Ultrasonic assisted tungsten inert gas (U-TIG) welding method was developed. Both U-TIG and conventional TIG welding of AISI 304 stainless steel with 5 mm thickness were experimentally studied in this paper. The results show that the penetration depth is increased up to 300% for weld made with U-TIG welding compared with conventional TIG welding. Ultrasonic energy enhances arc push force, causes a continual high frequency oscillation in the arc plasma and increases welding penetration. These effects are thought to be responsible for enhancing the welding efficiency and improving the appearance of stainless steel weld joints.

Intermetallic layer of dissimilar tungsten inert gas welding-brazing butt joint of aluminium alloy/ stainless steel has been studied. A visible unequal thickness intermetallic layer has formed in welded seam/steel interface, and the thickness of the whole layer is ,10 mm. The interface with Al-12Si filler metal consists of t 5 -Al 8 Fe 2 Si layer in welded seam side and h-(Al,Si) 13 Fe 4 layer in steel side with the hardness values of 1025 and 835 HV respectively, while the interface with Al6Cu filler metal consists of h-Al 13 (Fe,Cu) 4 layer with the hardness of 645 HV. The average tensile strength of the joint with Al-12Si filler metal is 100-120 MPa, and the fracture occurs at h-(Al,Si) 13 Fe 4 layer, while the joint with Al-6%Cu filler metal presents high crack resistance with tensile strength of 155-175 MPa, which reaches more than 50% of aluminium base metal strength.

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Docetaxel (DTX), a paclitaxel analogue, can efficiently inhibit proliferation of vascular smooth muscle cells and has broadly been used as an antiangiogenesis drug. However, as a candidate drug of drug-eluting stent, the effects of DTX on human umbilical vein endothelial cells (HUVECs) are still not well understood. Herein, we investigated the effects of DTX on proliferation, apoptosis, adhesion, migration and morphology of HUVECs in vitro. We found that DTX had the cytostatic and cytotoxic effects at low and high concentrations, respectively. DTX could inhibit the proliferation and migration of HUVECs, induce HUVECs apoptosis, delay HUVECs adhesion and decrease spreading area and aspect ratio of individual cells. The signaling pathway that DTX led to the migration inhibition, adhesion delay and shape change of HUVECs is the VE-cadherin mediated integrin β1/FAK/ROCK signaling pathway. The study will provide a theoretical basis for the clinical application of DTX.