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R Moller

Publications and source records attributed to R Moller.

At least 19 recordsLinked to original sources
PubMed2004

Development and evaluation of a new ELISA for the detection and quantification of antierythropoietin antibodies in human sera.

Assays for the analysis of antierythropoietin antibodies (anti-EPO Abs) currently suffer from a high degree of nonspecificity or are cumbersome and time consuming to perform. They are therefore not well suited for the analysis of large numbers of human sera samples, a task that has become increasingly important due to an increase in the number of patients developing anti-EPO Abs. The objective of this study was to develop and validate a sensitive and specific ELISA for the determination of anti-EPO Abs that would suit these purposes. In this new double antigen bridging ELISA, anti-EPO Abs bind via one site to recombinant human erythropoietin (rhEPO)-biotin immobilized to streptavidin-coated microtiter plates (MTPs) and by a second site to rhEPO labelled with digoxigenin (DIG). The amount of bound antibody is determined using an anti-DIG antibody coupled to peroxidase. A rabbit polyclonal anti-EPO Ab purified by immunoadsorption is used as reference antibody preparation. The dynamic range of this ELISA was 1-75 ng/ml per assay calibrated with the reference antibody preparation. The assay was specific for anti-EPO Abs and did not react with other immunoglobulins (Ig) present in human serum. The lower limit of detection (LLD) of the assay was 0.5 ng/ml, and the lower limit of quantitation (LLQ) was 1.0 ng/ml. Anti-EPO Abs could be detected in the sera of pure red cell aplasia (PRCA) patients. In contrast to previous reports, no anti-EPO Abs could be detected in the sera of patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Sjogren's syndrome (SS), or in the sera of dialysis patients.

Animals↗
PubMed1993

Effect of a high fat diet on phospholipid class distribution and fatty acid composition in rat liver.

1. Long term consumption (20 weeks) of a high fat diet (65% of the energy content as fat) rich in either saturated [30% (w/w) coconut oil] or unsaturated [30% (w/w) sunflower oil] fatty acids resulted in strikingly similar alterations in the phospholipid class distribution and fatty acid composition in the liver of male Wistar rats. 2. The effect of these two diets was compared to a control group maintained on a 2% fat diet (w/w) for the same time interval. 3. In spite of the difference in the PUFA/SFA (polyunsaturated fatty acid/saturated fatty acid) ratio between the two high fat diets (0.1, saturated fatty acid diet; 5.4, unsaturated fatty acid diet), both diets resulted in a similar PUFA/SFA ratio in liver phospholipids, a similar reduction in palmitic acid (16:0), oleic acid (18:1, n-9) and arachidonic acid (20:4, n-6) and an elevation in stearic acid (18:0), linoleic acid (18:2, n-6) and docosahexaenoic acid (22:6, n-3). 4. Further, changes in the phospholipid classes were also similarly affected by both high fat diets.

Animals↗
PubMed1990

Cardiac electrophysiologic properties of bupivacaine and lidocaine compared with those of ropivacaine, a new amide local anesthetic.

Ropivacaine is a new amino-amide local anesthetic whose anesthetic profile appears similar to that of bupivacaine. Moreover, in intact animals ropivacaine was reportedly less arrhythmogenic than bupivacaine. These experiments evaluated the cardiac transmembrane electrophysiologic effects of ropivacaine compared with those of lidocaine and bupivacaine in an isolated rabbit Purkinje fiberventricular muscle preparation. Only bupivacaine (3-5 micrograms/ml, 0.92-1.5 x 10(-5) m) significantly decreased Purkinje fiber maximum diastolic potential. Action potential amplitude and maximal rate of depolarization (Vmax) were significantly decreased by all agents in the following order: bupivacaine, ropivacaine, lidocaine. High concentrations of bupivacaine and ropivacaine caused premature depolarizations during phase 3 in some preparations. In addition, bupivacaine altered the action potential configuration by producing "notching" not seen with either ropivacaine or lidocaine. This may reflect effects caused by changes in Ca2+, K+, or electrotonic effects. Ropivacaine and bupivacaine (30 micrograms/ml, 9.2 x 10(-5) m) and lidocaine (100 micrograms/ml, 3.74 x 10(-4) m) caused Purkinje fiber inexcitability and Purkinje fiber-ventricular muscle conduction block. However, the duration of PF inexcitability following exposure to ropivacaine and lidocaine was significantly shorter than in bupivacaine-treated preparation. Duration of PF-VM conduction block also tended to be shorter for ropivacaine than bupivacaine, but significantly longer than lidocaine. In general, ropivacaine is less potent than bupivacaine but more potent than lidocaine in terms of its depressant effect on cardiac excitation and conduction.

