Dinitrogen Activation by Heteronuclear Bimetallic Cluster Anion FeV- in the Gas Phase.

Nitrogen activation is a significant but difficult project in the chemical area. Photoelectron spectroscopy (PES) and calculated results are used to investigate the reaction mechanism of the heteronuclear bimetallic cluster FeV- toward N2 activation. The results clearly show that N2 can be fully activated by FeV- at room temperature, forming the FeV(µ2-N)2- complex with the totally ruptured N≡N bond. Electronic structure analysis reveals that the activation of N2 by FeV- is achieved by the electron transfer of bimetallic atoms and electron back-donation to the metal core, which demonstrates that heteronuclear bimetallic anionic clusters are very important to nitrogen activation. This study provides important information for the rational design of synthetic ammonia catalysts.

Photothermal Superhydrophobic Chitosan-Based Cotton Fabric for Rapid Deicing and Oil/Water Separation.

Superhydrophobic cotton fabrics have a lot of potential for use in practical settings. The majority of superhydrophobic cotton fabrics, however, only serve one purpose and are made from fluoride or silane chemicals. Therefore, it remains a challenge to develop multifunctional superhydrophobic cotton fabrics using environmentally friendly raw materials. In this study, chitosan (CS), amino carbon nanotubes (ACNTs), and octadecylamine (ODA) were used as raw materials to create CS-ACNTs-ODA photothermal superhydrophobic cotton fabrics. The cotton fabric that was created showed a remarkable superhydrophobic property with a water contact angle of 160.3°. The surface temperature of CS-ACNTs-ODA cotton fabric can rise by up to 70 °C when exposed to simulated sunlight, demonstrating the fabric's remarkable photothermal capabilities. Additionally, the coated cotton fabric is capable of quick deicing. Ice particles (10 µL) melted and began to roll down in 180 s under the light of "1 sun". The cotton fabric exhibits good durability and adaptability in terms of mechanical qualities and washing tests. Moreover, the CS-ACNTs-ODA cotton fabric displays a separation efficacy of more than 91% when used to treat various oil and water mixtures. We also impregnate the coating on polyurethane sponges, which can quickly absorb and separate oil and water mixtures.

Comparison of clinical outcomes of using the nonirradiated and irradiated allograft for anterior cruciate ligament (ACL) reconstruction: A systematic review update and meta-analysis.

BACKGROUND: This study was a systematic review comparing the clinical outcomes of using the nonirradiated and irradiated allograft for anterior cruciate ligament (ACL) reconstruction. METHODS: A comprehensive literature search was conducted using multiple databases, including Medline, Embase, and Cochrane. All databases were searched from the earliest records through August 2019 using the following Boolean operators: irradiated AND nonirradiated AND ACL AND allograft. All prospective and retrospective controlled trials were retrieved that directly compared physical examination and knee function scores and patient-rated outcomes between the nonirradiated and irradiated allograft for ACL reconstruction. RESULTS: Three prospective and 2 retrospective articles were identified by the search, and the findings suggested that the nonirradiated allografts were superior to the irradiated allografts based on improved knee joint functional scores and decreased failure rate, even though there was no significantly difference with respect to overall IKDC, range of motion, vertical jump test, and one-leg hop test. CONCLUSIONS: Irradiated allograft should be limited to be used in ACL surgery and further research into new alternative sterilization techniques are needed to avoiding the disease transmission without interference with the biomechanical properties of the grafts.

Iridium Dimer Anion-Mediated C≡C Triple Bond Cleavage and Successive Dehydrogenation of Acetylene in the Gas Phase.

The reactions of the iridium dimer anion [Ir2]- with acetylene have been studied by mass spectrometry in the gas phase, which indicate that the [Ir2]- anion can consecutively react with C2H2 molecules to form the [Ir2C2x]- (x = 1, 2) and [Ir2C2yH2]- (y = 3-5) anions as major products with the successive release of H2 molecules at room temperature. The reactions are confirmed by the reactions of the mass-selected product [Ir2C2]- anion with C2H2 to produce [Ir2C4]- and [Ir2C2yH2]- (y = 3-5). Photoelectron spectra and quantum chemistry calculations confirm that the [Ir2C2x]- (x = 1, 2) product anions possess cyclic [Ir(µ-C)2Ir]- and [Ir(µ-C)(µ-C3)Ir]- structures, implying that the robust C≡C triple bond of acetylene can be completely cleaved by the [Ir2]- anion.

