Biomedical subjects
Publications and source records attributed to C Bauer.
A case of erysipelas-like symptoms in a 26-year-old female student of medicine having returned from Nicaragua to Germany is reported. On the removal of the scurf covering the supposed entrance of the erysipelas, a larva of Dermatobia hominis, the human bot fly, was extracted from the head skin, and the inflammation completely disappeared within a short period of time.
Incubation of rat renal mesangial cells with angiotensin II (0.1 microM) resulted in transient breakdown of phosphatidylinositol 4,5-bisphosphate, rapid generation of diacylglycerol and phosphatidic acid, increased 45Ca2+ influx, increased intracellular [Ca2+] as measured by quin 2, and increased prostaglandin E2 synthesis. All of these processes were markedly inhibited time- and dose-dependently by prior exposure of cells to pertussis toxin. In contrast, the effects of the ionophore A23187 on 45Ca2+ influx and prostaglandin E2 synthesis were not altered by the exposure of the cells to pertussis toxin. The action of the toxin was not associated with alterations in cellular concentrations of cyclic AMP. Incubation of membrane fraction of mesangial cells with pertussis toxin resulted in ADP-ribosylation of Mr-42,000 protein. From all these results, it is likely that a G protein is involved in receptor-mediated signal transduction in renal mesangial cells.
It was the aim of the present study to find out if a common mechanism exists by which the vasoconstrictive hormones angiotension II, noradrenaline and 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (AGEPC) increase prostaglandin E2 (PGE2) synthesis in cultures of rat renal mesangial cells. Angiotension II, noradrenaline and AGEPC stimulated PGE2 synthesis and uptake of 45Ca2+ in cultured mesangial cells. Both of these effects could be completely suppressed by the calcium channel blocker verapamil. Angiotensin II, noradrenaline and AGEPC caused a rapid breakdown of phosphatidylinositol 4,5-bisphosphate with a concomitant increase of 1,2-diacylglycerol and inositol trisphosphate, indicating an activation of phospholipase C by these hormones. Addition of verapamil had no effect on the hormone-induced stimulation of phospholipase C. The synthetic analogue of diacylglycerol, 1-oleoyl-2-acetylglycerol, and the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA), both of which are known to stimulate protein kinase C, enhanced PGE2 synthesis. Chelation of extracellular calcium with EDTA or addition of verapamil abolished the effect of 1-oleoyl-2-acetylglycerol and phorbol ester on PGE2 synthesis. 1-Oleoyl-2-acetylglycerol and phorbol ester increased the uptake of 45Ca2+ by the cells in a dose-dependent manner and this effect could be blocked by verapamil. The entirety of these data leads us to suggest that vasoconstrictor-evoked synthesis of PGE2 in rat mesangial cells is mediated by the subsequent activation of phospholipase C and protein kinase C. The activation of protein kinase C by diacylglycerol is likely to be involved in the increase of the calcium permeability of the plasma membrane which is a prerequisite for PGE2 synthesis induced by vasoconstrictive hormones.
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The prevalence of benzimidazole-resistant small strongyles was determined in a survey, conducted on 14 thoroughbred studs, which compared the faecal egg counts of groups of horses before and after treatment with the recommended doses of cambendazole (20 mg kg-1 b.w.) or febantel (6 mg kg-1 b.w.). Benzimidazole-resistant cyathostomes were found on all farms examined. Pyrantel pamoate (19 mg kg-1 b.w.), oxibendazole (10 mg kg-1 b.w.) and ivermectin (0.2 mg kg-1 b.w.) reduced the strongyle egg counts on these studs by 97-100% at 2 weeks post-treatment. However, 6 weeks after dosing the reduction of the strongyle egg output had decreased to an average of 67.8% (8.7-97.1%) with pyrantel pamoate and 51.2% (0-95.8%) with oxibendazole, whereas ivermectin still suppressed the egg counts by 98.2% (95-100%).
We have examined the effect of a synthetic analogue of human alpha-atrial natriuretic peptide (ANP), APII, on renin release in cultured renal juxtaglomerular cells (JGA cells). Using cell cultures containing 80-90% renal juxtaglomerular cells, we found that ANP (10(-13)-10(-9) M) strongly inhibited renin release from the cells in a dose-dependent fashion (ki, 10 pM) to about 10% of control. Inhibition of renin release by ANP was paralleled by an increase in cellular cGMP levels; while in the presence of the cGMP-phosphodiesterase inhibitor M&B 22948 (1 mM), concentrations of ANP lower by a factor of 100 were required to obtain the same effects on renin release and cGMP levels. The guanylate cyclase inhibitor methylene blue (10 microM), on the other hand, shifted the dose-response curves for renin release and cGMP levels to 100-fold higher concentrations of ANP. Neither the influx of 45Ca into the cells nor the intracellular quin-2 signal, which is a measure for changes of intracellular Ca concentration, was in any way altered by ANP. Our results suggest that ANP inhibits renin release from juxtaglomerular cells by a cGMP-dependent process that does not involve changes in intracellular calcium.
