@article{WaagaKrzymanskiUlrichsetal.1993,
  author    = {Waaga, AM and Krzymanski, M. and Ulrichs, Karin and Wierusz-Wysocka, Bogna and M{\"u}ller-Buchholtz, Wolfgang},
  title     = {Hematological effects of the new immunosuppressive drug 15-deoxyspergualin},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-44701},
  year      = {1993},
  abstract  = {Since systematic hematological studies on blood and bone marrow changes after treatment with 15-Deoxyspergualin (DOS) are lacking, a quantitative assessment was performed fourteen or twenty eight days after intraperitoneal application of DOS to rats. Further observations done 7 and 14 days after discontinuation of DOS administration allowed analysis of banc marrow regeneration. DOS induced lymphocytopenia, granUlocytopenia and anemia with a decrease of bone marrow cellularity due to suppression of cell maturation. The effect was dose-dependent and bone marrow as well as blood changes were observed in animals treated with doses from 0.5 to 10.0 mg/kg DOS. Within 14 days after termination of the treatment, rapid recovery with normalization of all hematological parameters was observed. In the light of our data, these hematological side effects may not be a major disadvantage, if DOS is used in doses below 2.5 mg/kg, and for a course of therapy which is limited to 7 to 14 days.},
  subject      = {Chirurgie},
  language  = {en}
}
@article{RottlaenderKuerten2015,
  author    = {Rottlaender, Andrea and Kuerten, Stefanie},
  title     = {Stepchild or prodigy? Neuroprotection in multiple sclerosis (MS) research},
  series = {International Journal of Molecular Sciences},
  volume    = {16},
  journal   = {International Journal of Molecular Sciences},
  doi       = {10.3390/ijms160714850},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-148416},
  pages     = {14850-14865},
  year      = {2015},
  abstract  = {Multiple sclerosis (MS) is an autoimmune disorder of the central nervous system (CNS) and characterized by the infiltration of immune cells, demyelination and axonal loss. Loss of axons and nerve fiber pathology are widely accepted as correlates of neurological disability. Hence, it is surprising that the development of neuroprotective therapies has been neglected for a long time. A reason for this could be the diversity of the underlying mechanisms, complex changes in nerve fiber pathology and the absence of biomarkers and tools to quantify neuroregenerative processes. Present therapeutic strategies are aimed at modulating or suppressing the immune response, but do not primarily attenuate axonal pathology. Yet, target-oriented neuroprotective strategies are essential for the treatment of MS, especially as severe damage of nerve fibers mostly occurs in the course of disease progression and cannot be impeded by immune modulatory drugs. This review shall depict the need for neuroprotective strategies and elucidate difficulties and opportunities.},
  language  = {en}
}
@article{SchampelKuerten2017,
  author    = {Schampel, Andrea and Kuerten, Stefanie},
  title     = {Danger: high voltage - the role of voltage-gated calcium channels in central nervous system pathology},
  series = {Cells},
  volume    = {6},
  journal   = {Cells},
  number    = {4},
  doi       = {10.3390/cells6040043},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-172653},
  year      = {2017},
  abstract  = {Voltage-gated calcium channels (VGCCs) are widely distributed within the central nervous system (CNS) and presumed to play an important role in the pathophysiology of a broad spectrum of CNS disorders including Alzheimer's and Parkinson's disease as well as multiple sclerosis. Several calcium channel blockers have been in clinical practice for many years so that their toxicity and side effects are well studied. However, these drugs are primarily used for the treatment of cardiovascular diseases and most if not all effects on brain functions are secondary to peripheral effects on blood pressure and circulation. While the use of calcium channel antagonists for the treatment of CNS diseases therefore still heavily depends on the development of novel strategies to specifically target different channels and channel subunits, this review is meant to provide an impulse to further emphasize the importance of future research towards this goal.},
  language  = {en}
}
@article{StratosBehrendtAnselmetal.2022,
  author    = {Stratos, Ioannis and Behrendt, Ann-Kathrin and Anselm, Christian and Gonzalez, Aldebarani and Mittlmeier, Thomas and Vollmar, Brigitte},
  title     = {Inhibition of TNF-α restores muscle force, inhibits inflammation, and reduces apoptosis of traumatized skeletal muscles},
  series = {Cells},
  volume    = {11},
  journal   = {Cells},
  number    = {15},
  issn      = {2073-4409},
  doi       = {10.3390/cells11152397},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-286094},
  year      = {2022},
  abstract  = {Background: Muscle injuries are common in humans and are often associated with irrecoverable damage and disability. Upon muscle injury, TNF-α signaling pathways modulate the healing process and are predominantly associated with tissue degradation. In this study we assumed that TNF-α inhibition could reduce the TNF-α-associated tissue degradation after muscle injury. Materials and methods: Therefore, the left soleus muscle of 42 male Wistar rats was injured using a standardized open muscle injury model. All rats were treated immediately after injury either with infliximab (single i.p. injection; 10 mg/kg b.w.) or saline solution i.p. Final measurements were conducted at day one, four, and 14 post injury. The muscle force, the muscle cell proliferation, the muscle cell coverage as well as the myofiber diameter served as read out parameters of our experiment. Results: Systemic application of infliximab could significantly reduce the TNF-α levels in the injured muscle at day four upon trauma compared to saline treated animals. The ratio of muscle weight to body weight was increased and the twitch muscle force showed a significant rise 14 days after trauma and TNF-α inhibition. Quantification of myofiber diameter in the penumbra zone showed a significant difference between both groups at day one and four after injury, indicated by muscle hypertrophy in the infliximab group. Planimetric analysis of the injured muscle at day 14 revealed increased muscle tissue fraction in the infliximab group compared to the control animals. Muscle cell proliferation did not differ between both groups. Conclusions: These data provide evidence that the TNF-α blockade positively regulates the restauration of skeletal muscles upon injury.},
  language  = {en}
}