University of Erlangen-Nuremberg

About: University of Erlangen-Nuremberg is a education organization based out in Erlangen, Bayern, Germany. It is known for research contribution in the topics: Population & Immune system. The organization has 42405 authors who have published 85600 publications receiving 2663922 citations.

High-performance direct conversion X-ray detectors based on sintered hybrid lead triiodide perovskite wafers

Abstract: Methyl ammonium lead triiodide perovskite wafers for application in direct conversion X-ray detectors are fabricated by a room-temperature sintering process. A conversion efficiency of 2,527 mC Gyaircm–2 under 70 kVp X-ray exposure is obtained.

Clinical fit of all-ceramic three-unit fixed partial dentures, generated with three different CAD/CAM systems

Abstract: In this study, the hypothesis was tested that the marginal and internal fit of CAD/CAM fabricated all-ceramic three-unit fixed partial dentures (FPDs) can be as good as in metal-ceramic FPDs. Twenty-four all-ceramic FPDs were fabricated and randomly subdivided into three equally sized groups. Eight frameworks were fabricated using the Digident CAD/CAM system (DIGI), another eight frameworks using the Cerec Inlab system (INLA). Vita Inceram Zirkonia blanks were used for both groups. In a third group frameworks were milled from yttrium-stabilized Zirconium blanks using the Lava system (LAVA). All frameworks were layered with ceramic veneering material. In addition, six three-unit metal-ceramic FPDs served as control group. All FPDs were evaluated using a replica technique with a light body silicone stabilized with a heavy body material. The replica samples were examined under microscope. The medians of marginal gaps were 75 microm for DIGI, 65 microm for LAVA and INLA and 54 microm for the conventional FPDs. Only the DIGI data differed significantly from those of the conventional FPDs. Within the limits of this study, the results suggest that the accuracy of CAD/CAM generated three-unit FPDs is satisfactory for clinical use.

Roles of the Candida albicans Mitogen-Activated Protein Kinase Homolog, Cek1p, in Hyphal Development and Systemic Candidiasis

Abstract: Extracellular signal-regulated protein kinase (ERK, or mitogen-activated protein kinase [MAPK]) regulatory cascades in fungi turn on transcription factors that control developmental processes, stress responses, and cell wall integrity. CEK1 encodes a Candida albicans MAPK homolog (Cek1p), isolated by its ability to interfere with the Saccharomyces cerevisiae MAPK mating pathway. C. albicans cells with a deletion of the CEK1 gene are defective in shifting from a unicellular budding colonial growth mode to an agar-invasive hyphal growth mode when nutrients become limiting on solid medium with mannitol as a carbon source or on glucose when nitrogen is severely limited. The same phenotype is seen in C. albicans mutants in which the homologs (CST20, HST7, and CPH1) of the S. cerevisiae STE20, STE7, and STE12 genes are disrupted. In S. cerevisiae, the products of these genes function as part of a MAPK cascade required for mating and invasiveness of haploid cells and for pseudohyphal development of diploid cells. Epistasis studies revealed that the C. albicans CST20, HST7, CEK1, and CPH1 gene products lie in an equivalent, canonical, MAPK cascade. While Cek1p acts as part of the MAPK cascade involved in starvation-specific hyphal development, it may also play independent roles in C. albicans. In contrast to disruptions of the HST7 and CPH1 genes, disruption of the CEK1 gene adversely affects the growth of serum-induced mycelial colonies and attenuates virulence in a mouse model for systemic candidiasis.

Mend Your Fences: The Epithelial Barrier and its Relationship With Mucosal Immunity in Inflammatory Bowel Disease

Abstract: The intestinal epithelium can be easily disrupted during gut inflammation as seen in inflammatory bowel disease (IBD), such as ulcerative colitis or Crohn's disease. For a long time, research into the pathophysiology of IBD has been focused on immune cell-mediated mechanisms. Recent evidence, however, suggests that the intestinal epithelium might play a major role in the development and perpetuation of IBD. It is now clear that IBD can be triggered by disturbances in epithelial barrier integrity via dysfunctions in intestinal epithelial cell-intrinsic molecular circuits that control the homeostasis, renewal, and repair of intestinal epithelial cells. The intestinal epithelium in the healthy individual represents a semi-permeable physical barrier shielding the interior of the body from invasions of pathogens on the one hand and allowing selective passage of nutrients on the other hand. However, the intestinal epithelium must be considered much more than a simple physical barrier. Instead, the epithelium is a highly dynamic tissue that responds to a plenitude of signals including the intestinal microbiota and signals from the immune system. This epithelial response to these signals regulates barrier function, the composition of the microbiota, and mucosal immune homeostasis within the lamina propria. The epithelium can thus be regarded as a translator between the microbiota and the immune system and aberrant signal transduction between the epithelium and adjacent immune cells might promote immune dysregulation in IBD. This review summarizes the important cellular and molecular barrier components of the intestinal epithelium and emphasizes the mechanisms leading to barrier dysfunction during intestinal inflammation.