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C Bauer

Publications and source records attributed to C Bauer.

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

[Critical aspects in determining total radioactivity of biological samples].

During measurements of radioactivity in some milk samples with liquid scintillation counter (about one year after the nuclear accident of Chernobyl) we have observed an increase of the values of scintillation fluid with the passing of time. Although this enhancement is absolutely small (about 2 c.p.m. in 500 min), it is very important for an exact measurement of samples at low counting, as those tested. Our protocol of measure provides for insertion of alternate blanks and samples in the automatic sample-holders of liquid scintillation counter. The values of measurement of samples are taken during the increase phase subtracting the value of blank interpolated on the increasing straight line from c.p.m. of sample. Finally, we report the collected values of the whole radioactivity in some milk samples: at least 5-6 nCi/L contrary to about 1 nCi/L of 137Cs reported by USL. In our opinion it is important to consider the whole radioactivity as measure of the overall biological danger of radioactive samples. In fact, this measurement takes into account also biologically very dangerous radionuclides as 3H, 14C, 90Sr.

Animals↗
PubMed1988

Evaluation of the stability of human erythropoietin in samples for radioimmunoassay.

Radioimmunoassays for erythropoietin are limited so far to a few specialized laboratories and this requires transport and storage of samples. We therefore tested the stability of immunoreactive erythropoietin in serum and plasma samples obtained from a uremic and a nonuremic anemic patient. No significant change in the concentration of immunoreactive erythropoietin was found in either serum or plasma samples for up to 14 days of storage. This type of stability was observed no matter whether the samples were stored at room temperature, 4 degrees C, or -20 degrees C. There was no difference between the estimates of erythropoietin in serum and heparinized plasma. Validity of the radioimmunoassay used in this study was demonstrated by parallelism of dilution curves of test specimens and the 2nd International Reference Preparation for erythropoietin and by a close correlation between the immunoreactivity and the bioactivity of the hormone, as assessed in the same samples by the exhypoxic polycythemic mouse bioassay. In conclusion the data obtained clearly indicate that the necessity of storage and transport of clinical samples does not limit the practicability of the radioimmunoassay for erythropoietin.

Anemia, Aplastic↗
PubMed1988

Cerebrospinal fluid antibodies to myelin basic protein in acute idiopathic optic neuritis.

Free and bound levels of anti-myelin basic protein (anti-MBP) antibodies were measured by radioimmunoassay in the cerebrospinal fluid of 20 patients with acute idiopathic optic neuritis, 133 patients with multiple sclerosis (MS) divided into three clinical subgroups, and 76 normal control subjects. Patients with idiopathic optic neuritis had elevated levels of anti-MBP predominantly in free form, resulting in an elevated (above unity) free/bound anti-MBP ratio similar to that of MS patients with acute relapses. These data suggest that acute idiopathic optic neuritis, like active MS, is associated with anti-MBP.

Autoantibodies↗
PubMed1988

Expression of a cloned beta-glucanase gene from Bacillus amyloliquefaciens in an Escherichia coli relA strain after plasmid amplification.

Amino acid starvation of cells of the Escherichia coli relA strain, CP79, which cannot accumulate guanosine tetraphosphate (ppGpp) in response to amino acid limitation, increased the pEG1 plasmid content about 5- to 7-fold in comparison with exponentially growing cells (pEG1:pBR322 with an insertion of Bacillus amyloliquefaciens DNA coding for beta-glucanase). In contrast, no pEG1 amplification occurred in E. coli CP78, the stringently controlled counterpart, after amino acid starvation. In order to verify these results, the plasmid DNA content was monitored by measuring the expression of pEG1-encoded beta-glucanase from B. amyloliquefaciens both before and after plasmid amplification. When amino acid starved CP79 cells were given an additional dose of amino acids, a more than 10-fold increase in pEG1-encoded beta-glucanase activity (per cell mass) was measured. This increase in enzyme activity correlates with pEG1 amplification during amino acid limitation. Under comparable conditions the activity of beta-glucanase was not increased in strain CP78, which did not amplify the plasmid. We suggest that the replication of pEG1 in amino acid starved E. coli cells is somehow under negative control by ppGpp. Moreover, we found the Bacillus beta-glucanase in E. coli relA cells to be excreted into the growth medium after starvation and overexpression.

Amino Acids↗
PubMed1988

Besnoitia besnoiti: studies on the definitive host and experimental infections in cattle.

