Long Noncoding RNA LINC01207 Promotes Colon Cancer Cell Proliferation and Invasion by Regulating miR-3125/TRIM22 Axis.

Increasing study has validated that long noncoding RNAs (lncRNAs) are involved in the growth and metastasis of colon cancer. LINC01207 has been reported to play vital roles in certain types of cancer, while the precise function of LINC01207 in the progression of colon cancer remains unclear. The objective of this study was to investigate the effect of LINC01207 on the growth and metastasis of colon cancer cells and to explore the underlying mechanism. We found that the expression of LINC01207 was significantly upregulated in colon adenocarcinoma tissues compared with normal tissues by the GEPIA database. Notably, silencing of LINC01207 significantly suppressed the proliferation, migration, and invasion abilities of SW480 and HT-29 cells. Mechanistically, our data demonstrated that LINC01207 could sponge miR-3125 in colon cancer cells. Moreover, miR-3125 could directly target TRIM22 and negatively regulate its expression. Rescue assays revealed that miR-3125 inhibitor or TRIM22 overexpression significantly reversed the repressive role of LINC01207 knockdown in colon cancer cell proliferation and invasion. In conclusion, LINC01207 exerts an oncogenic role in the progression of colon cancer by absorbing miR-3125 to modulating TRIM22 expression.

Minimally invasive beating heart technique for mitral valve surgery in patients with previous sternotomy and giant left ventricle.

PURPOSE: To analyze the efficacy of minimally invasive beating heart technique for mitral valve surgery in the cardiac patients with previous sternotomy and giant left ventricle. METHODS: Eighty cardiac patients with previous sternotomy and giant left ventricle according to the diagnostic criteria that left ventricular end diastolic diameter (LVEDD) was ≥70 mm, who underwent mitral valve surgery at our center from January 2006 to January 2019 were analyzed. We divided all patients into minimally invasive beating heart technique group (n = 30) and conventional median resternotomy arrested heart technique group (n = 50) according to the surgical methods. Preoperative, intraoperative, and postoperative variables were compared between two groups. RESULTS: Minimally invasive beating heart technique compared to the conventional median resternotomy arrested heart technique for mitral valve surgery in the cardiac patients with previous sternotomy and giant left ventricle had significant differences in operation time(P = 0.002), cardiopulmonary bypass (CPB) time(P < 0.001), intraoperative blood loss(P < 0.001), postoperative transfusion ratio(P = 0.01), postoperative transfusion amount(P < 0.001), postoperative drainage volume(P = 0.001), extubation time(P = 0.04), intensive care unit (ICU) stay time(P = 0.04) and postoperative hospital stay time(P < 0.001), but no significant differences in re-exploration for bleeding, postoperative 30-day mortality, postoperative complications and 6 months postoperative echocardiographic parameters. CONCLUSIONS: Using the method of minimally invasive beating heart technique for mitral valve surgery in the cardiac patients with previous sternotomy and giant left ventricle is effective and reliable, meanwhile reduce the operation time and CPB time, decrease the transfusion ratio and transfusion amount, shorten postoperative ICU stay and hospital stay time, promote the early extubation so that accelerate the patients' early recovery. All of these show a benefit of minimally invasive beating heart technique compared to conventional median resternotomy arrested heart technique.

[Diagnosis and treatment of a case of acute severe Stanford type A aortic dissection].

OBJECTIVE: Patients with acute myocardial infarction (AMI) complicated with acute Stanford type A aortic dissection after percutaneous coronary intervention (PCI) are critically ill, with a very high fatality rate, and few cases are successfully treated clinically. A case with AMI admitted to the First Affiliated Hospital of Zhengzhou University complicated with acute left cardiac insufficiency after PCI, Stanford type A aortic dissection, pericardial and pleural infection, recurrent AMI was reviewed. In the condition of coexistence of many diseases, through timely adjustment of treatment strategy and exploratory application of drugs to improve cardiac function, the patient successfully received operation and discharged from the hospital. By presenting the successful treatment experience of this case, the author aims to improve the overall treatment of AMI patients with acute Stanford type A aortic dissection after PCI.

