Einfluss von Fluorid-Ionen auf die Dynamik der galvanischen Korrosion im System Titan-Implantat / Abutment / Suprakonstruktion (Titan / Titan und Titan / Co-Cr-Mo-Legierung)

Die Fluoridexposition im Rahmen der täglichen Zahnpflege kann das galvanische Korrosionsverhalten von Implantatmaterialien empfindlich beeinflussen. Von besonderem Interesse ist dabei die Dynamik der Reaktion auf eine spontane Fluoridexposition. Zur Untersuchung dieser Dynamik wurde die Reaktion der Kopplungen Ti/Ti und Ti/CoCrMo auf die Zugabe verschiedener Fluoridkonzentrationen sowohl im neutralen als auch im sauren Milieu mittels elektrochemischer Rauschmessungen aufgezeichnet. Anschließend erfolgten eine optische Oberflächenbewertung und eine Ermittlung des Massenverlustes an den Proben. Während sich Ti/CoCrMo nicht beeinflussen ließ, zeigte Ti/Ti – abhängig von pH-Wert und Fluoridkonzentration – Veränderungen im galvanischen Korrosionsverhalten. Diese reichten von einer temporären Beeinträchtigung der Passivierungsschicht mit anschließender Repassivierung bis zur aktiven Korrosion mit signifikantem Massenverlust. Aus den Untersuchungen folgt, dass bei Ti/Ti die Kombination von hoher Fluoridkonzentration und niedrigem pH-Wert zu vermeiden ist – insbesondere bei längerer Expositionsdauer. Dagegen ist Ti/CoCrMo gegenüber Fluoriden äußerst unempfindlich

„Letzlich ist es die Liebe, die alles zusammenhält.”: Interview mit Dževad Karahasan

Ein Gespräch mit dem Autor Dževad Karahasan über seine Liebe zur Kunst, die Liebe in seinem Roman "Der nächtliche Rat (Noćno vijeće)" und über die besondere Spannung in seinem Heimatland Bosnien-Herzegovina

From insect to man: Photorhabdus sheds light on the emergence of human pathogenicity

Photorhabdus are highly effective insect pathogenic bacteria that exist in a mutualistic relationship with Heterorhabditid nematodes. Unlike other members of the genus, Photorhabdus asymbiotica can also infect humans. Most Photorhabdus cannot replicate above 34°C, limiting their host-range to poikilothermic invertebrates. In contrast, P. asymbiotica must necessarily be able to replicate at 37°C or above. Many well-studied mammalian pathogens use the elevated temperature of their host as a signal to regulate the necessary changes in gene expression required for infection. Here we use RNA-seq, proteomics and phenotype microarrays to examine temperature dependent differences in transcription, translation and phenotype of P. asymbiotica at 28°C versus 37°C, relevant to the insect or human hosts respectively. Our findings reveal relatively few temperature dependant differences in gene expression. There is however a striking difference in metabolism at 37°C, with a significant reduction in the range of carbon and nitrogen sources that otherwise support respiration at 28°C. We propose that the key adaptation that enables P. asymbiotica to infect humans is to aggressively acquire amino acids, peptides and other nutrients from the human host, employing a so called “nutritional virulence” strategy. This would simultaneously cripple the host immune response while providing nutrients sufficient for reproduction. This might explain the severity of ulcerated lesions observed in clinical cases of Photorhabdosis. Furthermore, while P. asymbiotica can invade mammalian cells they must also resist immediate killing by humoral immunity components in serum. We observed an increase in the production of the insect Phenol-oxidase inhibitor Rhabduscin normally deployed to inhibit the melanisation immune cascade. Crucially we demonstrated this molecule also facilitates protection against killing by the alternative human complement pathway

The balance between the intronic miR-342 and its host gene Evl determines hematopoietic cell fate decision

Protein-coding and non-coding genes like miRNAs tightly control hematopoietic differentiation programs. Although miRNAs are frequently located within introns of protein-coding genes, the molecular interplay between intronic miRNAs and their host genes is unclear. By genomic integration site mapping of gamma-retroviral vectors in genetically corrected peripheral blood from gene therapy patients, we identified the EVL/MIR342 gene locus as a hotspot for therapeutic vector insertions indicating its accessibility and expression in human hematopoietic stem and progenitor cells. We therefore asked if and how EVL and its intronic miRNA-342 regulate hematopoiesis. Here we demonstrate that overexpression (OE) of Evl in murine primary Lin- Sca1+ cKit+ cells drives lymphopoiesis whereas miR-342 OE increases myeloid colony formation in vitro and in vivo, going along with a profound upregulation of canonical pathways essential for B-cell development or myelopoietic functions upon Evl or miR-342 OE, respectively. Strikingly, miR-342 counteracts its host gene by targeting lymphoid signaling pathways, resulting in reduced pre-B-cell output. Moreover, EVL overexpression is associated with lymphoid leukemia in patients. In summary, our data show that one common gene locus regulates distinct hematopoietic differentiation programs depending on the gene product expressed, and that the balance between both may determine hematopoietic cell fate decision