Action Potentials↗
PubMed1990

[Enzyme immunoassays for the quantification of human gamma-gamma-enolase (NSE)].

A direct two-site binding assay on the basis of antibodies from sheep for the quantification of human gamma-gamma enolase is described. The antibody was produced by immunization with human NSE coupled to horse spleen ferritin. The assay shows two feature: a decreased reactivity with NSE from rat and NSE from human serum in spite of 100% recovery of purified human brain NSE. The sheep antibody seems to react with epitopes less accessible on the rat NSE and on the NSE of human serum. The assay is characterized by gamma-gamma enolase specificity, a high sensitivity (2 pg) and a precision of CV = 3-7%.

Animals↗
PubMed1986

Influence of a perinatal hypoxia on the carbonic anhydrase activity in different brain regions of the rat.

Homogenates of striatum, hippocampus and cerebral cortex of the rat brain were investigated for carbonic anhydrase activities. During ontogeny the enzyme activities increase with proceeding gliogenesis. At the 5th postnatal day (PD) prenatal hypoxia (17th day of gestation (GD)--birth) is followed by a 4-fold increase of carbonic anhydrase (CA) activity in the hippocampus. After postnatal hypoxia (2nd-10th day of life) CA activity in all investigated brain regions rise. At the 11th PD the values were 190 (cerebral cortex), 242 (striatum) and 176 (hippocampus) per cent of control. Noradrenaline (10(-6)M) enhanced CA activity in cerebral cortex and hippocampus about 2-fold. Dopamine (10(-6)M) caused an increase in the striatum up to 210% of control. The increased CA activity after hypoxia is assumed to be a functional response to activation of the glia by catecholamines.

Aging↗
PubMed1986

Effect of early and late postnatal hypoxia on subcellular synaptosomal fractions from cerebral cortex of rats. I. An electron-microscopical and biochemical study.

Synaptosomal fractions of brain cortex of rats exposed to moderate intermittent hypobaric hypoxic conditions during the first or second decade of the postnatal life were investigated electron microscopically one day or up to one week after the hypoxia experiment. Mitochondria and synaptosomes with impaired morphology were observed to occur more frequently in fractions obtained from hypoxic animals. Synaptosomes showed lesions of the outer membrane and loss of the synaptoplasmatic content, or condensation of the synaptosomal content with increasing electron density, deformation of the synaptosomes in size and shape, disappearance of structural details, degeneration of intrasynaptosomal mitochondria in form of strong condensation and, finally, formation of intrasynaptosomal vacuoles with dense core inclusions. The mitochondrial reaction was characterized by two antagonistic configurations: condensation of the matrix with secondary enlargement of the intracistal spaces and of the outer compartment and, finally, the decay of the matrix condensate in several crumbs. On the other hand, swelling of the matrix with strong enlargement of the whole mitochondrium, later defects in the outer membrane and the degeneration into empty mitochondrial ghosts, appearing in the upper fractions. Some characteristic marker enzymes were tested in the fractions. The results hint at an elevated vulnerability of synaptosomes obtained from animals exposed to postnatal hypoxia, as indicated by the lowered quotient of LDH activities after and before addition of Triton X-100. Furthermore, there are clues to a decrease in the number of synaptic connections within the cortex of hypoxia exposed animals, as is concluded from the diminished AChE activity in the subcellular fractions of these animals. However, no different effect of early or late postnatal hypoxia exposition was evident in the biochemical parameters.

Acetylcholinesterase↗
PubMed1986

Effect of early and late postnatal hypoxia on subcellular synaptosomal fractions from cerebral cortex of rats. II. A quantitative ultrastructural study.

