Biomedical subjects

B Bergmann

Publications and source records attributed to B Bergmann.

14 recordsLinked to original sources

PubMed1992

Formation of the semiquinone anion radical from tert-butylquinone and from tert-butylhydroquinone in rat liver microsomes.

The tert-butylsemiquinone anion radical is formed from tert-butylhydroquinone and from tert-butylquinone in rat liver microsomes. In the presence of oxygen, the quinone and, less extensively, the hydroquinone induce excess production of superoxide in microsomes. It is concluded that autoxidation of the semiquinone formed from the quinone by microsomal enzyme activity is responsible for superoxide formation and that the hydroquinone enters the redox cycle via autoxidation. tert-Butylquinone induces injury of the hepatocyte plasma membrane. tert-Butylhydroquinone and tert-butylquinone are metabolites of the antioxidant butylated hydroxyanisole. The semiquinone-dependent superoxide formation may contribute to the toxic actions of butylated hydroxyanisole.

Animals↗

PubMed1991

Pyrimethamin-resistant Plasmodium falciparum lack cross-resistance to methotrexate and 2,4-diamino-5-(substituted benzyl) pyrimidines.

Methotrexate resistance induced in cultured Plasmodium falciparum depends on an altered dihydrofolate reductase with decreased affinity for methotrexate as well as for pyrimethamine. In contrast, pyrimethamine-resistant field isolates of P. falciparum lack cross-resistance to methotrexate and 2,4-diamino-5-(substituted benzyl) pyrimidines. The structure of the latter class was optimized by the use of trimethoprim as a lead and the substitution of methoxy groups at the benzyl ring by 3-(4'-aminophenyl-4-sulfonylphenylamino)propoxy or by (4'-aminophenyl-4-sulfonylphenyl)methoxy, which resulted in antimalarials of high potency. The efficiency of these newly designed 2,4-diamino-5-(substituted benzyl) pyrimidines was confirmed by their strong inhibitory effect on plasmodial dihydrofolate reductase as well as by in vitro screening against drug-sensitive and -resistant strains of P. falciparum.

Animals↗

PubMed1991

N-acetylglucosaminyltransferase from Ascaris suum.

The occurrence of N-acetylglucosaminyltransferase, the initial step in the synthesis of the carbohydrate moiety of N-linked glycoproteins, is demonstrated in the microsomal fraction of the nematode Ascaris suum. Phosphatidylglycerol stimulated enzyme activity three- to six-fold without affecting the Km values of either substrates, uridinediphospho-N-acetylglucosamine or dolichylphosphate. The Km values were determined to be about 12 microM and 100 micrograms ml-1, respectively. The enzyme activity was strongly inhibited by tunicamycin acting as a competitive inhibitor with respect to the substrate uridinediphospho-N-glucosamine.

Animals↗

PubMed1991

Characterization and molecular cloning of a Cu/Zn superoxide dismutase from the human parasite Onchocerca volvulus.

Evidence suggests that the helminth antioxidant enzyme superoxide dismutase (SOD) may play a role in parasite's defense against the cellular immune mechanisms of the host. In order to investigate this for the human parasite Onchocerca volvulus, the enzyme activity was characterized, the release of SOD by the parasite was examined, and a complete cDNA encoding the O. volvulus SOD was identified. The SOD activity in adult O. volvulus was found to be 8.1 +/- 4.2 U/mg of protein. A Cu/Zn-containing enzyme was demonstrated by its sensitivity towards cyanide, azide, and hydrogen peroxide. Isoelectric focusing, combined with an enzyme activity assay, revealed two activities at pI 6.8 and 7.6, with both activities inhibited by KCN. Adult parasites, maintained in vitro, released SOD into the culture medium, which was detected by enzyme activity. In parallel, lactate production was measured to ensure the viability of the parasite. Oligonucleotides (based upon conserved sequences in the SOD genes of other organisms) and the polymerase chain reaction were used to identify a portion of the SOD gene from O. volvulus genomic DNA. A cDNA library was constructed in lambda unizapII and screened with the genomic polymerase chain reaction fragment. A complete cDNA encoding the Cu/Zn SOD was identified, and its nucleotide sequence was determined. Southern blot hybridization experiments indicated that the Cu/Zn SOD is encoded by a single-copy gene with at least one intron.

Amino Acid Sequence↗

PubMed1991

[Changes in the endothelial cell density after perforating keratoplasty].

