Water Jet flow was projected at normal human aortic walls and human chronic obstructive iliac arteries in the air or in the ordinary saline solution. Ordinary saline solution was used for the jet, which was projected at a pressure of 10kg·f/cm² through a nozzle 0.10mm in diameter. When the Water Jet was projected at the normal aortic intima, damage to the wall was more severe with duration of fluid projection, and projection for ten sec ruprured the elastic fiber of the media. But when the fluid jet projected ordinary saline, damage to the aortic wall was slight and projection for 30sec only dissected the surface of the intima. Water Jet projection in air showed slight effect on thrombi of the chronic obstructive iliac arteries, and projection for 60sec only made small irregular holes in the thrombi. When the Water Jet was projected in ordinary saline solution, however, destructive effects on thrombi were stronger and the projection for 40sec could remove almost all the thrombi for a distance of 2cm, while damage to the initima was very slight. This study demonstrated that fluid jet projection using ordinary saline solution could remove thrombi in chronically obstructive artery safely and effectively and suggested the possibility of the Water Jet angioplasty.

GIPC1, GIPC2 and GIPC3 consist of GIPC homology 1 (GH1) domain, PDZ domain and GH2 domain. The regions around the GH1 and GH2 domains of GIPC1 are involved in dimerization and interaction with myosin VI (MYO6), respectively. The PDZ domain of GIPC1 is involved in interactions with transmembrane proteins [IGF1R, NTRK1, ADRB1, DRD2, TGFbetaR3 (transforming growth factorbeta receptor type III), SDC4, SEMA4C, LRP1, NRP1, GLUT1, integrin alpha5 and VANGL2], cytosolic signaling regulators (APPL1 and RGS19) and viral proteins (HBc and HPV-18 E6). GIPC1 is an adaptor protein with dimerizing ability that loads PDZ ligands as cargoes for MYO6-dependent endosomal trafficking. GIPC1 is required for cell-surface expression of IGF1R and TGFbetaR3. GIPC1 is also required for integrin recycling during cell migration, angiogenesis and cytokinesis. On early endosomes, GIPC1 assembles receptor tyrosine kinases (RTKs) and APPL1 for activation of PI3K-AKT signaling, and G protein-coupled receptors (GPCRs) and RGS19 for attenuation of inhibitory Galpha signaling. GIPC1 upregulation in breast, ovarian and pancreatic cancers promotes tumor proliferation and invasion, whereas GIPC1 downregulation in cervical cancer with human papillomavirus type 18 infection leads to resistance to cytostatic transforming growth factorbeta signaling. GIPC2 is downregulated in acute lymphocytic leukemia owing to epigenetic silencing, while Gipc2 is upregulated in estrogen-induced mammary tumors. Somatic mutations of GIPC2 occur in malignant melanoma, and colorectal and ovarian cancers. Germ-line mutations of the GIPC3 or MYO6 gene cause nonsyndromic hearing loss. As GIPC proteins are involved in trafficking, signaling and recycling of RTKs, GPCRs, integrins and other transmembrane proteins, dysregulation of GIPCs results in human pathologies, such as cancer and hereditary deafness.
Adaptor Proteins, Signal Transducing/chemistry/genetics/*metabolism ; Amino Acid Sequence ; Evolution, Molecular ; Humans ; Molecular Sequence Data ; *Multigene Family ; Neoplasms/*genetics ; Protein Binding ; *Proteomics