KLF2 inhibits cell growth via regulating HIF-1α/Notch-1 signal pathway in human colorectal cancer HCT116 cells.

The transcription factor Krüppel-like factor 2 (KLF2) has been shown to function as a tumor suppressor and regulate biological processes of cancer cells, such as cell growth, cell apoptosis and angiogenesis. However, the function and mechanism of KLF2 in colorectal cancer (CRC) is still unknown. In the present study, we show that the expression of KLF2 is diminished in a cohort of CRC cell lines. Also, KLF2 overexpression remarkably inhibits HCT116 and SW480 cell survival and proliferation. Moreover, cell death detection ELISA plus assay showed that KLF2 overexpression increased HCT116 cell proliferation. Caspase-3/7 activity also increased in HCT116 cells transfected with PcDNA3.1-KLF2. Further studies showed that KLF2 significantly suppresses the expression of Notch-1 and is dependent on the decline of the HIF-1α level. Most importantly, silencing Notch-1 expression or HIF-1α level both impair the action of KLF2 overexpression in CRC cells. Collectively, we demonstrated that KLF2 mediates CRC cell biological processes including cell growth and apoptosis via regulating the HIF-1α/Notch-1 signal pathway. These results indicated that KLF2 plays an important role in CRC and provided novel insight on the function of KLF2 in tumor progression.

Nicotinic α7 receptor inhibits the acylation stimulating protein­induced production of monocyte chemoattractant protein­1 and keratinocyte­derived chemokine in adipocytes by modulating the p38 kinase and nuclear factor­κB signaling pathways.

Obesity is associated with chronic low­grade inflammation, which is characterized by increased infiltration of macrophages into adipose tissue. Acylation stimulating protein (ASP) is an adipokine derived from the immune complement system, which constitutes a link between adipocytes and macrophages, and is involved in energy homeostasis and inflammation. The purpose of the present study was to preliminarily investigate in vitro, whether functional α7nAChR in adipocytes may suppress ASP­induced inflammation and determine the possible signaling mechanism. Studies have reported associations between the expression of α7 nicotinic acetylcholine receptor (α7nAChR) and obesity, insulin resistance and diabetes. Additionally, α7nAChRs are important peripheral mediators of chronic inflammation, which is a key contributor to health problems in obesity. The primary aim of the present study was to evaluate the impact of exogenous ASP and α7nAChR on macrophage infiltration in adipose tissue and to examine the potential underlying molecular mechanism. Western blot analysis revealed that recombinant ASP increased the expression levels of monocyte chemoattractant protein­1 (MCP­1) and keratinocyte­derived chemokine (KC) by 3T3­L1 adipocytes. However, nicotine significantly inhibited the production of ASP­induced cytokines via the stimulation of α7nAChR. It was also found that α7nAChR inhibited the ASP­induced activation of p38 kinase and nuclear factor­κB (NF­κB), and the production of MCP­1 and KC. These data indicated that α7nAChR caused the inhibition of ASP­induced activation of p38 kinase and NF­κB to inhibit the production of MCP­1 and KC.

Pulmonary artery closure in combination with patch technique for treating congenital heart disease combined with large patent ductus arteriosus: A clinical study of 9 cases.

