Functions of long non-coding RNA LNC11649 in non-small cell lung cancer cells as a reprocessed form of MALAT1.

Long non-coding RNAs (lncRNAs) have received much attention concerning their expression mechanisms in tumor formation. It is known that lncRNAs are involved in the occurrence, development, and prognosis of various tumors, including lung cancer. In our study, one non-coding RNA, LNC11649 (649 nt in length), was identified in non-small cell lung cancer (NSCLC) by PacBio third-generation sequencing technology. Both northern blot and quantitative PCR analyses confirmed the presence of LNC11649 in NSCLC tissues and cells with high expression. Its sequence was found to be highly homologous to lncRNA MALAT1. Knocking down MALAT1 could lead to a significant downregulation of LNC11649 content, revealing the possibility that LNC11649 could originate from MALAT1 reprocessing. RNA immunoprecipitation and electrophoretic mobility shift assays confirmed an interaction between LNC11649 and the MSI1 protein. Further experiments revealed that LNC11649 promoted the cytoplasmic distribution of MSI1 through its interaction with MSI1 and then activated the Akt signaling pathway to regulate the proliferation and migration of NSCLC cells. Our study reveals the possibility that LNC11649 plays a cancer-promoting role as a reprocessed form of MALAT1 in NSCLC cells and suggests that the MALAT1/LNC11649/MSI1/Akt regulatory axis becomes a potential therapeutic target for lung cancer.

Significance of the lipid profile and endothelium-dependent vasodilatation in the pathogenesis of microvascular angina.

BACKGROUND: To investigate the significance of lipid disorders and endothelial dysfunction in the pathogenesis of microvascular angina. METHODS: Levels of plasma lipids, lipoproteins and apolipoproteins were assessed in 21 patients with microvascular angina and 24 healthy subjects as controls. Also, the endothelium-dependent vasodilatation function was determined with high-resolution ultrasound in both groups. RESULTS: Levels of serum total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C), apolipoprotein B(100) (ApoB(100)) and lipoprotein(a) [Lp(a)] in microvascular angina group were significantly higher than those in healthy subjects (each p < 0.05). The flow-mediated dilatation (FMD) in brachial arteries in patients with microvascular angina declined significantly as compared with that in control subjects (4.7 +/- 1.9% vs. 12.8 +/- 3.7%, p < 0.001). However, no significant difference was observed in response to nitroglycerin between groups (19.7 +/- 8.1% vs. 21.2 +/- 6.6%; p > 0.05). Linear correlation analysis revealed a significant negative correlation between the FMD of brachial arteries and the serum levels of LDL-C and Lp(a) in the microvascular angina group (r = -0.5125 and -0.4271, respectively, both p < 0.001). Subsequently, all subjects were pooled and divided into two groups (groups A and B) according to the degree of FMD in brachial arteries (A pound 4% and B > 4%). The serum LDL-C level was found to be significantly higher in group A than in group B (4.09 +/- 0.65 mmol/L vs. 2.59 +/- 0.49 mmol/L; p < 0.05). CONCLUSIONS: Plasma lipid disorders and vascular endothelial dysfunction may play important roles in the development of microvascular angina. The dysfunction of endothelium-dependent vasodilation was mainly associated with anomalies in LDL-C and Lp(a), and myocardial endothelial dysfunction was aggravated by lipid abnormalities in patients with microvascular angina.

Atrioventricular block: a serious complication in and after transcatheter closure of perimembranous ventricular septal defects.

