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Tissue-Engineering stellt eine vielversprechende Methode zur Herstellung autologer Knorpeltransplantate fur die rekonstruktive Chirurgie dar. Ein Problem hierbei ist die Dedifferenzierung der Chondrozyten. In der vorliegenden Studie wurde die Genexpression verschiedener Marker einerseits wahrend der Dedifferenzierung humaner Chondrozyten (HC) aus Septumknorpel und andererseits wahrend der chondrogenen Differenzierung von mesenchymalen Stammzellen (hMSC) aus Knochenmarkproben in Zellkultur mittels Microarrays analysiert. Kollagen 1α1, 2α1, 3α1, 4α1, 11α1, Biglykan, Fibromodulin und Lumican wurden wahrend der Dedifferenzierung der HC aktiviert, Kollagen 9α2, 9α3, 10α1 und Chondroadherin inaktiviert. Wahrend der chondrogenen Differenzierung der MSC wurden die Gene fur Kollagen 3α1, 9α2, 9α3, 10α1, 11α1 aktiviert, die fur Kollagen 4α1 und Fibromodulin inaktiviert, sowie die Gene fur Col 1α1, Biglykan und Chondroadherin konstant exprimiert. Das Genprofil von chondrogen differenzierten Stammzellen entspricht hinsichtlich der untersuchten Marker dem von humanen differenzierten Chondrozyten. Kollagen 2α1, 9α2, 9α3, 10α1 konnten Marker fur die Differenzierung von Knorpelgewebe sein, Col 1α1, 3α1 und 4α1, Biglykan, Fibromodulin und Lumican fur die Dedifferenzierung.

Interleukin-12 (IL-12), a heterodimeric cytokine, is important in the generation of a Th1-biased immune response. Several polymorphisms have been described in IL12B, the gene encoding the p40 subunit of IL-12. A bi-allelic polymorphism within the IL12B promoter region has been reported to show association with diseases as diverse as severe childhood asthma and fatal cerebral malaria. In order to define the molecular basis for these disease associations, we investigated the secretion of IL-12 by human monocyte-derived dendritic cells. Homozygotes for the IL12B promoter polymorphism showed a 10-fold difference in median p70 secretion in response to CD40 ligation. Remarkably, this difference resulted from the inability of most allele 1 homozygotes to secrete heterodimeric IL-12. In contrast, most of the donors homozygous for allele 2 had detectable secretion. These findings are important for the understanding of the highly complex regulation of IL-12 secretion, and its consequent impact on disease susceptibility, in humans.

Background: Anatomic and functional results of macularholes using vitrectomy and platelet-concentrate (PC) or autologous whole blood (WB) were investigated without peeling any epiretinal membrane in order to minimize retinal trauma. Methods: 44 patients with macular holes stage II, III and IV underwent a vitrectomy with removal of posterior cortical vitreous (in stage II and III) and C2F6 gas endotamponade. No peeling of any epiretinal membrane or the ILM was performed. In 14 patients autologous WB was injected and in 30 patients autologous PC. The mean follow-up time was 9.3 months.Results: An anatomic closure was observed in 36.4%of patients in the WB-group and in 93.9% of patients in the PC-group. SLO-microperimetry showed a reduction of absolute scotomas in 80% of the WB- and in 75% of the PC-group. In the WB- group 1 retinal detachment and 1 branch vein occlusion occurred; in the PC-group 3 retinal detachments, 1 central artery occlusion, 1 macular pucker,1 cystoid macular edema, 1 late reopening and 1 secondary glaucoma were observed. Inboth groups no endophthalmitis occurred. Conclusion: If autologous platelet concentrate is available, high anatomic success rates can be achieved without aggressive membrane removal,which may cause retinal damage. Autologous whole blood cannotbe recommended as an alternative adjunct for the treatment of macular holes without membrane removal.

Coated membranes and vesicles play an important role in receptor-mediated endocytosis and intracellular trafficking in various cell types, and are also present in blood platelets. Platelets take up certain proteins from the blood plasma, such as von Willebrand factor and fibrinogen, and these substances are transferred to storage granules. The receptors for these plasma proteins on the platelet plasma membrane have been well characterized, but morphological evidence for their transport to the storage granules is not yet available. In an attempt to clarify this aspect, we employed postembedding immunocytochemistry on platelets embedded in the acrylic resin LR White. Clathrin as the major coat component of coated vesicles was localized in the cytoplasm, on the plasmic faces of alpha-granules and the open canalicular system, and on the plasmic face of the plasma membrane. Colocalizations of the adhesive proteins, von Willebrand factor, fibrinogen and fibronectin, with clathrin could be observed at the same typical locations as coated vesicles were seen in Araldite-embedded material. These colocalizations have not been reported to date and furnish further evidence for a coated vesicle-mediated transport of blood plasma-derived adhesive proteins from their receptors on the outer plasma membrane to the alpha-granules.