未经改性的聚丙烯纤维织物的染色

描述了德国邓肯道夫纺织化学与化学纤维研究所开发的对未经改性的聚丙烯纤维织物还原染色的新工艺.该工艺的关键是在还原染料染色前利用等离子技术对PP纤维进行预处理.用还原染料染PP纤维,除了获得较深的颜色和优异的色牢度性能外,这一工艺的显著特点还在于它摒弃了还原剂,如保险粉.染料的固色在高温蒸箱或利用热定型工艺可连续完成.     

Einfaches und spezifisches HPLC-Verfahren zur Bestimmung von Cyclamat in fruchtsafthaltigen Getr?nken nach Derivatisierung zu N,N-Dichlorcyclohexylamin

Zusammenfassung Es wird eine HPLC-Methode zur Bestimmung von Cyclamat in fruchtsafthaltigen Getränken vorgestellt, welche auf der Umsetzung von Cyclamat zuN,N-Dichlorcyclohexylamin beruht. Die HPLC-Analyse erfolgt an einer RP 18-Trennsäule mit Hilfe der Detektion bei 314 nm. Es lassen sich Gehalte von 10 bis 800 mg/1 mit einer relativen Standardabweichung von weniger als 2% analysieren. Bei verschiedenen fruchtsafthaltigen Getränken lag die Wiederfmdungsrate für Cyclamat bei 96 bis 99%. Die Einfachheit und Schnelligkeit (Gesamtanalysenzeit ca. 30 min) lassen die Methode insbesondere für die Routineanalytik geeignet erscheinen. Daneben wird eine Methode zur Isolierung von Cyclamat mittels Festphasenextraktion an Amino-Anionenaustauscher beschrieben.

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Simple and specific HPLC procedure for determination of cyclamate in fruit juice beverages after conversion to N,N-dichlorcyclohexylamine

Summary A high pressure liquid chromatography (HPLC) procedure for the determination of cyclamate in fruit juice beverages is described, which depends on the conversion of cyclamate toN,N-dichlorcyclohexylamine. For HPLC analysis an RP 18 separation system with detection at 314 nm is used. Contents of 10 to 800 mg/L can be detected in about 30 min with a relative standard deviation of less than 2%. Recovery of cyclamate from several fruit juice beverages amounts to 96–99%. This simple and rapid method seems to be very well suited for routine analysis. A method for solid-phase extraction of cyclamate with amino-anion-exchange columns is also presented.

     

Policies to support renewable energies in the heat market

Whereas the contribution from renewable energies in the electrical power market is increasing rapidly, similar progress in the heat market is yet to be made. A prerequisite for progress is the development of innovative support instruments that transcend the usual support through public subsidies or tax reductions. We present an overview of the various classes of possible instruments. Some particularly interesting instruments will be selected and evaluated, comparing them qualitatively and quantitatively for the case of Germany. The most favourable model is found to be a new, allocation-financed¹ model known as the Bonus Model. This model will be described in more detail.     

Vitamin C blocks inflammatory platelet-activating factor mimetics created by cigarette smoking

Cigarette smoking within minutes induces leukocyte adhesion to the vascular wall and formation of intravascular leukocyte-platelet aggregates. We find this is inhibited by platelet-activating factor (PAF) receptor antagonists, and correlates with the accumulation of PAF-like mediators in the blood of cigarette smoke-exposed hamsters. These mediators were PAF-like lipids, formed by nonenzymatic oxidative modification of existing phospholipids, that were distinct from biosynthetic PAF. These PAF-like lipids induced isolated human monocytes and platelets to aggregate, which greatly increased their secretion of IL-8 and macrophage inflammatory protein-1alpha. Both events were blocked by a PAF receptor antagonist. Similarly, blocking the PAF receptor in vivo blocked smoke-induced leukocyte aggregation and pavementing along the vascular wall. Dietary supplementation with the antioxidant vitamin C prevented the accumulation of PAF-like lipids, and it prevented cigarette smoke-induced leukocyte adhesion to the vascular wall and formation of leukocyte-platelet aggregates. This is the first in vivo demonstration of inflammatory phospholipid oxidation products and it suggests a molecular mechanism coupling cigarette smoke with rapid inflammatory changes. Inhibition of PAF-like lipid formation and their intravascular sequela by vitamin C suggests a simple dietary means to reduce smoking-related cardiovascular disease.     

Investigation of the adhesive strength of PMMA structures on substrates obtained by deep X-ray lithography

The adhesive strength of PMMA structures obtained by deep X-ray lithography with synchrotron radiation is a decisive factor for effective structure replication in subsequent electroforming processes. The adhesion depends on various factors, in particular on the interaction of radiation and secondary electrons at the boundary resist/substrate. We have determined the adhesion strength of PMMA microcolumns as a function of the dose deposited below the mask absorber by breaking tension measurements applying a new experimental method. Care has been taken to separate degradation effects in the resist due to the primary photon beam from the loss of adhesion at the boundary substrate/resist caused by secondary electrons. This has been studied quantitatively by utilizing different substrate materials like glassy carbon, wet oxidized titanium, copper and gold.