BACKGROUND: Transcatheter closure is an effective approach for perimembranous ventricular septal defects (PMVSD). However, atrioventricular blocks (AVB) emerged possibly due to the close proximity of the PMVSD to the conduction system, but concern for the complication was not adequately emphasized. In this study, we report the incidence of AVBs, in and after transcatheter closure of a PMVSD, and the outcome of the complication in our center. METHODS: One hundred and sixty-eight PMVSD patients were accepted for transcatheter closure with Amplazter PMVSD occluder (AGA Medical, Plymouth, Minn., USA). The procedure was discontinued when a second- or third-degree AVB occurred. A steroid was administered to all patients who developed AVBs. Temporary pacemakers were inserted in patients who developed a complete AVB or Mobitz type II AVB during or after the procedure. RESULTS: During the follow-up period of 6-24 mo (mean 10.6 +/- 3.9), the incidence of AVBs occurring during or after transcatheter closure of PMVSD was 3.5%. The AVB disappeared quickly after discontinuing the procedure in patients who developed AVBs during the procedure, whereas the AVBs disappeared between 2 and 21 d (mean 8.0 +/- 8.8) in the patients who developed AVBs after the procedure. However, complete right bundle branch block (CRBBB) was observed, and a transient complete AVB emerged after 8 mo in 1 case, incomplete right bundle branch block (IRBBB) in 1 case, and CRBBB and left anterior hemiblock (LAH) in 1 case. CONCLUSIONS: The AVB is a serious complication during and after transcathter closure of PMVSD. More attention should be paid to the complication, and multicentres are required to monitor the complication.

Complications associated with transcatheter closure of perimembranous ventricular septal defects.

OBJECTIVES: To identify the complications associated with transcatheter closure of perimembranous ventricular septal defects (PmVSD) using the Amplazter PmVSD occluder (AGA Medical, USA). METHODS: Between October 2002 and November 2006, transcatheter closure PmVSD was attempted in 210 patients and performed in 206 patients. Those patients were followed-up for 6-24 months (mean, 10.6 +/- 3.9 months) to identify the complications. RESULTS: Device implantation was successfully accomplished in 206 of the 210 patients (98%). Serious complications such as high degree atrioventricular block (AV block), infective endocarditis, and device embolization occurred in eight cases (3.8%). Other complications including mild aortic or tricuspid regurgitation, femoral pseudoaneurysm, and femoral arteriovenous fistula occurred in four cases. CONCLUSIONS: Transcatheter closure of PmVSD can be performed safely and successfully. But further studies should continue to evaluate the potential complications associated with this procedure.

[Characterizations of atrial contractions triggering paroxysmal atrial fibrillation and the effect of atrial fibrillation prevention pacing].

OBJECTIVE: To evaluate the electrocardiographic characterizations of atrial contractions(AC) triggering paroxysmal atrial fibrillation(AF), and to explore the effects of AF prevention pacing on their electrocardiographic characterizations. METHODS: Twenty-four patients with the implantation of AF therapy pacemaker(Vitatron 900E) were analyzed by AC triggering paroxysmal AF with Holter monitoring in the study. AC compluing interval, compensatory pause and frequency 2 minutes before the AF or during the AC were compared between the induced paroxysmal AF group and noinduced paroxysmal AF group, and the preventive effect of AF on the post-PAC response program was investigated. RESULTS: There was significant difference in the AC compluing interval [(352.3 +/-30.4) vs (421.8 42.5)ms], compensatory pause [(963 +/-109) vs (733 +/-124) ms], and frequency [(34.8 +/-18.9) vs (12.7 +/-8.7)/min] 2 minutes before the AF or during the AC in the induced paroxysmal AF group, compared with those in the noinduced paroxysmal AF group (all P<0.05). The AF of 7 patients were controlled by atrial overdrive pacing therapy, 17 patients by post-AC-response or/and post-exercise control therapy, 6 patients by the above therapy combining with cordarone (0.2g/d). CONCLUSION: AC triggering paroxysmal AF is related to the compluing interval, compensatory pause and frequency 2 minutes before the paroxysmal AF or during the AC, AF prevention pacing may be helpful for the paroxysmal AF induced by AC.

[Peripheral vascular complications after the cardiac catheterization].

OBJECTIVE: To explore the cause, the clinical manifestation and the management of peripheral vascular complications after cardiac catheterization. METHODS: Clinical data of patients with peripheral vascular complications were analyzed retrospectively. RESULTS: Of the 4,531 patients, 122 (2.7%) had peripheral vascular complications, including local hematoma (86 cases, 1.90%), pseudoaneurysm (15 cases, 0.33%), arteriovenous fistula (8 cases, 0.18%), femoral venous thrombosis (5 cases, 0.11%), excessive hemorrhage (5 cases, 0.11%), femoral arterial thrombosis (2 cases, 0.04%), and femoral nerve malfunction (1 case, 0.02%). All complications were relieved after conservative therapy except that one case needed surgery. CONCLUSION: Peripheral vascular complications are associated with anticoagulation, diabetes, and hypertension. Prognosis of overwhelming complications is good, as long as patients are treated timely and appropriately.

