Über die Polymerisation des Isobutylens durch Aluminiumjodid in Anwesenheit einiger Alkylhalogenide

An investigation was made on the effect of some n-alkyl halides (n-butyl fluoride, n-butyl chloride, and n-butyl bromide) and some benzyl halides (benzyl fluoride, benzyl chloride, and benzyl bromide) on the polymerization of isobutene in heptane, catalyzed by aluminium iodide. It was found that n-butyl fluoride and benzyl halides raise the rate of polymerization considerably. It was also established, from the dependence of the rate of polymerization and of the molecular weights on the concentration of alkyl halides and aluminium iodide, that alkyl halides do not act as cocatalysts, but that the increase in the rate of polymerization is due to the formation of catalytically active products of halogen exchange between aluminium iodide and alkyl halides. The results are discussed in terms of our present knowledge concerning the polymerization of isobutene with catalytic systems consisting of two FRIEDEL-CRAFTS halides.     

Partial purification and characterization of anhydrotetracycline oxygenase of Streptomyces aureofaciens

Anhydrotetracycline oxygenase was purified both by affinity chromatography and by hydrophobic interaction chromatography. Molecular weight of anhydrotetracycline oxygenase was determined to be 115,000 by Sephadex G-200 gel filtration. Using preparative isoelectric focusing the isoelectric point of the enzyme was estimated to be 5.3. The enzyme showed a sensitivity to thiol-specific inhibitors. During the hydrophobic interaction purification step, the activity dropped considerably. Reactivation occurred when a heat treated crude extract was added to the reaction mixture.     

Properties of visual evoked potentials to onset of movement on a television screen

In 80 subjects the dependence of movement-onset visual evoked potentials on some measures of stimulation was examined, and these responses were compared with pattern-reversal visual evoked potentials to verify the effectiveness of pattern movement application for visual evoked potential acquisition. Horizontally moving vertical gratings were generated on a television screen. The typical movement-onset reactions were characterized by one marked negative peak only, with a peak time between 140 and 200ms. In all subjects the sufficient stimulus duration for acquisition of movement-onset-related visual evoked potentials was 100ms; in some cases it was only 20ms. Higher velocity (5.6°/s) produced higher amplitudes of movement-onset visual evoked potentials than did the lower velocity (2.8°/s). In 80% of subjects, the more distinct reactions were found in the leads from lateral occipital areas (in 60% from the right hemisphere), with no correlation to handedness of subjects. Unlike pattern-reversal visual evoked potentials, the movement-onset responses tended to be larger to extramacular stimulation (annular target of 5°–9°) than to macular stimulation (circular target of 5° diameter).Abbreviation PREP pattern-reversal visual evoked potentials     

SORB-GEL method of analysis of 99mTc-labelled compounds

A SORB-GEL method has been worked out for analysing ^99mTc-labelled compounds which (in a few minutes) enables the pertechnetate content to be determined in a preparation. The method is based upon a different tupe of behaviour of ^99mTc-labelled compound, pertechnetate in the columns packed with Sephadex G-10, and with alumina during elution with saline.Polythene syringes 4.7 cm long and 1 cm in diameter were used as chromotographic columns. A syringe packed with Sephadex G-10 transferred 0.1 ml of ^99mTc-labelled compound into the column, and the activity of the column was then measured in the ionisation chamber. Using a syringe, 20 ml of saline was foreced through this column. The eluate was then removed. Using an injection needle, a second column, packed with alumina, was connected with the first. Similarly, a third column, packed with Sephadex G-10, was connected to the second. Through all of them 40 ml of saline was forced. The third column containing Sephadex G-10 was then disconnected and its activity was measured in the ionisation chamber. The pertechnetate content in the preparation was then calculated from the measured values.The method is suitable for determinating the free pertechnetate content in strong and weak chelate compounds and in particle preparations.     

