Über die Blutkapillaren und perivaskulären Strukturen der Area postrema des Kaninchens und über ihr Verhalten im Pentamethylentetrazol-(„Cardiazol“-)Krampf

Zusammenfassung Die sinusförmigen Kapillaren der Area postrema werden von zwei Basalmembranen umgeben, die einen Raum einschließen, in dem Makrophagen liegen. Verästelte Ausläufer der äußeren Basalmembran dringen tief zwischen die Gliafortsätze ein und bilden ein Membranlabyrinth. Das Kapillarendothel ist fenestriert. Nach Cardiazolkrampf entsteht ein perivaskuläres Oedem, das das Membranlabyrinth öffnet und den perivaskulären Raum vergrößert. Das Endothel zeigt hierbei starke Cytopempsis. Die funktionelle Bedeutung der Strukturen wird diskutiert.

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Summary The sinusoid capillaries of the area postrema are surrounded by two basement membranes enclosing a perivascular space, in which macrophages are found. Ramified extensions of the outer basement membrane penetrate deeply between the glial processes forming a labyrinth of basement membranes. The capillary endothelium is fenestrated. After a Cardiazolinduced convulsion a perivascular edema opens the basement membrane labyrinth and the perivascular space is greatly enlarged. The endothelium shows pinocytotic activity. The functional significance of these structures is discussed.

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Mit dankenswerter Unterstützung durch die Deutsche Forschungsgemeinschaft.     

Zur Frage einer intraventrikulären Neurosekretion

Zusammenfassung In der vorderen Wand des IV. Ventrikels und des Canalis centralis gegenüber der Area postrema liegen beim Kaninchen Nervenzellen, deren Fortsätze intraventrikulär mit 6 großen Protoplasmakugeln endigen, die mit Mitochondrien angefüllt sind. Das Perikaryon ist reich an Ergastoplasma, alle Teile der Zelle enthalten leere, 600 bis 1500 Å messende, und ein dichtes Granulum enthaltende, 650–1000 Å große Bläschen. Vermutlich werden Stoffe in den Liquor cerebrospinalis abgegeben. Dem Plasmalemm der Nervenzellen liegen Synapsen an.

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Summary In the anterior wall of the IVth ventricle, opposite to the area postrema, nerve cells are found. Their processes end with spheroid swellings extending into the ventricle. These bulbs contain a large number of mitochondria, while ergastoplasm is seen in the perikaryon. The cytoplasm of the whole cell shows vesicles (600–1500 Å) and dense-core vesicles (650–1000 Å) which might be extruded into the liquor cerebrospinalis. The plasmalemma of the perikaryon is in contact with synapses.

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Die Untersuchung wurde mit dankenswerter Unterstützung durch die Deutsche Forschungsgemeinschaft durchgeführt.     

Antioxidant Activity of 5-Hydroxytryptophan, 5-Hydroxyindole, and Dopa Against Microsomal Lipid Peroxidation and Its Dependence on Vitamin E

The antioxidant capacity of 5-hydroxy-tryptophan. 5-hydroxy-indole. and DOPA (3,4-dihydroxy-phenyI-alanine) was tested in the Fe-induced lipid peroxidation of liver microsomes of normal- and vitamin E-deficient rats, using ascorbate as a reductant. Lipid peroxidation was monitored as low-level chemilu-minescence, indicative of generation of electronically-excited states arising from the recombination of secondary lipid peroxyl radicals.     

Chemiluminescent oxidation of ribose catalyzed by horseradish peroxidase in presence of hydrogen peroxide

The reaction of ribose with horseradish peroxidase in the presence of H₂O₂ is accompanied by light emission. The detection of horseradish peroxidase Compound II (FeO²⁺) indicates that the enzyme participates in a normal peroxidatic cycle. Hydrogen peroxide converts horseradish peroxidase into Compound I (FeO³⁺) which in turn is converted into Compound II by abstracting a hydrogen atom from ribose forming a ribosyl radical. In aerated solutions oxygen rapidly adds to the ribosyl radical. Based on the spectral characteristics and the enhancement of the chemiluminescence by chlorophyll-a, xanthene dyes, D₂O and DABCO, it is suggested that the excited species, apparently triplet carbonyls and ¹O₂, are formed from the bimolecular decay of the peroxyl radicals via the Russell mechanism.     

