer disease.

Ranitidine, 300 mg daily, was given to 92 patients with duodenal ulcer (DU), 38 with prepyloric ulcer (PPU), and 21 with gastric corporeal ulcer (GCU). The healing rates at 4 weeks differed for the different types of ulcers (P less than 0.01), being 91% for DU, 68% for PPU, and 81% for GCU. After established ulcer healing, maintenance treatment with either ranitidine, 100 mg twice daily or 150 mg at night, or placebo was given for 1 year or until ulcer relapse in a total of 108 patients--71 with DU, 24 with PPU, and 13 with GCU. There were no significant differences in relapse rates between the two groups treated with active drug or between the three ulcer groups. However, the overall relapse rate in the active drug groups was 16%, against 72% in the placebo group (P less than 0.001).

Antacids↗
PubMed1985

Observations during long-term plasma exchange in primary biliary cirrhosis.

Plasma exchange was performed weekly during 6 months in two patients with symptomatic primary biliary cirrhosis. At the end of the treatment period improvement of liver demethylating capacity was noted, along with reduced C3 activation and a decrease in serum concentrations of IgM and procollagen III aminopeptide. Serum concentrations of aminotransferases, alkaline phosphatases, and anti-mitochondrial antibodies were not affected. These data suggest that long-term plasma exchange may improve liver function and possibly retard the progression of fibrosis in primary biliary cirrhosis.

Aged↗
PubMed1985

Ultrasonographic screening for gallstone disease in middle-aged women. Detection rate, symptoms, and biochemical features.

Five hundred and forty-seven middle-aged women, selected at random from the population of Malmö, Sweden, were invited to a screening survey for gallstone disease; 424 participated (77.5%). Forty-one had previously been operated on for gallbladder disease. The prevalence of gallstone disease, on the basis of a positive finding at ultrasonography and cholecystography, was 11%. The predictive value of a positive finding at ultrasonography was 86%. Six out of 10 women with gallstone were classified as asymptomatic. Body weight, blood pressure, liver enzymes, fasting blood glucose, and blood lipids, including apolipoprotein-A, did not differ significantly in women with and without gallstone disease. At least 9 out of 10 gallstones appeared to be cholesterol stones. Approximately half were of a size that would make them accessible for dissolution therapy.

Cholecystography↗
PubMed1985

Long-term immunosuppressive treatment in Crohn's disease.

We studied the clinical effects of long-term immunosuppressive treatment in 42 patients with severe Crohn's disease and extensive colonic involvement. Mean observation period before and after start of therapy exceeded 5 years. All but one of the patients receiving azathioprine or 6-mercaptopurine improved, and 11 of 42 attained complete remission during therapy. Cyclophosphamide was substituted for azathioprine with inferior results in four patients with pancreatitis soon after initiation of azathioprine therapy. The frequency of both local and systemic complications decreased significantly during the period of therapy. Prednisolone could be withdrawn in 25 patients and reduced to less than 7.5 mg every other day in the others. The average remission period after withdrawal of all drugs in 10 patients was 40 months. The results were superior to those in a surgical series with comparable observation time drawn from the same background population. Aside from pancreatitis in four patients, no serious side effects were seen. Fertility was unaffected. The data demonstrate the feasibility of long-term azathioprine (6-mercaptopurine) treatment in extensive Crohn's disease.

Adolescent↗