Analysis of Adenosine Vascular Effect in Isolated Rat Aorta: Possible Role of Na+/K+‐ATPase

Abstract: The present experiments were undertaken in order to examine the effect of adenosine in isolated rat aorta, to investigate the possible role of intact endothelium and endothelial relaxing factors in this action and to determine which population of adenosine receptors is involved in rat aorta response to adenosine. Adenosine (0.1–300 μM) produced concentration‐dependent (intact rings: pD₂=4.39±0.09) and endothelium‐independent (denuded rings: pD₂=4.52±0.12) relaxation of isolated rat aorta. In the presence of high concentration of K⁺ (100 mM) adenosine‐evoked relaxation was significantly reduced (maximal relaxation in denuded rings: control – 92.1±9.8 versus K⁺– 54.4±5.0). Similar results were obtained after incubation of ouabain (100 μM) or glibenclamide (1 μM). In K⁺‐free solution, K⁺ (1–10 mM)‐induced rat aorta relaxant response was significantly inhibited by ouabain (100 μM). Application of indomethacin (10 μM), N^G‐nitro‐L‐arginine (10 μM) or tetraethylammonium (500 μM) did not alter the adenosine‐elicited effect in rat aorta. 8‐(3‐Chlorostyril)‐caffeine (0.3–3 μM), a selective A_2A‐receptor antagonist, significantly reduced adenosine‐induced relaxation of rat aorta in a concentration‐dependent manner (pK_B=6.57). Conversely, 1,3‐dipropyl‐8‐cyclopentylxanthine (10 nM), an A₁‐receptor antagonist, did not affect adenosine‐evoked dilatation. These results indicate that in isolated rat aorta, adenosine produces endothelium‐independent relaxation, which is most probably dependent upon activation of smooth muscle Na⁺/K⁺‐ATPase, and opening of ATP‐sensitive K⁺ channels, to a smaller extent. According to receptor analysis, vasorelaxant action of adenosine in rat aorta is partly induced by activation of smooth muscle adenosine A_2A receptors.     

Aryl hydrocarbon receptor-activating polychlorinated biphenyls and their hydroxylated metabolites induce cell proliferation in contact-inhibited rat liver epithelial cells.

Polychlorinated biphenyls (PCBs) exhibit tumor-promoting effects in experimental animals. We investigated effects of six model PCB congeners and hydroxylated PCB metabolites on proliferation of contact-inhibited rat liver epithelial WB-F344 cells. The 'dioxin-like' PCB congeners, PCB 126, PCB 105, and 4'-OH-PCB 79, a metabolite of the planar PCB 77 congener, induced cell proliferation in a concentration-dependent manner. In contrast, the 'non-dioxin-like' compounds that are not aryl hydrocarbon receptor (AhR) agonists, PCB 47, PCB 153, and 4-OH-PCB 187, an abundant noncoplanar PCB metabolite, had no effect on cell proliferation at concentrations up to 10 muM. The concentrations of dioxin-like PCBs leading to cell proliferation corresponded with the levels inducing the expression of cytochrome P450 1A1 mRNA, suggesting that the release from contact inhibition was associated with AhR activation. The effects of PCB 126 and PCB 153 on expression of proteins controlling G0/G1-S-phase transition and S-phase progression were compared. Only PCB 126 was found to upregulate cyclin A and D2 protein levels, and to increase both total cyclin-dependent kinase 2 (cdk2) and cyclin A/cdk2 complex activities. Despite the observed upregulation of cyclin D2, no increase in cdk4 activity was observed. The expression of cdk inhibitor p27Kip1 was not affected by either PCB 126 or PCB 153. These results suggest that dioxin-like PCBs can induce cell proliferation of contact-inhibited rat liver epithelial cells by increasing cyclin A protein levels, a process that then leads to upregulation of cyclin A/cdk2 activity and initiation of DNA replication. This mechanism could be involved in tumor-promoting effects of dioxin-like PCBs.