Potential and recycling strategies for LCD panels from WEEE

Indium is one of the strategically important materials, which have been characterized as critical by various industrialized countries. Despite its high relevance, only low recycling rates are realized. Its main application is in indium tin oxide (ITO), which is used in the production of liquid crystal displays (LCD). However, recovery strategies for indium from LCDs are not yet being implemented in recycling practices. Although LCDs consist of a sandwich compound with additional materials such as glass (80% ± 5%) and polarizer foils (20% ± 5%), recently published recycling approaches focus mainly on the recovery of indium exclusively. This study, first of all, provides information about the quantity and quality of the materials applied in the LCD panels of the various equipment types investigated, such as notebooks, tablets, mobile phones, smartphones, PC monitors, and LCD TVs. The highest indium mass fraction per mass of LCD was determined in mobile phones and the least indium was found in smartphones. Additionally, we found the significant use of contaminating metals like antimony, arsenic, lead, and strontium in the glass fraction. Thus, specific recovery strategies should focus on selected equipment types with the highest indium potential, which is directly related to the sales of new devices and the number of collected end-of-life devices. Secondly, we have developed and successfully tested a novel recycling approach for separating the sandwich compound to provide single output fractions of panel glass, polarizer foils, and an indium concentrate for subsequent recycling. Unfortunately, the strongly varying content of contaminating metals jeopardizes the recycling of this output fraction. Nonetheless, economic recycling approaches need to address all materials contained, in particular those with the highest share in LCD panels such as polarizer foils and panel glass

Perturbed soliton excitations in DNA molecular chain

We study nonlinear dynamics of a periodic inhomogeneous DNA double helical chain under dynamic plane-base rotator model by considering angular rotation of bases in a plane normal to the helical axis. The dynamics is governed by a perturbed sine-Gordon equation. The perturbed soliton solution is obtained using a multiple scale soliton perturbation theory. The perturbed kink-antikink solitons represent formation of open state configuration with fluctuation in DNA.Comment: 20 Pages, 5 figure

Wirkung der AT2-Überexpression auf Collagen I alpha 2-mRNA-Gehalt und Migration porciner kardialer Fibroblasten