Domestic cats, 11 other species of carnivorous mammals, 6 species of snakes, and white-backed vultures were tested for their possible role as definitive hosts of Benoitia besnoiti by feeding with cystic material from chronically infected bovines. None of the species tested is a definitive host; hence, the life cycle of this parasite remains obscure. In attempts to produce clinical cases of besnoitiosis by experimental infection, bovines were inoculated IV, SC, and IP with cystozoites or tachyzoites. Immunosuppression of the animals was essential for the development of severe cases and skin lesions; cystozoites proved to be more pathogenic than tachyzoites.

Animals↗
PubMed1988

In vivo induction of gliadin-mediated enterocyte damage in rats by the mannosidase inhibitor, swainsonine: a possible animal model for celiac disease.

Simultaneous feeding of gliadin and swainsonine, an inhibitor of alpha-D-mannosidases, in rats disturbed enterocytic maturation as shown by a marked loss of activities of alkaline phosphatase and gamma-glutamyltransferase. Morphologically, simultaneous treatment with gliadin and swainsonine caused destruction and decreased density of microvilli, as shown by electron microscopy. Neither gliadin nor swainsonine when given alone had significant effects on enterocytic enzyme activities or enterocytic morphology. Binding of enterocytic glycoproteins to both gliadin-Sepharose and concanavalin A-Sepharose was significantly increased in rats treated with swainsonine. Because swainsonine causes the formation of hybrid-type oligosaccharides with a high binding affinity to mannose-specific lectins, the observed alterations of enterocytic maturation and morphology are presumably caused by the increased binding of gliadin to enterocytic glycoproteins. A possible analogy in the etiology of celiac disease is discussed.

Alkaline Phosphatase↗
PubMed1988

EDTA affects cytochrome P450-dependent biotransformation reactions during incubations for the liver microsomal assay.

In order to optimize the condition of the liver microsomal assay (LMA), studies were carried out to determine the effects of EDTA on mixed-function oxidase activity and its stability under the exact incubation conditions for the LMA. Aminopyrine N-demethylase (APD) and p-nitroanisole O-demethylase (p-NAD) activities as well as lipid peroxidation development (LP) in S9 liver fractions from beta-naphthoflavone and sodium phenobarbital (beta-NF + PB)- or Aroclor 1254 (AC)-treated mice were examined during a period of preincubation with EDTA ranging from 1 to 40 mM. At 5 mM EDTA, we obtained a strong inhibition of the microsomal LP as well as the greatest value of the mean specific activity (Asp) for both APD and pNAD activities. In agreement with the biochemical data, the presence of 5 mM EDTA in the incubation mixtures for the LMA significantly increased the mitotic gene conversion, mitotic crossing-over and point-reverse mutation of the well-known premutagen cyclophosphamide (30 mM) on the diploid D7 strain of Saccharomyces cerevisiae as the outcome of a greater metabolic activity. We concluded that the systematic use of 5 mM EDTA in LMA mixtures could improve the reliability and sensitivity of such a test.

Aminopyrine N-Demethylase↗
PubMed1988

Prevalence of Eimeria leuckarti (Flesch, 1883) and intensity of faecal oocyst output in a herd of horses during a summer grazing season.

The prevalence of Eimeria leuckarti infection and the intensity of faecal oocyst output were determined in a herd of 14 mares and their foals in northwest Germany using a sedimentation technique at weekly intervals during a summer grazing season from May to September. None of the mares, but all foals shed oocysts on at least one occasion. The patent periods lasted up to 16 weeks. The mean intensity of oocyst output (0.1-33 o.p.g.) was very low. No clinical signs of gastrointestinal disorder were noticed in any of the foals during this study.

Animals↗
PubMed1988

Role of cGMP as second messenger of adenosine in the inhibition of renin release.

Adenosine is known to be a potent inhibitor of renin release from the kidneys. The aim of this study was to investigate the transmembrane signalling avenue that the second messenger of adenosine causes inhibition of renal renin release. Using short term cultures of juxtaglomerular cells isolated from rat kidneys, we found that adenosine inhibited spontaneous renin release from these cells up to 40% of control, in a dose dependent fashion between 10(-10) M to 10(-6) M. Half maximal inhibition was observed at 2 X 10(-8) M adenosine. The inhibitory effect of adenosine on renin release could be mimicked by the A1-receptor agonist N6-cyclohexyladenosine (CHA) and could be attenuated by the A-receptor antagonist theophylline (5 X 10(-5) M). The A2-receptor agonist 5'-N-ethylcarboxamideadenosine (NECA) had no inhibitory effect on renin release. These findings indicate that the inhibitory effect of adenosine is mediated by A1-receptors on juxtaglomerular cells. Adenosine had no effect on either transmembrane calcium influx or the cytosolic free calcium concentration in the isolated juxtaglomerular cells. Adenosine also did not alter the cellular level of cyclic AMP in the concentration range employed. However, adenosine led to a dose dependent increase of the cellular level of cyclic GMP. Half maximal increase of cGMP was observed at 10(-8) M adenosine. The effect of adenosine on cyclic GMP could be mimicked by the A1-receptor agonist CHA and could be attenuated by the A-receptor antagonist, theophylline.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1988

Insulin-like growth factor I stimulates erythropoiesis in hypophysectomized rats.