Monte Carlo simulations have been carried out to simulate the deposited dose at the surface layer of different substrates. The corresponding results are supplemented by deep lithography experiments, which may be used as a means to directly conclude the deposited resist dose from secondary electrons emitted from the substrate surface.

All the irradiation experiments have been performed with specially designed masks for deep X-ray lithography at the storage ring DCI (Orsay/France).     

Oxidized LDL-induced leukocyte/endothelium interaction in vivo involves the receptor for platelet-activating factor

Leukocyte adhesion and subendothelial emigration, constant hallmarks of early atherogenesis, have been ascribed to the action of oxidized low-density lipoprotein (oxLDL). Using intravital fluorescence microscopy in the skinfold-chamber model in hamsters, we have previously shown that systemic administration of oxLDL stimulates leukocyte adhesion in vivo through a mechanism that depends on the generation and/or action of both leukotrienes and superoxide radicals. On the basis of the fact that oxygen radical-catalyzed peroxidation of phospholipids results in the generation of fragments with short sn2 residues, which besides authentic platelet-activating factor (PAF), activate the receptor for PAF on leukocytes and thereby induce leukocyte adhesion, we asked whether pretreatment of hamsters with a specific PAF receptor antagonist (WEB2170; 1 mg/kg of body weight IV, 10 minutes before oxLDL) attenuates leukocyte adhesion after injection of oxLDL (4 mg/kg of body weight IV, oxidized by 7.5 mumol/L Cu2+ for 18 hours at 37 degrees C). We demonstrate herein that in contrast to untreated control animals in which oxLDL elicited rolling and adhesion of circulating leukocytes to the endothelium of venules and arterioles, oxLDL-induced leukocyte adhesion was significantly attenuated in WEB2170-pretreated animals. These changes cannot be ascribed to alterations of microhemodynamic parameters and, hence, wall shear conditions. This finding indicates that oxLDL-induced leukocyte/endothelium interaction involves the PAF receptor, which may function both as a receptor for authentic PAF or for PAF-like lipids that are generated in a free radical-catalyzed peroxidation of phospholipids.     

Fatigue crack propagation and strain cycling properties

A mechanical model of fatigue crack propagation was studied. It is hypothesized that propagation is caused by cumulative damage due to strain cycling of the material at a crack tip. With Miner's cumulative damage law and Manson and Coffin's strain cycle fatigue: law, crack propagation rate of a material can be calculated. The calculated values are compared with data on 7075-T6 Al, 2024-T4 Al, AM 350 stainless steel, and 18 Ni maraging steel. The calculated and experimental values correlate reasonably well. The results indicate that fatigue crack propagation resistance of a material is related to its capability to sustain strain cycling, i.e. its cyclic ductility.

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Zusammenfassung Ein mechanisches Modell der Rißfortpflanzung in Ermüdung wurde untersucht. Es wird angenommen, daß Rißfortpflanzung durch einen akkumulierten Schädigungsprozeß, zufolge der Dehnungsschwingungen des Materials am Rißgrund, verursacht wird. Die Rißfortpflanzungsgeschwindigkeit cities Materials kann, mit Hilfe des Schädigungsgesetzes von Miner und des Manson-Coffin Gesetzes für Ermüdung durch Dehnungsschwingungen, berechnet werden. Die so errechneten Werte werden mit den experimentellen Ergebnissen für Aluminium Legierungen 7075-T6, 2024-T4, rostfreiem Stahl AM 350 und Marageing Stahl 18% Ni verglichen. Die Übereinstimmung zwischen experimentellen und errechneten Werten ist verhältnismßig gut. Die Ergebnisse zeigen, daß der Widerstand eines Werstoffes gegen Rißfortpflanzung in Ermüdung mit seiner Dehnungschwingungsfestigkeit, d.h. mit seinem dynamischen Dehnungsvermögen im Zusammenlrang steht.

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Résumé Un modelé mécanique de la propagation des fractures de fatigue a été étudié. On suppose que la propagation provient l'accumulation des défauts en tête de la fissure durant la déformation alternée du matériau. On peut calculer la vitesse de propagation des fractures d'un matérial donné à l'aide de la loi de l'accumulation des défauts de Miner et de la loi de Manson et Coffin sur la fatigue en déformation alternée. On compare les valeurs calculées avec les résultats obtenus avec les aciers inoxydables 7075-T6 Al, 2024-T4 Al AM 350 et l'acier martensitique vieilli 18 Ni.La correlation entre les valeurs calculées et expérimentales est assez bonne. Les résultats obtenus montrent que la résistance d'un matériau à la propagation des fractures de fatigue depend de sa capacité à soutenir les déformations alternées, c'est-à-dire de sa ductilité en déformation cyclique.