Integrated coupled systems as biodegradability enhancement of textile wastewater by photo-fenton process

Photo-Fenton process was explored as photochemicalpre-treatment to enhance and improve the biodegradabilityand complete mineralization of a wastewater coming from a textile industry located in the east of Germany containing reactive dyes which was characterized as biorecalcitrant,non-biodegradable and refractory organic compounds.Wastewater treatment was carried out including a series of bench scale experiments, to identify optimum operating conditions for the treatment of textile wastewater at the end of the pipe effluent. The effect of operating parameters as: pH, irradiation time and initial concentrations of both H2O2 and Fe2+ on the photomineralization processes as a pretreatment step have been studied and the optimal conditions were found. Chemical oxygen demand (COD), total organic carbon (TOC) and colour removal are the parameters used to trace the experiments course.The color removal of the textile wastewater reached to above 100% within 30 min of photocatalytic treatment. The wastewater was completely degraded by a photo-Fenton treatment after 60 min irradiation time by using a 50 mg/L of Fe2+ catalyst concentration and the H2O2 concentration was 1000 mg/L and pH=3 at 25°C. At these optimum operating conditions % removal of TOC, COD and colour removal were 89, 95 and 100 respectively of photo-mineralization. The experimental results show that the ratio of BOD5/COD of the wastewater increased from original 0.09 up to 0.7 after 60 min. The result implies that photocatalytic oxidation enhanced the biodegradability of the dye-containing wastewater and therefore relationship between decolorization and biodegradability exists.When the color disappeared completely, the wastewaterbiodegraded normally and could be discharged for furthertreatment. The biodegradability tests also demonstratedthat photo-treated effluents within a short time of startingthe photo-Fenton process were biodegradable with a BOD5/COD ratio of 0.4 after 30 min of irradiation time.The experimental results demonstrate that it is possible tocombine photocatalysis with conventional biological treatmentfor the remedy of wastewater containing generally non-biodegradable azo dyes. The results of the present study revealed that the treated effluent by photo-Fenton process is complying with the environmental regulations for discharge of textile wastewater in Germany

How is GABA_A receptor mediated central inhibition enhanced by nitrous oxide, xenon and isoflurane?