Stimulation of erythropoiesis during growth is necessary to ensure proportionality between erythrocyte mass and body mass. However, the way by which erythrocyte formation is adapted to body growth is still unknown. Growth arrest in hypophysectomized rats is accompanied by decreased erythropoiesis. We have, therefore, examined whether insulin-like growth factor I (IGF-I), the mediator of growth hormone effects on body growth, is able to restore erythropoiesis in these animals. Subcutaneous infusions of 120 micrograms of recombinant human IGF-I per day in hypophysectomized rats led to increases in body weight, 59Fe incorporation into erythrocytes, and the number of reticulocytes that were similar to increases caused by infusions of 28 milliunits of human growth hormone per day. Body weight gain and 59Fe incorporation were linearly correlated. Like growth hormone, IGF-I also caused a significant rise in serum erythropoietin concentrations. However, the stimulatory effect on erythropoiesis occurred before serum erythropoietin levels had risen. These results demonstrate that IGF-I mediates the stimulatory effect of growth hormone on erythropoiesis in vivo and thus further support the somatomedin concept. They also show that IGF-I can stimulate erythropoiesis in an endocrine manner, and they suggest two possible routes of action: a direct one and an indirect one by means of enhanced erythropoietin production.

Animals↗
PubMed1988

[Capsular lesions in extracapsular cataract operation and implantation of posterior chamber lenses].

The present paper reports follow-up findings up to five years postoperatively in 41 cases following capsular-zonular rupture with implantation of a posterior chamber lens after extracapsular cataract extraction. Capsular disruption occurred most frequently (in 32 cases) during cortical aspiration. The capsular defects were localized in the periphery in 18 cases and in the central area in ten. Dialysis of the zonular fibers was seen in 13 cases. The intraocular lens (IOL) was well centered in 30 eyes and slightly off-center in seven. Only two cases with decentered IOLS required surgical centering of the lenses. In two eyes dislocation of the IOL into the vitreous was observed. Cystoid macular edema developed in two cases. In five cases retinal detachment occurred.

Cataract Extraction↗
PubMed1987

Different effects of phorbol ester on angiotensin II- and stable GTP analogue-induced activation of polyphosphoinositide phosphodiesterase in membranes isolated from rat renal mesangial cells.

Pretreatment with pertussis toxin inhibits angiotensin II-induced activation of polyphosphoinositide phosphodiesterase in rat renal mesangial cells [Pfeilschifter & Bauer (1986) Biochem. J. 236, 289-294]. Furthermore, activation of protein kinase C by the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) and by 1-oleoyl-2-acetylglycerol (OAG) abolishes angiotensin II-induced formation of inositol trisphosphate (IP3) in mesangial cells [Pfeilschifter (1986) FEBS Lett. 203, 262-266]. Using membrane preparations of [3H]inositol-labelled mesangial cells we tried to obtain further insight as to the step at which protein kinase C might interfere with the signal transduction mechanism in mesangial cells. Angiotensin II (100 nM) stimulates IP3 formation from membrane preparations of [3H]inositol-labelled mesangial cells with a half-maximal potency of 1.1 nM. The angiotensin II-induced formation of IP3 is enhanced by GTP. This effect of angiotensin II is completely blocked by the competitive antagonist [Sar1,Ala8]angiotensin II. Guanosine 5'-[gamma-thio]triphosphate (GTP gamma S) and guanosine 5'-[beta gamma-imido]triphosphate (Gpp[NH]p), non-hydrolysable analogues of GTP, stimulate IP3 production in the absence of angiotensin II with Kd values of 0.19 microM and 2.4 microM, respectively. Angiotensin II augments the increase in IP3 formation induced by GTP gamma S. However, when mesangial cells were pretreated with TPA there was a dose-dependent inhibition of the synergistic action of angiotensin II on GTP gamma S-induced IP3 production. Comparable results are obtained with OAG, while the non-tumour-promoting phorbol ester 4 alpha-phorbol 12,13-didecanoate is without effect. These results suggest that activation of protein kinase C in mesangial cells does not impair phosphoinositide hydrolysis by stable GTP analogues but somehow seems to interfere with the stimulatory interaction of the occupied angiotensin II receptor with the transducing G-protein.

Angiotensin II↗