Coronary Artery-Left Ventricular Fistula with Giant Right Coronary Aneurysm: A Case Report and Literature Review.

Right coronary artery-left ventricular (RCA-LV) fistula with associated giant right coronary artery aneurysm (CAA) is an extremely rare cardiac condition. This case study presents a patient with a large left ventricle (LV) and a giant right CAA with a maximal inner diameter of approximately 56.6 mm and an inner diameter of approximately 22 mm at its communication with the left ventricle. The patient underwent surgical management, involving suturing of the proximal end of the CAA and coronary artery bypass grafting (CABG). RCA-LV fistula with a giant right CAA may involve serious complications, such as thrombosis, rupture, and heart failure. Therefore, it is necessary to establish effective management strategies for this condition. Although this case is not unique, it serves as an illustrative example of the implementation of a classic surgical treatment method.

MicroRNA-221 Upregulates the Expression of P-gp and Bcl-2 by Activating the Stat3 Pathway to Promote Doxorubicin Resistance in Osteosarcoma Cells.

MicroRNA-221 (miRNA-221) is upregulated in several malignant tumors and is associated with poor patient prognosis. Therefore, the present study aimed to investigate the role and underlying mechanism of miRNA-221 in doxorubicin (DOX) resistance in osteosarcoma cells. We constructed DOX-resistant Saos-2/DOX cells and treated them with DOX. Cell viability was determined by performing a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cells were transfected with either miRNA-221 mimic or miRNA-221 inhibitor; quantitative (q)RT-PCR was performed to detect the expression of miRNA-221. Flow cytometry and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-digoxigenin nick-end labeling (TUNEL) staining were used to detect cell apoptosis. The immunofluorescence method was also used to detect cell signal transduction and activator of transcription 3 (Stat3) protein expression distribution. In addition, Western blotting was used to detect changes in the expression of each protein. We found that miRNA-221 was upregulated in Saos-2/DOX cells. Moreover, the miRNA-221 mimic induced DOX resistance in Saos-2 cells, whereas the miRNA-221 inhibitor enhanced DOX sensitivity in Saos-2/DOX cells. The miRNA-221 mimic upregulated the expression of phosphorylated-Stat3, P-glycoprotein (P-gp), and B-cell lymphoma-2 (Bcl-2) proteins in Saos-2 cells and induced the entry of Stat3 into the nucleus, whereas the miRNA-221 inhibitor exerted the opposite effect. Pretreatment with the Stat3 chemical inhibitor, STAT3-IN-3, significantly inhibited the upregulation of P-gp and Bcl-2 protein expression induced by the miRNA-221 mimic in Saos-2 cells; it also caused the Saos-2 cells to overcome DOX resistance induced by the miRNA-221 mimic. Thus, miRNA-221 increased the expression of P-gp and Bcl-2 by activating the Stat3 pathway to promote DOX resistance in osteosarcoma cells, indicating a potential use of miRNA-221 in osteosarcoma treatment.

Suppression of PAPP-A mitigates atherosclerosis by mediating macrophage polarization via STAT3 signaling.

