Several dry and wet surface treatment methods are explored for a selective SiGe epitaxial film used to fabricate embedded SiGe pMOSFETs. Pre-clean conditions for the device wafers used in this study were limited by a realistic CMOS process window with tight thermal and chemical budgets due to dopant diffusion and hardmask erosion concerns. The effectiveness of these pre-clean methods is evaluated by SiGe epitaxial film quality and SIMS profiles of key residual contaminants such as C and O at the SiGe-Si substrate interface. As an effective low-temperature dry surface treatment, chemical bake in HCl/H 2 at temperature below 800 • C is found to reduce interface C and O peak concentrations by an order of magnitude. Wet clean in multiple cycles of DIW-O 3 (ozonated water), SC1 and diluted HF (DHF) is also presented to prepare epitaxial growth surfaces with accumulated damage and chemical residues from previous process steps. SiGe epitaxial film morphology is also observed to improve by increasing DHF clean time. For further improvement of film quality on the most difficult surfaces, Si seed layer was employed to initiate SiGe film nucleation and yield smooth film growth.

Introduction. Urotensin II (U II) is a kind of active peptide with a variety of biological effects, such as promoting cell proliferation and endocrine effects. The aim of this study is to investigate the effect of urotensin II on the proliferation and secretion of vascular endothelial growth factor (VEGF) in cultured rat dermal papilla cells (DPCs), and to explore its molecular mechanism. Materials and Methods. We used the DPCs isolated from the thoracic aortas of Wistar-Kyoto rats to run the CCK8 and ELISA assay, RC-PCR and Western blotting techniques to identify the effect of Urotensin II on the proliferation and secretion of VEGF in DPCs, data were analyzed by one-way ANOVA or t-test. Results. U II can increase the mRNA expression of proliferation markers Ki67 and PCNA. In addition, the Wnt/β-catenin pathway was activated by U II, but Wnt inhibitor DKK1 reversed the effect of U II. Conclusions. U II promoted the proliferation and secretion of VEGF in rat DPCs through activation of the Wnt-β-catenin signaling pathway.