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Biomedical subjects

W Meyer

Publications and source records attributed to W Meyer.

At least 289 records · Page 16Linked to original sources
PubMed1985

Inactivation of bacteria and viruses in water: passage of germicidal ultraviolet light through Teflon.

Teflon pipe as used in a water purification system transmitted germicidal ultraviolet (UV) light to inactivate Pseudomonas aeruginosa and poliovirus. The information is useful for animal care workers and others concerned with the prevention of microbial growth in water systems such as deionizers and distilled water. Of special significance is that there is a plastic that transmits UV light.

Poliovirus↗
PubMed1985

Effects of the benzimidazole derivatives pimobendan and 2-(4-hydroxy-phenyl)-5-(5-methyl-3-oxo-4,5-dihydro-2H-6- pyridazinyl) benzimidazole . HCl on phosphodiesterase activity and force of contraction in guinea-pig hearts.

The effects of pimobendan (UD-CG 115 BS) and UD-CG 212 Cl (2-(4-hydroxy-phenyl)-5-(5-methyl-3-oxo-4,5-dihydro-2H-6- pyridazinyl)benzimidazole X HCl) on force of contraction, beating frequency, and on adenylate cyclase and phosphodiesterase activity were investigated in isolated preparations from guinea-pig hearts. Both benzimidazole derivatives exerted a concentration-dependent positive inotropic effect in guinea-pig papillary muscles. The efficacies were similar to that of dihydroouabain. The positive inotropic effect of both benzimidazoles was accompanied by an enhancement of the rate of force development and a prolongation of the contraction. Both benzimidazole derivatives inhibited phosphodiesterase (PDE) activity in a crude preparation from guinea-pig ventricles. However, at the concentrations producing maximal positive inotropic effects in papillary muscles, pimobendan and UD-CG 212 Cl diminished PDE activity only by about 20-30%. Since both benzimidazoles did not affect adenylate cyclase in a particulate membrane preparation a stimulation of the cAMP synthesis can be ruled out. As recently reported for pimobendan, this study provides functional evidence that the positive inotropic effect of UD-CG 212 Cl is also at least partially mediated by cAMP. Firstly, the positive inotropic effect of UD-CG 212 Cl was inhibited by carbachol, adenosine and (-)-N6-phenyl-isopropyladenosine. Secondly, UD-CG 212 Cl potentiated the inotropic effects of isoprenaline and histamine. UD-CG 212 Cl had no positive chronotropic effect and pimobendan increased the beating frequency only slightly.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1985

Cardiac effects of adenosine and adenosine analogs in guinea-pig atrial and ventricular preparations: evidence against a role of cyclic AMP and cyclic GMP.

The effects of adenosine, the Ri site adenosine receptor agonist (-)-N6-phenylisopropyladenosine (PIA), the Ra site agonist 5'-N-ethylcarboxamideadenosine (NECA) and the P site agonist 2',5'-dideoxyadenosine (DIDA) on force of contraction, cyclic AMP (cAMP) and cyclic GMP (cGMP) content and on transmembrane action potential were studied in isolated electrically driven left auricles and papillary muscles from guinea pigs. Furthermore, the effects on adenylate cyclase activity in a particulate membrane preparation were investigated. In the auricles, adenosine, PIA and NECA had negative inotropic effects which were accompanied by a shortening of the action potential. Theophylline antagonized these effects which are likely mediated by R site adenosine receptors. DIDA was ineffective. Except for a small positive inotropic effect of adenosine the analogs were ineffective in the papillary muscles. None of the mechanical effects was accompanied by a change in cAMP and cGMP content in the intact preparations. In the broken cell preparation PIA and NECA had no effect on adenylate cyclase activity. Adenosine and DIDA inhibited the enzyme. The latter effects can be classified as P site-mediated effects. In conclusion, distinct mechanical, i.e., negative inotropic effects of adenosine and its analogs in the heart are observed in auricular preparations only. These effects are unlikely to be related to the cAMP and/or cGMP system. Instead, they are probably due to a direct shortening of the action potential which, in turn, is conceivably due to an increase in K+ outward current and a secondary decrease in Ca++ inward current. This effect is apparently mediated by cardiac R site adenosine receptors which are not detectably coupled to adenylate cyclase.