Synaptosomal subfractions were isolated by discontinuous sucrose gradient centrifugation from the P2-fraction of cerebral cortices of juvenile rats exposed to moderate intermittent hypobaric hypoxia from day 2-11 (early postnatal period) or from day 12-21 (late postnatal period) after birth. Ultrastructural investigations were carried out on fractions A and E of the preparation. Quantitative parameters of synaptosomes and mitochondria (volume density, numerical density, profile size frequency distribution) were estimated in a stereological analysis. Early postnatal hypoxia exposition strengthened the irreversible swelling of mitochondria. The effect on synaptosomes was less pronounced, very large synaptosomes showed significant condensation. Late postnatal hypoxia exposition resulted in strong condensation of synaptosomes in all size classes and similar reaction in mitochondria. Both hypoxia experiments produced an enhanced vulnerability of the synaptosomal membranes against the fractionation procedure and the appearance of monstrous large condensed synaptosomes. The results are discussed in view of hypothetical biochemical mechanisms underlying these changes.

Age Factors↗
PubMed1985

Effect of chronic postnatal hypoxia on dopamine uptake by synaptosomes from striatum of adult rats.

The exposure of rats to an early postnatal hypoxia (pO2 11.3 kPa, 12 h daily, 2nd-11th day of life) causes not only long lasting changes in the dopamine (DA) release from striatum slices but also in the DA uptake by striatal synaptosomes. Adult controls have a synaptosomal DA uptake of about 5 pmoles per mg protein and per min (males 4.99, females 5.69). Rats which have been exposed to an early postnatal hypobaric hypoxia exhibit a DA uptake of 2.71 (males) and 4.53 (females) pmoles per mg protein and per min. This long-lasting effect on the dopaminergic system of the striatum must be caused by a hypoxic alteration of gene expression in a critical period of the neonatal rat brain development, with permanent effects on the DA-metabolism and/or on the function of synaptic membranes.

Animals↗
PubMed1984

Symptomatic radiation-induced pericarditis in Hodgkin's disease.

This is a retrospective review of 193 evaluable patients treated with radiation therapy to the mediastinum for Stages I, II and III-A Hodgkin's disease. Eligible patients were those receiving 3000 rad or more to the mediastinum and no chemotherapy prior to the radiation. During the study period, 13 patients developed symptomatic pericarditis. The interval post treatment to the development of symptoms was six to 34 months. The incidence of pericarditis was studied as a function of: (1) the dose of radiation at a depth of 2 cm, 5 cm and the midplane of the mediastinum; (2) the ratio of anterior to posterior weighting of dose; (3) the presence or absence of intrathoracic tumor; (4) the size of the tumor when present; and (5) the fraction of the heart exposed to the radiation beam. There was a significant increase in the incidence of pericarditis with an increased dose of radiation at 2 cm, 5 cm and midplane depths and also with the presence of a large intrathoracic tumor. A reduction in mediastinal dose is recommended.

Heart↗
PubMed1984

Effects of piracetam on brain development in newborn rats exposed to hypoxia.

Perinatal hypoxia is one of the main causes of disturbances of the function of the CNS during childhood. In this study the protective effect of the nootropic drug piracetam (oxo-2-pyrrolidinyl-1)-2-acetamide was tested. One-day-old Wistar rats were exposed together with their mothers to hypoxia up to the 10th day of life (11 h daily, pO2 = 9.86 kPa). On the 11th day a 48% decrease of body weight and a 30% decrease of brain weight was found in the hypoxic animals. The protein/DNA ratio and the AChE activity in the brain cortex were decreased indicating retarded brain development. Piracetam (daily 100 mg/kg, s. c., before hypoxic exposure) did not affect the mortality rate, the somatic development of the animals, or the estimated basic neurochemical markers in the cortex of the brain. At the age of 3 months the fractional efflux rate (FER) of dopamine (DA) evoked chemically or electrically as a characteristic functional feature of chemical synaptic transmission, was examined. It was found that postnatal hypoxia induces a long lasting increase of FER of DA of striatum slices. Animals exposed postnatally to hypoxia and treated with piracetam showed an increased FER of DA (potassium as stimulus) by comparison with those animals also exposed postnatally to hypoxia but left untreated with piracetam.

