Sorption of tetracycline and chlortetracycline on K- and Ca-saturated soil clays, humic substances, and clay-humic complexes

Tetracycline (TC) and chlortetracycline (CTC) are used extensively for growth promotion and therapeutic purposes in livestock production. The sorption of TC and CTC on clays, humic substances (HS), and clay-humic complexes (clay-HC) derived from two agricultural soils was quantified using dilute CaCl2 (Ca) and KCI (K) as background solutions. In all systems, the soil components sorbed > 96% of added tetracyclines. Strongest sorption was observed for clays, followed by HS, and then clay-HC. Greater sorption by the Ca systems than the K systems and decreased sorption with increasing pH suggests that cation bridging and cation exchange contribute to sorption. X-ray diffraction analysis showed that TC and CTC were sorbed in the interlayers of smectites and that the presence of HS reduced interlayer sorption of tetracyclines by smectites in clay-HC. The results indicate that tetracyclines are dominantly sorbed on soil clays and that HS in clay-HC either mask sorption sites on clay surfaces or inhibit interlayer diffusion of tetracyclines.     

CXCR4 and CXCR7 Inhibition Ameliorates the Formation of Platelet–Neutrophil Complexes and Neutrophil Extracellular Traps through Adora2b Signaling

Peritonitis and peritonitis-associated sepsis are characterized by an increased formation of platelet–neutrophil complexes (PNCs), which contribute to an excessive migration of polymorphonuclear neutrophils (PMN) into the inflamed tissue. An important neutrophilic mechanism to capture and kill invading pathogens is the formation of neutrophil extracellular traps (NETs). Formation of PNCs and NETs are essential to eliminate pathogens, but also lead to aggravated tissue damage. The chemokine receptors CXCR4 and CXCR7 on platelets and PMNs have been shown to play a pivotal role in inflammation. Thereby, CXCR4 and CXCR7 were linked with functional adenosine A2B receptor (Adora2b) signaling. We evaluated the effects of selective CXCR4 and CXCR7 inhibition on PNCs and NETs in zymosan- and fecal-induced sepsis. We determined the formation of PNCs in the blood and, in addition, their infiltration into various organs in wild-type and Adora2b−/− mice by flow cytometry and histological methods. Further, we evaluated NET formation in both mouse lines and the impact of Adora2b signaling on it. We hypothesized that the protective effects of CXCR4 and CXCR7 antagonism on PNC and NET formation are linked with Adora2b signaling. We observed an elevated CXCR4 and CXCR7 expression in circulating platelets and PMNs during acute inflammation. Specific CXCR4 and CXCR7 inhibition reduced PNC formation in the blood, respectively, in the peritoneal, lung, and liver tissue in wild-type mice, while no protective anti-inflammatory effects were observed in Adora2b−/− animals. In vitro, CXCR4 and CXCR7 antagonism dampened PNC and NET formation with human platelets and PMNs, confirming our in vivo data. In conclusion, our study reveals new protective aspects of the pharmacological modulation of CXCR4 and CXCR7 on PNC and NET formation during acute inflammation.     

Bewertung der Weiterverwendung einer alten Stahlbrücke auf der Grundlage bruchmechanischer Methoden

Evaluation of the further use of an old steel bridge on the basis of fracture‐mechanics methods. By the example of the bridge at the Dornheimer Weg in Darmstadt, which was built at the beginning of the 20^th century, the application of a fracture‐mechanics analysis procedure for the further use of old steel bridges is presented in this paper. Therefore the so‐called critical components of the bridge are determined, and for these elements the cross‐section items are represented by fracture‐mechanics models (cracked plates). By the assumption of a starting damage in form of a crack the remaining endurance of the component up to achieving the crack length leading to the failure can be determined by using a fatigue crack growth calculation. As far as possible a refinement of the models can be made, in order to avoid a too conservative estimation of the remaining endurance after the first run of the procedure. After iterative application of this method the final calculated endurance of the critical components arises, and it is possible to make a recapitulatory evaluation for the further use of the bridge.     

