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Biomedical subjects

H Böhm

Publications and source records attributed to H Böhm.

At least 55 records · Page 3Linked to original sources
PubMed1989

Molecular cloning, sequencing and expression in Escherichia coli of the 25-kDa growth-related protein of Ehrlich ascites tumor and its homology to mammalian stress proteins.

The growth-related 25-kDa protein (p25) of Ehrlich ascites tumor (EAT) has been characterized by molecular cloning and sequencing of cDNA clones detected by hybridization with oligonucleotide probes synthesized according to the amino acid sequence of a tryptic peptide of p25. Detection of p25 mRNA in EAT of the exponential growth phase and of the stationary phase using cDNA-derived RNA probes demonstrated that the abundance of p25 mRNA is also growth-related. High-level expression of p25 in Escherichia coli has been established by oligonucleotide-directed mutagenesis of cDNA and insertion of the mutated cDNA into a T7-promoter expression vector. Recombinant p25 from the expressed cDNA sequence has been shown to comigrate with EAT p25 in electrophoresis and to react with antibodies against the EAT p25. On the amino acid level, p25 shows about 80% sequence homology to the human stress protein hsp27. Furthermore, p25 has similar isoforms of phosphorylation as demonstrated for small mammalian stress proteins from rat and human. From the results obtained, it is concluded that p25 is a mammalian stress protein, the abundance of which is related to growth characteristics of the Ehrlich ascites tumor.

Amino Acid Sequence↗
PubMed1989

The growth-related protein P23 of the Ehrlich ascites tumor: translational control, cloning and primary structure.

p23 is a protein of Ehrlich ascites tumor cells, preferentially synthesized in the exponentially growing tumor. In vitro, serum and actinomycin D rapidly induce p23 synthesis. Using transcription inhibitors and a wheat germ cell-free translation system, evidence is provided that the synthesis of p23 is under translational control. Actinomycin D even results in superinduction of p23. Polymerase chain reaction, cloning and sequencing of p23 cDNA suggest p23 to be identical with a 21 kDa protein of mouse erythroleukemia cells, the synthesis of which was shown to be controlled also at the translational level (Chitpatima, S. T., Makrides, S., Bandyopadhyay, R., and Brawerman, G. (1988) Nucleic Acids Res. 16, 2350).

Amino Acid Sequence↗
PubMed1989

[Correction of Bechterew kyphosis].

The derangement of posture in advanced flexion deformity due to ankylosing spondylitis, as well as operative correction procedures are analysed. The "Dorsal Lordosating Spondylodesis", DLS, according to Zielke is introduced. This method of polysegmental correction and transpedicular fixation via USIS implants allows the recreation of a balanced upright posture by restoration of smooth lumbar lordosis. We present results of 173 patients corrected by DLS. Since the total amount of correction is split into 5-7 osteotomy sites, complication rates are substantially lower than in the monosegmental methods. Besides the gain of body height and immediate pain relief, the restoration of a horizontal axis of vision could be achieved. The latter, for all patients the most important feature, was maintained as up to 5 years follow-up's show.

Adult↗
PubMed1988

Purification of the growth-related protein p25 of the Ehrlich ascites tumor and analysis of its isoforms.

1. Two of the three isoforms of the growth-related protein p25 of the Ehrlich ascites tumor have been purified to homogeneity by giant two-dimensional polyacrylamide gel electrophoresis. 2. Antibodies raised against the isoform p25/1 react also with isoforms p25/2 and p25/3. 3. Limited tryptic digestion of p25/1 and p25/2 resulted in similar oligopeptide patterns. Corresponding oligopeptides of both isoforms have identical amino acid sequences. 4. The isoforms p25/2 and p25/3 are phosphorylated derivatives of unphosphorylated p25/1. The phosphorus is bound to serine and a further unknown phosphorylation site.

Amino Acid Sequence↗
PubMed1987

Atrial natriuretic peptide release due to physical exercise in healthy persons and in cardiac patients.

Plasma levels of human atrial natriuretic peptide were determined during different stages of a symptom-limited bicycle ergometer stress test. Eight healthy persons and three patients suffering from well-defined cardiac disorders were examined. Measurements of the peptide were performed before the exercise, at 75 watts, at maximal work load, and 10 and 30 min after ceasing the exercise. In healthy persons plasma levels of the peptide increased from preexercise levels of 4-41 ng/l to 16-59 ng/l at maximal work load, but remained in the normal range (10-70 ng/l). In contrast, in the cardiac patients, levels of the peptide were up to 8-fold higher at maximal physical exertion (154-270 ng/l) than at rest (34-86 ng/l). Within a recovery period of 30 min hormone concentrations returned almost to preexercise levels.

Aged↗
PubMed1986

[Immune complexes in myocardial infarct].

604 patients were investigated with C1q solid phase RIA in regard to circulating immune complexes (CIC) shortly after myocardial infarction. 118 (19.6%) of these 604 patients had CIC, which disappeared in 99 patients (83.7%) or decreased significantly in 9 cases (7.6%) after 2-4 weeks. Only 10 patients (8.3%) showed persisting CIC. 12 parameters assessing clinical features and laboratory data were compared with the results of CIC investigation in altogether 251 patients, of whom 54 (21.5%) were CIC-positive. No differences between CIC-positive and CIC-negative patients were observed with regard to generally accepted factors predisposing to infarction. However, CIC-positive patients differed significantly from CIC-negative cases in the higher incidence of a history of respiratory tract infection before infarction (p less than 0.001) and the more frequent absence of a family history of cardiac and circulatory disease (p less than 0.0005). Interpretation of these results indicates a transient appearance of CIC after liberation of heart - tissue antigens during infarction, but does not exclude the possible existence of a group of patients manifesting CIC already before the onset of infarction, whereby the CIC may have contributed towards triggering off the infarction. In this case persistence of CIC after infarction may be regarded as an unfavourable sign.