OBJECTIVE: To document clinical experience of treating congenital heart disease combined with large patent ductus arteriosus with pulmonary artery closure in combination with patch technique. METHODS: Thirty-six patients (8 males and 28 females) who suffered from congenital heart disease and underwent hybrid surgery in the First Affiliated Hospital of Zhengzhou University from October 2010 to February 2014 were selected for this study. They aged 14 to 39 years and weighed 32.20 to 61.50 kg. Diameter of arterial duct was between 10 mm and 13 mm; 28 cases were tube type, 4 cases were funnel type and four cases were window type. All patients had moderate or severe pulmonary arterial hypertension; besides, there were 28 cases of ventricular septal defect, 16 cases of atrial septal defect, eight cases of aortic insufficiency, four cases of mitral stenosis and insufficiency and four cases of infectious endocarditis. Cardz Pulmonary Bypass (CPB) was established after chest was opened along the middle line. With the help of Transesophageal echocardiography, large patent ductus arteriosus was blocked off through pulmonary artery. Pulmonary artery was cut apart after blocking of heart. Large patent ductus arteriosus on the side of pulmonary artery was strengthened with autologous pericardial patch. RESULTS: Of 36 patients, 32 patients had patent ductus arteriosus closure device and four patients had atrial septal defect closure device. Pulmonary arteries of 36 cases were all successfully closed. Systolic pressure declined after closure ((54.86±19.23) mmHg vs (96.05±23.07) mmHg, p<0.05); average pulmonary arterial pressure also declined after closure ((39.15±14.83) mmHg vs (72.88±15.76) mmHg, p<0.05). The patients were followed up for one to fifty one months (average 11.5 months). Compared to before surgery, left atrial diameter, left ventricular diameter and pulmonary artery diameter all narrowed after surgery. Besides, clinical symptoms were relieved and cardiac function of the patients also improved. CONCLUSION: Hybrid surgery is feasible and safe in treating patients with large patent ductus arteriosus and congenital heart disease, which decreases surgical problems, shortens surgical time and lowers the incidence of complications.

Right coronary artery fistula misdiagnosed as right atrial cardiac myxoma: A case report.

The current study describes a case of right coronary artery fistula (CAF) misdiagnosed as right atrial myxoma (RAM). A 33-year-old man presented with a 13-year history of intermittent chest pain, and aggravation for 3 days. Echocardiography revealed an occupying lesion in the right atrium producing a partial dynamic tricuspid obstruction. The initial diagnosis was RAM, which causes partial right ventricular inflow tract obstruction. During cardiopulmonary bypass surgery, a giant mass was detected in the anterior wall of the right ventricle and an abnormal vascular fistula was observed at the bottom of the mass. Successful excision of the mass and closure of the fistula completely relieved the patient's presenting symptoms. The disease was subsequently diagnosed as right CAF draining to the myocardial void. The surgical management and misdiagnosis of the case are discussed herein.

Combined use of transmyocardial laser revascularization and endothelial progenitor cells enhances neovascularization and regional contractility in a canine model of ischemic hearts.

The purpose of this study was to determine the combined effect of transmyocardial laser revascularization (TMLR) and the implantation of endothelial progenitor cells (EPCs) on cardiac function of ischemic hearts in canines. The left anterior descending artery (LAD) was occluded to establish the canine model of acute myocardial infarct (AMI). Four weeks later, the animals were randomly divided into four groups: TMLR group, in which transmyocardial laser-induced channels were established at the ischemic region; EPCs+TMLR group, in which EPCs were locally transplanted into laser-induced channels at the ischemic region; EPCs group, in which the EPCs were injected into the ischemic region; control group, in which the AMI animals received neither TMLR nor EPCs. The peripheral blood (50 mL) was sampled in all groups. Mononuclear cells from the peripheral blood were separated and cultured to obtain spindle-shaped attaching (AT) cells in vitro. AT cells were labeled with 1, 1'-dioctadecyl-1 to 3,3, 3',3'-tetramethyl-indocarbocyanine perchlorate (DiI) before injecting into the laser-induced channels or ischemic region. Four weeks after the first operation, TMLR was performed in the TMLR group and EPCs+TMLR group, and at the same time, the EPCs originating from the AT cells were mixed with calcium alginate (CA). Then the EPCs-CA composites were implanted into myocardial channels induced by laser in the EPCs+TMLR group, and into the myocardial infarct area in the EPCs group. All dogs underwent echocardiography at second month after LAD occlusion. Finally the samples of myocardium around the LAD were subjected to histochemical and immunohistologic examinations. The results showed there was no significant difference in the diameter of left atrium and ventricle before treatment among all groups (P>0.05). Eight weeks after modeling, the regional contractility in the LAD territory in the EPCs+TMLR group was increased as compared with control group and TMLR group, but there was no significant difference between control group and TMLR group. Neoangiogenesis was observed in the EPCs+TMLR group, and the fibrosis was seen in the TMLR group. There was no significant difference in neoangiogenesis around the channels induced by laser among EPCs+TMLR, EPCs and TMLR groups. It was concluded that TMLR combined with EPCs could improve the regional and global cardiac function in AMI, and augment neovascularizaiton in channels of ischemic myocardium induced by laser.

