Grundlagen der Solarenergieumwandlung auf der Basis von Fluoreszenzkollektoren.

Der Schwerpunkt der Arbeiten lag in der Messung und Untersuchung von Fluoreszenzfarbstoffen und transparenten Matrixmaterialien hinsichtlich ihrer Eignung für den Einsatz in Fluoreszenzkollektoren. Im sichtbaren Spektralbereich konnte dabei auf neue Farbstoffentwicklungen aus dem Displayanwendungsgebiet zurückgegriffen werden. Insgesamt zeigte es sich, daß im sichtbaren Spektralbereich die Kombination von organischem Farbstoff und Plexiglas zu brauchbaren Ergebnissen sowohl hinsichtlich des Wirkungsgrades wie auch der Stabilität führen kann. In beiden Teilbereichen konnten im Laufe des Vorhabens Verbesserungen erzielt werden. Ein praktischer Einsatz ist jedoch.derzeit noch nicht möglich. Erste Versuchskollektoren befinden sich im Dauerversuch auf einem Freiluftmeßstand. Im roten bzw. infraroten Spektralbereich sind die Eigenschaften der Farbstoffe bzw. Kollektoren noch nicht ausreichend. Eine spezielle Farbstoffentwicklung auf diesem Gebiet hat im Frühjahr 1980 bei der Industrie begonnen

Respiratory chain signalling is essential for adaptive remodelling following cardiac ischaemia

Abstract Cardiac ischaemia-reperfusion (I/R) injury has been attributed to stress signals arising from an impaired mitochondrial electron transport chain (ETC), which include redox imbalance, metabolic stalling and excessive production of reactive oxygen species (ROS). The alternative oxidase (AOX) is a respiratory enzyme, absent in mammals, that accepts electrons from a reduced quinone pool to reduce oxygen to water, thereby restoring electron flux when impaired and, in the process, blunting ROS production. Hence, AOX represents a natural rescue mechanism from respiratory stress. This study aimed to determine how respiratory restoration through xenotopically expressed AOX affects the re-perfused post-ischaemic mouse heart. As expected, AOX supports ETC function and attenuates the ROS load in post-anoxic heart mitochondria. However, post-ischaemic cardiac remodelling over 3 and 9 weeks was not improved. AOX blunted transcript levels of factors known to be up-regulated upon I/R such as the atrial natriuretic peptide (Anp) whilst expression of pro-fibrotic and pro-apoptotic transcripts were increased. Ex vivo analysis revealed contractile failure at nine but not 3 weeks after ischaemia whilst label-free quantitative proteomics identified an increase in proteins promoting adverse extracellular matrix remodelling. Together, this indicates an essential role for ETC-derived signals during cardiac adaptive remodelling and identified ROS as a possible effector.Peer reviewe

Respiratory chain signalling is essential for adaptive remodelling following cardiac ischaemia

Abstract Cardiac ischaemia-reperfusion (I/R) injury has been attributed to stress signals arising from an impaired mitochondrial electron transport chain (ETC), which include redox imbalance, metabolic stalling and excessive production of reactive oxygen species (ROS). The alternative oxidase (AOX) is a respiratory enzyme, absent in mammals, that accepts electrons from a reduced quinone pool to reduce oxygen to water, thereby restoring electron flux when impaired and, in the process, blunting ROS production. Hence, AOX represents a natural rescue mechanism from respiratory stress. This study aimed to determine how respiratory restoration through xenotopically expressed AOX affects the re-perfused post-ischaemic mouse heart. As expected, AOX supports ETC function and attenuates the ROS load in post-anoxic heart mitochondria. However, post-ischaemic cardiac remodelling over 3 and 9 weeks was not improved. AOX blunted transcript levels of factors known to be up-regulated upon I/R such as the atrial natriuretic peptide (Anp) whilst expression of pro-fibrotic and pro-apoptotic transcripts were increased. Ex vivo analysis revealed contractile failure at nine but not 3 weeks after ischaemia whilst label-free quantitative proteomics identified an increase in proteins promoting adverse extracellular matrix remodelling. Together, this indicates an essential role for ETC-derived signals during cardiac adaptive remodelling and identified ROS as a possible effector.Peer reviewe

Coi1 is a novel assembly factor of the yeast complex III–complex IV supercomplex

The yeast bc1 complex (complex III) and cytochrome oxidase (complex IV) are mosaics of core subunits encoded by the mitochondrial genome and additional nuclear-encoded proteins imported from the cytosol. Both complexes build in the mitochondrial inner membrane various supramolecular assemblies. The formation of the individual complexes and their supercomplexes depends on the activity of dedicated assembly factors. We identified a so far uncharacterized mitochondrial protein (open reading frame YDR381C-A) as an important assembly factor for complex III, complex IV, and their supercomplexes. Therefore, we named this protein Cox interacting (Coi) 1. Deletion of COI1 results in decreased respiratory growth, reduced membrane potential, and hampered respiration, as well as slow fermentative growth at low temperature. In addition, coi1Δ cells harbour reduced steady-state levels of subunits of complexes III and IV as well as of the assembled complexes and supercomplexes. Interaction of Coi1 with respiratory chain subunits seems transient, as it appears to be a stoichiometric subunit neither of complex III nor of complex IV. Collectively, this work identifies a novel protein that plays a role in the assembly of the mitochondrial respiratory chain

