Integrated use of virtual bronchoscopy and endobronchial ultrasonography on the diagnosis of peripheral lung lesions.

Endobronchial ultrasound (EBUS) improves bronchoscopic diagnosis of peripheral lung lesions (PLLs). The procedure time is lengthened by the search through multiple bronchial branches to PLLs. Virtual bronchoscopy (VB) provides endobronchial views that simulate findings at bronchoscopy. An open source software can be employed to study VB and hence the endobronchial route to a PLL. It allows VB to be studied in a Macintosh platform such as a laptop computer. Our purpose was to test if VB generated by this software could shorten procedure time of EBUS-guided bronchoscopy as compared with no VB assistance. The most feasible route to a PLL was manually selected using this software to study VB (VB group). For non-VB group, 2D CT axial +/- coronal images were reviewed to plan bronchoscopy. Before bronchoscopic biopsies, the location of PLL was confirmed by EBUS. Thirty-three subjects were recruited including 16 in VB group and 17 in non-VB group. The mean EBUS examination time and mean total procedure time were reduced in the VB group compared with non-VB group: 5.3 versus 10.5 minutes (P=0.04) and 22.4 versus 29.9 minutes (P=0.044), respectively. There was no complication in the VB group. Although the diagnostic yield was higher in the VB group than non-VB group, our study was not powered to test the difference. This pilot study suggests that VB assistance is safe and shortens procedural time of EBUS-guided bronchoscopy for PLL. Further study is warranted to confirm these findings.

Ginsenoside-Rg1 mediates a hypoxia-independent upregulation of hypoxia-inducible factor-1α to promote angiogenesis.

Hypoxia-inducible factor (HIF-1) is the key transcription regulator for multiple angiogenic factors and is an appealing target. Ginsenoside-Rg1, a nontoxic saponin isolated from the rhizome of Panax ginseng, exhibits potent proangiogenic activity and has the potential to be developed as a new angiotherapeutic agent. However, the mechanisms by which Rg1 promotes angiogenesis are not fully understood. Here, we show that Rg1 is an effective stimulator of HIF-1α under normal cellular oxygen conditions in human umbilical vein endothelial cells. HIF-1α steady-state mRNA was not affected by Rg1. Rather, HIF-1α protein synthesis was stimulated by Rg1. This effect was associated with constitutive activation of phosphatidylinositol 3-kinase (PI3K)/Akt and its effector p70 S6 kinase (p70(S6K)), but not extracellular-signal regulated kinase 1/2. We further revealed that HIF-1α induction triggered the expression of target genes, including vascular endothelial growth factor (VEGF). The use of small molecule inhibitors LY294002 or rapamycin to inhibit PI3K/Akt and p70(S6K) activities, respectively, resulted in diminished HIF-1α activation and subsequent VEGF expression. RNA interference-mediated knockdown of HIF-1α suppressed Rg1-induced VEGF synthesis and angiogenic tube formation, confirming that the effect was HIF-1α specific. Similarly, the angiogenic phenotype could be reversed by inhibition of PI3K/Akt and p70(S6K). These results define a hypoxia-independent activation of HIF-1α, uncovering a novel mechanism for Rg1 that could play a major role in angiogenesis and vascular remodeling.