Ein wesentlicher Wirkmechanismus von Allgemeinanästhetika besteht in der Verstärkung neuronaler Inhibition. Gamma-Aminobuttersäure (GABA) ist der vorherrschende inhibitorische Neurotransmitter im ZNS. Der GABAA-Rezeptor, der die schnelle inhibitorische synaptische Transmission vermittelt, gilt als ein wichtiger Angriffsort für Allgemeinanästhetika. Die vorliegende Dissertation beschreibt den Effekt der gasförmigen Anästhestika Lachgas (N2O) und Xenon (Xe) sowie des volatilen Anästhetikums Isofluran (ISO) auf den GABAA-Rezeptor. Hierfür wurden mittels Patch-Clamp-Technik GABA-induzierte Ströme von HEK 293 Zellen, die einen rekombinanten Alpha1Beta2Gamma2L-GABAA-Rezeptor der Ratte exprimieren, gemessen. Die gemessenen Ströme wurden anhand eines kinetischen Modells des GABAA-Rezeptors simuliert, um den Effekt der Anästhetika qualitativ und quantitativ zu beschreiben. N2O, Xe und ISO erhöhen die Wirksamkeit von GABA am GABAA-Rezeptor. Anhand des kinetischen Modells lässt sich zeigen, dass N2O und Xe diesen Effekt durch Verstärkung der GABA-Assoziation bewirken, ISO hingegen durch Verminderung der GABA-Dissoziation. Gleichzeitig blockiert ISO den offenen GABAA-Kanal, ein Effekt, der sich insbesondere bei höheren ISO-Konzentrationen zeigt. Die verzögerte GABA-Dissoziation durch ISO erklärt die Verlängerung des Zeitverlaufs GABAA-Rezeptor-vermittelter postsynaptischer Ströme. Der Offenkanalblock erklärt die Verminderung deren Amplitude. Bei klinisch relevanten Konzentrationen von ISO überwiegt dabei möglicherweise die Verlängerung des Zeitverlaufs, was insgesamt zu einer vermehrten postsynaptischen GABAergen Hyperpolarisation führt. Die untersuchten Anästhetika verstärken die GABAAerge synaptische Transmission durch direkte postsynaptische Wirkung. GABAerge Interneurone sind, insbesondere im Hippocampus, divergent verschaltet. Insgesamt kann dies die deutlich verstärkte neuronale Inhibition im Zustand der Allgemeinanästhesie miterklären.Enhancement of central inhibition is one major mechanism of general anaesthetics. gamma-aminobutyric acid (GABA) is the predominant inhibitory neurotransmitter, and the GABAA receptor is an important target for general anaesthetics. The present thesis investigates the effect of the gaseous anaesthetics nitrous oxide (N2O) and xenon (Xe), and the volatile anaesthetic isoflurane (ISO) on the GABAA receptor. We used the patch-clamp technique to record GABA-induced whole-cell currents from HEK 293 cells expressing a rat recombinant alpha1beta2gamma2L-GABAA receptor. The measured currents were simulated with a kinetic model of the GABAA receptor to detail the effects of the anaesthetics. N2O, Xe, and ISO increase the efficacy of GABA to evoke GABAA receptor-mediated currents. Kinetic modelling suggested that N2O and Xe mediate this effect by enhancing the GABA binding, whereas ISO reduces the GABA unbinding. Simultaneously, ISO blocks the opened GABAA receptor channel, an effect which is more prominent at higher concentrations of ISO. The reduced GABA-unbinding by ISO explains the prolonged time course of GABAA receptor-mediated postsynaptic currents. The open channel block explains the decrease in amplitude of these currents. At clinically relevant concentrations of ISO, the prolonging effect might outweigh the blocking effect and, thus, result in increased GABA-mediated postsynaptic hyperpolarisation. Our data are in favour of a direct postsynaptic effect of the investigated anaesthetics on GABAA receptor-mediated synaptic transmission. This could explain in part the enhanced central inhibition during the state of anaesthesia

Sevoflurane Anesthesia Improves Cognitive Performance in Mice, but Does Not Influence In Vitro Long-Term Potentation in Hippocampus CA1 Stratum Radiatum

BACKGROUND: Whether the occurrence of postoperative cognitive dysfunction is a result of the effects of surgery or anesthesia is under debate. In this study, we investigated the impact of sevoflurane anesthesia on cognitive performance and cellular mechanisms involved in learning and memory. METHODS: Male C57Bl6/J mice (4–5 months) were exposed to one minimum alveolar concentration sevoflurane for two hours. After 24 h, cognitive performance of mice was assessed using the modified hole board test. Additionally, we evaluated hippocampal long-term potentiation and expression levels of different receptor subunits by recording excitatory postsynaptic field potentials and using the western blot technique, respectively. Non-anesthetized mice served as controls. RESULTS: In anesthetized mice, neither cognitive performance nor long-term potentiation was impaired 24 h after anesthesia. Interestingly, sevoflurane anesthesia induced even an improvement of cognitive performance and an elevation of the expression levels of N-methyl-D-aspartate (NMDA) receptor type 1 and 2B subunits in the hippocampus. CONCLUSIONS: Since NMDA receptor type 1 and 2B subunits play a crucial role in processes related to learning and memory, we hypothesize that sevoflurane-induced changes in NMDA receptor subunit composition might cause hippocampus-dependent cognitive improvement. The data of the present study are in favor of a minor role of anesthesia in mediating postoperative cognitive dysfunction

Key characteristics impacting survival of COVID-19 extracorporeal membrane oxygenation