Prevalence and Severity of Potential Drug–Drug Interactions in Patients with Multiple Sclerosis with and without Polypharmacy

Polypharmacy (PP) is a common problem in modern medicine, especially known to affect patients with chronic diseases such as multiple sclerosis (MS). With an increasing number of drugs taken, the risk of potential drug–drug interactions (pDDIs) is rising. This study aims to assess the prevalence and clinical relevance of polypharmacy and pDDIs in patients with MS. Pharmacological data of 627 patients with MS were entered into two drug–drug-interaction databases to determine the number and severity of pDDIs for each patient. The patients were divided into those with and without PP (total PP and prescription medication PP (Rx PP)). Of the 627 patients included, 53.3% and 38.6% had total PP and Rx PP, respectively. On average, every patient took 5.3 drugs. Of all patients, 63.8% had at least one pDDI with a mean of 4.6 pDDIs per patient. Less than 4% of all pDDIs were moderately severe or severe. Medication schedules should be checked for inappropriate medication and for possible interacting drugs to prevent pDDIs. Physicians as well as pharmacists should be more sensitive towards the relevance of pDDIs and know how they can be detected and avoided

Spatially resolved solid-state reduction of graphene oxide thin films

Re-establishment of electrical conductivity in graphene oxide (GO), the insulating form of graphene, is (partially) accomplished by reduction through high temperature treatments in a reducing atmosphere, or using strongly reducing chemicals or electrolytic processes. The reduction methods are suited for bulk graphene oxide. Spatially resolved reduction of thin films of graphene oxide is important for a wide range of applications such as in microelectronics, where an electrolyte-free, room temperature reduction process is needed. Here, we present spatially resolved solid-state reduction of graphene oxide thin films. We demonstrate that the reduction mechanism is based on electrolysis of water that is adsorbed on the graphene oxide thin film. The reduced graphene oxide thin-films show sheet resistance of only several kOhm, with weak temperature dependence. Graphene oxide can be produced on a large scale and processed using low-cost solution casting techniques. Spatially resolved re-establishment of conductivity in GO can be used in electrically controlled water permeation or in micro- and nanoelectronic applications for instance as an anti-fuse.Novel Aerospace Material

A salvage pathway maintains highly functional respiratory complex I

Regulation of the turnover of complex I (CI), the largest mitochondrial respiratory chain complex, remains enigmatic despite huge advancement in understanding its structure and the assembly. Here, we report that the NADH-oxidizing N-module of CI is turned over at a higher rate and largely independently of the rest of the complex by mitochondrial matrix protease ClpXP, which selectively removes and degrades damaged subunits. The observed mechanism seems to be a safeguard against the accumulation of dysfunctional CI arising from the inactivation of the N-module subunits due to attrition caused by its constant activity under physiological conditions. This CI salvage pathway maintains highly functional CI through a favorable mechanism that demands much lower energetic cost than de novo synthesis and reassembly of the entire CI. Our results also identify ClpXP activity as an unforeseen target for therapeutic interventions in the large group of mitochondrial diseases characterized by the CI instability. Maintenance and quality control of the mitochondrial respiratory chain complexes responsible for bulk energy production are unclear. Here, the authors show that the mitochondrial protease ClpXP is required for the rapid turnover of the core N-module of respiratory complex I, which happens independently of other modules in the complex

Respiratory chain signalling is essential for adaptive remodelling following cardiac ischaemia.

Cardiac ischaemia-reperfusion (I/R) injury has been attributed to stress signals arising from an impaired mitochondrial electron transport chain (ETC), which include redox imbalance, metabolic stalling and excessive production of reactive oxygen species (ROS). The alternative oxidase (AOX) is a respiratory enzyme, absent in mammals, that accepts electrons from a reduced quinone pool to reduce oxygen to water, thereby restoring electron flux when impaired and, in the process, blunting ROS production. Hence, AOX represents a natural rescue mechanism from respiratory stress. This study aimed to determine how respiratory restoration through xenotopically expressed AOX affects the re-perfused post-ischaemic mouse heart. As expected, AOX supports ETC function and attenuates the ROS load in post-anoxic heart mitochondria. However, post-ischaemic cardiac remodelling over 3 and 9 weeks was not improved. AOX blunted transcript levels of factors known to be up-regulated upon I/R such as the atrial natriuretic peptide (Anp) whilst expression of pro-fibrotic and pro-apoptotic transcripts were increased. Ex vivo analysis revealed contractile failure at nine but not 3 weeks after ischaemia whilst label-free quantitative proteomics identified an increase in proteins promoting adverse extracellular matrix remodelling. Together, this indicates an essential role for ETC-derived signals during cardiac adaptive remodelling and identified ROS as a possible effector