Search PubMed⌕ Search

Biomedical subjects

A Richter

Publications and source records attributed to A Richter.

At least 361 records · Page 20Linked to original sources
PubMed1989

[Detection of mycoplasmas in experimentally-infected bull sperm].

Bull sperm pellets experimentally infected with various concentrations of Mycoplasma (M.) bovis, M. bovigenitalium, and M. californicum were stored several months at -196 degrees C and were subsequently tested for mycoplasmas, using different methods and culturing media. M. bovis was reliably identified by laboratory diagnosis up to a concentration of 10(2) cfu/pellet. M. bovigenitalium and M. californicum were found to make higher demands on the quality of culturing substrates. Recommended are 1-h broth incubation and 5-d broth breeding.

Animals↗
PubMed1989

Genetic homogeneity at the Friedreich ataxia locus on chromosome 9.

Classical Friedreich ataxia, a progressive, neurodegenerative disorder involving both the central and peripheral nervous systems, has been subclassified according to the observed clinical heterogeneity. The variations in the age at onset and in the spectrum and severity of symptoms have previously been interpreted as evidence of genetic heterogeneity. We have studied the linkage between the disorder and closely linked DNA markers in families of distinct ethnic origins, including the "typical" French-Canadians and the Acadian population of Louisiana. The disease in these two populations, both of continental French origin, has a very similar initial clinical picture. However, a marked difference in the rate of progression of the obligatory symptoms after 10 years of apparent disease is observed. A total of 553 individuals from 80 families with 202 affected members have been typed with the chromosome 9 marker MCT112, which we have previously shown to be closely linked to the disease locus. Evidence for linkage was observed in all families with the generation of a combined total lod score of 25.09 at a recombination fraction of theta = .00, providing strong evidence for genetic homogeneity at this locus for the classical form of this disease.

Canada↗
PubMed1988

Monoclonal antibodies neutralizing mammalian DNA topoisomerase I activity.

We have isolated three different monoclonal antibodies specific for mammalian type-I DNA topoisomerase. The antibodies react with three closely adjacent epitopes located in a central section of the enzyme (between amino acid residues 344 and 483). Two of the antibodies inhibit an early step of the nicking/closing pathway. We provide evidence showing that the antibodies do not block the association of the enzyme with DNA. The antibodies are useful for immunocytochemical investigation and for further exploration of the biochemical function of mammalian type-I DNA topoisomerase.

Amino Acid Sequence↗
PubMed1988

Effects of VM26, a specific inhibitor of type II DNA topoisomerase, on SV40 chromatin replication in vitro.

We have examined the influence of VM26 (teniposide), a specific inhibitor of mammalian type II DNA topoisomerase, on the replication of SV40 minichromosomes in vitro. The replication system we used consists of replicative intermediate SV40 chromatin as substrate which is converted to mature SV40 chromatin in the presence of ATP, deoxynucleotides and a protein extract from uninfected cells. The addition of 100 microM VM26 to this system reduces DNA synthesis to 70 to 80 percent of the control and leads to an accumulation of 'late replicative intermediates'. The VM26 induced block of replication was not released by the addition of large quantities of type I DNA topoisomerase. We conclude, that type II DNA topoisomerase is essential for the final replication steps leading from late Cairns structures of replicative intermediates to monomeric minichromosomes. It appears that type I DNA topoisomerase can function as a swivelase during most of the replicative elongation phase, but must later be replaced by type II DNA topoisomerase.

Animals↗
PubMed1988

Prediction of rupture in acute myocardial infarction.

