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Biomedical subjects

E Thomassen

Publications and source records attributed to E Thomassen.

18 recordsLinked to original sources
PubMed1995

Secreted and membrane-bound isoforms of T1, an orphan receptor related to IL-1-binding proteins, are differently expressed in vivo.

The murine T1 gene encodes a membrane-bound glycoprotein (T1-M), highly similar to interleukin-1 (IL-1) receptor type I, and a soluble variant (T1-S) representing its isolated extracellular domain. In vivo, the expression pattern of both T1 isoforms differs drastically. The T1-M receptor is abundantly expressed in single cells of the major hemopoietic organs (embryonic liver, spleen, bone marrow). It is restricted to few hemopoietic cell types throughout ontogenesis. By contrast, the soluble T1-S protein is predominantly expressed in selected nonhemopoietic embryonic tissues (developing skin, bone, and retina) and deposited in extracellular matrix. Despite the similarity of the T1 ligand-binding domain to all IL-1-binding proteins, it does not exhibit affinity to either IL-1 alpha or -beta. Thus, T1-M likely represents a novel orphan receptor of selected hemopoietic cells. The matrix-associated T1-S variant might act to create a reservoir of the putative T1 ligand in some differentiating tissues.

3T3 Cells↗
PubMed1995

Role of cell type-specific promoters in the developmental regulation of T1, an interleukin 1 receptor homologue.

Murine T1, an orphan receptor related to interleukin 1 receptors, exhibits a bimodal expression in mouse development. The molecular analysis of cultured cell lines now reveals the contribution of alternate promoters of the T1 gene to its differential expression. In nonhemopoietic cell types, where T1 synthesis in vivo is restricted to organogenesis and neoplasia, a recently characterized AP-1-dependent promoter directs a proliferation-associated expression of the gene. In hemopoietic cells, which express the T1 receptor throughout ontogenesis in vivo, T1 gene activity is driven by a novel serum factor-independent, constitutive promoter. The tissue-specific use of constitutive versus growth factor-dependent alternate promoters thus directs the permanent activity of the T1 gene in hemopoietic tissue versus the developmentally restricted expression of the gene in nonhemopoietic tissues in vivo.

Animals↗
PubMed1986

Kienböck's disease--late results by non-surgical treatment. A follow-up study.

Two groups of patients with Kienböck's disease were followed. Twenty-three wrists had been immobilised with plaster and twenty-six had no treatment. At follow up there was a marked improvement in both groups. Eighty-three percent of the wrists in the new treated group were pain free, or reported pain only on heavy work, and in the nontreated group this was valid for 77%. Examining X-rays at follow up we did not find a single wrist in which the lunate was normal or less deformed than at the time of diagnosis. In all forty-nine wrists the lunate was deformed and in 67% osteoarthrosis in the radiocarpal joint was evident. It is concluded, that Kienböck's disease has a naturally benign course, the remaining symptoms at follow-up might be caused by osteoarthrosis and nothing seems to be gained by rigorous immobilisation. If pain persists efficient treatment must be based on surgical methods.

Adolescent↗
PubMed1986

Ulnar variance determination.

Surgical procedures concerning the distal articular surfaces of the radius and ulna, demand an accurate method of measurement of ulnar variance. A new method, which is a modification of the method described by Palmer (1982), is introduced. 100 randomly selected healthy persons were submitted to X-ray of the wrist and the ulnar variance was determined independently by three observers using both methods. By "weighted kappa" statistics the results, expressed in intra- and interobserver agreement, showed a significantly higher reliability in favour of the Modified method.

Humans↗
PubMed1986

Ulnar variance in Kienböck's disease.

Forty four patients with forty seven wrists suffering from Kienböck's disease were re-examined. The mean observation time was 20.5 years. In all forty seven wrists the treatment had been immobilization. Using a standard X-ray projection, and a reliable method of ulnar variance measuring, the ulnar variance was determined by three observers independently. Comparing the result with the ulnar variance in normal wrists we found the so-called "ulnar minus variant" overrepresented in patients with Kienböck's disease. However, comparing X-rays taken at the time of diagnosis with X-rays at re-examination, we found in eight out of forty seven wrists that a subchondral bone formation in the distal radium opposite the lunate bone had taken place. This bone formation will tend to enhance the negative value of ulnar variance measurements, and suggests an explanation of the overrepresentation of "ulnar minus variants" in Kienböck's disease. Excluding these eight wrists from the material and comparing the mean ulnar variance value in the remaining thirty nine wrists with the mean value in normal wrists no statistical difference was shown. Based on these observations it seems unlikely that the "ulnar minus variant" has any bearing on the cause of Kienböck's disease.

Adolescent↗
PubMed1978

Two thymidylate synthetases in Bacillus subtilis.

Bacillus subtilis grown at temperatures below 37 degrees contains two thymidylate synthetases, TSaseA and TSaseB. Their presence is dependent on functional thyA and thyB genes, respectively. When cells are grown at 46 degrees they only contain TSaseA activity. This allous an easy positive selection for thyA and thyA, THYB mutants. The two TSases have been physically separated, and they show similar overall requirements for activity. However, they differ significantly in both their kinetic and their physicochemical properties.

Bacillus subtilis↗
PubMed1977

Thymidine-requiring mutants of Salmonella typhimurium that are defective in deoxyuridine 5'-phosphate synthesis.

