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Biomedical subjects

C Bauer

Publications and source records attributed to C Bauer.

At least 91 records · Page 5Linked to original sources
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↗
PubMed1987

Efficacy of four anthelmintics against benzimidazole-resistant cyathostomes of horses.

In order to confirm benzimidazole resistance as recommended at a workshop of the Commission of the European Communities the isolate 'E' of cyathostome strongyles originating from a stud where benzimidazole resistance had been demonstrated by egg hatch tests and by egg count reduction tests was investigated in two series of critical tests. Each of 11 foals reared strongyle-free was infected with 130,000 third stage cyathostome larvae. One animal remained untreated, two pairs of foals were treated with paste formulations of the (pro)benzimidazoles cambendazole (20 mg/kg bodyweight) or febantel (6 mg/kg bodyweight) and two groups of three foals were given pastes containing the non-benzimidazole drugs pyrantel pamoate (19 mg/kg bodyweight) or ivermectin (0.2 mg/kg bodyweight) either at 101 days (trial 1) or at 59 to 62 days (trial 2) after infection. Strongyles were counted in faecal samples collected daily between treatment and post mortem examination five or seven days later and worm burdens were counted in the intestinal contents and mucosal digests. Nine species of the cyathostome subfamily were found in the infected foals. The numbers of luminal stages were reduced by only 3.1 and 20.2 (mean 7.9) per cent by cambendazole and by 13.6 and 32.8 (mean 21.3) per cent by febantel in the individual animals. However, pyrantel pamoate (93.6 to 98.2, mean 96.3 per cent reduction) and ivermectin (100 per cent reduction) were highly effective. These trials provide the first report of benzimidazole resistant Cylicostephanus poculatus anywhere in the world and demonstrate (pro)benzimidazole resistance in seven other species for the first time in Europe.

Animals↗
PubMed1987

Effect of aerobic training quantity on the VO2 max of circumpubertal swimmers.

Maximal oxygen uptake (VO2 max) was measured in 38 swimmers aged 10-14 years. Thirty of 38 boys participated in this study for at least 2 consecutive years. Group 1 consisted of 23 subjects (48 measures) who trained for 7 h/week while group 2 consisted of 15 subjects (27 measures) who trained for 14 h/week. In group 2, VO2 max normalized to body weight was significantly higher at 14 years of age than at 10, whereas the increase was nonsignificant during this period in group 1. The subjects of group 2 showed a large increase of VO2 max/kg body weight from the age of 13, which corresponded in this study to the age of peak height growth velocity. The differences between the two groups were statistically significant at both 13 (P less than 0.02) and 14 years of age (P less than 0.05). At 13 and 14, the most trained subjects also showed significantly higher (P less than 0.05) values of maximal oxygen pulse/kg body weight (VO2 max/kg/HR max). Maximal heart rate (HR max) was similar in the two groups between 10 and 14 years of age. Therefore, we conclude that an increase in a training program of the aerobic type induces a large increase in VO2 max from the age of peak height growth velocity. This is likely due to an increase in the stroke volume.

Adolescent↗
PubMed1987

Stability of drug metabolizing enzymes during the incubation conditions of the liver microsomal assay with non-induced and induced mouse liver S-9 fractions.