M3 muscarinic acetylcholine receptor dysfunction inhibits Rac1 activity and disrupts VE-cadherin/ß-catenin and actin cytoskeleton interaction.

The objective was to investigate whether M3 muscarinic acetylcholine receptor (mAChR) dysfunction disrupts the linkage between the vascular endothelial (VE)-cadherin in the adherens junctional complex and the actin-based cytoskeleton, increasing vascular permeability in atherosclerosis. Western blotting revealed that a selective M3 receptor antagonist, 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP), and M3 receptor siRNA decrease VE-cadherin and ß-catenin in Triton X-100-insoluble fractions, indicating that M3 receptor inhibition weakens the linkage between the VE-cadherin/ß-catenin complex and the actin cytoskeleton. Co-immunoprecipitation assays showed that M3 receptor inhibition reduces Rac1 activity and the association of IQ motif-containing GTPase-activating protein 1 (IQGAP1) with Ras-related C3 botulinum toxin substrate 1 (Rac1), while increasing the interaction between IQGAP1 and ß-catenin. Using IQGAP1 siRNA, we found that IQGAP1 is required for stable interaction between VE-cadherin/ß-catenin and the actin cytoskeleton in quiescent endothelial cells; IQGAP1 siRNA augments the M3 receptor inhibition-induced dissociation between them. Moreover, S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide (NO) donor, attenuates this disassociation and Rac1 activity inhibition. The M3 receptor facilitates interaction of the VE-cadherin-based adherens junctional complex and the actin-based cytoskeleton by maintaining Rac1 activity, which regulates the interaction between IQGAP1/Rac1 and IQGAP1/ß-catenin, and may contribute to endothelial barrier function under physiological conditions.

Type 3 muscarinic acetylcholine receptor stimulation is a determinant of endothelial barrier function and adherens junctions integrity: role of protein-tyrosine phosphatase 1B.

The main purpose of this study was to investigate whether type 3 muscarinic acetylcholine receptor (M3R) dysfunction induced vascular hyperpermeability. Transwell system analysis showed that M3R inhibition by selective antagonist 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) and small interfering RNA both increased endothelial permeability. Using coimmunoprecipitation and Western blot assay, we found that M3R inhibition increased VE-cadherin and ß-catenin tyrosine phosphorylation without affecting their expression. Using PTP1B siRNA, we found that PTP1B was required for maintaining VE-cadherin and ß-catenin protein dephosphorylation. In addition, 4-DAMP suppressed PTP1B activity by reducing cyclic adenosine monophosphate (cAMP), but not protein kinase Cα (PKCα). These data indicate that M3R preserves the endothelial barrier function through a mechanism potentially maintaining PTP1B activity, keeping the adherens junction proteins (AJPs) dephosphorylation.

Uterine leiomyoma extension into right atrium.

We report a case of an intravenous leiomyomatosis of uterine origin extending into the right atrium, which was treated by two-stage surgery.

[Ventricular septal plication for post infarction anterior and anterior-septal aneurysm of the left ventricle].

