Effects of botulinum toxin A on patient-specific keloid fibroblasts in vitro.

Objectives/hypothesis: To test whether therapeutic effects of botulinum toxin A on patient- specific keloid tissue can be reproduced on the cellular level. Specifically, effects on cell proliferation and expression of growth factors and cytokines relevant for wound healing were to be tested.

Study Design: Experimental study including patient specific cell cultures of keloids.

Effects of external radiation in a co-culture model of endothelial cells and adipose-derived stem cells.

Background: The inflammatory response clinically observed after radiation has been described to correlate with elevated expression of cytokines and adhesion molecules by endothelial cells. Therapeutic compensation for this microvascular compromise could be an important approach in the treatment of irradiated wounds. Clinical reports describe the potential of adipose-derived stem cells to enhance wound healing, but the underlying cellular mechanisms remain largely unclear.

Wound healing after radiation therapy: review of the literature.

Radiation therapy is an established modality in the treatment of head and neck cancer patients. Compromised wound healing in irradiated tissues is a common and challenging clinical problem. The pathophysiology and underlying cellular mechanisms including the complex interaction of cytokines and growth factors are still not understood completely.

Effects of botulinum toxin a on cytokine synthesis in a cell culture model of cutaneous scarring.

Objective: To evaluate possible botulinum toxin A effects in a cell culture model.

Methods: In a cell culture model with dermal fibroblasts and microvascular endothelial cells, possible botulinum toxin A effects were evaluated. Cell proliferation and cytokine expression were analyzed using viability assays and enzyme-linked immunosorbent assay techniques.

Altered lipid metabolism in a Drosophila model of Friedreich's ataxia.

Friedreich's ataxia (FRDA) is the most common form of autosomal recessive ataxia caused by a deficit in the mitochondrial protein frataxin. Although demyelination is a common symptom in FRDA patients, no multicellular model has yet been developed to study the involvement of glial cells in FRDA. Using the recently established RNAi lines for targeted suppression of frataxin in Drosophila, we were able to study the effects of general versus glial-specific frataxin downregulation.