Background Severe COVID-19 induced acute respiratory distress syndrome (ARDS) often requires extracorporeal membrane oxygenation (ECMO). Recent German health insurance data revealed low ICU survival rates. Patient characteristics and experience of the ECMO center may determine intensive care unit (ICU) survival. The current study aimed to identify factors affecting ICU survival of COVID-19 ECMO patients. Methods 673 COVID-19 ARDS ECMO patients treated in 26 centers between January 1st 2020 and March 22nd 2021 were included. Data on clinical characteristics, adjunct therapies, complications, and outcome were documented. Block wise logistic regression analysis was applied to identify variables associated with ICU-survival. Results Most patients were between 50 and 70 years of age. PaO2/FiO2 ratio prior to ECMO was 72 mmHg (IQR: 58–99). ICU survival was 31.4%. Survival was significantly lower during the 2nd wave of the COVID-19 pandemic. A subgroup of 284 (42%) patients fulfilling modified EOLIA criteria had a higher survival (38%) (p = 0.0014, OR 0.64 (CI 0.41–0.99)). Survival differed between low, intermediate, and high-volume centers with 20%, 30%, and 38%, respectively (p = 0.0024). Treatment in high volume centers resulted in an odds ratio of 0.55 (CI 0.28–1.02) compared to low volume centers. Additional factors associated with survival were younger age, shorter time between intubation and ECMO initiation, BMI > 35 (compared to < 25), absence of renal replacement therapy or major bleeding/thromboembolic events. Conclusions Structural and patient-related factors, including age, comorbidities and ECMO case volume, determined the survival of COVID-19 ECMO. These factors combined with a more liberal ECMO indication during the 2nd wave may explain the reasonably overall low survival rate. Careful selection of patients and treatment in high volume ECMO centers was associated with higher odds of ICU survival

Xenon reduces N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-mediated synaptic transmission in the amygdala.

BACKGROUND: The neuronal and molecular targets of the inhalational general anesthetic xenon are a matter of debate. The current knowledge is largely based on studies using neurons in culture or heterologous expression systems. In the current study, the authors evaluated for the first time the effect of xenon on synaptic transmission in the basolateral amygdala in an in vitro brain slice preparation of the mouse. METHODS: A patch clamp technique was used to evaluate the effects of xenon on N-methyl-d-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated excitatory postsynaptic currents (EPSCs), as well as on gamma-aminobutyric acid type A receptor-mediated inhibitory postsynaptic currents. The currents were either evoked upon electrical stimulation (NMDA-eEPSCs, AMPA-eEPSCs) or upon focal, laser-guided photolysis of caged l-glutamate (p-NMDA-Cs, p-AMPA-Cs). In addition, the authors investigated the effects of xenon on miniature EPSCs. RESULTS: Xenon reversibly reduced basal synaptic transmission but had no effect on gamma-aminobutyric acid type A receptor-mediated inhibitory synaptic transmission. Xenon concentration-dependently diminished NMDA-eEPSCs and p-NMDA-Cs to the same amount. Likewise, xenon-induced reduction of AMPA-eEPSCs and p-AMPA-Cs did not differ. Xenon did not affect the frequency of miniature EPSCs but reduced their amplitude. CONCLUSIONS: In the current study, xenon considerably depressed NMDA and AMPA receptor-mediated synaptic transmission in the basolateral amygdala without affecting inhibitory synaptic transmission. The results provide evidence that the effects of xenon on NMDA- and AMPA-EPSCs are primarily mediated via postsynaptic mechanisms