Pregnancy-associated plasma protein-A (PAPP-A), a type of metalloproteinase in the insulin-like growth factor (IGF) system, has been implicated in atherosclerosis progression, but its function and mechanism in atherosclerosis is not fully understood. The study was performed to further explore the effects of PAPP-A on inflammation, macrophage polarization and atherosclerosis. In mouse macrophages stimulated by oxidized low-density lipoprotein (ox-LDL), PAPP-A expression was significantly increased. Its knockdown markedly mitigated inflammatory response and polarized macrophages to an M2-like phenotype in RAW264.7 cells upon ox-LDL treatment. Additionally, ox-LDL-induced activation of nuclear factor-κB (NF-κB) signaling pathway was dramatically restricted by PAPP-A knockdown in macrophages. However, JAK2/STAT3 activation was significantly up-regulated in RAW264.7 cells with PAPP-A inhibition after ox-LDL treatment. Importantly, we found that PAPP-A knockdown-induced polarization of M2-like phenotype in macrophages was mainly dependent on STAT3 activation. Clinical studies showed that serum PAPP-A levels were higher in patients with coronary artery disease (CAD) than that of healthy individuals. Apolipoprotein E-knockout (ApoE-/-) mice with high fat diet (HFD)-induced atherosclerosis exhibited higher expression of PAPP-A in aortas, which was mainly colocalized with F4/80. Subsequently, we found that PAPP-A deficiency greatly alleviated plaque formation, lesion burden and collagen accumulation in HFD-fed ApoE-/- mice. Consistent with in vitro macrophage phenotype, PAPP-A-/- reduced F4/80 expression, NF-κB activation and inflammatory response, while improved janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling and polarized macrophages to an M2-like phenotype in aortas of ApoE-/- mice after HFD feeding. In conclusion, these findings identified PAPP-A as a positive regulator of atherosclerosis by regulating macrophage polarization via STAT3 signal, and thus could be considered as a potential therapeutic target for atherosclerosis treatment.

APPBP2 enhances non-small cell lung cancer proliferation and invasiveness through regulating PPM1D and SPOP.

BACKGROUND: The influence of amyloid protein-binding protein 2 (APPBP2) on lung cancer is unknown. METHODS: The function and mechanisms of APPBP2 were investigated in the NSCLC cell lines A549 and H1299. The ectopic expression of APPBP2, PPM1D and SPOP in NSCLS were examined in samples collected from ten pairs of human lung adenocarcinoma cancer tissues and adjacent normal lung tissues. shRNA vector was used for APPBP2 knockdown. Quantitative PCR and western blot assays quantified the mRNA and protein level of APPBP2, PPM1D, and SPOP. Cell proliferation was measured with BrdU, MTT, colony formation assays, and xenograft tumour growth experiments. Cell migration and invasion were analysed with transwell and wound healing assays. Co-Immunoprecipitation assay detected protein-protein interactions. FINDINGS: APPBP2 was upregulated in NSCLC tissues. Silencing APPBP2 in A549 and H1299 cells resulted in the inhibition of cell proliferation, migration, and invasion, enhancement of apoptosis, and a significant decrease in the expression of PPM1D and SPOP. Overexpression of PPM1D and SPOP attenuated the APPBP2-knockdown inhibition of NSCLC cells. Co-IP assay showed that PPM1D interacted with APPBP2. INTERPRETATION: The expression level of APPBP2 positively correlates with NSCLC cell proliferation, migration, and invasiveness. APPBP2 contributes to NSCLC progression through regulating the PPM1D and SPOP signalling pathway. This novel molecular mechanism, underlying NSCLC oncogenesis, suggests APPBP2 is a potential target for diagnosis and therapeutic intervention in NSCLC. FUND: Key Program of Natural Science Research of Higher Education of Anhui Province (No. KJ2017A241), the National Natural Science Foundation of China (No. 81772493).

The diagnosis and treatment of cardiac lymphangioma: A case report and literature review.

RATIONALE: Cardiac lymphangioma is a rare disease. Until now, there have been only a few cases of cardiac lymphangioma reported in the literature. PATIENT CONCERNS: We report the case of a 57-year-old female patient with cardiac lymphangioma from atrial septum. DIAGNOSIS: Color Doppler echocardiography was performed, which revealed a tumor occupying a large amount of space in the left and right atrium. INTERVENTIONS: The patient underwent thoracoscopic cardiac tumor resection under general anesthesia according to the procedure used for benign tumors. OUTCOMES: The patient recovered completely and was discharged home. Follow-up color Doppler echocardiography scans obtained from 6 months to 2 years after the operation showed no recurrent mass. LESSONS: Once the tumor is detected, surgical treatment should be implemented as soon as possible.

Knockdown of TBRG4 affects tumorigenesis in human H1299 lung cancer cells by regulating DDIT3, CAV1 and RRM2.

