@article{KaluzaWallaceHeardetal.2018,
  author    = {Kaluza, Benjamin F. and Wallace, Helen M. and Heard, Tim A. and Minden, Vanessa and Klein, Alexandra and Leonhardt, Sara D.},
  title     = {Social bees are fitter in more biodiverse environments},
  series = {Scientific Reports},
  volume    = {8},
  journal   = {Scientific Reports},
  number    = {12353},
  doi       = {10.1038/s41598-018-30126-0},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-177231},
  year      = {2018},
  abstract  = {Bee population declines are often linked to human impacts, especially habitat and biodiversity loss, but empirical evidence is lacking. To clarify the link between biodiversity loss and bee decline, we examined how floral diversity affects (reproductive) fitness and population growth of a social stingless bee. For the first time, we related available resource diversity and abundance to resource (quality and quantity) intake and colony reproduction, over more than two years. Our results reveal plant diversity as key driver of bee fitness. Social bee colonies were fitter and their populations grew faster in more florally diverse environments due to a continuous supply of food resources. Colonies responded to high plant diversity with increased resource intake and colony food stores. Our findings thus point to biodiversity loss as main reason for the observed bee decline.},
  language  = {en}
}
@article{BreyerGruenerKleinetal.2024,
  author    = {Breyer, Maximilian and Gr{\"u}ner, Julia and Klein, Alexandra and Finke, Laura and Klug, Katharina and Sauer, Markus and {\"U}{\c{c}}eyler, Nurcan},
  title     = {\(In\) \(vitro\) characterization of cells derived from a patient with the GLA variant c.376A>G (p.S126G) highlights a non-pathogenic role in Fabry disease},
  series = {Molecular Genetics and Metabolism Reports},
  volume    = {38},
  journal   = {Molecular Genetics and Metabolism Reports},
  issn      = {22144269},
  doi       = {10.1016/j.ymgmr.2023.101029},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-350295},
  year      = {2024},
  abstract  = {Highlights • The GLA variant S126G is not associated with Fabry symptoms in the presented case • S126G has no effect on α-GAL A activity or Gb3 levels in this patient • S126G sensory neurons show no electrophysiological abnormalities Abstract Fabry disease (FD) is a life-limiting disorder characterized by intracellular globotriaosylceramide (Gb3) accumulations. The underlying α-galactosidase A (α-GAL A) deficiency is caused by variants in the gene GLA. Variants of unknown significance (VUS) are frequently found in GLA and challenge clinical management. Here, we investigated a 49-year old man with cryptogenic lacunar cerebral stroke and the chance finding of the VUS S126G, who was sent to our center for diagnosis and initiation of a costly and life-long FD-specific treatment. We combined clinical examination with in vitro investigations of dermal fibroblasts (HDF), induced pluripotent stem cells (iPSC), and iPSC-derived sensory neurons. We analyzed α-GAL A activity in iPSC, Gb3 accumulation in all three cell types, and action potential firing in sensory neurons. Neurological examination and small nerve fiber assessment was normal except for reduced distal skin innervation. S126G iPSC showed normal α-GAL A activity compared to controls and no Gb3 deposits were found in all three cell types. Baseline electrophysiological characteristics of S126G neurons showed no difference compared to healthy controls as investigated by patch-clamp recordings. We pioneer multi-level cellular characterization of the VUS S126G using three cell types derived from a patient and provide further evidence for the benign nature of S126G in GLA, which is of great importance in the management of such cases in clinical practice.},
  language  = {en}
}