Adenosine↗
PubMed1985

Studies on tissue distribution of glutathione and on activities of glutathione-related enzymes after carbon tetrachloride-induced liver injury.

After an initial decrease following CCl4-application (1.0 ml/kg bodyweight, i.p.), in the liver of male Wistar rats, values of reduced glutathione (GSH) are at a maximum 6 and 12 h after treatment. Oxidized glutathione (GSSG) increases up to 24 h after intoxication. Malondialdehyde (MDA) is at a low level, when GSH is high. Glutathione peroxidase has a clear initial increase of activity, but otherwise shows only slight deviations from control values. Cytosolic and microsomal glutathione-S-transferases reach minimum values at 6 and 12 h, respectively. The histochemical demonstration of GSH reveals an uneven distribution in the liver lobule, with higher amounts of reaction products in the periphery. With increasing time after intoxication the typical lobular distribution pattern changes and the accumulation of GSH reaction products becomes patchy. Other parts, however, remain rather normal. 12 h after intoxication most of the hepatic lobules are relatively free of GSH, while the content of the central venules and sublobular veins is strongly stained. Lipid histochemistry shows a fat accumulation already 3 h after CCl4. Central lobular cells are particularly affected. Biochemical and histochemical results are discussed with respect to the regional differences.

Animals↗
PubMed1985

Some remarks on preinvasive cervical neoplasia--an image analysis study.

By means of automated microscope image analysis 5275 normal cells as well as dyscaryotic cells were investigated in cytologic preparations from 53 cervical smears (26 negative cases, 27 positive cases). In this way, visually not conspicuous differences between normal cell populations of positive and negative cases could be demonstrated with multivariate statistic analysis of discriminant features. The examination of this phenomenon in 2910 epithelial cells from tissue sections of portio conizations has shown that the subvisually changed epithelial cells originate from circumscript regions in the margin and surroundings of CIN-lesions. The biological role of these changes in the formal genesis of cervical neoplasias has been discussed.

Cell Differentiation↗
PubMed1984

Alpha-adrenoceptor-mediated positive inotropic effect of phenylephrine in isolated human ventricular myocardium.

In isolated human ventricular myocardium the alpha-adrenoceptor agonist phenylephrine had a positive inotropic effect in preparations from 9 of 14 patients. This effect was seen in the presence of the beta-adrenoceptor-blocking agent propranolol but was nearly abolished by the alpha-adrenoceptor blocking agent prazosin. In contrast to the beta-adrenoceptor-mediated positive inotropic effect, the effect of phenylephrine was accompanied by a prolongation of the isometric contraction. The results suggest that alpha-adrenoceptors exist in human ventricular myocardium.

Adult↗
PubMed1984

Human ballistic finger flexion: uncoupling of the three-burst pattern.

In isotonic and isometric goal-directed index finger movements made as fast as possible, the "braking hypothesis" ascribed to the antagonist burst was tested. Under isotonic conditions, the extensor burst often failed to occur in small angle movements with low inertial load. It regularly occurred, however, in small angle movements with high inertial load and in wide angle movements with both low and high inertial loads. Such features suggest, indeed, the antagonist burst as being part of braking strategies. Under isometric conditions, the antagonist burst - if it occurred - exhibited characteristics which suggested a rapidly alternating movement rather than a braking strategy.

Electromyography↗
PubMed1984

Adenosine and adenosine analogs inhibit phosphodiesterase activity in the heart.

Adenosine and its analogs (-)-N6-phenylisopropyladenosine and 5'-N-ethylcarboxamideadenosine inhibit cAMP and cGMP phosphodiesterase activity in guinea-pig atrial and ventricular preparations at concentrations of 100 mumol l-1 and higher. These effects are probably unrelated to the inotropic effects of these substances. However, inhibition of cAMP breakdown may compensate for the adenosine-induced inhibition of adenylate cyclase and may thus at least partially explain why with this drug no changes in cAMP or cGMP content have previously been observed in intact cardiac tissue.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1984

Comparative quantitative aspects of putative neurotransmitters in the central nervous system of spiders (Arachnida: Araneida).