The transforming growth factor ß regulator 4 (TBRG4) gene, located on the 7p14-p13 chromosomal region, is implicated in numerous types of cancer. However, the contribution(s) of TBRG4 in human lung cancer remains unknown. In the present study, the expression of TBRG4 mRNA was investigated in the H1299 lung cancer cell line using the quantitative polymerase chain reaction (qPCR) following the knockdown of TBRG4 by a lentivirus-mediated small interfering RNA (siRNA). Results identified that the expression of TBRG4 within H1299 cells was significantly suppressed (P<0.01) by RNA interference, and 586 genes were differentially expressed following TBRG4 silencing. Ingenuity Pathway Analysis (IPA) revealed that these genes were often associated with infectious diseases, organismal injury, abnormalities and cancer functional networks. Further IPA of these networks revealed that TBRG4 knockdown in H1299 cells deregulated the expression of 21 downstream genes, including the upregulation of DNA damage-inducible transcript 3 (DDIT3), also termed CCAAT/enhancer-binding protein homologous protein, and downregulation of caveolin 1 (CAV1) and ribonucleotide reductase regulatory subunit M2 (RRM2). Results were validated using qPCR and western blotting. Furthermore, immunohistochemical staining of TBRG4 protein identified that expression was markedly increased in carcinoma compared with in normal tissue. In conclusion, TBRG4 serves a role in the tumorigenesis of lung cancer via deregulation of DDIT3, CAV1 and RRM2. The results of the present study may be important in contributing to our understanding of TBRG4 as a target for lung cancer treatment.

Histone deacetylase inhibitor SAHA-induced epithelial-mesenchymal transition by upregulating Slug in lung cancer cells.

SAHA, a member of histone deacetylase inhibitors (HDACIs), which emerged as a class of novel antitumor drug, has been used in clinical treatment of cancers. However, clinical experience of SAHA in solid tumors has been disappointing. Nevertheless, the underlying mechanism of this deficiency is not clearly understood. In the present study, we found that SAHA could induce epithelial-mesenchymal transitions (EMT) in lung cancer A549 cells, which was associated with increased migration capability and cellular morphology changes. We showed that SAHA decreased epithelial marker E-cadherin's expression and increased the expression of mesenchymal marker vimentin. SAHA upregulated the protein and mRNA expression of transcription factor Slug in a time-dependent manner and promoted its nuclear translocation. We further demonstrated that SAHA upregulated Slug expression by promoting Slug acetylation but not influencing the phosphorylation of GSK-3ß, a main kinase-controlled Slug expression. Finally, silencing of Slug by siRNA reversed EMT marker expressions and cellular morphology change induced by SAHA, suggesting that Slug plays a crucial role in SAHA-mediated EMT in A549 cells. Our research study provided a better understanding of treatment failure of SAHA in patients with solid tumors. Therefore, more attention should be paid to cancer treatment using SAHA and strategies for reversing EMT before using SAHA would be better if the value of SAHA in the treatment of solid tumors, especially lung cancer, is realized.

Wnt5a promotes epithelial-to-mesenchymal transition and metastasis in non-small-cell lung cancer.

A recent study indicated that high Wnt5a expression is associated with poor prognosis in non-small-cell lung cancer (NSCLC) patients; however, the underlying mechanism was not clear yet. Immunohistochemistry and Western blotting were performed to examine the protein expression level in NSCLC tissues and cell lines. The role of Wnt5a in clone formation, invasiveness, migration, and epithelial-to-mesenchymal transition (EMT) of NSCLC cells was studied. Luciferase reporter assay was used to evaluate the Tcf/Lef transcriptional activity. For assessing the effects of Wnt5a on tumor growth and metastasis in vivo, A549 cells transfected with sh-Wnt5a were subcutaneously or orthotopically injected into nude mice. In NSCLC tissues, higher expression levels of Wnt5a and ROR2 were found, ß-Catenin was expressed exceptionally, and EMT was prompted. Wnt5a overexpression increased clone formation, migration, and invasion, as well as prompted EMT of NSCLC cell in vitro, whereas Wnt5a knockdown showed the absolutely reversed results. Wnt5a overexpression enhanced the Tcf/Lef transcriptional activity and elevated the nuclear ß-catenin level in NSCLC cells, without altering the ROR2 expression. We also demonstrated that si-ß-catenin antagonized Wnt5a overexpression nduced EMT and invasiveness. Besides, in vivo experiment showed that sh-Wnt5a significantly increased tumor volume and tumor weight, and prompted EMT in A549 tumor-bearing mice as compared with the control. No metastasis was found in the liver tissue after sh-Wnt5a-transfected cells were orthotopically injected into nude mice as compared with the control. In conclusion, Wnt5a promotes EMT and metastasis in NSCLC, which is involved in the activation of ß-catenin-dependent canonical Wnt signaling.