Neuronale Wirkmechanismen von Inhalationsanästhetika

Die Mechanismen, die auf neuronaler Ebene für die Wirkung der Inhalationsanästhetika Xenon und Isofluran verantwortlich sind, sind bisher nicht geklärt. Im Rahmen dieses Habilitationsvorhabens wurde mit elektrophysiologischen Methoden die Wirkung der beiden Substanzen auf verschiedene Komponenten der synaptischen Transmission in Nagetier-Hirnschnittpräparaten Anästhesie-relevanter ZNS-Regionen untersucht. Die Wirkung der beiden Anästhetika auf die inhibitorische synaptische Transmission unterschied sich deutlich: Während Isofluran diese verstärkte, zeigte Xenon keinen Einfluss darauf. Eine deutliche Hemmung der glutamatergen exzitatorischen synaptischen Transmission konnte hingegen unter beiden Substanzen festgestellt werden, wobei Xenon diese über postsynaptische, Isofluran dagegen über präsynaptische Mechanismen vermittelte. Entsprechend den physiologischen Funktionen der untersuchten ZNS-Areale Amygdala, Kortex und Rückenmarks-Hinterhorn könnten die gezeigten Wirkungen den amnestischen, hypnotischen und analgetischen Eigenschaften der Substanzen zu Grunde liegen

[Postoperative cognitive dysfunction. Possible neuronal mechanisms and practical consequences for clinical routine].

Postoperative cognitive dysfunction (POCD) presents as a long-lasting decline in cognitive function after a surgical procedure, predominantly occurring in elderly patients. The causes are most likely multifactorial with the exact mechanisms still unknown. Hypotheses of the causes of POCD are based on experimental evidence that anesthetics can impair mechanisms of learning and memory on a neuronal level and might lead to neurodegeneration. Additionally, surgery can result in neuroinflammation which could also underlie POCD. The most important strategy to avoid POCD is to maintain the patient's physiological homeostasis perioperatively. According to the presently available clinical studies recommendations in favor or against certain anesthesiological procedures cannot be given

Design and implementation of interaction interfaces into a realtime VR application for the presentation of CAD interiors

In dieser Arbeit werden mehrere Interaktionskonzepte zur Steuerung einer VR-Anwendung entworfen und implementiert. Um ihre Gebrauchstauglichkeit zu bewerten, erfolgt die Evaluation der Konzepte durch Nutzergruppen der Anwendung. Die Anwendung dient der Visualisierung von Raumplanungen aus CAD-Daten

The xenon-mediated antagonism against the NMDA receptor is non-selective for receptors containing either NR2A or NR2B subunits in the mouse amygdala.

In pharmacological studies using cultured neurones or heterologous expression systems, the N-methyl-d-aspartate (NMDA) receptor has been found as a major target for the inhalational anaesthetic xenon (Xe). NMDA receptors play a crucial role in behavioural and cellular processes related to learning and memory, and NMDA receptor subunits type 2A (NR2A) and type 2B (NR2B) are critical determinants for synaptic plasticity. In the present study, we investigated in an acute mouse brain slice preparation of the basolateral amygdala whether the antagonism of Xe is subunit-selective against the NR2A or NR2B subunit. From principal neurones, pharmacologically isolated NMDA receptor-mediated currents (p-NMDA-Cs) were evoked upon focal photolysis of caged L-glutamate and recorded using the whole-cell patch-clamp technique. To test whether the Xe-induced inhibition of NMDA receptor-mediated currents is selective for NR2A or NR2B subunits, p-NMDA-Cs were recorded in the presence of the NR2A or NR2B subunit antagonists R-S-1-4-bromophenylethylamino-2,3-dioxo-1,2,3,4-tetrahydroquinoxalin-5-yl-methylphosphonic acid (NVP-AAM077, 50 nM) or R-R*,S*-alpha-4-Hydroxyphenyl-beta-methyl-4-phenylmethyl-1-piperidinepropanol hydrochloride (Ro 25-6981, 0.5 microM), respectively. The Xe-induced reduction under these conditions was not significantly different from that without NR2A or NR2B blockade. These results provide evidence, that the Xe-induced antagonism against NMDA receptors is non-selective against NR2A- or NR2B-containing receptors