Antigen-Antibody Complex↗
PubMed1984

Generation, characterization and ELISA of monospecific antibodies against the subunits of a Ca2+-dependent protein kinase and a Ca2+-transport ATPase from rabbit skeletal muscle.

Monospecific precipitating sheep antibodies were generated for the first time against the purified, homogeneous alpha-, beta- and gamma-subunits of the Ca2+-dependent protein kinase, phosphorylase kinase, from rabbit muscle. As reference, antibodies against the holoenzyme and the CA2+-transport ATPase of sarcoplasmic reticulum were induced. In all cases antibody titers could be quantitated (standard error 5-10%) by enzyme-linked immunosorbent assay. Differentiation of antibody binding was achieved by quantitative precipitation and complement fixation assays. In general maximal antibody titers were reached 56 days after primary immunization and high titers (approximately 5000) were maintained for several weeks. Anti-alpha, anti-beta and anti-gamma avidly precipitate the denatured subunits employed as immunogens as well as the native enzyme. No cross-reactivity between antibodies against a specific subunit and any of the other heterologous subunits was demonstrable in double immunodiffusion assays providing no evidence for immunologically identical sites on the alpha-, beta- and gamma-subunits. Since anti-alpha, anti-beta and anti-gamma strongly inhibit enzyme activity, it is likely that they do so primarily by sterically interfering with the binding of the large substrate phosphorylase b (Mr 2.0 X 10(5)) to phosphorylase kinase (Mr 1.3 X 10(6)). It cannot be excluded, however, that anti-beta and anti-gamma bind to the active sites on these 2 subunits.

Animals↗
PubMed1983

Exercise induces in vivo platelet activation in patients with coronary artery disease and in healthy individuals.

Recently, conflicting results have been published about a possible relationship between platelet activity and exercise-induced myocardial ischemia. The present study was performed to investigate platelet behavior during a graded symptom-limited bicycle ergometer test both in relation to the intensity of exercise and to exercise-induced myocardial ischemia. Plasma concentrations of platelet factor 4 (PF4) and beta-thromboglobulin (beta-TG) were measured by radioimmunoassays in 53 patients who had had acute myocardial infarction 10 weeks before the study and, for comparison, in 9 healthy individuals. In the whole group of the 53 patients there was no significant alteration in platelet-specific proteins during exercise, whereas physical activity induced a 2- to 3-fold increase in beta-TG and PF4 levels in the controls. However, on differentiation of the patients as to their individual exercise performance, significant exercise-associated platelet activation was demonstrable in those who reached more than 75% of their calculated maximal working capacity, whereas no correlation was found between platelet activity and exercise-induced myocardial ischemia. Thus, the results from this study indicate that in vivo platelet activation is a physiological phenomenon which occurs when a certain degree of physical intensity is exceeded, independent of the precipitation of myocardial ischemia.

Adult↗
PubMed1981

[Ergometric dose-effect study of bunitrolol (Stresson) in patients with coronary heart disease (author's transl)].

20 patients with coronary heart disease and ergometrically provocable stenocardias and electrocardiographic signs of ischemia were tested ergometrically with two different dosages (5 mg:20 mg) of the beta-blocking agent bunitrolol (Stresson) in a double-blind-test. The results obtained are in accordance with literature: The greater the ergometric stress the more effective is Stresson and vice versa. For treatment of coronary heart disease can be considered: Low dosage of Stresson in patients with stenocardias and hypoxias in high-grade exercise, high dosage of Stresson in patients with stenocardias or ischemias in low-grade exercise or rest.

Clinical Trials as Topic↗
PubMed1980

[Ergometric double-blind study, Isoket-spray versus placebo-spray, in patients with coronary heart disease (author's transl)].

In a double-blind study 40 patients with coronary heart disease, who all complained of typical exertion-dependent angina pectoris symptoms and showed ECG changes after work in conformity with a myocardiac hypoxia, were examined in ergometric exertion tests before as well as immediately and 60 minutes after a single dose of 3.75 mg of Isoket-spray or Placebo-spray respectively. The Isoket-spray group was compared with the placebo group, furthermore, within the Isoket-spray group, the original ergometry (without medication) and the subsequent ergometries. The ST-depression, the time until reattainment of the original electrocardiographical situation after cessation of exertion and the subjective complaints showed highly significant improvements after use of the Isoket-spray in both repeated ergometries. Rapid and long-term relief after application of Isoket-spray were thus impressively shown in this double-blind study.

Aerosols↗
PubMed1980

[Acebutolol in coronary heart disease: an ergometric double-blind study (author's transl)].

In 20 patients with coronary heart disease and typical changes in the exercise ECG (evidence of myocardial hypoxia), which disappeared completely on second ergometry after isosorbid dinitrate, the effect of a single dose of 400 mg acebutolol (Prent) was tested on exercise. Ergometrically induced cardiac work was significantly reduced in all patients, compared with leg exercise (little change in lower, more marked change in the higher ranges of exercise) so that repeat ergometry at the same ergometric level of exercise produced neither signs of hypoxia nor angina. There were no significant changes after a placebo.

Acebutolol↗