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Notes: Tectonomagmatic similarities between the modern Chilean flat-slab region and pre-Neogene magmatic episodes suggest that they represent analogues to flat subduction. Evolutionary patterns in each magmatic suite include (i) increasing La/Yb ratios and Sr-and Nd-isotopic enrichment through time, (ii) eastward-migration of magmatism after periods of transpressional/transtensional intra-arc deformation, and (iii) subsequent termination and virtual absence of main-arc activity for 5–10 Myr. These patterns may reflect slab shallowing followed by flat subduction and thickening of the overlying crust. If repeated, they require interchanging episodes of slab steepening. Increasing convergence rates force slab kinking and eventual failure of the oversteepened slab, followed by rebound of the slab tip (owing to lack of further slab pull), flat subduction and termination of subduction-related magmatism. Rapid subduction leads to shallow overriding of the detached slab fragment. Eclogitization of the gradually steepening slab tip at depth and subsequent slab pull permits asthenospheric corner flow and subduction-related magmatism.

Notes: Erythrocyte sedimentation rates from 40 suspensions of packed red blood cells in modified fluid gelatin, 4% albumin solution, 6% hydroxyethyl starch and normal saline were measured at room temperature using Westergren's method. The erythrocyte sedimentation rate was extremely high in gelatin and this increase was significant after 10–60 min when compared with the other fluids. Erythrocyte sedimentation rates in albumin, hydroxyethyl starch and normal saline were low and there were no differences between these fluids [erythrocyte sedimentation after 60 min, median (interquartile range): gelatin 128 (111.2–130.0) mm, albumin 2 (1.5–2.0) mm, hydroxyethyl starch 1.5 (1.0–1.6) mm, normal saline 2 (1.9–2.5) mm, p 〈 0.0001]. The addition of twice the volume of modified fluid gelatin to a volume of red blood cells leads to rapid acceleration of the erythrocyte sedimentation rate. This is caused by increased erythrocyte aggregation, and in clinical practice this effect may be useful for the haemoconcentration of diluted blood from cardiopulmonary bypass circuits or cell-saver autotransfusion in paediatric surgery.

Notes: Abstract Isoprene emission from plants represents one of the principal biospheric controls over the oxidative capacity of the continental troposphere. In the study reported here, the seasonal pattern of isoprene emission, and its underlying determinants, were studied for aspen trees growing in the Rocky Mountains of Colorado. The springtime onset of isoprene emission was delayed for up to 4 weeks following leaf emergence, despite the presence of positive net photosynthesis rates. Maximum isoprene emission rates were reached approximately 6 weeks following leaf emergence. During this initial developmental phase, isoprene emission rates were negatively correlated with leaf nitrogen concentrations. During the autumnal decline in isoprene emission, rates were positively correlated with leaf nitrogen concentration. Given past studies that demonstrate a correlation between leaf nitrogen concentration and isoprene emission rate, we conclude that factors other than the amount of leaf nitrogen determine the early-season initiation of isoprene emission. The late-season decline in isoprene emission rate is interpreted as due to the autumnal breakdown of metabolic machinery and loss of leaf nitrogen. In potted aspen trees, leaves that emerged in February and developed under cool, springtime temperatures did not emit isoprene until 23 days after leaf emergence. Leaves that emrged in July and developed in hot, midsummer temperatures emitted isoprene within 6 days. Leaves that had emerged during the cool spring, and had grown for several weeks without emitting isoprene, could be induced to emit isoprene within 2 h of exposure to 32°C. Continued exposure to warm temperatures resulted in a progressive increase in the isoprene emission rate. Thus, temperature appears to be an important determinant of the early season induction of isoprene emission. The seasonal pattern of isoprene emission was examined in trees growing along an elevational gradient in the Colorado Front Range (1829–2896 m). Trees at different elevations exhibited staggered patterns of bud-break and initiation of photosynthesis and isoprene emission in concert with the staggered onset of warm, springtime temperatures. The springtime induction of isoprene emission could be predicted at each of the three sites as the time after bud break required for cumulative temperatures above 0°C to reach approximately 400 degree days. Seasonal temperature acclimation of isoprene emission rate and photosynthesis rate was not observed. The temperature dependence of isoprene emission rate between 20 and 35°C could be accurately predicted during spring and summer using a single algorithm that describes the Arrhenius relationship of enzyme activity. From these results, it is concluded that the early season pattern of isoprene emission is controlled by prevailing temperature and its interaction with developmental processes. The late-season pattern is determined by controls over leaf nitrogen concentration, especially the depletion of leaf nitrogen during senescence. Following early-season induction, isoprene emission rates correlate with photosynthesis rates. During the season there is little acclimation to temperature, so that seasonal modeling simplifies to a single temperature-response algorithm.