Clinical and biochemical studies in three patients with severe early infantile Cockayne syndrome

Summary We present clinical and biochemical data from three patients with severe Cockayne syndrome (CS) of very early onset. Unlike in classic CS, signs became evident in the first weeks of life and led to unusually early death. Fibroblasts from two of the patients showed a complete defect of the repair of UV-induced thymine dimer lesions. They were unable to remove thymine dimer lesions from their DNA, had a severe reduction of the RNA synthesis rates after UV irradiation, and showed no reactivation of an UV-inactivated indicator gene and no DNA recondensation after UV irradiation. DNA repair investigated in these two fibroblast cell strains resembled that of xeroderma pigmentosum cells of complementation group A. In contrast, fibroblasts from the third patient showed the same in vitro repair characteristics as classic CS cells.     

Fetal cells in maternal blood: recovery by charge flow separation

Fetal blood cells can be recovered from the maternal circulation by charge flow separation (CFS), a method that obviates the risks associated with amniocentesis and chorionic villus sampling. By CFS, we processed blood samples from 13 women carrying male fetuses, 2 carrying fetuses with trisomy 21, and 1 who had delivered a stillborn infant with trisomy 18. On average more than 2000 fetal nucleated red blood cells were recovered per 20-ml sample of maternal blood. Recovery of fetal cells was confirmed by fluorescence in situ hybridization with probes for chromosomes Y, 18 and 21. After culturing of CFS-processed cells, amplification by the polymerase chain reaction revealed Y-chromosomal DNA in clones from four of six women bearing male fetuses, but not in clones from three women bearing female fetuses. Received: 8 January 1996 / Revised: 22 March 1996     

Bicyclic carbo- and heterocycles from an allylidene complex and cyclic 1,3-dienes by tandem cyclopropanation/cope rearrangement

The allylidene complex (CO)₅W=CH---C(Ph)=C(Ph)H (4) reacts with cyclopentadiene by stereospecific transfer of the carbene ligand to one of the two double bonds of cyclopentadiene to give a cis-divinylcyclopropane complex 5. The divinylcyclopropane ligand coordinates to the metal via the unsubstituted double bond. Addition of bromide to solutions of 5 gives rise to the formation of [(CO)₅WBr]⁻ and a bicyclo[3.2.1]octadiene (6), the Cope rearrangement product of the free divinylcyclopropane. Thermolysis of 5 affords 6 and its (CO)₅W complex. The reaction of 4 with furan (8a), 2-methylfuran (8b) and 3-methylfuran (8c) affords the (CO)₅W(bicyclo[3.2.1]oxahepta- diene) complexes (9a–c), The formation of 9a–c which is chemo-, regio- and stereospecific is explained by a tandem cyclopropanation/Cope rearrangement sequence. The bicyclic ligands 10a–c are liberated from the metal either by thermolysis of solutions of 9a–c or by addition of bromide.     

α2-Adrenoceptor-Mediated Inhibition of Electrically Evoked [3H]Noradrenaline Release from Chick Sympathetic Neurons: Role of Cyclic AMP

Abstract: This study explores the role of cyclic AMP in electrically evoked [³H]noradrenaline release and in the α₂-adrenergic modulation of this release in chick sympathetic neurons. Along with an increase in stimulation-evoked tritium overflow, applications of forskolin enhanced the formation of intracellular cyclic AMP. Both effects of forskolin were potentiated by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine. The forskolin-induced increase in overflow was abolished by the Rp-diastereomer of cyclic AMP-thioate, an antagonist at cyclic AMP-dependent protein kinases, and 1,9-dideoxy-forskolin, an inactive analogue at adenylyl cyclase, had no effect on the evoked overflow. A 24-h pretreatment with either cholera toxin or forskolin reduced the subsequent forskolin-induced accumulation of cyclic AMP and inhibited the stimulation-evoked release. Basal cyclic AMP production, however, remained unaltered after forskolin treatment and was enhanced after 24 h of cholera toxin exposure. The α₂-adrenergic agonist bromoxidine did not affect the formation of cyclic AMP stimulated by forskolin but reduced electrically evoked release. However, effects of bromoxidine on ³H overflow were attenuated by forskolin as well as by 8-bromo-cyclic AMP. Effects of bromoxidine on [³H]noradrenaline release were paralleled by an inhibition of voltage-activated Ca²⁺ currents, primarily through a delayed time course of current activation. This effect was abolished when either forskolin or 8-bromo-cyclic AMP was included in the pipette solution. Both substances, however, failed to affect Ca²⁺ currents in the absence of bromoxidine. These results suggest that the signaling cascade of the α₂-adrenergic inhibition of noradrenaline release involves voltage-activated Ca²⁺ channels but not cyclic AMP. Elevated levels of cyclic AMP, however, antagonize this α₂-adrenergic reduction, apparently through a disinhibition of Ca²⁺ channels.