Kinetics of polymerization of 1,3-dioxepane with the Al(C2H5)3/H2O catalyst system

The kinetics of the polymerization of 1,3-dioxepane (DH) with the catalytic system Al(C₂H₅)₃/H₂O was studied. The dependence of the polymerization rate R₀ of the monomer DH(M) may be represented by the equation: The kinetic scheme which verifies the obtained results is that which takes into consideration in the starting period of the polymerization the existence of chain transfer to the monomer. The decrease of the polymerization rate and the diminishing of the intrinsic viscosity at high conversions points to the existence of chain transfer to the polymer in this stage of the reaction. The reaction rate constants of the chain transfer to the monomer are one order of magnitude higher than those of the transfer reaction to the polymer.     

Ethylene/propene copolymerization in the presence of the homogeneous catalyst system Ti(Oi-C3H7)4/Al(C2H5)2F

The behaviour of the homogeneous catalyst system Ti(Oi-C₃H₇)₄/Al(C₂H₅)₂F in ethylene/propene copolymerization was studied. The copolymer structure is discussed in view of the stereoregulation mechanism previously proposed for vanadium-based homogeneous catalyst systems.     

Phospholipase D and priming of the respiratory burst by H(2)O(2) in NR8383 alveolar macrophages

Previous investigation showed that preincubation within a range of nontoxic H(2)O(2) concentrations enhanced subsequently stimulated superoxide production by rat alveolar macrophages in response to various stimuli. In the present study, the NR8383 rat alveolar macrophage cell line was used to further investigate the priming effect of H(2)O(2). Using nitroblue tetrazolium, which formed an insoluble formazan when reduced by superoxide, modulation of the respiratory burst was visualized in a cell population exposed to a concentration gradient of H(2)O(2) before stimulation. This model system illustrates how H(2)O(2) may constitute a signaling molecule for a feed-forward regulation of the respiratory burst during inflammation. n-Butanol, which allows consumption of phosphatidic acid by the transphosphatidylation reaction, and propanolol, which inhibits phosphatidic acid phosphohydrolase, were used to investigate the possible involvement of phospholipase D in this phenomenon. These two agents were found to inhibit the basal adenosine diphosphate-stimulated respiratory burst. Inhibition of the H(2)O(2)-enhanced respiratory burst was equally or slightly less effective when expressed as percentage of controls. Furthermore, phospholipase D was not activated by H(2)O(2) concentrations that enhance superoxide production. Thus, phospholipase D does not mediate the enhancement of the respiratory burst by H(2)O(2), although it may be activated by high concentrations of this hydroperoxide.     

Preliminary results on ethylene/propene copolymerization in the presence of Cp2Ti(CH3)2/Al(CH3)3/H2O

Ethylene/propene copolymerizations were carried out in the presence of the catalyst system Cp₂Ti(CH₃)₂/Al(CH₃)₃/H₂O (Cp = cyclopentadienyl group), and the reactivity ratios r₁, r₂ were determined through the Fineman and Ross equation and via ¹³C NMR. A nearly alternating copolymer structure was pointed out. The yields as well as the molecular weights of the copolymers strongly decrease with increasing propene mole fraction in the copolymers.     

Effect of Medium on H(2)O(2) Levels and Peroxidase-Like Activity by Mycoplasma pneumoniae

H₂O₂ levels accumulated by Mycoplasma pneumoniae can be influenced by carbon source, different horse sera, yeast extract, thallium acetate, or growth in a simplified, dialyzed medium. Thus, increased levels of H₂O₂ were detected by growth in glycerol, by omission of thallium acetate, and by the use of dialyzed medium. The ability of M. pneumoniae in the presence of glucose, but not with fructose, mannose, or glycerol, to remove both endogenous and exogenous H₂O₂ suggests an inducible peroxidase similar to bacterial enzymes in streptococci. This peroxidase-like activity is in turn influenced by the complex interplay of medium components, explaining perhaps some of the variability of H₂O₂ accumulations observed with glucose. A survival value has been suggested for this “peroxidase-like” activity.     

