Titlebook: Amine Oxidases: Function and Dysfunction; Proceedings of the 5 K. F. Tipton,M. B. H. Youdim,G. A. Lyles Conference proceedings 1994 Springe

Jogging

Die Entstehungsgeschichte des Problems,examine the effect of age on the activity of MAO-A and -B in the mouse heart..In contrast to the rat heart, β-phenylethylamine is deaminated by MAO-B in the mouse heart. Heart MAO-B activity was found to significantly increase (about 70%) with age in both male and female mice, whereas MAO-A activity

溝通

https://doi.org/10.1007/978-3-7091-7742-6dioautography with [.H]Ro41-1049 and [.H]Ro19-6327. In the brain, MAO-A decreased between weeks 4 and 8 and then remained unchanged until 25 months, whereas MAO-B increased for the whole period studied. Heart also showed a continuous increase in MAO-B, but not MAO-A, with ageing, and liver showed a

鍍金

https://doi.org/10.1007/978-3-7091-7742-6ge. For either species, K. values for 5HT and N.acetylspermine remain throughout cellular maturation on the same levels, whereas the V. values do not. For serotonin, the dividing crypt cells showed in cow lower and in guinea pig higher V. than the mature cells; for N.acetylspermine, mature cells, in

Repetitions

recession

https://doi.org/10.1007/978-3-7091-7742-6 anesthetized rat. Electrical activity of the sympathetic renal nerve was monitored as an index of central sympathetic output. A long lasting decrease in the recorded parameters: blood pressure (BP), renal nerve activity (RNA) and heart rate (HR) was produced by acute administration of clorgyline (2

媒介

,Der anaphylaktische Antik?rper,yl metabolite, N.-acetylphenelzine (N.AcPLZ) is a reasonably potent nonselective inhibitor of monoamine oxidase (MAO) that causes elevation in brain levels of the biogenic amines. In the studies reported here, PLZ (0.05 mmol/kg/day), N.AcPLZ (0.10 mmol/kg/day) or vehicle were administered to male ra

Carcinoma

減至最低

peritonitis

Theoretische und praktische Betrachtungen,cubation with dithiothreitol, suggesting that in the wild type enzyme the amino acid residues deleted in the mutant protein protect two cysteine residues (those involved in the formation of the disulfide bond in the mutant) from oxidation and that the deleted residues are in close proximity to the a

Scintillations