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Biomedical subjects

P Edelmann

Publications and source records attributed to P Edelmann.

9 recordsLinked to original sources
PubMed1992

Brace treatment in idiopathic scoliosis.

A German multicenter study with consequent long-term follow-up of patients with idiopathic scoliosis after Milwaukee brace treatment in one out of seven Orthopaedic Clinics showed that brace weaning at the bone age of Risser 4 is followed by early loss of curve correction. According to Oberthaler et al. patients, who were furnished with a brace as outpatients, are inclined to practice a part-time wearing with different brace free intervals. In a longterm follow-up study of 328 patients with idiopathic scoliosis treated at the North German Scoliosis Center in Cuxhaven 123 compliant patients were examined 4 1/2 years after brace weaning. All were asked to wear their braces 23 hours a day and were weaned only at Risser 4-5 or Risser 5. The control rate was 93%. A gain of correction between 9 and 22% was the result. We analysed the composition of the group of 81 noncompliant patients. As far as we could find out the percentage of really non-compliant patients was only 19% compared with a total of 212 patients, who had finished their brace treatment at least 5 years ago. Eight patients (4%) with prebrace values of over 40 degrees Cobb had to be operated, though they were compliant. Based on these results, strict brace treatment in progressive idiopathic scoliosis is recommended, unless no more physiologic way of treatment is available.

Braces↗
PubMed1987

Nonsense suppression context effects in Escherichia coli bacteriophage T4.

Nonsense suppression by supE44 has been examined in a collection of 14 T4 gene 22 and gene 23 UAG mutants, for which the precise gene location is known. In concordance with previous studies, UAG followed by a pyrimidine was inefficiently suppressed. However, among positions with similar 3' nucleotides, there was considerable variation in suppression efficiency. The competition between supE44 and Release Factor 1 (RF 1) was also investigated following the introduction of a multicopy RF 1 plasmid. An inverse relationship between the efficiency of suppression and RF 1 competition was observed.

Codon↗
PubMed1977

Mistranslation in E. coli.

Flagellin, the protomeric subunit of bacterial flagella, contains no cysteine. We have detected the incorporation of trace quantities of 35S-cysteine into flagellin, highly purified and then resolved by SDS polyacrylamide gel electrophoresis, to measure mistranslation in vivo. Under normal conditions, this value is about 6 X 10(-4) pmoles cysteine per pmole flagellin. This value is greatly increased during growth in low concentrations of streptomycin and neomycin, antibiotics which are known to stimulate misreading in vitro. Of the specific types of misreading which streptomycin stimulates in vitro, only misreading of the CGU and CGC arginine codons could give rise to illegitimate incorporation of cysteine. In agreement, partial arginine starvation increases the incorporation of 35S-cysteine into flagellin in a relA- mutant, with or without streptomycin, but has no such effect in its isogenic relA+ partner- Assuming from these results that 35S-cysteine incorporation into flagellin reflects misreading of CGU/C coda, we deduce a misreading probability per codon in the range of 10(-4).

Arginine↗
PubMed1977

On the translational error theory of aging.

Theoretical treatments of error feedback in translation have revealed that two different modes of behavior are possible, depending on the values of certain parameters. In mode I, the error frequency will rise steadily toward randomness, inevitably reaching whatever value is catastrophic for cell survival; the "error catastrophe" theory of aging implicitly assumes this mode of behavior. In mode II, the error frequency will converge to a stable value, which may or may not have toxic consequences. We have performed an experimental test of the behavior of the translation system in Escherichia coli cells: we altered the system's intrinsic fidelity by means of the error-promoting drug streptomycin, and monitored the kinetics of change in error frequency by means of a specific assay of one kind of mistranslation (incorporation of cysteine into flagellin). We find that the system behaves according to mode II. Moreover, E. coli cells in which the error frequency has stabilized at a value as high as 50 times greater than normal continue to proliferate, albeit abnormally slowly, and their viability is not detectably reduced. Earlier results by Gorini and his associates point in the same direction. These observations diminish the plausibility of the error catastrophe theory of aging.

Aging↗