Evaluation of stability of deep venous thrombosis of the lower extremities using Doppler ultrasound.

OBJECTIVE: This study aimed to assess using Doppler ultrasound for analyzing stability of deep venous thrombosis (DVT) of the lower extremities. METHODS: Patients with DVT of the lower extremities who were treated from August 2017 to December 2019 were selected. The patients were divided into stable and unstable groups according to whether thrombus was collected in a filter. Related ultrasound and blood test results were analyzed and compared. RESULTS: A total of 126 patients with DVT of the lower extremities were included, of whom 74 were in the stable group and 52 were in the unstable group. There were significant differences in the prothrombin time (PT), and lipoprotein alpha, D-dimer, and triglyceride levels between the groups. D-dimer levels >2800 ug/L, smoking, history of venous thrombosis, PT >13.15 s, and body mass index >24.45 kg/m2 were independent risk factors for stability of DVT of the lower extremities. The area under the curve with combined detection of DVT was significantly higher than that for body mass index, PT, and D-dimer alone. CONCLUSION: Doppler ultrasound may be reliable for analyzing the stability of DVT of the lower extremities. Related strategies targeting risk factors are required for reducing DVT of the lower extremities.

The Protective Effect of Safinamide in Ischemic Stroke Mice and a Brain Endothelial Cell Line.

Stroke is one of the leading causes of mortality in cardiovascular diseases. The disruption of the brain-blood barrier is the common feature of stroke-related complications. Safinamide is a newly approved add-on drug to treat Parkinson's disease, and previously studies suggest safinamide could have a potential role on neuroprotection. In this study, we investigated its preventive effect in both acutely induced stroke animals and brain endothelial cells. By the induction of middle cerebral artery occlusion (MCAO) in mice, we established a transit stroke model. Mice were administered 90 mg/kg/day safinamide prior to MCAO and during ischemia and reperfusion. Results indicate that the administration of safinamide significantly ameliorated MCAO-caused cerebral infarction volume, neurological deficit, disruption of the brain-blood barrier (BBB), and impaired expression of tight junction protein occludin and ZO-1. In cultured brain endothelial cell line bEND.3, pre-treatment with safinamide alleviated oxygen and glucose deprivation/reperfusion (OGD/R) caused cytotoxicity and favored cell survival. Transwell assay showed safinamide prevented OGD/R-induced hyperpermeability and the reduction of occludin and ZO-1. Moreover, safinamide treatment suppressed OGD/R-caused induction of metalloproteinase 2 (MMP-2) and 9 (MMP-9). Collectively, our data conclude safinamide has a preventive neuroprotection in acute stroke animals. The protective effect of safinamide on brain endothelial cells suggests the drug may ameliorate BBB disruption and improve vascular integrity in ischemia stroke.

Aminophylline promotes mitochondrial biogenesis in human pulmonary bronchial epithelial cells.

Recently, mitochondrial dysfunction has been linked to the development of common airway disorders, such as chronic obstructive pulmonary disease (COPD) and asthma. Phosphodiesterase inhibitors are therapeutic agents for various diseases. Aminophylline is a nonselective phosphodiesterase inhibitor used to treat common lung diseases. In this study, we show that aminophylline promotes mitochondrial biogenesis in cultured human pulmonary bronchial epithelial cells (HPBECs). Aminophylline treatment induces the expression of transcriptional coactivator PGC-1α and transcriptional factors NRF1 and TFAM. The effect of aminophylline on mitochondrial biogenesis can be revealed by its promotion of the ratio of mitochondrial DNA to nuclear DNA (mtDNA/nDNA), mitochondrial protein cytochrome B and mitochondrial mass. At the cellular level, aminophylline increases the mitochondrial respiration rate and ATP production but reduces oxygen content. Consistently, we show that aminophylline activates the CREB-PGC-1α signaling pathway to promote mitochondrial biogenesis. The inhibition of CREB activation by its specific inhibitor H89 obscures the induction of PGC-1α, NRF1, and TFAM by aminophylline, and also abolishes the action of aminophylline on the mtDNA/nDNA ratio and respiration rate, suggesting that the activation of CREB is required for the action of aminophylline. Collectively, our study supports that aminophylline is a potent metabolic inducer of mitochondrial biogenesis in epithelial cells. Aminophylline could have a therapeutic effect on epithelial mitochondrial function in lung diseases.