We examined 590 endothelial photomicrographs of 327 patients with computerized morphometry; these patients had undergone penetrating keratoplasty in the period from 1981 to 1987. We found a weak negative correlation of r = -0.39 between postoperative endothelial cell density and the postoperative period. The endothelial cell density in the interval 12-24 months postoperatively averaged 1624 cells/mm. This is approximately 380 cells/mm more than described in other studies of that kind. We found significantly higher cell densities for cultured corneas and for corneas of young donors (age up to 39 years) up to 1 year postoperatively. Comparison of the diagnosis groups showed no relevant differences in postoperative cell density.

Cell Count↗

PubMed1987

Myocardial biopsy in patients with hypertrophic cardiomyopathy: correlations between morphologic and clinical parameters and development of myocardial hypertrophy under medical therapy.

Left ventricular biopsies from 38 patients with hypertrophic cardiomyopathy (HOCM 28, HNCM 10) were investigated to evaluate possible correlations between morphological and clinical parameters. No correlation was found between the degree of myocardial hypertrophy (muscle cell diameter), nuclear size of the myocytes, fibrous tissue content and various clinical data such as pressure gradient, left ventricular end-diastolic pressure, Sokolow index and heart volume. In 11 patients with HOCM, a second biopsy was performed after medical therapy (verapamil, n = 9; propranolol, n = 2) over 33 +/- 12 months. Increasing myocardial hypertrophy (cell diameter 16.2 +/- 4.4 mu vs. 20.3 +/- 4.2 mu) was observed in all 11 patients. The interstitial fibrous tissue content increased from 5.7 +/- 6.3 to 12.7 +/- 6.8%. The volume fraction of myofibrils decreased (48.8 +/- 2.7 vs. 43.6 +/- 5.3%). The morphological changes were observed regardless of the clinical outcome which was improved in four, unchanged in five and worsened in two cases. The underlying hypertrophic process in HCM seems to be slowly progressive in most patients and cannot be influenced by medical treatment.

Adult↗

PubMed1987

Period-amplitude analysis of rat electroencephalogram: effects of sleep deprivation and exercise.

Electroencephalogram (EEG) wavelength and amplitude within NREM sleep, paradoxical sleep (PS), and wake were measured by computer in five intact rats and four rats with suprachiasmatic nucleus (SCN) lesions for the first recovery day following 24-h total sleep deprivation (TSD) achieved by keeping them on a rotating cylinder over water. To assess exercise effects, EEG within NREM was also analyzed in four intact rats for 8 h after separate 4-h TSD sessions at low and high rates of cylinder rotation (high rate = 12 times low rate). During recovery from 24-h TSD, EEG changed most dramatically in NREM. The number of slow waves per unit time (1-4 Hz wave incidence) and the amplitude at all wavelengths from 1 to 16 Hz were increased for up to 12 h and then fell below baseline levels for most of the next 12 h. Fast (5-16 Hz) wave incidence changed inversely with slow wave incidence. Wake and PS also showed initially increased amplitude, but shifts in incidence were from slow to fast waves. Relative to baseline, intact and SCN-lesioned rats showed similarly shaped recovery functions, indicating that EEG responses to sleep loss are largely independent of diurnal rhythms. Four-hour TSD at a low rotation rate affected NREM EEG similarly to 24-h TSD, but more mildly. The high rotation rate further increased slow wave incidence during recovery without further increasing slow wave amplitude. The results suggest that both EEG wave incidence and amplitude are responsive to prior wakefulness, but only incidence is responsive to prior exercise.

Animals↗

PubMed1977

Ir gene control of carrier recognition II. Unexpected low immunogenicity of guinea pig insulin.

The immune response of mice to guinea pig insulin (as well as to insulins from other species) is controlled by immune response genes. The immunogenicity of guinea pig insulin is generally much lower than that of bovine insulin, through there are 14 sequence differences between mouse insulin and guinea pig insulin as compared to 5 sequence differences between mouse insulin and bovine insulin, respectively. The low immunogenicity of guinea pig insulin is indicated by a low frequency of responder strains and the requirement for high antigen doses for immunisation. Guinea pig and bovine insulin do not cross-react at the antibody level, but there seems to be some cross-recognition at the carrier level, as indicated by the capability of guinea pig insulin primed spleen cells to provide help for the pig insulin carrier in cooperative cell transfer.

Animals↗

PubMed1974