[Changes of plasma CD40L and PAPP-A in patients with acute coronary syndrome after the PCI operation].

OBJECTIVE: To observe the changes and significance of plasma CD40L and pregnancy-associated plasma protein-A (PAPP-A) in acute coronary syndrome (ACS) patients after percutaneous coronary intervention (PCI) operation. METHODS: According to the occurrence of primary heart events or restenosis 6 months after the PCI, 68 patients were divided into the ACS group and the stable angina pectoris (SAP) group. Plasma CD40L and PAPP-A after the PCI operation were measured and compared. Thirty-six patients underwent repeated angiography after the PCI. Their baseline and follow up angiograms were compared by quantitative coronary angiography to assess the incidence of restenosis. RESULTS: CD40L and PAPP-A after the PCI operation were higher in the ACS group than that in the SAP group.The group having primary heart events within 6 months had higher level of PAPP-A after the PCI. The group having restenosis 6 months had higher level of PAPP-A after the PCI. The change of later loss index of coronary artery lumen diameter was correlated with PAPP-A level after the PCI. CONCLUSION: CD40L and PAPP-A were higher in the ACS group, indicating the possible mechanism by which CD40L facilitates the plaque rupture via up-regulating the PAPP-A expression.Plasma PAPP-A level after the PCI possibly for cases the occurrence of primary heart events or restenosis within 6 months.

[Transcatheter closure for patent ductus arteriosus in children].

OBJECTIVE: To evaluate the results of transcatheter closure for patent ductus arteriosus (PDA) by different devices in children. METHODS: Seventy-eight cases of PDA in children (7 months to 14 years old), diagnosed by physical examination and transthoracic 2-dimensional echocardiography (TTE), were included in the study. The examination included the cardiac catheterization, photograph of the thoracic aorta and conventional technique of PDA closure. Among these patients, 16 were treated with coils, 9 with Amplatzer duct occluder (ADO), and 53 with native produced PDA occluders. RESULTS: TTE examination on the next day of the operation showed that PDAs were completely occluded in 76 cases, while the other 2 cases treated by coil had minimal residual shunt. Sixty-four patients, who were detected enlargement of the left ventricle before the operation, showed obvious diminishment of the cardiac size. By the end of 3 months, TTE examination showed that the closure of PDA was complete, and the left ventricle size was normal in 77 cases, while one case treated with coil had minimal residual shunt, which persisted for more than 4 years. The 3 - 80 months follow-up showed that the closure of PDA was complete in 77 cases, the configurations of the left ventricle, the thoracic aorta,and the left pulmonary artery were all normal. The occluders were well remained in situ. CONCLUSION: The usual procedures of transcatheter closure for PDA are effective and safe with ADO, native produced occluders and coil in children. Interventional method, which shows minute insult, few complications, and few adverse effects, can substitute the thoracic surgery.

[Oxidative stress and inflammation with angiographic morphology of coronary lesions in patients with coronary heart disease].

OBJECTIVE: To evaluate the role of oxidative stress and inflammation in the development of plaque rupture. METHODS: One hundred and ten patients enrolled in this study. All patients underwent coronary angiography. It included 85 patients with coronary heart disease (CHD) and 25 controls. The angiographic morphology of plaques was analyzed. According to the morphologic types of plaque, CHD patients were divided into Type I (smooth borders) group (n=31), Type II (irregular lesions) group (n=35), and Type III (long lesions) group (n=19). All patients were measured of MDA-LDL, hs-CRP, creatine kinase (CK), and MB isoenzyme of CK (CK-MB) in the plasma. RESULTS: Plasma MDA-LDL and hs-CRP in the Type II group were significantly higher than those in the control group, Type I group, and Type III group (P<0.01). The plasma levels of MDA-LDL were not correlated to LDL and HDL in patients in Type II group (P>0.05). The plasma levels of MDA-LDL and hs-CRP had a significant positive correlation in patients in Type II group (r=0.630, P<0.01). CONCLUSION: Oxidative stress and inflammation may cause plaque rupture in CHD patients. The oxidative stress is likely to either induce or intensify the inflammatory action, and may co-affect with inflammation factors to cause or accelerate plaque rupture.