It was the aim of the present study to get insight into some of the intracellular mechanisms by which the vasoconstrictor hormones angiotensin II (ANG II), arginine vasopressin (AVP), and norepinephrine (NE) inhibit renin release from renal juxtaglomerular cells. To this end a primary cell culture from rat renal cortex was established that consisted of 50% juxtaglomerular cells. The cultured juxtaglomerular cells contained prominent renin granules closely resembling those in the intact kidney and responded to a number of stimuli of renin release. By using these cultures, we found that ANG II (10(-7) M), AVP (10(-6) M), and NE (10(-5) M) inhibited renin release and increased the calcium permeability of the plasma membrane of the cultured cells. Both the effects on renin release and on calcium permeability could be diminished or even be abolished by the calcium channel blocker verapamil (Vp) (10(-5) M). ANG II, AVP, and NE led to an increased formation of diacylglycerol (DAG), a well-known stimulator of protein kinase C (PKC). Moreover, a direct stimulation of PKC by 12-O-tetradecanoylphorbol-13-acetate (TPA) (10(-8)-10(-6) M) also inhibited renin release and increased the calcium permeability of the cell membrane. Similar to ANG II, AVP, and NE, the effects of TPA on calcium permeability and renin release could be diminished by Vp. In conclusion, these results point toward a common mechanism by which vasoconstrictors inhibit renin release from renal juxtaglomerular cells: ANG II, AVP, and NE activate a phospholipase C, which generates DAG.(ABSTRACT TRUNCATED AT 250 WORDS)
Prostaglandins (PGs) can modulate a variety of renal functions, including Na+ and Cl- reabsorption. However, it is not known if a direct interdependence exists between PG synthesis and transport activity. The present study was done to find out whether or not the rate of NaCl transport has an influence on PG synthesis in renal tubular cells. For our studies we used cultures of so-called high-resistance MDCK cells, which were originally derived from canine kidney. This cell type has a loop diuretic- and ouabain-sensitive NaCl transport that can be enhanced by activation of the adenylate cyclase (AC). In MDCK cell cultures we found that each state of increased NaCl transport during stimulation of AC by either epinephrine (10(-6) M), isoprenaline (10(-5) M), or forskolin (10(-5) M) was accompanied by a twofold increase in PG release. During inhibition of NaCl transport by furosemide (10(-4) M) or ouabain (2 X 10(-4) M), stimulation of AC failed to increase PGE2 release, whereas basal PG production was not inhibited by either furosemide or ouabain. Furthermore, PG formation during activation of AC was dependent on the concentration of extracellular Na+, whereas PG formation in the absence of activators of AC was independent of extracellular Na+. These results suggest that increased NaCl transport stimulates PG formation in cultures of high-resistance MDCK cells.
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This study was done to investigate aspects of control of extrarenal erythropoietin (Ep) production. To this end we studied the effects of three stimuli of renal Ep production in the adult, i.e. hypoxia, cobalt, and activation of adenylate cyclase on Ep generation by cultured fetal mouse liver cells. The fetal liver was taken as a model for extrarenal Ep production because this organ is considered the predominant site of extrarenal Ep production. We found that Ep production by the cells increased as the oxygen concentration was decreased in the incubation atmosphere from 20% to 1%. Cobalt (10(-4)-10(-5) M) had no effect on Ep production. Activation of adenylate cyclase by forskolin (10(-5) M) or isoproterenol (10(-5) M) greatly enhanced Ep production. These findings indicate that the Ep-stimulating effect of cobalt is specific for the kidney. However, oxygen depletion and activation of adenylate cyclase seem to be more general stimuli in Ep-producing cells. Furthermore we found that Ep production in hypoxia correlated with lactate formation in the cultured liver cells. This finding suggests that Ep production in fetal livers under hypoxic conditions parallels the shift from aerobic to anaerobic cellular energy metabolism.
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We examined the effect of synthetic atrial natriuretic peptide (ANP) on unstimulated renin release from rat renal juxtaglomerular cells. Using renal cortical cell cultures containing 80-90% juxtaglomerular cells, we found that ANP strongly inhibited renin release from the cells in a dose-dependent fashion. Half-maximal inhibition was observed at 10(-11) mol/l ANP. Furthermore, ANP produced a rise in the intracellular concentration of cyclic guanosine monophosphate (cGMP) and a fall in the concentration of cyclic adenosine monophosphate (cAMP). Data indicated that the inhibition of renin release by ANP was related to the rise in cGMP and not to the fall of cAMP. Atrial natriuretic peptide (10(-10) mol/l) had no influence on the transmembrane calcium influx nor did it alter the intracellular calcium concentration of the juxtaglomerular cell. We found, however, that the inhibitory effect of ANP on renin release could be attenuated by the calcium channel blocker verapamil. Our results suggest that ANP inhibits renin release from juxtaglomerular cells by a mechanism that is mediated by cGMP; the mechanism is not linked to any alteration in intracellular calcium concentration but requires a normal level of calcium.