Notes: Summary The adult respiratory distress syndrome (ARDS) is characterized by extended inflammatory processes in the lung microvascular, interstitial, and alveolar compartments, resulting in vasomotor disturbances, plasma leakage, cell injury, and complex gas exchange disturbances. Abnormalities in the alveolar surfactant system have long been implicated in the pathogenetic sequelae of this life-threatening syndrome. This hypothesis is supported by similarities in pulmonary failure between patients with ARDS and preterm babies with infant respiratory distress syndrome, known to be triggered primarily by lack of surfactant material. Mechanisms of surfactant alterations in ARDS include: (a) lack of surface-active compounds (phospholipids, apoproteins) due to reduced generation/release by diseased pneumocytes or to increased loss of material (this feature includes changes in the relative composition of the surfactant phospholipid and/or apoprotein profiles); (b) inhibition of surfactant function by plasma protein leakage (inhibitory potencies of different plasma proteins have been defined); (c) “incorporation” of surfactant phospholipids and apoproteins into polymerizing fibrin upon hyaline membrane formation; and (d) damage/inhibition of surfactant compounds by inflammatory mediators (proteases, oxidants, nonsurfactant lipids). Alterations in alveolar surfactant function may well contribute to a variety of pathophysiological key events encountered in ARDS. These include decrease in compliance, ventilation-perfusion mismatch including shunt flow due to altered gas flow distribution (atelectasis, partial alveolar collapse, small airway collapse), and lung edema formation. Moreover, more speculative at the present time, surfactant abnormalities may add to a reduction in alveolar host defense competence and an upregulation of inflammatory events under conditions of ARDS. Persistent atelectasis of surfactant-deficient and in particular fibrin-loaded alveoli may represent a key event to trigger fibroblast proliferation and fibrosis in late ARDS (“collapse induration”). Overall, the presently available data on surfactant abnormalities in ARDS lend credit to therapeutic trials with transbronchial surfactant administration. In addition to the classical goals of replacement therapy defined for preterm infants (rapid improvement in lung compliance and gas exchange), this approach will have to consider its impact on host defense competence and inflammatory and proliferative processes when applied in adults with respiratory failure.

Notes: [Auszug] This event occurred at approximately 11 a.m. in the entrance hall of the Plockenhaus, a restaurant below the Plockenpass in the Carnic Alps (Austria). Students from a field trip of the Geology Department of the Universitat Heidelberg were staying inside this restaurant because of a thunderstorm ...

Notes: Abstract The optical and structural properties of films deposited from laser sintered Zirconia (ZrO2), Hafnia (HfO2), and Yttria (Y2O3) and from the commercially available (unprocessed material) Zirconia, Hafnia and Yttria, were studied and compared. All the films had low absorption. Films deposited from the laser sintered material had very low optical inhomogeneity. ZrO2 films showed negative inhomogeneity for films deposited from the unprocessed material. The refractive index increased for ZrO2 films deposited from the laser sintered material. HfO2 and Y2O3 films showed positive inhomogeneity when deposited from the unprocessed material. The refractive index of the films of these materials decreased when deposited from the laser sintered material. The thin films of ZrO2 and Y2O3 prepared from laser sintered material had stable monoclinic and cubic structures respectively while HfO2 films were found to be amorphous.

Notes: Abstract The thermal decomposition of polytetrafluoroethylene (TFE, Teflon), high and low density polyethylene (HDP and LDP), Delrin Acetal (DA), AVCO Phenolic Fiberglass (APFG), and carbon phenolic (CP), were studied by a thermogravimetric technique which utilized a constant heating rate. Loss in sample weight was recorded as a function of time or temperature from room temperature to approximately 700°. Reaction orders were established from logarithmic rate versus temperature plots. Arrhenius frequency factors and overall activation energies were determined from computerized integrations of the appropriate rate equations in which the results were treated on the basis of first-order reaction mechanisms for specific temperature regions. Zero-order mechanisms were estimated by the usual graphical methods.

Notes: Abstract Emissions of sulfur gases from both natural and anthropogenic sources strongly influence the chemistry of the atmosphere. To assess the relative importance of these sources we have combined the measurements of sulfur gases and fluxes during the past decade to create a global emission inventory. The inventory, which is divided into 12 latitude belts, takes into account the seasonal dependence of sulfur emissions from biogenic sources. The total emissions of sulfur gases from natural sources are approximately 0.79 Tmol S/a. These emissions are 16% of the total sulfur emissions in the Northern Hemisphere and 58% in the Southern Hemisphere. The inventory clearly shows the impact of anthropogenic sulfur emissions in the region between 35° and 50°N.

Notes: Summary Adult respiratory distress syndrome (ARDS) is characterized by extended inflammatory processes in the lung microvascular, interstitial and alveolar compartments, resulting in vasomotor disturbances, plasma leakage, cell injury and complex gas exchange disturbances. Abnormalities of the alveolar surfactant system have since long been implicated in the pathogenetic sequelae of this life-threatening syndrome. This hypothesis is supported by similarities in pulmonary failure between patients with ARDS and preterm babies with infant respiratory distress syndrome (IRDS), which is known to be triggered primarily by a lack of surfactant material. Mechanisms of surfactant alterations in ARDS include: lack of surface-active compounds, changes in the relative composition of the surfactant constituents, alteration of the extracellular surfactant subtype distribution, inhibition of surfactant function by plasma protein leakage, and damage/inhibition of surfactant compounds by inflammatory mediators.¶   Alterations in alveolar surfactant function may well contribute to a variety of pathophysiological key events encountered in ARDS. These include decrease in compliance, ventilation-perfusion mismatch including shunt-flow due to altered gas flow distribution (atelectasis, partial alveolar collapse, small airway collapse) and lung edema formation. Persistent atelectasis of surfactant-deficient and, in particular, fibrin-loaded alveoli may represent a key event to trigger fibroblast proliferation and fibrosis in late ARDS (collapse induration).¶   Overall, the presently available data on surfactant abnormalities in ARDS lend credit to therapeutic trials with transbronchial surfactant application. Accordingly, acute improvement of gas exchange was encountered in two recently performed pilot studies addressing the safety and efficacy of a transbronchial application of large quantities of exogenous surfactant material. In parallel to a far reaching, but yet not complete restoration of „physiological” surfactant properties in BALF, re-opening of formerly collapsed lung regions with concomitant reduction of intrapulmonary shunt flow was noticed. Although not the primarily goal in these pilot studies, a tendency towards lower mortality in the surfactant treatment groups was noted. At present, a controlled study enrolling higher patient numbers is being performed to probe the impact of a transbronchial surfactant administration on the outcome of ARDS patients.