Rapid microarray processing using a disposable hybridization chamber with an integrated micropump.

We present a disposable microarray hybridization chamber with an integrated micropump to speed up diffusion based reaction kinetics by generating convective flow. The time-to-result for the hybridization reaction was reduced from 60 min (standard protocol) down to 15 min for a commercially available microarray. The integrated displacement micropump is pneumatically actuated. It includes two active microvalves and is designed for low-cost, high volume manufacturing. The setup is made out of two microstructured polymer parts realized in polycarbonate (PC) separated by a 25 µm thermoplastic elastomer (TPE) membrane. Pump rate can be controlled between 0.3 µl s(-1) and 5.7 µl s(-1) at actuation frequencies between 0.2 Hz and 8.0 Hz, respectively.

Angiogenic effects of injected VEGF165 and sVEGFR-1 (sFLT-1) in a rat flap model.

BACKGROUND: Injections of single-dose vascular endothelial growth factor (VEGF)(165) have been advocated as a therapeutic tool for angiogenesis in ischemic flaps. We challenged this thesis by employing both VEGF(165) and vascular endothelial growth factor receptor-1 (VEGFR-1) (for competitive inhibition of VEGF signal transduction) in different experimental settings of an ischemic rat flap model. MATERIAL AND METHODS: 80 isogenic rats were divided in two groups of 40 animals (groups 1A-1D and 2A-2D). The ischemic target was a 7 x 7-cm epigastric island flap, based on the right inferior epigastric pedicle. Group 1 received flap treatment 1 week prior to flap elevation by test substance injection into its flap panniculus carnosus: 1 ml NaCl 0.9% (1A), 1 ml Dulbecco's modified Eagle's medium (1B), 1.0 microg VEGF(165) (1C), and 10 microg sFLT-1 with 1.0 microg VEGF(165) (1D). sFLT-1 is a soluble receptor for VEGF and is able to prevent VEGF signaling through the cell surface receptor. Group 2 had the same flap treatment at the day of flap elevation. RESULTS: In group 1C we found the most vital flap tissue, without reaching significance. Compared with group 1D, however, significantly more flap tissue maintained vital. In groups 2A-2D, no significant results were found with respect to flap survival. CONCLUSIONS: Local application of single-dose VEGF(165) 1 week prior to ischemia dose not have significant clinical angiogenic effects. In this experimental setting, VEGF(165)-induced angiogenic effects can be significantly inhibited by adding sFLT1 in vivo. A single-dose of VEGF(165) under ischemic conditions causes no significantly better flap survival in this model.