@article{RommelMildeEberleetal.2020,
  author    = {Rommel, Marcel G. E. and Milde, Christian and Eberle, Regina and Schulze, Harald and Modlich, Ute},
  title     = {Endothelial-platelet interactions in influenza-induced pneumonia: A potential therapeutic target},
  series = {Anatomia, Histologia, Embryologia},
  volume    = {49},
  journal   = {Anatomia, Histologia, Embryologia},
  number    = {5},
  doi       = {10.1111/ahe.12521},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-213610},
  pages     = {606 -- 619},
  year      = {2020},
  abstract  = {Every year, influenza viruses spread around the world, infecting the respiratory systems of countless humans and animals, causing illness and even death. Severe influenza infection is associated with pulmonary epithelial damage and endothelial dysfunction leading to acute lung injury (ALI). There is evidence that an aggressive cytokine storm and cell damage in lung capillaries as well as endothelial/platelet interactions contribute to vascular leakage, pro-thrombotic milieu and infiltration of immune effector cells. To date, treatments for ALI caused by influenza are limited to antiviral drugs, active ventilation or further symptomatic treatments. In this review, we summarize the mechanisms of influenza-mediated pathogenesis, permissive animal models and histopathological changes of lung tissue in both mice and men and compare it with histological and electron microscopic data from our own group. We highlight the molecular and cellular interactions between pulmonary endothelium and platelets in homeostasis and influenza-induced pathogenesis. Finally, we discuss novel therapeutic targets on platelets/endothelial interaction to reduce or resolve ALI.},
  language  = {en}
}
@article{LauknerTruchetManukjanetal.2021,
  author    = {Laukner, Anna and Truchet, Laura and Manukjan, Georgi and Schulze, Harald and Langbein-Detsch, Ines and Mueller, Elisabeth and Leeb, Tosso and Kehl, Alexandra},
  title     = {Effects of cocoa genotypes on coat color, platelets and coagulation parameters in French Bulldogs},
  series = {Genes},
  volume    = {12},
  journal   = {Genes},
  number    = {7},
  issn      = {2073-4425},
  doi       = {10.3390/genes12071092},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-242745},
  year      = {2021},
  abstract  = {A nonsense variant in HPS3, c.2420G>A or p.Trp807*, was recently discovered as the cause for a brown coat color termed cocoa in French Bulldogs. Here, we studied the genotype-phenotype correlation regarding coat color in HPS3 mutant dogs that carried various combinations of mutant alleles at other coat color genes. Different combinations of HPS3, MLPH and TYRP1 genotypes resulted in subtly different shades of brown coat colors. As HPS3 variants in humans cause the Hermansky-Pudlak syndrome type 3, which in addition to oculocutaneous albinism is characterized by a storage pool deficiency leading to bleeding tendency, we also investigated the phenotypic consequences of the HPS3 variant in French Bulldogs on hematological parameters. HPS3 mutant dogs had a significantly lowered platelet dense granules abundance. However, no increased bleeding tendencies in daily routine were reported by dog owners. We therefore conclude that in dogs, the phenotypic effect of the HPS3 variant is largely restricted to pigmentation. While an effect on platelet morphology is evident, we did not obtain any indications for major health problems associated with the cocoa coat color in French Bulldogs. Further studies will be necessary to definitely rule out very subtle effects on visual acuity or a clinically relevant bleeding disorder.},
  language  = {en}
}