Acetylglyceryl ether phosphorylcholine (AGEPC), commonly known as platelet activating factor, was found to strongly inhibit renin secretion in cultures rich in juxtaglomerular cells. This inhibitory action of AGEPC was accompanied by an enhanced calcium permeability of the cell membrane as evaluated from measurements of the uptake of 45Ca. Simultaneous addition of the calcium channel blocker verapamil abolished the effects of AGEPC on both renin secretion and calcium permeability. Furthermore, addition of AGEPC to the cell cultures led to a decrease of 32P-labeled phosphatidylinositol 4,5-bisphosphate and to an increase in 3H-labeled diacylglycerol, indicating an activation of phospholipase C by AGEPC.
The volatile acids extracted by pentane/dichloromethane (2 + 1) from tropical fruit pulps were identified and determined by capillary gas chromatography (HRGC) and combined capillary gas chromatography-mass spectrometry using EI- and CI mode (HRGC-EI/CIMS). In cherimoya (A. cherimolia, Mill.) fruit pulp 47 acids were characterized; major compounds were hexanoic (3 mg/kg) and octanoic (1 mg/kg) acid. Fifty one acids were identified in guava (P. guajava, L.), 54 in mango (M, indica, L., var. Alphonso) and 56 in papaya (C. papaya, L.). (E)-cinnamoic acid (0.4 mg/kg) and (Z)-3-hexenoic acid (0.2 mg/kg) were determined as major constituents in guava; in mango 5-hydroxy-(Z)-7-decenoic acid (2 mg/kg) and 3-hydroxyoctanoic acid (1.1 mg/kg) and in papaya pulp butanoic acid (1.2 mg/kg) were established as major constituents.
Altogether 30 different sugar analogues have been tested in a cell free system from rat liver or, in part, in freshly prepared hepatocytes. It is our aim to find suitable compounds which are able either to interfere with the metabolization of L-fucose, galactose and N-acetylmannosamine or, alternatively, to block the attachment of these sugars to the nascent oligosaccharide chain. 1-Methylfucoside inhibits the fucokinase by a competitive mode (Ki = 1.1 mmol/l). Both the fucokinase and fucose-1-phosphate pyrophosphorylase activity are impaired by Clobenoside, a chloro-containing glucofuranoside (Ki values between 5 to 10 mmol/l). In hepatocytes this inhibition leads to a drastic reduction of fucoprotein biosynthesis and secretion. 1-Methylenegalactose proved to be a promising competitive inhibitor of the galactokinase (Ki = 4.1 mmol/l), while the efficacy of 2-deoxy-2-fluoro-galactose and 6-deoxy-6-fluoro-galactose is less pronounced. Part of these sugar analogues could become a suitable tool in order to elucidate the biological significance of terminal and subterminal sugars.
The effect of temperature on enzymatic activity and stability was studied with respect to the monooxygenase activities of aminopyrine-N-demethylase (APD) and p-nitroanisole O-demethylase (pNAD) under incubation conditions for the liver microsomal assay. The activities of S9 liver fractions of mice induced with sodium phenobarbital and beta-naphthoflavone were determined during a period of preincubation in a range of temperatures from 30 to 44 degrees C. The greatest value of the mean specific activity was found at 40-42 degrees C for both APD and pNAD. The rapid increase of lipid peroxidation after 1 h of incubation at temperatures higher than 42 degrees C can provide an explanation of the enhancement of the rate of inactivation. In order to determine whether biological response is affected by the modifications induced by temperature in the metabolic activating system, tester strain D7 of Saccharomyces cerevisiae was used to assay the genetic activity of the well known premutagenic agent cyclophosphamide by incubating the mixtures both at the traditional temperature of 37 degrees C and at 42 degrees C. We suggest that the use of more favourable conditions for LMA with respect to enzymatic activity, than the traditional ones could improve the reliability and the sensitivity of such tests.
The proliferation of epithelial cells in colonic mucosa was studied in humans at varying degrees of risk for colon cancer. Seventh-Day Adventist vegetarians, known to have significantly lower mortality from colon cancer than the general U.S. population, had the most quiescent proliferative activity of mucosal epithelial cells. Increased replication and expansion of the proliferative compartment accompanied increased colon cancer risk. The analytical methods of this study may be useful in assessing the influence of dietary components involved in the initiation, promotion or inhibition of colon cancer, and in developing strategies for nutritional intervention.
In view of recent findings which suggest that renal prostaglandins mediate the effect of hypoxia on erythropoietin production, we have studied whether hypoxia is a stimulus for in vitro prostaglandin synthesis. Studies were carried out in rat renal mesangial cell cultures which produce erythropoietin in an oxygen-dependent manner. Production rates of PGE2 and in specified samples also of 6-keto-PGF1 alpha, as a measure of PGI2, and PGF2 alpha were determined by radioimmunoassay after incubation at either 20% O2 (normoxic) or 2% O2 (hypoxic) in gas permeable dishes for 24 hrs. Considerable variation in PGE2 production was noted among independent cell lines. PGE2 production appeared to be inversely correlated to the cellular density of the cultures. In addition, PGE2 production was enhanced in hypoxic cell cultures. The mean increase was 50 to 60%. PGF2 alpha and 6-keto-PGF1 alpha increased by about the same rate. These results indicate that hypoxia is a stimulus for in vitro prostaglandin production.