Cystic fibrosis transmembrane conductance regulator(CFTR)is an ATP-gated,cAMP-dependent chloride channel. The basic biophysical and pathological functions of CFTR are related with the secretion of chloride ion in epithelial cells and tissues. Mutations in CFTR cause cystic fibrosis(CF),which is a rare but fatal autosomal recessive inheritant disease ,mainly affecting glan?dular epithelial function in respiratory tract ,intestinal and reproductive system. New drugs targeting human CFTR gene mutations have been developed to significantly prolong lifeand improve respiratory symptoms of CF patients. Recent evidence suggested that CFTR plays a functional role in vasoconstriction and the formation of myocardial action potential. As a channel protein ,CFTR may al?so functions as a multiprotein/channel complex ,which has been demonstrated in the development of cardiovascular diseases such as myocardial ischemia and pulmonary hypertension.

Myocardial hypertrophy is the complication of many cardiovascular diseases that induce cardiac remodeling.The molecular mechanism of cardiac remodeling involves abnormal changes in various transmembrane ionic currents in the heart.Recent studies suggest the potential involvement of volume-regulated Cl-current(ICl.Vol)in cardiac hypertrophy.Although the molecular basis of ICl.Vol remains to be elucidated,recent progress is reviewed in the potential role of ICl.Vol in cardiac remodeling.

The effects of drugs on intracellular calcium concentration(［Ca2+］i) were investigated with fura-2 fluorescence technique to investigate ATP and thrombin-induced Ca2+ entry in bovine aortic endothelial cells(BAEC). It was found that application of ATP and thrombin gave rise to biphasic ［Ca2+］i elevation. ATP or thrombin only triggered a fraction of cyclopiazonic acid(CPA)-sensitive Ca2+ store, which was enough to activate Ca2+ entry. The Ca2+ release induced by thrombin resulted from the activation of phospholipase C(PLC), whereas the PLC-independent mechanism was involved in ATP-induced Ca2+ release. Nifedipine had no effect on ATP and thrombin- induced Ca2+ entry. SK&F 96365 and ginsenoside-2A inhibited both ATP and CPA-induced Ca2+ entry, however no effect of them on thrombin-induced Ca2+ entry was found. The inhibitory effects of SK&F 96365 and ginsenoside-2A on CPA-induced Ca2+ entry were less than that on ATP-induced Ca2+ entry. The Ca2+ influx sensitive to SK&F 96365 was not the same as that to ginsenoside-2A. These observations suggest that both ATP and thrombin evoke Ca2+ release and Ca2+ influx by activation of different receptor. However their mechanisms appear different.

Objective:To evaluate the outcomes of lesser arc perilunate injuries (Perilunate disloca-tions)treated with arthroscopically assisted mini-invasive reduction and fixation.Methods:Between 2012 and 2014,5 patients who had a perilunate dislocation were treated with arthroscopically assisted re-duction and percutaneous fixation.The mean follow-up was 17.8 months (range,10 to 32 months). Clinical outcomes were evaluated on the basis of range of motion;grip strength;Mayo wrist score;Quick disabilities of the arm,shoulder and hand questionnaire;and patient-rated wrist evaluation score.Radio-graphic evaluations included carpal alignments and any development of arthritis.Results:The range of flexion-extension motion of injured wrist averaged 84% of the values for contralateral wrist.The grip strength of the injured wrist averaged 90% of the values for the contralateral wrists.The mean Quick Disabilities of the arm,shoulder and hand score was 1 ,and the mean Patient-Rated Wrist Evaluation score was 5 .According to the Mayo wrist scores,the overall functional outcomes were rated as excellent in all the patients.Reduction obtained during the operation was maintained within normal ranges in all the patients.Arthritis had not developed in any patient at the end of the follow-up.Conclusion:Arthroscopic mini-invasive reduction with percutaneous fixation is a reliable and favorable alternative in the treatment of perilunate dislocations according to our early results.

Objective To investigate the effect of LncRNA-p21 on the proliferation, migration and invasion of non-small cell lung cancer A549 cells by regulating Notch signaling pathway. Methods The pcDNA-lincRNA-p21 and empty plasmid pcDNA were transfected into A549 cells, and they were divided into overexpression group and empty vector group. Cells from the stably-transfected overexpression group were added with the Notch signaling pathway specific activator Jagged1 protein and set as the Notch activator group. In addition, the cells without treatment were taken as the control group. Cell proliferation, migration and invasion of each group were detected by MTT method, scratch test and Transwell cell test. The expressions of Notch 1, HES-1, NICD, E-cadherin, Vimentin mRNA and protein were detected by RT-qPCR and Western blot. Results The A value of MTT test at 24, 48 and 72 hours in the overexpression group was lower than those in the control group, empty vector group and Notch activator group, and the Notch activator group was higher than the control group and the empty vector group (P < 0.05). The cell migration rate, the number of transmembrane cells and the relative expressions of Notch1, HES-1, NICD, Vimentin mRNA and protein of overexpression group at 48 hours were lower than those of the control group, empty vector group and Notch activator group, and the Notch activator group was lower than the control group and the empty vector group (P < 0.05). The relative expressions of E-cadherin mRNA and protein of overexpression group were higher than those of control group, empty vector group and Notch activator group, and the Notch activator group was higher than the control group and the empty vector group (P < 0.05). Conclusion Overexpression of LncRNA-p21 gene could inhibit the proliferation, migration and invasion of non-small cell lung cancer A549 cells. Its regulatory mechanism may be related to inhibiting Notch signaling pathway, thereby blocking the epithelial-mesenchymal transition of A549 cells.

[This corrects the article DOI: 10.1016/j.apsb.2021.04.013.].

Vascular smooth muscle cell (VSMC) migration plays a critical role in the pathogenesis of many cardiovascular diseases. We recently showed that TMEM16A is involved in hypertension-induced cerebrovascular remodeling. However, it is unclear whether this effect is related to the regulation of VSMC migration. Here, we investigated whether and how TMEM16A contributes to migration in basilar artery smooth muscle cells (BASMCs). We observed that AngII increased the migration of cultured BASMCs, which was markedly inhibited by overexpression of TMEM16A. TMEM16A overexpression inhibited AngII-induced RhoA/ROCK2 activation, and myosin light chain phosphatase (MLCP) and myosin light chain (MLC20) phosphorylation. But AngII-induced myosin light chain kinase (MLCK) activation was not affected by TMEM16A. Furthermore, a suppressed activation of integrin

[This corrects the article DOI: 10.1016/j.apsb.2021.04.013.].