Enhanced crystallization by annealing of poly(phenylene sulfide) in presence of CO2 and N2O

Crystallization of amorphous poly(phenylene sulfide) was carried out upon annealing in the presence of sorbed CO₂ and N₂O at pressures of 50 bar. Thermal crystallization at the same pressure allows the comparison of crystallization rates. From the results of IR-spectroscopy, wide angle X-ray diffraction, differential scanning calorimetry and density measurements, it is seen that in the presence of sorbed gas molecules crystallization occurs even at temperatures below the glass transition measured at atmospheric conditions. At a given temperature, gas sorption yields accelerated crystallization. The results, show the considerable plasticizing influence of sorbed gas molecules. From the crystallization rate at sorbed gas conditions the plasticizing ability of the gas may be estimated. That of N₂O exceeds that of CO₂ by a factor of three. Assuming a simple two-phase model for the crystalline polymer the comparison of heat of melting and density values for t → ∞ allows the conclusion that parts of the noncrystalline volume fraction become less dense by annealing in the presence of sorbed gas molecules. An increased free volume fraction which may be formed in the non-crystalline regions is discussed. It is possible that the remaining lower density results from a hindered relaxation of chain molecules from the dilated state they take due to gas sorption. In this context the influence of decreased mobility of non-crystalline chains is discussed in terms of the “rigid amorphous phase” concept.     

The phenoloxidase activity in the presence of H2O2, EDTA, and copper (author's transl)]

Investigations performed with cryostat sections of the gut, spleen and lung of the rat have shown, that the substrate of PER H2O2 inhibits the PO activity in dependence of the concentration, and that obvious the PO substrate DOPA is no suitable H2-donator for the PER reaction. Therefore a false positive reaction by the PO proof is not to be expected. Copper sulfat does not influence the PO reaction, but it accelerates melanin formation, which causes an unspecific colouring of the tissue.     

Differential modulation of MAP kinases by zinc deficiency in IMR-32 cells: role of H(2)O(2)

The influence of zinc deficiency on the modulation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK1/2), p38, and c-Jun N-terminal kinase (JNK) was studied. Using human IMR-32 cells as a model of neuronal cells, the role of oxidants on MAPKs and activator protein-1 (AP-1) activation in zinc deficiency was investigated, characterizing the participation of these events in the triggering of apoptosis. Relative to controls, cells incubated in media with low zinc concentrations showed increased cell oxidants and hydrogen peroxide (H(2)O(2)) release, increased JNK and p38 activation, high nuclear AP-1-DNA binding activity, and AP-1-dependent gene expression. Catalase addition to the media prevented the increase of cellular oxidants and inhibited JNK, p38, and AP-1 activation. Low levels of ERK1/2 phosphorylation were observed in the zinc-deficient cells in association with a reduction in cell proliferation. Catalase treatment did not prevent the above events nor the increased rate of apoptosis in the zinc-deficient cells. It is first demonstrated that a decrease in cellular zinc triggers H(2)O(2)-independent, as well as H(2)O(2)-dependent effects on MAPKs. Zinc deficiency-induced increases in cellular H(2)O(2) can trigger the activation of JNK and p38, leading to AP-1 activation, events that are not involved in zinc deficiency-induced apoptosis.     

The effect of preparation conditions on the catalyst Nd(P507)3/H2O/Al(i-Bu)3 for the polymerization of styrene

The catalyst system neodymium phosphonate Nd(P₅₀₇)₃ /H₂O/Al(i-Bu)₃ for the polymerization of styrene was examined. Effects of the addition order of the catalyst components, catalyst aging time and aging temperature on the catalyst activity and the polymer characteristics were investigated. The catalyst activity for isospecific polymerization of styrene increases with aging time and reaches the maximum with a catalyst aged for 45 min at 70°C. The aging time that the catalyst needs to reach the highest activity for isospecific polymerization decreases with increasing aging temperature. The preformed catalyst and the in situ catalyst were compared with respect to the kinetic behavior of the styrene polymerization and the polymer characteristics.     