OBJECTIVE: To determine the use of septal plication with Dor or Cooley procedure for post infarction anterior and anterior-septal aneurysm of the left ventricle. METHODS: A total of 23 patients with post infarction anterior and anterior-septal aneurysm of the left ventricle underwent septal plication and Dor or Cooley procedure along with coronary artery bypass grafting concomitantly. Data of NYHA grading, left ventricular end diastolic volume index (LVEDVI), left ventricular end systolic volume index (LVESVI) and left ventricular ejection fraction (LVEF) were recorded before the surgery, before discharge and 3 months after the surgery. RESULTS: Compared with the preoperative data, the NYHA grading before the discharge and 3 months after the surgery improved from 3.21 ± 0.62 to 1.72 ± 0.31 and 1.57 ± 0.23(P<0.05); LVEDVI decreased from (102.31 ± 18.71) mL/m² to (62.11 ± 6.21) mL/m² and (54.63 ± 4.54) mL/m² (P<0.05); LVESVI decreased from (69.32 ± 17.48) mL/m² to (30.23 ± 3.25)mL/m² and (28.34 ± 3.12) mL/m²; while LVEF increased from (32.92 ± 8.12)% to (48.78 ± 4.51)% and (50.52 ± 4.68)% (P<0.05), respectively. CONCLUSION: Ventricular septal plication combined with Dor or Cooley procedure can remarkably improve the left heart function in patients with post infarction ventricular aneurysm.

[Treatment of superior lobe central lung cancer with lung replantation].

BACKGROUND: Patients suffering from lung cancer often have poor quality of life after pneumonectomy. It has clinical significances to preserve maximum lobes of the "healthy" lung. The aim of this study is to report the applications of lung replantation in treatment of superior lobe central lung cancer. METHODS: Three lung cancer cases were included and analysed. The bronchus and margin of lower lung lobe were encroached by cancer. Pulmonary artery was invaded and surrounded by metastatic lymph node. Complete pneumonectomy, antegrade perfusion and retroperfusion with low-potassium dextran (LPD) solution in vitro were performed. The retainable lower pulmonary lobe was selected from the isolated lung and superior pulmonary vein was replaced with inferior pulmonary veins. The bronchus and pulmonary artery were inosculated by turns. RESULTS: The operative cumulative time ranged from 220 min to 250 min. The isolated time of lobus inferior pulmonary ranged from 120 min to 150 min. The chest tube was pulled out after chest X-ray confirmed the reimplant lung full re-expansion. The patients were followed up for 4 months to 8 months and accomplished adjuvant chemotherapy for 3 or 4 periodicities. The patients had a sound quality of life. CONCLUSIONS: Lung replantation removing the extensive tumor tissue and retaining the maximum pulmonary normal tissue is an useful method for treatment of lung cancer.

[Pretreatment of donor dendritic cells with NBD-peptide prolongs mouse cardiac allograft survival].

OBJECTIVE: To observe the effects of NBD-peptide pretreatment of the donor dendritic cells in immune tolerance induction in mouse allograft recipients and investigate the mechanisms. METHODS: BALB/c mouse DCs pretreated with NBD-peptide (NBD-Peptide-DC) were injected into the recipient C57BL/6 mice 7 days before transplantation. Cervical heterotopic heart transplantation model was established using the cuff technique and the cardiac allograft survival time was observed. Pathological analysis were performed to examine the graft injection and the responsiveness of the recipient spleen T cell to the donor alloantigen was determined by mixed lymphocyte reaction (MLR). The serum levels of cytokines were determined using ELISA. RESULTS: The cardiac allograft survival time in the NBD-Peptide-DC-treated group (21.83-/+3.54 days) was significantly longer than that in the Day9-DC group (13.33-/+2.58 days) and PBS-treated group (6.66-/+1.21 days) (P<0.01), with also significantly lower pathological grade for graft rejection (P<0.01). The donor-derived NBD-Peptide-DCs induced alloantigen-specific T-cell hyporesponsiveness. In the NBD-Peptide-DC-treated group, the serum levels of IL-12 and IFN-gamma decreased significantly (P<0.01), but the levels of IL-4 and IL-10 increased significantly (P<0.01). CONCLUSION: Injection of donor-derived NBD-Peptide-DCs can leads to donor-specific tolerance in the transplant recipients, and the induction of recipient T-cell hyporesponsiveness and polarization of Th2 response may play important roles in immune tolerance to cardiac allografts.