In der vorliegenden Arbeit wurde der Einfluss der humanen AT2-Rezeptorexpression und -stimulation auf den Collagen I alpha 2-mRNA-Gehalt und die Migration von porcinen kardialen Fibroblasten untersucht, um die Frage zu klären, ob AT2-Rezeptoren in kultivierten kardialen Fibroblasten AT1-antagonistische antifibrotische und migrationshemmende Effekte auf den Collagen I alpha 2-mRNA-Gehalt bzw. die Migration ausüben. Um die Funktion der AT2-Rezeptoren in der Zellkultur untersuchen zu können, wurde die AT2-cDNA durch adenovirale Transduktion in die Fibroblasten übertragen und so der AT2-Rezeptor überexprimiert. Mittels RT-PCR wurden die relativen Änderungen im Collagen I alpha 2-mRNA-Gehalt in TGF-beta1- bzw. TGF-beta1 plus Ang II-stimulierten Fibroblasten im Vergleich zur unstimulierten Kontrolle bestimmt. Alle Werte wurden auf ein Referenzgen (beta-Actin) bezogen. Die AT2-Stimulation änderte den relativen Collagen I alpha 2-mRNA-Gehalt der Fibroblasten nicht signifikant gegenüber den Antisense-(Ad5TA2)-transduzierten Fibroblasten. In der modifizierten Boyden-Kammer wurde der AT2-vermittelte Effekt von Ang II, hPDGF-BB sowie der Kombination beider Stoffe auf die Migration untersucht. Die alleinige Stimulation von AT2-Rezeptoren mit Ang II verhinderte die Migration gegenüber nichttransduzierten Fibroblasten. In Kombination mit hPDGF-BB änderte Ang II die Migration in AT2-überexprimierenden Fibroblasten nicht gegenüber den Antisense-(Ad5TA2)-transduzierten Fibroblasten. Bei ausschließlicher Stimulation durch hPDGF-BB wurde aber in AT2-exprimierenden Fibroblasten eine signifikant geringere Migration als in Antisense-(Ad5TA2)-transduzierten Fibroblasten festgestellt. Die zugrunde liegende Hypothese, dass AT2-Expression und Stimulation den relativen Collagen I alpha 2-mRNA-Gehalt hemmt, konnte in den vorliegenden Experimenten nicht bestätigt werden. Dies ließ keine inhibitorische AT2-vermittelte Wirkung von Ang II im Bezug auf den TGF-beta1-induzierten Collagen I alpha 2-mRNA-Gehalt erkennen. Dagegen führte die Ang II-Stimulation überexprimierter AT2-Rezeptoren zu einer verringerten Migration und vermittelte so einen AT1-antagonistischen Effekt.In this work the influence of expression and stimulation of the human AT2 receptor on Collagen I alpha 2-mRNA-content and migration of porcine cardiac fibroblastst was tested to clarify the question if AT2 receptors promote AT1 antagonistic antifibrotic and antimigratory effects on collagen I alpha 2-mRNA content and migration. To examine the AT2 receptor function in the cell culture AT2 cDNA was transferred into fibroblasts by adenoviral transduction and the AT2 receptor was overexpressed. Through the use of RT-PCR the relative changes in collagen I alpha 2-mRNA content in TGF-beta1 stimulated and TGF-beta1 plus Ang II stimulated fibroblasts were assayed and compared to the unstimulated control. All values were referred to a reference gene (beta-actin). Stimulation of AT2 receptors did not change the relative collagen I alpha 2-mRNA content of the fibroblasts significantly compared to antisense-(Ad5TA2) transduced fibroblasts. In the modified Boyden-chamber the AT2 mediated effect of Ang II, hPDGF-BB and the combination of both on migration was assessed. The stimulation of AT2 receptors with Ang II inhibited migration compared to nontransduced fibroblasts. In combination with hPDGF-BB Ang II did not change the migration in AT2 overexpressing fibroblasts compared to antisense-(Ad5TA2)-transduced fibroblasts. In the case of exclusive stimulation of AT2-expressing fibroblasts with hPDGF-BB a significantly lower migration was found compared to antisense-(Ad5TA2)-transduced fibroblasts. The underlying therory that AT2 expression and stimulation inhibits the relative collagen I alpha 2-mRNA content could not be confirmed in this work. This did not reveal an inhibitory AT2 mediated effect of Ang II in respect to the TGF-beta1 induced collagen I alpha 2-mRNA content. In contrast to that Ang II stimulation of overexpressed AT2 receptors led to a decreased migration and mediated an AT1 antagonistic effect

The carnitine status does not affect the contractile and metabolic phenotype of skeletal muscle in pigs

Abstract Background Recently, supplementation of L-carnitine to obese rats was found to improve the carnitine status and to counteract an obesity-induced muscle fiber transition from type I to type II. However, it has not been resolved if the change of muscle fiber distribution induced in obese rats and the restoration of the “normal” muscle fiber distribution, which is found in lean rats, in obese rats by supplemental L-carnitine is causally linked with the carnitine status. In the present study we hypothesized that fiber type distribution in skeletal muscle is dependent on carnitine status. Methods To test this, an experiment with 48 piglets which were randomly allocated to four groups (n = 12) was performed. All piglets were given orally either 60 mg sodium bicarbonate/kg body weight (group CON), 20 mg L-carnitine and 60 mg sodium bicarbonate/kg body weight (group CARN), 30 mg pivalate (dissolved in sodium bicarbonate)/kg body weight (group PIV) or 20 mg L-carnitine and 30 mg pivalate/kg body weight (group CARN + PIV) each day for a period of 4 weeks. Results Concentrations of total carnitine in plasma, liver and longissimus dorsi and biceps femoris muscles were 2.0–2.7 fold higher in group CARN than in group CON, whereas these concentrations were 1.9–2.5-fold lower in group PIV than in group CON. The concentrations of total carnitine in these tissues did not statistically differ between group CARN + PIV and group CON. Fiber type distribution of longissimus dorsi and biceps femoris muscles, mRNA and protein levels of molecular regulators of fiber distribution in longissimus dorsi and biceps femoris muscles and mRNA levels of genes reflecting the metabolic phenotype of longissimus dorsi and biceps femoris muscles did not differ between groups. Conclusion Changes in the systemic carnitine status and the muscle carnitine concentration induced by either supplementing L-carnitine or administering pivalate have no impact on the contractile and metabolic phenotype of skeletal muscles in pigs