Modulation of somatodendritic dopamine release by endogenous H(2)O(2): susceptibility in substantia nigra but resistance in VTA

We showed previously that dopamine (DA) release in dorsal striatum is inhibited by endogenously generated hydrogen peroxide (H(2)O(2)). Here, we examined whether endogenous H(2)O(2) can also modulate somatodendritic DA release in the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA), with companion measurements in DA terminal regions. Evoked DA release was monitored in brain slices using carbon-fiber microelectrodes with fast-scan cyclic voltammetry. Exogenous H(2)O(2) decreased DA release by 50-60% in SNc and VTA but only by 35% in nucleus accumbens. Whether endogenous H(2)O(2) also modulated somatodendritic release was examined using the glutathione peroxidase inhibitor, mercaptosuccinate (MCS), which should increase stimulation-evoked H(2)O(2) levels. In the presence of MCS, DA release was suppressed by 30-40% in SNc as well as in dorsal striatum and nucleus accumbens. In striking contrast, DA release in the VTA was unaffected by MCS. These data are consistent with stronger H(2)O(2) regulation or lower H(2)O(2) generation in VTA than in the other regions. Importantly, oxidative stress has been linked causally to Parkinson's disease, in which DA cells in SNc degenerate, but VTA cells are spared. The present data suggest that differences in oxidant regulation or generation between SNc and VTA could contribute to this.     

Measurements of energy expenditure using isotope-labelled water (2H2 180) during an Arctic expedition

Summary Estimates of energy expenditure using both isotope-labelled (²H₂ ¹⁸0) water and dietary intake/body composition changes were made during an attempt by two men (MS and RF) to walk to the North Pole. The isotope-labelled water technique gave mean estimates of daily energy expenditure for the 48-day expedition of 28.05 MJ (MS) and 32.38 MJ (RF), which compared with estimates of 25.66 MJ (MS) and 24.86 MJ (RF) from the intake/body composition measurements. Fluid retention and peripheral oedema probably caused a considerable underestimate of the losses in body energy stores when applying the energy balance method, whereas in the isotope method, uncertainty in the measurements of isotopic background led to minimum errors of –4.9% to +4.0% of the means for MS and –12.7% to +8.2% for RF (95% confidence limits).     

Polymerization of propylene to syndiotactic polymer. III. Behaviour of the catalyst system VCl4-Al(C2H5)2Cl in the presence of lewis bases

Polymerizations of propylene to syndiotactic polymer have been carried out in the presence of the catalyst system VCl₄-Al(C₂H₅)₂Cl-anisole. The data obtained have been related to those previously reported concerning the catalyst system, VCl₄-Al(C₂H₅)₂Cl. It was thus possible to propose a mechanism of formation of the catalytic complexes and to put forward or confirm some hypotheses on their constitution. A polymerization mechanism is also proposed that can justify both the type of stereoregularity of the polymer and the variation of steric regularity on varying the polymerization conditions.     

Preparation and properties of polyaniline doped with poly(thiophenylenesulfonic acid)

A novel polyaromatic acid, poly(thiophenylenesulfonic acid) (PTPSA), prepared from a soluble precursor of poly(arylenesulfonium salt) was employed as a dopant for polyaniline (PAn). The electro-oxidative polymerization of aniline in PTPSA aqueous solution gives an electroactive PAn/PTPSA composite with three redox couples at 0.16, 0.53, and 0.71V (vs. SCE). Composites of different molar ratio ([SO₃H]/[An] = 0.10, 0.21, 0.42, 0.50, 0.83, 1.67) was prepared in order to confirm the transformation from the emeraldine base to its PTPSA salt, where a quantitative doping reaction was observed by means of UV-VIS and IR measurements. The thermogravimetric analysis revealed that the composites do not decompose up to 200°C in nitrogen atmosphere. The composite ([SO₃H]/[An] = 0.50) shows an electrical conductivity of 1.5 S·cm^–1 at 30°C and 3.0×10^–1 S·cm^–1 at 170°C. The composite retains its conductivity after heating at 150°C for 24 h.     

