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Chloride intracellular channel 1 (CLIC1) has been demonstrated to be overexpressed in gastric cancer, and elevated CLIC1 expression levels are markedly associated with the processes of tumor cell migration and invasion. However, the regulatory mechanism and signaling pathway underlying these processes have remained to be elucidated. The present study examined the impact of N-acetyl cysteine (NAC), indanyloxyacetic acid (IAA)-94 and SB203580, inhibitors of reactive oxygen species (ROS), as well as CLIC1 and p38 mitogen-activated protein kinase (MAPK) on the migration and invasion of SGC-7901 gastric cancer cells in a hypoxia-reoxygenation (H-R) microenvironment. The results demonstrated that intracellular ROS and CLIC1 levels were increased under H-R conditions, and that functional inhibition of CLIC1 significantly decreased the H-R-elevated ROS generation and p-p38 MAPK levels in SGC-7901 cells, as well as inhibited the migration and invasion of SGC-7901 cells. In addition, the expression levels of MMP-2 and MMP-9 were inhibited by NAC, IAA-94 and SB203580. These results indicated that CLIC1 regulates gastric cancer-cell migration and invasion via the ROS-mediated p38 MAPK signaling pathway.

Background. Abdominal aortic aneurysm (AAA) belongs to a progressive, gradual aortic rupture, which can lead to death without surgical intervention. The key factors regulating the occurrence and progress of AAA are not clear. Increasing studies have indicated that microRNA (miRNA) plays an important role in cancer development. miR-124a serves as a tumor suppressor in several neoplasms, and its upregulation can greatly inhibit the life activities such as malignant growth and migration of tumor cells. Aim. The objective of this study is to explore the association of miR-124a with AAA and to uncover the regulated mechanism of miR-124a on AAA progression. Methods. The specimens from the AAA patients were used for observing the miR-124a expression, and human aortic endothelial cells (hAoECs) were treated with AngII to establish the AAA cell models. The quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR), CCK-8, transwell assay, flow cytometry assay, and western blot were conducted to unearth the regulation mechanism of miR-124a on AAA, and the dual-luciferase reporter assay was employed to investigate the downstream target of miR-124a. Results. miR-124a was significantly downregulated in the whole blood of the patients, and the decreased miR-124a was also observed in AAA cell models. Overexpressing miR-124a could effectively inhibit the proliferation and migration and promote the apoptosis of the AAA cells. The dual-luciferase reporter assay confirmed that BRD4 was a downstream target of miR-124a, and BRD4 upregulation could obviously reverse the effects of miR-124a on the phenotype of AAA cells. Moreover, it was found that miR-124a could regulate the activities of Wnt/β-catenin and P53 pathways via targeting the BRD4. Conclusion. Our data suggested that miR-124a could regulate the activities of Wnt/β-catenin and P53 to suppress the AAA progression via targeting the BRD4.

Objective Deep vein thrombosis of the lower limbs is a common disease in vascular surgery. Approximately 20–50% of deep vein thrombosis patients develop post-thrombotic syndrome, which can severely affect the patient's quality of life. However, the precise science of the pathophysiology of the progression of the post-thrombotic syndrome remains unclear. Studies have demonstrated that patients with post-thrombotic syndrome of the lower limbs have impaired arterial wall endothelial function. Nevertheless, there is little research on the different impacts of post-thrombotic syndrome on the arterial wall endothelial function between the affected limbs and the healthy limbs. This study aims to assess this difference. Methods A total of 60 patients treated for the post-thrombotic syndrome of the lower limbs were included. The flow-mediated dilation (FMD%) and nitroglycerin-mediated dilation (NMD%) were measured to assess the different endothelial function alterations of the common femoral arterial wall between the affected limb and the healthy limb. Results No significant differences in the common femoral artery diameter between the affected limbs and the healthy limbs were discovered (8.94  ±  0.92 mm vs 8.75  ±  1.0 mm, P = 0.710). The flow-mediated dilation of the common femoral artery of the affected limbs were significantly lower compared to the healthy limbs (FMD%: 3.21  ±  1.07% vs 5.19  ±  1.35%, P  =  0.001). However, there was no significant difference in the nitroglycerin-mediated dilation of the common femoral artery between the affected limbs and the healthy limbs（ NMD%: 13.37  ±  1.78% versus 14.45  ±  2.14%, P = 0.083). Conclusions Our results demonstrated the association between post-thrombotic syndrome and deteriorated endothelial functional properties of the arterial wall of the lower limbs. Endothelial dysfunction of the arteries wall was more severe in the affected lower limbs with the post-thrombotic syndrome than in the healthy limbs. The mentioned findings may partly explain the pathophysiology of the progression post-thrombotic syndrome of the lower limbs. Highlights tudies have demonstrated that patients with post-thrombotic syndrome of the lower limbs have impaired arterial wall endothelial function. Our results demonstrated the endothelial dysfunction of the arteries wall was more severe in the affected lower limbs with the post-thrombotic syndrome than in the healthy limbs. Our findings may partly explain the pathophysiology of the progression post-thrombotic syndrome of the lower limbs.

Objective The present study aims to compare the changes of venous flow parameters of the lower limbs under the assessment based on the duplex ultrasound scanning in obese and non-obese individuals by complying with body mass index during laparoscopic cholecystectomy. Methods A prospective cohort study was conducted in non-obese (body mass index <25 kg/m2) and obese individuals (body mass index >30 kg/m2) during laparoscopic cholecystectomy to analyze venous hemodynamics of the lower limbs. The assessment was conducted on Femoral vein diameter, Femoral vein cross-sectional area, Femoral vein peak velocity, and Femoral vein volume flow. The change values (%) of venous flow parameters of the lower limbs were calculated as a percentage by: (intra-operative parameter-pre-operative parameter)/ pre-operative parametersX100%. Results 45 right lower limbs were examined in 45 non-obese individuals and 33 right lower limbs in 33 obese individuals during laparoscopic cholecystectomy. The statistically significant difference was identified in the pre-operative and intra-operative values of Femoral vein diameter, Femoral vein cross-sectional area, Femoral vein peak velocity, as well as Femoral vein volume flow in both groups when these were analyzed independently ( p = .00). When the change values of venous flow parameters of the lower limbs of the two groups were compared, more changes were identified significantly in the obese group, Femoral vein diameter ( p = .042), Femoral vein cross-sectional area ( p = .013), Femoral vein peak velocity ( p = .002), and Femoral vein volume flow ( p = .032). Conclusion The changes of lower limb venous flow parameters showed more significant difference in obese than in non-obese individuals during laparoscopic cholecystectomy. The mentioned findings may in part explain why obese patients undergoing laparoscopic cholecystectomy have a higher rate of post op deep venous thrombosis.