It has been reported that it is the expression levels of Rho GTPases, but not their mutations, that govern change of cancer cell activities, such as metastasis. Furthermore, it has been shown that LIG can inhibit ERK-MAP kinase, which is an upstream regulator of RhoA and Rac1 in colon carcinoma cells, and suppress tumor necrosis factor-alpha, which can effectively activate RhoA and ROCK in human pulmonary microvascular endothelial cells. Moreover, in PC12 cells, LIG can activate PI3K/Akt pathways, which directly up-regulate Rho GTPases. The study provides a clear perspective that explains the inhibitive effect of Z-ligustilide on T98G cell migration and suggests that Z-ligustilide may be an effective agent for protecting the central nervous system against GBM diseases, partially through the modulation of Rho GTPase expression. Furthermore, this study also shows that cell migration can be used to understand the outcome of altered Rho GTPase activity as a potential approach for drug screening. Pulmonary hypertension is defined as mean pulmonary arterial pressure $25 mmHg at rest. If untreated, the vasculopathy often progresses and leads to right ventricular 
failure and premature death. Optimal assessment of RV morphology and function is thus critical in the management of PH. Cardiac magnetic resonance imaging is an established modality for the objective assessment of RV geometry and function. To date, CMR studies of PH have described increased size and impaired function of the right ventricle. Recent CMR studies have also demonstrated late gadolinium enhancement at ventricular insertion points. LGE is commonly seen in patients with coronary and myocardial diseases and is thought to emerge as a result of contrast leakage and pooling in fibrotic or severely damaged myocardium. In PH, however, the underlying mechanisms of LGE at VIPs are insufficiently understood. Regarding this, a possible explanation is that LGE at VIPs develops as a result of elevated RV pressure and resultant RV remodeling in PH. Indeed, previous studies have shown significant associations between LGE volume at VIPs and measurements of pulmonary hemodynamics and RV morphology. Interestingly, however, we have recently experienced and reported a case in which paradoxical motion of the interventricular septum alone caused LGE at VIPs without PH. This paradoxical IVS movement has been described in PH and, thus, it can be assumed that altered IVS motion might be the predominant mechanism of LGE at IVS rather than increased RV pressure and/or remodeling. The present study investigated the underlying mechanisms of LGE at IVSs in PH by evaluating the association between LGE at VIPs and clinical parameters. Particular focus was made on the possible contribution of paradoxical IVS motion assessed by speckle-tracking echocardiography to the development of LGE at IVSs. Recent studies have indicated significant associations between LGE at VIPs and AbMole Pteryxin various parameters of PH. For example, mean PAP, RV volume and RV mass index have been reported to positively correlate with LGE volume.