In two patient series including 809 and 327 patients, respectively, with acute myocardial infarction we have compared those who died in myocardial rupture (verified at autopsy, Group A) with those who died without rupture (autopsied, Group B), and those who survived hospitalization (Group C) with regard to previous history and clinical course in hospital. Rupture among autopsied patients was observed in 45% and 40% of the cases in the respective studies. Previous infarction was observed in each study as 0% and 0% in Group A compared with 25% and 31% in Group B, and 20% and 34% in Group C. Previous angina pectoris was observed in 26% and 22% in Group A compared with 50% and 54% in Group B and 52% and 54% in Group C. Maximum serum enzyme activity in Group A did not differ from Group B, but was higher than in Group C (p less than 0.001). Group A patients tended to have a higher initial pain score and a higher requirement of analgesics compared with other groups, whereas initial heart rate or systolic blood pressure did not differ in these patients compared to others. We thus conclude that patients with myocardial rupture have a very low occurrence of previous myocardial infarction and angina pectoris, and that their pain course appears to be particularly severe in the acute phase.

Aged↗
PubMed1988

Genetic variations of human serum beta 2-glycoprotein I demonstrated by isoelectric focusing.

Human serum beta 2-glycoprotein I was analyzed by isoelectric focusing followed by immunoprinting or immunoblotting with monospecific antiserum. Isoelectric focusing revealed a heterogeneous pattern consisting of 4 major and 4-5 minor bands with isoelectric points of the major bands between pH 5.4 and 6.2. Comparative analysis of sera from more than 400 healthy blood donors showed individual variations of band patterns: six different phenotypes were observed. A family study of 44 families with a total of 129 children demonstrated the genetic control of this variation. Presumably, three alleles, called B2G*1, B2G*2, and B2G*3, determine six phenotypes: B2G 1, 2, 3, 1-2, 1-3 and 2-3. The phenotype 3, however, has not been found in this study. An additional phenotype, noted in one serum specimen, was tentatively classified as B2G 2-4. The distribution of phenotypes and alleles in two populations, from Munich and from Tyrol, has been examined and the frequencies are presented. This genetic polymorphism appears not to be associated with inherited quantitative variations of beta 2-glycoprotein I found earlier. The inherited variations can still be recognized after treatment of sera with neuraminidase and with endoglycosidase F, although the banding pattern is altered and shifted towards the cathode. The genetic polymorphism can, therefore, not be ascribed to variations residing in the carbohydrate side chains.

Alleles↗
PubMed1988

Association of DNA topoisomerase I and RNA polymerase I: a possible role for topoisomerase I in ribosomal gene transcription.

RNA polymerase I preparations purified from a rat hepatoma contained DNA topoisomerase activity. The DNA topoisomerase associated with the polymerase had an Mr of 110,000, required Mg2+ but not ATP, and was recognized by anti-topoisomerase I antibodies. When added to RNA polymerase I preparations containing topoisomerase activity, anti-topoisomerase I antibodies were able to inhibit the DNA relaxing activity of the preparation as well as RNA synthesis in vitro. RNA polymerase II prepared by analogous procedures did not contain topoisomerase activity and was not recognized by the antibodies. The topoisomerase I: polymerase I complex was reversibly dissociated by column chromatography on Sephacryl S200 in the presence of 0.25 M (NH4)2SO4. Topoisomerase I was immunolocalized in the transcriptionally active ribosomal gene complex containing RNA polymerase I in situ. These data indicate that topoisomerase I and RNA polymerase I are tightly complexed both in vivo and in vitro, and suggest a role for DNA topoisomerase I in the transcription of ribosomal genes.

Animals↗
PubMed1988

In situ activation of human erythrocyte prolidase: potential for enzyme replacement therapy in prolidase deficiency.

Deficiency of prolidase is frequently associated with skin lesions and mental retardation. Biochemically, the condition is marked by iminodipeptiduria. We have investigated the feasibility of using donor erythrocytes to replace the deficient enzyme. Prolidase occurs in erythrocytes in an inactive form. If erythrocytes are incubated overnight at 37 degrees C in the presence of 1 mM MnCl2, the intracellular Mn++ concentration increases from 0.014 to 2.04 micrograms/ml. As a consequence, the activity of prolidase in hemolysates increases to 159 mumol glycyl-L-proline hydrolyzed/h/ml compared to 5 mumol/h/ml for hemolysates of cells incubated in the absence of Mn++. Hydrolysis of glycyl-L-proline by intact erythrocytes is reduced by the slow rate of iminodipeptide transport into the cell; however, intact cells hydrolyzed this substrate at a rate 10-20 times faster after preincubation with MnCl2. After exogenous MnCl2 is removed from the storage buffer, high levels of erythrocyte prolidase activity persist for at least 13 days. The kinetic parameters for intact activated erythrocyte-catalyzed hydrolysis of glycyl-L-proline have been estimated. These values predict that donor erythrocytes, activated with Mn++ before transfusion could play a significant role in the recovery of proline from dietary sources of iminodipeptides in patients with prolidase deficiency.