Animals↗
PubMed1983

Antiarrhythmic effects of tocainide and lidocaine in dogs.

To compare the antiarrhythmic activities of tocainide and lidocaine in dogs, a protocol was designed where the drug plasma levels were increased stepwise. This was achieved by computerizing bolus doses and infusion rates, using pharmacokinetic equations with constants, derived from previous experiments in similar animals. In conscious coronary-ligated dogs with ischaemic arrhythmias both compounds were active, causing a 50% reduction in VPB's at plasma concentrations of 5.0 micrograms/ml (tocainide) and 3.5 micrograms/ml (lidocaine). "Clearing" of catecholamine-induced arrhythmias was not obtained in any of six dogs given tocainide and only in two out of six dogs given lidocaine.

Animals↗
PubMed1981

Influence of drugs on the bilirubin UDP-glucuronyltransferase activity and the concentration of Y and Z acceptor proteins in rat liver.

The aim of this paper is to report on the influence of phenobarbital, the combination of phenobarbital/nikethamide, the racemate and (+) isomer of methylphenobarbital on the activity of bilirubin UDP-glucuronyltransferase and the concentration of intrahepatic Y and Z protein in rats. The activity of bilirubin DP-glucuronyltransferase increased after the treatment in all groups. Pretreatment with phenobarbital/nikethamide resulted in the highest enzyme activity, using wet weight as reference. (+) Methylphenobarbital isomer as well as the racemate showed effects similar to those of phenobarbital. The concentration of hepatic Y acceptor protein increased in all pretreated groups by about 30%. The drugs did not increase the concentration of Z protein. The (+) isomer of methylphenobarbital seems better suited as an inductive drug in the prophylaxis of hyperbilirubinemia and in the treatment of nonconjugated hyperbilirubinemia than phenobarbital or phenobarbital/nikethamide since it has no sedative effect.

Animals↗
PubMed1980

[Development of bilirubin-UDP-glucuronosyltransferase (EC 2.4.1.17) and the concentration of transport proteins Y and Z of rat liver under postnatal hypoxia].

The development of bilirubin-UDP-glucuronyltransferase (bili.-UDP-GT) activity and the concentration of transport proteins Y and Z from the livers of Sprague-Dawley rats were studied in the first 20 days from birth and compared to the findings obtained on postnatally hypoxic rat newborns. The activity of bili.-UDP-GT is very low immediately after birth, and rises within the first 4 days to values distinctly exceeding adult values. Onset of hypoxia within the first 3 h of life inhibits the development of bili.-UDP-GT; later onset of hypoxia is without effect. The development of Y and Z transport proteins proceeds more slowly than that of bili.-UDP-GT. The binding properties of the Y protein in regard to substrate affinity. There is evidence in newborns for interactions in terms of cooperative binding. No influence of hypoxia on the development of Y and Z transport proteins is demonstrable.

Aging↗
PubMed1980

[Behavior of creatine in red blood cells and blood plasma of adult rats following exposure to hypoxia].

Adults rats exposed to hypoxia showed a definite increase of creatine concentration in red cells and plasma. The rise in cell creatine 37 h after the beginning of hypoxia had disappeared 2 days after the end of hypoxia. It is explained by the expulsion of preformed reticulocytes from the bone marrow. The increase of plasma creatine is supposed to be due to hypoxic damage to the muscles, which release creatine into the blood stream.

Animals↗
PubMed1978

[Bilirubin UDP-glucuronyltransferase activity in human fetal liver homogenates].

The bilirubin UDP GT-activity of the liver was studied from week 15 of pregnancy in 23 human fetuses and mature and immature dead newborns, respectively. No measurable bilirubin UDP GT-activity was found up to week 26 of pregnancy. The development of enzymatic activity presumably starts only postnatally, irrespective of gestational age of birth weight. Up to the fifth day the bilirubin UDP GT-activity is less than 0.2 mg of conjugated bilirubin/g liver/h, reaching in the second week values that correspond to approximately 20--30% of adult values. This activity is sufficient to prevent a clinically important hyperbilirubinemia because the concentration of unconjugated serum bilirubin was in all children below 12mg/100 ml.

Bilirubin↗