Long-term outcomes of minimally invasive Ivor Lewis esophagostomy for esophageal squamous cell carcinoma: Compared with open approach.

OBJECTIVE: To investigate the safety and long-term efficacy of combined thoraco-laparoscopic minimally invasive Ivor Lewis esophagostomy(MI-ILE) in the treatment of esophageal squamous cell carcinoma. METHODS: The clinical data of patients with esophageal squamous cell carcinoma who underwent Ivor Lewis esophagostomy of esophageal cancer from October 2011 to June 2013 were retrospectively analyzed. Of which 90 patients received MI-ILE, 95 patients underwent open Ivor Lewis esophagostomy (O-ILE). The clinicopathological features, intraoperative records and incidences of postoperative complications of the two groups were compared with t-test and χ2 test. The primary end point of the study was 3-year disease-free survival (DFS) and 3-year overall survival (OS) was a secondary end point. RESULTS: There were no statistically significant differences in gender, age, preoperative comorbidities, American Society of Anesthesiologists score and position of the tumor between the two groups. There was also no significant difference in clinicopathological characteristics, operation time, length of tumor resection margin and number of resected lymph nodes between the two groups (P > 0.05). In MI-ILE group, the blood loss was lower than in the O-ILE group [(159.1 + 97.4) ml vs. (191.7 + 141.9) ml, t = 1.811, P = 1.811]and the postoperative hospital stay was shorter [(11.5 + 4.5) d vs. (13.9 + 6.2) d, t = 2.944, P = 0.004]. There was no significant difference in the incidences of perioperative mortality and major morbidities (P > 0.05). Minor complications including incision infection rate (1.1% vs 8.4%, χ2 = 3.873, P = 0.049) and pulmonary infection incidence (3.3% vs 11.57%, χ2 = 4.492, P = 0.034) is lower in MIILE group. There was no significant difference in 3-year disease-free survival (DFS) and 3-year overall survival (OS) between the two groups. CONCLUSION: MI-ILE is a technically safe and feasible approach for esophageal squamous cell carcinoma treatment. The oncologic outcomes of MI-ILE are comparable to that of O-ILE 3 years after resection.

Reduced RKIP expression levels are associated with frequent non-small cell lung cancer metastasis and STAT3 phosphorylation and activation.

The current study examined the role of Raf kinase inhibitor protein (RKIP) in non-small cell lung cancer (NSCLC) metastasis. A total of 100 patients with NSCLC were recruited following pathological diagnosis in the First Affiliated Hospital of Bengbu Medical College. The patients were classified and statistically analyzed according to their clinicopathological characteristics and tumor-node-metastasis stage. Paired tumor tissue and adjacent non-tumor tissue samples were subject to pathological diagnosis and western blot analysis. Transient transfection and lentivirus particle vector-mediated RKIP overexpression, small interfering RNA-mediated silencing, Transwell assays and immunocytochemistry methods were employed to elucidate the role and underlying mechanisms of RKIP and the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway in NSCLC metastasis. Furthermore, in order to examine the in vivo effects of RKIP, recombinant lentivirus particles containing the RKIP gene were administrated in a mouse NSCLC tumor model via tail vein injection. The results revealed reduced RKIP expression levels in NSCLC tissue compared with corresponding non-cancer tissue. Additionally, RKIP expression levels were inversely associated with NSCLC intra-lung, lymph node and long-distance metastasis. The results also indicated that RKIP was able to block STAT3 activation via phosphorylation and inhibit NSCLC-cell metastasis in vitro. Furthermore, RKIP knockdown was able to promote STAT3 phosphorylation and cell metastasis in NSCLC cell lines. During in vivo experiments, RKIP overexpression was able to suppress xenograft tumor metastasis in nude mice. Therefore, RKIP may be an important factor in cancer cell metastasis in patients with NSCLC, and RKIP may inhibit NSCLC-cell invasion by blocking the activation of the JAK/STAT3 signaling pathway.