The amounts of eight putative neurotransmitters or modulators (acetylcholine, dopamine, noradrenaline, adrenaline, GABA, taurine, glutamic acid, glycine) were determined from the CNS of 12 species of five different spider families (Theraphosidae, Agelenidae, Araneidae, Lycosidae, Salticidae). Comparatively high contents of acetylcholine and noradrenaline could be found in the CNS of hunting spiders, higher contents of GABA and taurine were visible in the web-building spider families, while extraordinarily high amounts of glutamic acid were confined to the Theraphosidae. The results obtained are compared with findings from other arthropod groups and the role of putative transmitters or modulators in the spider CNS is discussed in relation to behavioural differences within the families investigated.

Acetylcholine↗
PubMed1984

Metastasizing APUD cell tumours of the human gastrointestinal tract. Light microscopic and karyometric studies.

A total of 11 metastasizing gastrointestinal APUD cell tumours from biopsy and autopsy files were reclassified according to Soga and Tazawa as well as to WHO Histologic Classification of Tumours. The much higher proportion of APUD cell tumours in autopsies (11 cases from 1000 autopsies in comparison with 22 cases from 22 000 biopsies) demonstrate that the majority of them will not be discovered during the patient's life. EC cell carcinoids (type A) predominate in both non-metastasizing and metastasizing gastrointestinal APUD cell tumours. Metastases from EC cell carcinoids occurred only in regional lymph nodes and in the liver. The APUD cell tumours originating in the pancreas represent the most frequently metastasizing gastrointestinal carcinoids. Besides in the liver and in regional lymph nodes metastases from pancreatic APUD cell tumours were seen in the skin, the brain and the skeleton. One case with two (pancreatic, bronchial) competitive primary APUD cell tumours and a skin metastasis was studied by means of automated cell image analysis. Cell populations of these three tumour sites were characterized by morphometric and densitometric nuclear parameters. It could be demonstrated that the skin metastasis consisted of a cell population, which occurred as a subpopulation in the primary tumour of the bronchus. The results of karyometric investigations supported the hypothesis that single components of tumours can metastasis selectively.

Adolescent↗
PubMed1984

Adenosine inhibition of catecholamine-induced increase in force of contraction in guinea-pig atrial and ventricular heart preparations. Evidence against a cyclic AMP- and cyclic GMP-dependent effect.

The antagonism between adenosine and isoprenaline on force of contraction, cyclic AMP (cAMP) and cyclic GMP (cGMP) content, adenylate cyclase activity and transmembrane action potential in isolated electrically driven atrial and ventricular muscle preparations from guinea-pig hearts was investigated. In atrial preparations adenosine added 5 min after isoprenaline decreased force of contraction. Adenosine abolished completely the positive inotropic effect of isoprenaline. Similarly, adenosine prevented the positive inotropic effect of isoprenaline when both substances were added simultaneously. In ventricular preparations adenosine also decreased the isoprenaline-induced increase in force of contraction. The effect was much smaller than it was in the atria. Adenosine reduced the isoprenaline-induced increase in force of contraction only by about 60%. Adenosine did not at all influence the positive inotropic effect of isoprenaline when both substances were added simultaneously. In both preparations the isoprenaline-induced increase in cAMP content of the intact contracting preparations was not diminished by adenosine. cGMP content remained unchanged too. Adenosine inhibited adenylate cyclase activity in broken cell preparations from both tissues. In atrial preparations the decrease in force of contraction of adenosine in the presence of isoprenaline was accompanied by a shortening of the action potential duration. In ventricular preparations adenosine failed to shorten the action potential. In conclusion, the effects of adenosine to inhibit the stimulatory action of isoprenaline on myocardial force of contraction are not due to changes in the cAMP and/or cGMP content. Instead, adenosine may inhibit a step beyond an increased cAMP level, e.g., may exert an inhibition of protein kinases. However, in the atria, but not in the ventricles, an additional direct effect of adenosine on transmembrane ion currents, most likely an increase in potassium conductance, probably is of even greater importance.

Adenosine↗