Increased release of hydrogen peroxide (H2O2) and superoxide anion (O-2) by murine macrophages in vitro after cis-platin treatment

When murine macrophage (M phi) monolayers are treated with cis-Platin (10 micrograms or 5 micrograms/ml) for 30 min, 1, 2, 4, 8 and 24 h a significant increase in the release of H2O2 and O-2 by M phi is observed. The release of H2O2 and O-2 was comparatively much more when M phi were treated with 5 micrograms/ml cis-Platin than 10 micrograms/ml. However, it is observed that 4 h cis-Platin treatment results in comparative inhibition in the release of H2O2 and O-2. Further, we compared the release of H2O2 and O-2 by M phi treated with cis-Platin, LPS and PMA.     

Sodium pyruvate protects against H(2)O(2) mediated apoptosis in human neuroblastoma cell line-SK-N-MC

Free radicals are involved in neuronal damage. The present study was aimed to investigate the protective effect of sodium pyruvate-a free radical scavenger against hydrogen peroxide (H(2)O(2)) induced apoptosis in human neuroblastoma cell line-SK-N-MC. On exposure to H(2)O(2) (0.025 mM) cells exhibited apoptosis within 24 h, demonstrating a high caspase 3 activity by 3 h followed by cleavage of PARP that was maximum at 24 h. A break down in the mitochondrial membrane potential was observed 3 h onwards. Sodium pyruvate protected cells significantly (P<0.05) against apoptosis in a dose dependent manner as assessed for cell viability by dye exclusion method and apoptosis by TUNEL. Sodium pyruvate significantly inhibited caspase 3 activity, cleavage of PARP and breakdown of mitochondrial membrane potential. These data suggest that sodium pyruvate protects neuronal damage caused by H(2)O(2).     

H(2)O(2) is a novel, endogenous modulator of synaptic dopamine release

Recent evidence suggests that reactive oxygen species (ROS) might act as modulators of neuronal processes, including synaptic transmission. Here we report that synaptic dopamine (DA) release can be modulated by an endogenous ROS, H(2)O(2). Electrically stimulated DA release was monitored in guinea pig striatal slices using carbon-fiber microelectrodes with fast-scan cyclic voltammetry. Exogenously applied H(2)O(2) reversibly inhibited evoked release in the presence of 1.5 mM Ca(2+). The effectiveness of exogenous H(2)O(2), however, was abolished or decreased by conditions that enhance Ca(2+) entry, including increased extracellular Ca(2+) concentration ([Ca(2+)](o); to 2.4 mM), brief, high-frequency stimulation, and blockade of inhibitory D(2) autoreceptors. To test whether DA release could be modulated by endogenous H(2)O(2), release was evoked in the presence of the H(2)O(2)-scavenging enzyme, catalase. In the presence of catalase, evoked [DA](o) was 60% higher than after catalase washout, demonstrating that endogenously generated H(2)O(2) can also inhibit DA release. Importantly, the Ca(2+) dependence of the catalase-mediated effect was opposite to that of H(2)O(2): catalase had a greater enhancing effect in 2.4 mM Ca(2+) than in 1.5 mM, consistent with enhanced H(2)O(2) generation in higher [Ca(2+)](o). Together these data suggest that H(2)O(2) production is Ca(2+) dependent and that the inhibitory mechanism can be saturated, thus preventing further effects from exogenous H(2)O(2). These findings show for the first time that endogenous H(2)O(2) can modulate vesicular neurotransmitter release, thus revealing an important new signaling role for ROS in synaptic transmission.