Diagnosis and surgical treatment of mediastinal solitary fibrous tumor.

AIM: The aim of this study was to investigate the clinical features as well as the diagnosis and treatment methods for mediastinal solitary fibrous tumor (MSFT). METHODS: The clinical data of 13 patients treated for pathologically confirmed MSFT were retrospectively analyzed. The clinical symptoms were mainly cough, chest tightness, chest pain and chest discomfort. It was difficult to distinguish MSFT from other types of tumors simply via imaging results, hence, the confirmative diagnosis required pathological and immunohistochemistry analysis. RESULTS: The tumors were completely resected for all patients. All patients were discharged after surgery and followed up for 2-85 months. One patient died of cerebral hemorrhage 2 months after the surgery, and the rest of the patients experienced no recurrence or metastasis during the follow-up period. CONCLUSIONS: MSFT is a rare type of mediastinal tumor, and the diagnosis requires pathological and immunohistochemical analysis. Surgical treatment is preferred, and a complete resection can achieve a good prognosis; however, postoperative adjuvant radiotherapy might be necessary for cases with extensive external invasion.

Reversal of galectin-1 gene silencing on resistance to cisplatin in human lung adenocarcinoma A549 cells.

This study aims to investigate reversal of Galectin-1 gene silencing on resistance to cisplatin in human lung adenocarcinoma A549 (or A549/DDP) in vivo and in vitro. The stably transfected lentivirus vector was used to silence Galectin-1 in human lung adenocarcinoma cell line A549 and A549/DDP cells and the cell lines were cultured and passaged. RT-PCR and western blot assay were used to test A549, A549/DDP cells, silenced Galectin-1A549 (A549/I) cells, Galectin-1 mRNA and protein expression levels, respectively, in A549/DDP (A549/DDP/I) cells. CCK8 assay was used to measure median inhibitory concentration (IC50) in each group and resistant index of A549/DDP cells and A549/DDP/I cells. Tumor model in nude mice was established by armpit injection of A549, A549/DDP, A549/I, A549/DDP/I cells. Cisplatin was injected intraperitoneally in tumor models and growth of tumor was observed in vivo model. Four weeks later, nude mice were killed and tumor weight and diameter was measured. mRNA and protein expression of Galectin-1 in A549/DDP cells was higher than that in A549 cells. mRNA and protein expression of Galectin-1 in A549/DDP/I cells was lower than that in A549/DDP cells. Moreover, IC50 values ​​and resistance index in A549/DDP cells was higher than that in A549 cells group and IC50 values ​​and resistance index A549/DDP/I cell group were lower than that in A549/DDP cells. Additionally, tumor weight and volume in A549/DDP/I cell group were lower than that in A549/DDP. In conclusion, Galectin-1 gene silencing would improve the sensitivity of A549/DDP cells to cisplatin in vivo and in vitro.

MicroRNA-181a regulates epithelial-mesenchymal transition by targeting PTEN in drug-resistant lung adenocarcinoma cells.

Chemoresistance is an inevitable occurrence in lung adenocarcinoma, which has been associated with decreased expression of the phosphatase and tensin homolog deleted on chromosome ten (PTEN). Therefore, it is important to identify novel molecular mechanisms to suppress chemoresistance in lung adenocarcinoma cells. Paclitaxel- and cisplatin-resistant A549 lung carcinoma cell derivatives were developed by long-term serial culture. The metastatic properties of the cells were assessed using wound-healing assays, migration assays, invasion assays, morphological examination, and western blot analysis/RT-PCR of genes associated with the epithelial-mesenchymal transition (EMT). To identify novel regulators of EMT in A549 cells, differentially expressed miRNAs in drug-resistant cells were identified by microarray analysis. The role of miR-181a was established by transfection with specific mimic and inhibitor followed by functional assays. Luciferase assays were performed to assess the ability of miR-181a to target the PTEN promoter, and regulation of PTEN expression by miR-181a was assessed by western blot analysis and RT-PCR. Paclitaxel- and cisplatin-resistant A549 cells acquired metastatic properties and EMT phenotype and had reduced PTEN expression as compared to sensitive cells. miR­181a was identified as a differentially expressed miRNA in drug-resistant A549 cells, and miR-181a mimic and inhibitor were shown to affect migration, invasion, morphology and expression of EMT-associated genes. PTEN was identified as a direct target of miR-181a. Our findings demonstrate that miR-181a expression in lung adenocarcinoma is associated with EMT progression, potentially through targeting of PTEN. Regulation of miR-181a may provide a novel strategy for overcoming resistance to paclitaxel and cisplatin in lung adenocarcinoma.