Dipeptidases↗
PubMed1988

[Lipoxygenase inhibitors and mast cell degranulation].

Lipoxygenase inhibitors block the release of histamine from protaminesulfate-stimulated peritoneal mast cells of the rat in vitro. The order of this inhibitory activity of the agents does not correlate with the order of this inhibitory activity of the agents does not correlate with the order of their inhibitory activity against lipoxygenases from reticulocytes and peas. Antioxidants/radical scavengers, which do not inhibit lipoxygenase activity (mannitol, hydrochinone) block the protaminesulfate-activated degranulation of peritoneal rat mast cells, too. Therefore we assume that activated oxygen radicals are generated by stimulation of pRMZ with protaminesulfate. These oxygen radicals could be promotors for the histamine secretion of the peritoneal mast cells. Consequently, lipoxygenase inhibitors with radical scavenging properties may influence degranulation of peritoneal mast cells of the rat by two mechanisms, namely by reduction of the synthesis of 5-LOX-products (promotors of the histamine release) and by reduction of the toxic effects of activated oxygen radicals.

Animals↗
PubMed1987

Effects of VM26 (teniposide), a specific inhibitor of type II DNA topoisomerase, on SV40 DNA replication in vivo.

Simian Virus 40 (SV40) infected cells were pulse labeled with (3H) thymidine and chased either in the absence or in the presence of the cytotoxic drug VM26 (teniposide). We investigated the structure of labeled SV40 DNA and found that VM26 had no significant effect on replicative chain elongation but strongly inhibited the conversion of late replication intermediates to mature DNA daughter molecules. The late replicative SV40 DNA intermediates which accumulate in VM26 treated cells contained essentially full length labeled DNA strands. These newly synthesized strands were not part of two catenated interlocked SV40 monomers suggesting that the block occurred prior to the final ligation reaction. Since VM26 is known to be a specific inhibitor of DNA topoisomerase II we conclude that this enzyme is dispensable for the chain elongation of replicating SV40 DNA, but that it is essential for the termination of SV40 DNA replication cycles.

Animals↗
PubMed1987

QRS complex recovery during one year after acute myocardial infarction.

The recovery of the ECG signs of anterior myocardial infarction has been studied in 70 patients. A significant increase in R-wave amplitude and decrease in Q-wave amplitude on 24-lead precordial mapping was observed during one year after infarction. Patients with lower initial heart rate showed a greater recovery of R- and Q-wave amplitudes, as did patients with smaller infarcts, as assessed by peak heat-stable lactate dehydrogenase (LDH).

Adult↗
PubMed1987

[Neuroautonomic organization of cardiac rhythm and of nonrhythmic oscillations in the frequency of cardiac contractions and respiration].

In 25 chronic adult rabbits, the functional organization of neurally mediated short-term rhythms and patterns of the heart rate (HR) were investigated. The respiration-unrelated arrhythmia seems to be vagally mediated only, being abolished with atropine. The respiration-related arrhythmia exists not only within the range of respiratory frequency but also in lower frequencies as discovered by spectral and coherence analysis. During motor activity, there is a systematic correlation among increasing premotor, motor and amygdaloid multispike activities, increasing HR and depressed HR-rhythms with limbic initiation of motor and concomitant autonomic patterns, "Immobile confrontations" alone produces vagally induced HR-decrease and increased amplitudes of vagal HR-rhythms with a concomitant cortical multispike depression, a mirror image of the autonomic patterns after nociceptive stimulation.

Action Potentials↗