ESBA105 potently inhibits inflammation and prevents cartilage damage triggered by TNFalpha. In contrast to a full length IgG, ESBA105 also penetrates into cartilage and can be expected to reverse the TNFalpha-induced catabolic state of articular cartilage in arthritides.

In this study we evaluate the performance of primary rat hepatocytes and HepG2 cells on chitosan-collagen hydrogel-coated textile scaffolds. Light microscopy and electron microscopic observations showed attachment and aggregate formation tendency of hepatocytes on the scaffolds. As tested by the tetrazolium reduction (MTT) assay it was evident that cells had preserved mitochondrial functionality. It was also observed that pure collagen and collagen blended scaffolds allowed higher cell growth than pure chitosan scaffold. Fluorescent live/dead staining showed a metabolically active, viable cell population on all scaffold compositions with occurrence of few dead cells. Cell functionality was confirmed by secretion of albumin, which was maintained throughout culture period. Take collectively our results suggests that hydrogel-coated textile scaffolds could be promising for tissue-engineering applications, as they allow favorable hepatocyte attachment, spheroid formation and maintenance of function. These scaffolds could be useful for co-culturing hepatocytes and non-parenchymal endothelial cells in bioartificial liver support systems.

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Photodynamic therapy (PDT) is a promising alternative method for clinical cancer treatment. In the present study, cells from four breast carcinomas, seven ovarian carcinomas of various stages of differentiation, and ascites from a diffuse metastatic tumor were treated by PDT in vitro. Tetra(m-hydroxyphenyl)-chlorin (m-THPC) was used as the photosensitizer. Surviving cell rate was evaluated by the ATP-Cell-Viability-Assay (ATP-CVA), which measures light production as an interaction of intracellular ATP with the luciferin-luciferase complex. The most effective PDT of the tumor cells was achieved at an m-THPC concentration of 0.2 microgram/ml following incubation of the cells with photosensitizer for 24 hours. PDT toxicity resulted in a cell survival rate of 1% to 42% compared to untreated control cells (survival rate of control = 100%). The inhibitor concentration IC50 of m-THPC was determined both in the dark (dark toxicity) and in combination with laser irradiation. IC50 was defined as the concentration of photosensitizer which caused 50% of cell death. The IC50 values were heterogeneous in all tumor specimens examined. IC50 values for dark toxicity were on average 0.14 microgram m-THPC/ml for primary ovarian carcinoma, 2.16 micrograms m-THPC ml for refractory ovarian carcinoma and 0.3 microgram m-THPC/ml for breast carcinoma. After PDT, average IC50 value for refractory ovarian carcinoma was 0.04 microgram m-THPC/ml, for primary ovarian carcinoma 0.05 microgram m-THPC/ml and for breast carcinoma 0.03 microgram m-THPC/ml. These data might indicate that clinical PDT of gynecological carcinoma requires individual treatment conditions to achieve optimal results.

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