The purpose of this work was to study the relative activities and stabilities of phase-I and phase-II drug metabolizing enzymes in incubation mixtures used in vitro genotoxicity testing in order to optimize the conditions of the assay, increase sensitivity and eliminate false negative results. Cytochrome P-450, NADPH-cytochrome P-450 (cytochrome c) reductase activity and various phase-I and phase-II enzyme activities of the drug-metabolizing system were determined in incubation mixtures used in liver microsomal assays. The behaviour of aminopyrine N-demethylase and p-nitroanisole O-demethylase activities as phase-I markers have been reported previously. Other activities measured were glutathione S-transferase, glutathione S-epoxide transferase and epoxide hydrase, and lipid peroxidation (LP) was determined. The experiments were carried out on liver S9 fractions derived from non-induced mice or mice induced with sodium phenobarbital (PB), and/or beta-naphthoflavone (beta-NF). The phase-II enzymes were much more stable (70-90% residual activity) than phase-I enzyme activities (35-60%) in all conditions tested. The residual cytochrome P-450 was approximately 70% stable and the remaining activity of NADPH-cytochrome c-reductase about 80%, indicating that this latter enzyme does not limit the rate of the monoxygenase system in these conditions. Phase-II enzymes were induced to a smaller extent (about 2 times) than in phase-I enzymes (5-6 times) by beta-NF + PB. NADPH-cytochrome c-reductase behaved as phase-II enzymes in this respect as well as for stability. LP was appreciably higher in non-induced than in induced animals. Treatment with the beta-NF + PB mixture, however, showed that induced enzymes were more stable than those obtained by simple induction with either beta-NF or PB alone. These results lead to the conclusion that prolonged incubation times in mutagenicity assays are unnecessary when considering the relative stabilities of the various phase-I and phase-II enzyme activities in the drug-metabolizing system.

Animals↗
PubMed1987

Mechanism of NaCl transport-stimulated prostaglandin formation in MDCK cells.

Recently we have found that stimulation of NaCl transport in high-resistance MDCK cells enhances their prostaglandin formation. In the present study, we investigated the mechanisms by which prostaglandin formation could be linked to the ion transport in these cells. We found that stimulation of transport caused a transient stimulation of prostaglandin formation lasting 5-10 min. The rise in prostaglandin formation was paralleled by a rise of free intracellular arachidonic acid. Analysis of membrane lipids revealed that the rise of free arachidonic acid was paralleled by a loss of arachidonic acid from polyphosphoinositides. We failed to obtain indications for the stimulation of calcium-dependent phospholipase A2. However, we did obtain evidence that the incorporation of arachidonic acid into phospholipids was diminished during stimulation of ion transport, indicating a decreased rate of reesterification. Despite the fact that there was no significant fall in total cellular ATP on stimulation of ion transport, we found a high and transient rise of lactate production of the cells on stimulation of the ion transport indicating an alteration of the ADP/ATP ratio. Moreover, prostaglandin formation and lactate formation were linearly correlated in this situation. When glucose utilization was inhibited by mannoheptulose, the rise in lactate formation was abolished, whereas that of PG formation was unaltered, indicating that lactate formation and prostaglandin formation were not causally linked on stimulation of ion transport. Our results suggest that an increase in the rate of sodium chloride transport by MDCK cells stimulates formation by an inhibition of reesterification of free arachidonic acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1987

[Typical recurrent disease behavior of NANB hepatitis. A computer-assisted analysis].

1013 ALAT-attacks--in addition to the frequent asymptomatic onset of the disease and the high tendency of chronicity a typical symptom of the non-A, non-B hepatitis--were statistically analysed on 333 patients (of these 216 with uniform parenteral source of infection). 52% of the patients showed a multiphasic course. The aim of the analysis was the exact mathematical description of the attack-behaviour and the discovery of presumed regularities. The investigation of the periodicity of the attacks showed a maxima of spectral density corresponding to a 7-day-rhythm. The trend function of the ALAT-amplitudes in the time-course was assessed as an exponential function. Between mono- and multiphasic ALAT-courses no significant differences existed concerning the clinical picture (icteric--anicteric--subclinical), but as regards the late prognosis the multiphasic courses exhibited highly-significantly more transitions into chronic hepatitis. From the time-serial analysis of the attacks can be deduced for practical application that the reliable detection of non-A, non-B hepatitis cannot be guaranteed with weekly screenings. Screenings at 2-day-intervals which take into consideration the attack-behaviour and the ascertained time of incubation are recommended.

Alanine Transaminase↗