[Effect of atrial pacing on the sleep apnea syndrome in elderly patients].

OBJECTIVE: To evaluate the efficacy of atrial pacing to increase the heart rate during sleep in elderly patients with sleep apnea syndrome. METHODS: Sixteen elderly patients with central type or obstructive type sleep apnea received permanent atrial-synchronous ventricular pacemakers for symptomatic sinus bradycardia were analysed in this study. All patients received polysomnographic evaluations for 3 consecutive nights. All patients were evaluated at the base-line, and then were randomly divided into 2 groups at the first night. In the following 2 nights, one group was monitored in spontaneous rhythm model and the other in dual-chamber pacing model with atrial overdrive (increasing by 15 beats per minute on the basic rate of the mean nocturnal sinus), and then the two groups were switched at the third night. The total duration and number of episodes of sleep apnea or hypopnea were analyzed, and compared between the two models. RESULTS: The mean 24 h sinus rate in the spontaneous rhythm mode was 55+/-9 beats per minute at the base line, as compared in the 72+/-4 beats per minute in the atrial overdrive pacing model. There was statistic significant difference between the 2 models (P<0.05). There was no difference in the total duration of sleep between spontaneous rhythm model and atrial overdrive pacing model [(322+/-48) minutes vs (330+/-52) minutes, P>0.05 ]. The hypopnea index reduced from 9+/-3 in the spontaneous rhythm model to 3+/-3 in the atrial overdrive pacing model (P<0.01). The index of apnea and hypopnea was 28+/-21 in the spontaneous rhythm model, as compared with 10+/-13 in the atrial overdrive pacing model (P<0.01). CONCLUSION: Atrial overdrive pacing can significantly reduce the number of episodes of central type or obstructive type sleep apnea, but doesn't decrease the total sleep time in elderly patients with sleep apnea syndrome.

The effect of atorvastatin on serum myeloperoxidase and CRP levels in patients with acute coronary syndrome.

BACKGROUND: Inflammation is involved in the atherogenesis and pathogenesis of acute coronary syndrome (ACS). As the acute-phase reaction proteins in ACS, myeloperoxidase (MPO) and C-reactive protein (CRP) may play critical roles. Anti-inflammation may be one of benefits of statin drugs in ACS. Studies have showed that statins can suppress serum CRP concentrations. However, whether statins also reduce serum MPO concentrations in patients with ACS is unknown. METHODS: Seventy-eight patients with ACS were randomly separated into Group A and Group B, the patients in Group A receiving conventional therapy, which include no cholesterol-lowering drugs, +atorvastatin (10 mg/day, n=40), the patients in Group B receiving conventional therapy (n=38). The serum concentrations of MPO were measured by enzyme-linked immunosorbent assay (ELISA) and CRP were measured by turbidimetric immunoassay. RESULTS: Serum concentrations of MPO were significantly lower after 1-week therapy in both groups of patients [Group A from 590+/-168 to 496+/-154 microg/l, Group B from 570+/-165 to 521+/-153 microg/l; P<0.01, respectively]. Serum concentrations of CRP also were markedly lower than pretreatment [Group A from 6.56+/-1.87 to 5.14+/-2.07 mg/l; Group B from 6.36+/-1.94 to 5.45+/-1.90 mg/l, P<0.05, respectively]. Compared with conventional therapy alone, atorvastatin significantly further reduced serum MPO [P=0.014] and CRP concentrations [P=0.032]. There were no correlations detected between the reduction of MPO and CRP (r=0.124, P=0.068). CONCLUSIONS: Atorvastatin reduced serum MPO and CRP concentrations in patients with ACS. These effects may explain some clinical benefits of statins in the treatment of these patients.