Identification of emotional facial expressions following recovery from depression.

This study investigated the identification of facial expressions of emotion in currently nondepressed participants who had a history of recurrent depressive episodes (recurrent major depression; RMD) and never-depressed control participants (CTL). Following a negative mood induction, participants were presented with faces whose expressions slowly changed from neutral to full intensity. Identification of facial expressions was measured by the intensity of the expression at which participants could accurately identify whether faces expressed happiness, sadness, or anger. There were no group differences in the identification of sad or angry expressions. Compared with CTL participants, however, RMD participants required significantly greater emotional intensity in the faces to correctly identify happy expressions. These results indicate that biases in the processing of emotional facial expressions are evident even after individuals have recovered from a depressive episode. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Structure-based synthetic mimicry of discontinuous protein binding sites: inhibitors of the interaction of Mena EVH1 domain with proline-rich ligands

The Mena EVH1 domain, a protein-interaction module involved in actin-based cell motility, recognizes proline-rich ligand motifs, which are also present in the sequence of the surface protein ActA of Listeria monocytogenes. The interaction of ActA with host Mena EVH1 enables the bacterium to actively recruit host actin in order to spread into neighboring cells. Based on the crystal structure of Mena EVH1 in complex with a polyproline peptide ligand, we have generated a range of assembled peptides presenting the Mena EVH1 fragments that make up its discontinuous binding site for proline-rich ligands. Some of these peptides were found to inhibit the interaction of Mena EVH1 with the ligand pGolemi. One of them was further characterized at the level of individual amino acid residues; this yielded information on the contribution of individual positions of the peptides to the interaction with the ligand and identified sites for future structure optimization.     

IL-18 But Not IL-1 Signaling Is Pivotal for the Initiation of Liver Injury in Murine Non-Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is rising in prevalence, and a better pathophysiologic understanding of the transition to its inflammatory phenotype (NASH) is key to the development of effective therapies. To evaluate the contribution of the NLRP3 inflammasome and its downstream effectors IL-1 and IL-18 in this process, we applied the true-to-life “American lifestyle-induced obesity syndrome” (ALiOS) diet mouse model. Development of obesity, fatty liver and liver damage was investigated in mice fed for 24 weeks according to the ALiOS protocol. Lipidomic changes in mouse livers were compared to human NAFLD samples. Receptor knockout mice for IL-1 and IL-18 were used to dissect the impact of downstream signals of inflammasome activity on the development of NAFLD. The ALiOS diet induced obesity and liver steatosis. The lipidomic changes closely mimicked changes in human NAFLD. A pro-inflammatory gene expression pattern in liver tissue and increased serum liver transaminases indicated early liver damage in the absence of histological evidence of NASH. Mechanistically, Il-18r^−/−- but not Il-1r^−/− mice were protected from early liver damage, possibly due to silencing of the pro-inflammatory gene expression pattern. Our study identified NLRP3 activation and IL-18R-dependent signaling as potential modulators of early liver damage in NAFLD, preceding development of histologic NASH.     

Impact of the crystallographic structure of epitaxially grown strained sodium–bismuth–titanate thin films on local piezo- and ferroelectric properties

Thin films of different phases of lead-free sodium–bismuth–titanate were epitaxially grown on SrTiO₃ and NdGaO₃ substrates by metal–organic chemical vapor deposition. Aurivillius phases with m = 3, m = 3.5 and m = 4 and the Na_0.5Bi_0.5TiO₃ perovskite phase were obtained by varying the substrate temperature and the Na/Bi ratio in the gas phase. Investigations of the impact of crystallographic structure and incorporated film lattice strain on local piezo- and ferroelectric properties were carried out by piezoresponse force microscopy experiments using dual AC resonance tracking combined with a tip-sample contact modeling procedure to determine an effective value for the piezoelectric coefficient for each sample. Comparative piezoresponse force microscopy measurements revealed a significant increase of the average effective piezoelectric coefficient d_zz when the film structure changed from an Aurivillius phase to the perovskite phase. Films of perovskite phase have also shown the possibility of local tip-induced polarization switching.