[Establishment of a cyanotic congenital heart defect porcine model with decreased pulmonary blood flow].

OBJECTIVE: To establish a porcine model of congenital heart disease with decreased pulmonary blood to explore the morphological changes of immature pulmonary vascular vessels. METHODS: Twenty piglets (one to two-month-old) were randomly divided into three groups: sham-operated group (group S, n = 6), small incisions on the right chest, produced a transient reduction in pulmonary blood; Operation group 1(group T(1), n = 7), small incisions on the right chest, producing artificial atrial defect with self-made dilator and simultaneous banding pulmonary artery to generate a systolic pressure gradient between 20 - 30 mm Hg (1 m Hg = 0.133 kPa); Operation group 2(group T(2), n = 7): operation procedure was similar as group T(1) with systolic pressure gradient between 30 - 50 mm Hg. Lung tissue from right middle lobe (1.0 cm×0.8 cm×0.8 cm) was taken immediately after thoracotomy, at the end of surgery and at 2 months after operation and stained by Weigert (elastic fiber) and van Gieson (collagen) methods to observe the morphological changes. RESULTS: Five animals survived in Group S, 6 animals survived in group T(1) and 5 animals survived in group T(2). The inside diameter of pulmonary arterioles after thoracotomy and at the end of surgery was similar among the three groups (P > 0.05). At 2 months after operation, the inside diameter of pulmonary artery was significantly higher in group T(1) and T(2) than in group S (all P < 0.05) while the number of pulmonary small artery per square centimeter (APSC) of group T(1) and T(2) was significantly lower than that of group S (all P < 0.05). Tunica media of pulmonary artery was thinner and vascular lumen was larger in group T(1) and T(2) compared to those of group S. CONCLUSION: In this piglets model with reduced pulmonary blood, the pulmonary arterioles underwent dysplastic changes. Thus, pulmonary blood flow is an important determinant for the physiological development of pulmonary artery.

[Detection of CEA mRNA on non-small lung cancer and it's significance.].

BACKGROUND: In recent years, many studies on micrometastasis in non-small cell lung cancer (NSCLC) have been reported, this study is to investigate the effect of operation on micrometastasis from NSCLC and evaluate the relation between micrometastasis and clincopathological parameters. METHODS: The blood samples were taken from 70 cases of NSCLC and 18 patients with benign diseases at 3 intervals during the operation from peripheral vein. The transcription of carcinoembryonic antigen messenger ribonucleic acid (CEA mRNA) was assayed by means of nested reverse transcriptase polymerase chain reaction (RT-PCR) and micro-fluid chip. RESULTS: The CEA mRNA positive rates of all 3 time spots were as follows: 50% at beginning of the operation (Time 1), 62.8% at ligating the pulmonary vein (Time 2) and 57.1% at 1 h after ligating pulmonary vein (Time 3). There is significant difference between Time 1 and Time 2 (Chi-Square=7.114, P <0.05). The positive rates of well-differentiation and middle-differentiation, stage I and state II, Tis, T1 and T2, N0 were significant less than non-differentiation and low-differentiation, stage III and state IV, T3 and T4, N1, N2 and N3, respectively. No negative control samples was found to be positive, and no positive control samples was found to be negative. The sensitivity of our test was 10 cells/mL. CONCLUSIONS: The cancer cells dissemination during operation was demonstrated indirectly in our study, the time of pulmonary vein ligation (earlier or later) may affect the quantity of tumor cells released into circulation; The patients with lower differentiation, advanced TNM stage, larger tumor size and metastasis of lymph node have higher rates of metastasis in peripheral, so the detection of CEA mRNA can guide the therapy of NSCLC to a certain extent.