In a Salmonella typhimurium strain made diploid for the thy region by introduction of the Escherichia coli episome, F'15, mutants resistant to trimethoprim in the presence of thymidine were selected. One was shown to be defective in deoxyuridine 5'-phosphate (dUMP) synthesis; it requires deoxyuridine or thymidine for growth and is sensitive to trimethoprim in the presence of deoxyuridine. Genetic studies showed that the mutant is mutated in two genes, dcd and dum, located at 70 and 18 min, respectively, on the Salmonella linkage map. The dcd gene cotransduces 95% with udk, the structural gene for uridine kinase. Both mutations are necessary to create a deoxyuridine requirement, providing evidence for the existence of two independent pathways for dUMP synthesis. Pool studies showed that a dum mutation by itself causes a small decrease in the deoxythymidine 5'-triphosphate (dTTP) pool of the cells, whereas a dcd mutation results in a much more marked decrease. The double mutant dcd dum, when incubated in the absence of deoxyuridine, contains barely detectable levels of dTTP. Enzyme analysis revealed that dcd encodes deoxycytidine 5'-triphosphate deaminase. The gene product of the dum gene has not yet been identified; it does not encode either subunit of ribonucleoside diphosphate reductase or deoxyuridine 5'-triphosphate pyrophosphatase. Mutants deleted for the dcd-udk region of the S. typhimurium chromosome were isolated.

Chromosome Mapping↗
PubMed1976

Altered deoxyribonucleotide pools in P2 eductants of Escherichia coli K-12 due to deletion of the dcd gene.

Deletion of the Escherichia coli K-12 chromosome associated with P2 mediated education extend through the structural gene for uridine kinase, udk, and the dcd gene encoding 2'-deoxycytidine 5'-triphosphate deaminase. The lack of uridine kinase makes a positive selection possible for these strains. Due to the dcd mutation, P2 eductants show large alterations in their deoxyribonucleoside triphosphate pools.

Deoxyribonucleotides↗
PubMed1974

Salmonella typhimurium mutants defective in cytidine monophosphate kinase (cmk).

Mutants of Salmonella typhimurium defective in cytidine 5'-monophosphate (CMP) kinase (cmk) have been isolated. The mutants also lack the ability to phosphorylate 2'-deoxyCMP, indicating that one enzyme is responsible for the phosphorylation of both CMP and deoxyCMP to the corresponding diphosphates. In glucose minimal medium the mutants grow at the same rate as the parental strain; however, they excrete large quantities of pyrimidines into the growth medium. Cytidine but not deoxycytidine has been identified among the excreted products. The mutant phenotype suggests that the physiological role of CMP kinase is that of rephosphorylating CMP arising from the breakdown of messenger ribonucleic acid. This proposed role of CMP kinase is supported by the fact that a cmk(-) mutant is much more sensitive to any partial impairment of cytidine 5'-triphosphate synthetase than is the cmk(+) parent strain. The gene cmk has been located on the Salmonella chromosome at 38.5 min. No markers which can be cotransduced with cmk by phage P22 have been found.

Autoradiography↗
PubMed1972

Metabolism of pyrimidines and pyrimidine nucleosides by Salmonella typhimurium.

The pathways by which uracil, cytosine, uridine, cytidine, deoxyuridine, and deoxycytidine are metabolized by Salmonella typhimurium are established. The various 5-fluoropyrimidine analogues are shown to exert their toxic effects only after having been converted to the nucleotide level, and these conversions are shown to be catalyzed by the same enzymes which similarly convert the natural substrates. Methods for isolating mutant strains blocked in various steps of metabolism of pyrimidine bases and nucleosides are described.

Aminohydrolases↗
PubMed1971

Deoxycytidine triphosphate deaminase: identification and function in Salmonella typhimurium.

The biosynthesis of 2'-deoxyuridine monophosphate (dUMP) has been studied in a cytidine- and uracil-requiring mutant of Salmonella typhimurium (DP-55). The dUMP pool and the thymidine monophosphate (dTMP) pool of DP-55, grown in the presence of (3)H-uracil and unlabeled cytidine, are found to have the same specific activities. However, only 30% of the dUMP and the dTMP is synthesized from a uridine nucleotide. Seventy per cent is derived directly from a cytosine compound. The identification and partial purification of a Mg(2+)-dependent 2'-deoxycytidine triphosphate (dCTP) deaminase from S. typhimurium suggests that the combined action of dCTP deaminase and 2'-deoxyuridine triphosphate pyrophosphatase accounts for 70% of the dUMP, and therefore the dTMP, synthesized in vivo. The introduction of a thymine requirement (i.e., a block in thymidylate synthetase) into DP-55 results in a 100-fold increase in the size of the dUMP pool. However, the relative contribution of the uridine and cytidine pathways to dUMP synthesis is unaltered. The high dUMP pool is accompanied by extensive catabolism of dUMP to uracil. Partial thymine starvation of the cells results in a significant increase in the dUMP and dCTP pools. Moreover, an increase in the contribution of the dCTP pathway to dUMP synthesis is observed. As a result of these changes the catabolism of dUMP to uracil is augmented.

Aminohydrolases↗
PubMed1971

Deoxycytidine triphosphate deaminase: characterization of an Escherichia coli mutant deficient in the enzyme.

A mutant of Escherichia coli, previously shown to contain abnormal nucleoside triphosphate pools, was found to be defective in its ability to synthesize thymidine nucleotides. The defect is not in the enzyme thymidylate synthetase but in deoxycytidine triphosphate deaminase, an enzyme that supplies deoxyuridine monophosphate, the substrate for thymidylate synthetase.

Aminohydrolases↗