Objective Vertigo is the main clinical feature and cerebral atherosclerosis is the major etiological factor and pathogenesy of posterior circulation ischemia (PCIV).The objective of this study was to observe the clinical effect of butylphthalide combined with naloxone on PCIV and hemodynamics . Methods One hundred and sixty two patients with PCIV were classified into treatment group and control group .In the treatment group , butylphthalide soft capsules were administrated by oral and naloxone 2.4 mg were administrated by intravenous drip per day .In the control group , Xueshuantong at the dose of 300 mg was given by intravenous drip per day.All the treatment lasted for 14 days.Transcranial doppler (TCD) examination was performed for all patients before and after the treatment.The mean velocity (Vm) and the systolic velocity (Vs) of bilateral vertebral arteries were recorded .Clinical cure rate was evaluated . Results Basilar artery Vm and Vs increased after treatment in the control group compared with those before treatment ([30.15 ±3.84])cm/s vs ([26.95 ±3.72])cm/s, ([40.87 ±4.54])cm/s vs ([37.16 ±4.72])cm/s.Basilar artery Vm and Vs increased after treatment compared with before treatment in the treatment group ([34.47 ±3.53]) cm/s vs ([27.53 ± 3.68])cm/s, ([42.25 ±5.29])cm/s vs ([35.87 ±4.85])cm/s, (P<0.05).Basilar artery Vm and Vs increased in the treatment group compared with the control group after the treatment ([34.47 ±3.53])cm/s vs ([30.15 ±3.84])cm/s, ([42.25 ±5.29])cm/s vs ([40.87 ±4.54])cm/s, (P<0.05).The cure rate and total effective rate in the treatment group (58.8%, 93.8%) were higher than thoes in the control group, respectively (31.7%, 75.6%)(P<0.05). Conclusion Butylphthalide soft capsules combined with naloxone have definite clinical curative effect and few side for PCIV treatment.

Metastasis is crucial for the mortality of non-small cell lung carcinoma (NSCLC) patients. The epithelial-mesenchymal transition (EMT) plays a critical role in regulating tumor metastasis. Glioma-associated oncogene 1 (Gli1) is aberrantly active in a series of tumor tissues. However, the molecular regulatory relationships between Gli1 and NSCLC metastasis have not yet been identified. Herein, we reported Gli1 promoted NSCLC metastasis. High Gli1 expression was associated with poor survival of NSCLC patients. Ectopic expression of Gli1 in low metastatic A549 and NCI-H460 cells enhanced their migration, invasion abilities and facilitated EMT process, whereas knock-down of Gli1 in high metastatic NCI-H1299 and NCI-H1703 cells showed an opposite effect. Notably, Gli1 overexpression accelerated the lung and liver metastasis of NSCLC in the intravenously injected metastasis model. Further research showed that Gli1 positively regulated Snail expression by binding to its promoter and enhancing its protein stability, thereby facilitating the migration, invasion and EMT of NSCLC. In addition, administration of GANT-61, a Gli1 inhibitor, obviously suppressed the metastasis of NSCLC. Collectively, our study reveals that Gli1 is a critical regulator for NSCLC metastasis and suggests that targeting Gli1 is a prospective therapy strategy for metastatic NSCLC.