@article{KrannichThereseBroscheitetal.2012,
  author    = {Krannich, Jens-Holger and Therese, Tobias and Broscheit, Jens and Leyh, Rainer and M{\"u}llges, Wolfgang},
  title     = {Diabetes severely affects attentional performance after coronary artery bypass grafting},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75320},
  year      = {2012},
  abstract  = {Background: Diabetes is a risk factor for (micro) vascular damage of the brain, too. Therefore cognitive performance after coronary artery bypass grafting may be hypothesized worse in diabetics. To avoid observational errors a reliable tool for testing attentional performance was used. We evaluated whether diabetes mellitus disposes to distinct cognitive dysfunction after coronary artery bypass grafting (CABG). Methods: Three aspects in attentional performance were prospectively tested with three different tests (alertness: composed of un-cued and cued reaction, divided attention, and selective attention) by a computerized tool one day before and seven days after CABG in a highly selected cohort of 30 males, 10 of whom had diabetes. Statistical comparisons were done with analysis of variance for repeated measurements and Fisher´s LSD. Results: Prior to CABG there was no statistically meaningful difference between diabetics and non-diabetics. Postoperatively, diabetic patients performed significantly worse than non-diabetics in tests for un-cued (p=0.01) and cued alertness (p=0.03). Test performance in divided attention was worse after CABG but independent of diabetes status. Selective attention was neither affected by diabetes status nor by CABG itself. Conclusions: Diabetes may have an impact on cognitive performance after CABG. More severe deficits in alertness may point to underlying microvascular disease.},
  subject      = {Medizin},
  language  = {en}
}
@article{BoehmTorsinTintetal.2017,
  author    = {B{\"o}hm, Lena and Torsin, Sanda and Tint, Su Hlaing and Eckstein, Marie Therese and Ludwig, Tobias and P{\´e}rez, J. Christian},
  title     = {The yeast form of the fungus Candida albicans promotes persistence in the gut of gnotobiotic mice},
  series = {PLoS Pathogens},
  volume    = {13},
  journal   = {PLoS Pathogens},
  number    = {10},
  doi       = {10.1371/journal.ppat.1006699},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-159120},
  pages     = {e1006699},
  year      = {2017},
  abstract  = {Many microorganisms that cause systemic, life-threatening infections in humans reside as harmless commensals in our digestive tract. Yet little is known about the biology of these microbes in the gut. Here, we visualize the interface between the human commensal and pathogenic fungus Candida albicans and the intestine of mice, a surrogate host. Because the indigenous mouse microbiota restricts C. albicans settlement, we compared the patterns of colonization in the gut of germ free and antibiotic-treated conventionally raised mice. In contrast to the heterogeneous morphologies found in the latter, we establish that in germ free animals the fungus almost uniformly adopts the yeast cell form, a proxy of its commensal state. By screening a collection of C. albicans transcription regulator deletion mutants in gnotobiotic mice, we identify several genes previously unknown to contribute to in vivo fitness. We investigate three of these regulators—ZCF8, ZFU2 and TRY4—and show that indeed they favor the yeast form over other morphologies. Consistent with this finding, we demonstrate that genetically inducing non-yeast cell morphologies is detrimental to the fitness of C. albicans in the gut. Furthermore, the identified regulators promote adherence of the fungus to a surface covered with mucin and to mucus-producing intestinal epithelial cells. In agreement with this result, histology sections indicate that C. albicans dwells in the murine gut in close proximity to the mucus layer. Thus, our findings reveal a set of regulators that endows C. albicans with the ability to endure in the intestine through multiple mechanisms.},
  language  = {en}
}