Terpen-derivate aus Senecio-arten

Investigation of about 50 Senecio species has afforded many new substances, in addition to known compounds. Present in these plants are 23 fura     

Single cellular origin of somatostatin and calcitonin in the rat thyroid gland

Summary Immunostaining of thin serial paraffin sections has shown that somatostatin is present in the same parafollicular cells as calcitonin in the adult rat thyroid gland. The number of cells containing both peptides is much smaller than the number containing calcitonin but not somatostatin.     

Compact Escherichia coli nucleoids in a highly supercoiled conformation.

Escherichia coli nucleoids were visualized in a compact, highly supercoiled conformation at 1 M NaCl. After the salt concentration was lowered to 0.15 M NaCl, the nucleoids uncoiled in beaded fibers in which RNA-mediated structural domains could be distinguished.     

BRAIN pH MEASUREMENTS USING A DIFFUSIBLE, LIPID SOLUBLE pH SENSITIVE FLUORESCENT INDICATOR

Brain tissue pH was measured in cats at normocapnia hypocapnia, hypercapnia, and death from anoxia using a pH sensitive fluorescent indicator (umbelliferone) with both molecular and ionic fluorophors. A ratio analysis of the indicator's calibrated 450 nm fluorescent tissue washout curves from 340 and 370 nm excitation permitted direct determinations using a nomogram. Possible errors in these measurements related to differential quenching, absorption, and changes in the redox state of the indicator were investigated in vitro and in vivo for brain tissue and blood. In animals with preserved autoregulation, brain pH varied linearly with arterial pH (art pH 7.0, brain pH 6.98: art pH 7.4, brain pH 7.24). Brain pH at death fell to 6.68. An analysis of the indicator clearance curves suggests these measurements reflect a component of the intracellular space and the lipid solubility of the indicator suggests this is a membranous component.     

Reduction methods for logical control networks

In this paper some earlier stated theorems on logical control networks are proved. It is proved that a cascade of elements is equivalent to a single positive or negative element with N, number of negative elements, respectively even or odd. A loop of elements may show a cyclic behaviour with N odd or may show two possible stationary states with N even. A grafted cascade on a loop destroys the typical behaviour of the loop if the cascade is a negative chain grafted with an AND or a positive chain grafted with an OR connection; the system then admits only one stable state. Grafting a negative chain with an OR or a positive chain with an AND connection leaves the general behaviour of the loop unaffected. The detailed behaviour of two interconnected loops is extensively described. Finally it is indicated that although a complex network can be formalized as a reduced graph, its topological properties cannot always predict the final possible behaviour.     

Cross inhibition models for the transmission of hormonal signals.

Implications of a model where the formation of two mediators interacting through cross inhibition is stimulated by the same hormone or by two specific hormones are analyzed at steady'state, first in the case where no co-operative processes are involved, secondly in the case where one of the inhibitory branches presents positive co-operativity characteristics. The possible occurrence of agonist concentration-mediators response curves with extrema of opposite type, multiple steady states, hysteresis and discontinuous transitions from one functional program to another is demonstrated. When steady-state hormonal levels fluctuate, it is shown that the cross inhibitory mediators may induce a strict temporal organization of the intracellular processes and result in both amplification and frequency multiplication of the fluctuations.     

β-endorphin-induced increase in striatal dopamine turnover

Human β-endorphin administered intracisternally in a dose of 15 μg per rat increased striatal concentrations of the dopamine metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) as well as producing catalepsy. These effects were inhibited by naloxone. Pargyline-induced decreases in striatal DOPAC and HVA were greater in endorphin-treated than in saline-treated animals, supporting the concept that β-endorphin increases striatal dopamine turnover. β-endorphin increased the rate of decline in striatal dopamine concentration following synthesis inhibition with α-methyltyrosine, further suggesting that endorphin increases striatal dopamine turnover. β-endorphin and probenecid interacted competitively to decrease the effects of each other to increase striatal HVA. Naloxone prevented the effect of endorphin to decrease the HVA response to probenecid. Thus, probenecid cannot be used to assess the effects of endorphin on striatal dopamine turnover. If β-endorphin acts presynaptically to decrease dopamine release in striatum, the increases in striatal DOPAC and HVA probably represent a compensatory attempt to increase dopamine synthesis. Although turnover of dopamine to its metabolites is increased, dopamine release may be suppressed by β-endorphin.     

Effects of β-endorphin on brain serotonin metabolism

Human β-endorphin (15 μg) administered intracisternally increased concentrations of serotonin (5HT) and its metabolite, 5-hydroxyindoleacetic. acid (5-HIAA), in brain stem and hypothalamus and decreased 5-HIAA concentrations in hippocampus. These data are compatible with the hypothesis that β-endorphin increases 5HT turnover in brain stem and hypothalamus and decreases 5HT turnover in hippocampus. β-endorphin increased in brain stem and hypothalamus and decreased in hippocampus the rate of pargyline-induced decline of 5-HIAA. β-endorphin decreased the rate of pargyline-induced accumulation of 5HT in all these brain regions. The probenecid-induced accumulation of 5-HIAA in brain stem was decreased by β-endorphin. These data are compatible with the hypothesis that β-endorphin increases release of 5HT from neurons in brain stem and hypothalamus and decreases release of 5HT from neurons in hippocampus. The data require further a hypothesis that β-endorphin either decreases 5HT reuptake in these three brain regions or increases 5-HIAA egress from brain.