Mechanism and correlated factors of SAM phenomenon after aortic valve replacement.

To investigate the mechanism and correlated factors of systolic anterior motion (SAM) phenomenon after aortic valve replacement, 48 patients with severe aortic valvular stenosis were studied. Tested by echo-Doppler one week after aortic valve replacement, the patients were divided into two groups: SAM group and non-SAM group. The data of the left ventricular end-diastolic diameters, the left ventricular end-systolic diameters, the left ventricular outflow diameters, the thickness of the interventricular septum, the posterior wall of left ventricle, the blood velocities of left ventricular outflow and intra-cavitary gradients were recorded and compared. The results showed that no patients died during or after the operation. The blood velocities of left ventricular outflow was increased significantly in 9 patients (>2.5 m/s), and 6 of them developed SAM phenomenon. There was significant difference in all indexes (P<0.05 or P<0.01) except the posterior wall of left ventricle (P>0.05) between two groups. These indicated that the present of SAM phenomenon after aortic valve replacement may be directly related to the increase of blood velocities of left ventricular outflow and intra-cavitary gradients. It is also suggested that smaller left ventricular diastolic diameters, left ventricular systolic diameters, left ventricular outflow diameters and hypertrophy of interventricular septum may be the anatomy basis of SAM phenomenon.

[Effects of right ventricular outflow tract reconstruction with modified autologous pericardial monocuspid valve in patients with tetralogy of Fallot: a clinical research].

OBJECTIVE: To evaluate the application value of right ventricular outflow tract (RVOT) reconstruction with an autologous pericardial monocuspid valve to prevent pulmonary regurgitation after total correction of tetralogy of Fallot (TOF). METHOD: Twenty patients suffering from TOF with pulmonary artery hypoplasia, 11 males and 9 females, aged (8.43+/-3.83), received surgical total correction with RVOT reconstruction with autologous pericardial monocuspid valve. During the operation, the RVOT was enlarged with the autologous pericardial patch, and a predesigned part of the pericardial patch was folded to form a big artificial valve, which was stitched along with the pericardial patch. Another 20 patients, 12 males and 8 females, aged (8.47+/-3.94), underwent traditional RVOT reconstruction with traditional pericardial monocuspid valve patch. Post-operational follow-up was conducted for 6 months. RESULTS: No surgical mortality was recorded after operation. The degree of pulmonary valve regurgitation in the research group was less than that in the control group. CONCLUSION: Modified autologous pericardial monocuspid valve can prevent pulmonary regurgitation better.

Diagnosis and surgical treatment of ruptured aneurysm in sinus of Valsalva.

OBJECTIVE: To evaluate the methods used to diagnose and surgically treat ruptured aneurysm in sinus of Valsalva (RASV). METHODS: Thirty-seven hospitalized patients with ruptured aneurysms in the sinus of Valsalva from September 1981 to April 2001, including 21 cases (56.7%) of RASV associated with ventricular septal defects (VSD) and 11 (29.7%) with aortic valvular prolapse were given surgical interventions. Under hypothermia and extracorporeal circulation, we successfully performed the surgical correction of RASV for all 37 patients VSD repair in 21 patients, aortic valvuloplasty in 6 and aortic valvular replacement in 2. RESULTS: There was no hospital deaths among these patients, although residual shunting occurred in two patients and acute renal failure was found one. Follow-up study of one month to 20 years in the patients undergoing repair of RASV revealed that the mostly individuals treated with operation obtained satisfactory cardiac function. CONCLUSION: Correct diagnosis of ruptured aneurysm in sinus of Valsalva should be confirmed immediately and surgical correction should be carried out as soon as possible.