In conclusion, all four systems for preparation of platelet-rich plasma investigated result in considerable growth factor release. In what extent the total content of PDGF-AB as a consequence of platelet yield has an impact on wound healing has to be further investigated.

Intensive endurance exercise is known to induce lymphocyte apoptosis, which might affect immune function. Less is known about the effects of resistance exercise on apoptosis and its underlying mechanisms. In this study, subjects performed an intensive resistance test (IRT) and a moderate resistance test, and lymphocyte apoptosis, apoptosis-related parameters, and underlying mechanisms were investigated. IRT induced a significant increase of lymphocyte apoptosis 3 h after exercise, which was accompanied by a significant decrease of mitochondrial membrane potential, a reduction of Bcl-2, and an upregulation of the CD95 receptor. Blood lactate, IL-6, C-reactive protein, and cortisol increased significantly 3 h after IRT. A significant correlation was observed between the increase of apoptosis and cortisol levels 3 h after IRT. Incubation of freshly isolated lymphocytes in IRT serum indicated an important role of serum correlates for apoptosis induction. Selective incubation of lymphocytes in concentrations of selected serum parameters corresponding to levels found post in IRT serum demonstrated a major role for cortisol in apoptosis induction. This result was confirmed by attenutation of apoptosis after addition of mifepristone before incubation in IRT serum. In summary, resistance exercise induced lymphocyte apoptosis in an intensity-dependent way. Furthermore, cortisol signaling via glucocorticoid receptors might be an important mechanism for lymphocyte apoptosis after resistance exercise.

Preliminary analysis of Atlantic salmon alpha- and beta-globin genes indicated that these genes are linked in a 3' to 3' orientation, with the RNA-coding sequences located on opposite strands. In this report, we show that two different alpha-globin genes have the same orientation and are encoded on the same strand whereas two different beta-globin genes are encoded on the opposite strand and also have the same orientation. This cluster of globin genes is divided into two subclusters: one for the Bohr globin genes and one for the non-Bohr globin genes. This is the first evidence for this type of arrangement found for globin genes. DNase I footprint analysis of two of the globin promoters show erythroid-specific transcription factor binding sites that have also been found in human and other mammalian globin genes.

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