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Evidence suggests that Tripartite Motif Containing 11 (TRIM11) has pro-tumor activity in human non-small cell lung cancer (NSCLC). However, the roles and underlying mechanisms of TRIM11 in NSCLC have not yet been fully elucidated. In this work, human lung cancer cell lines (A549, H446, and H1975) were transfected with siRNA or lentiviruses to knockdown or overexpress TRIM11 and dual-specificity phosphatase 6 (DUSP6). The cell tumor response was assessed by determining the rate of proliferation, apoptosis, the uptake of 2-[N-(7-nitrobenz-2-oxa-1, 3-diaxol-4-yl) amino]-2-deoxyglucose (2-NBDG), and the secretion of lactic acid (LD). Dominant-negative (dn)-MEK1 was used to block the ERK1/2 pathway. The mechanism was investigated by assessing the protein levels of pyruvate kinase isozymes M2 (PKM2) and DUSP6, as well as the activation of ERK1/2 pathway. Our data confirmed the anti-cancer effect of siTRIM11 in human lung cancer by demonstrating inhibition of cancer cell proliferation, induction of apoptosis, prevention of 2-NBDG uptake, suppression of LD production, and prevention of lung cancer cell (A549) tumorigenicity in nude mice. The underlying mechanism involved the up-regulation of DUSP6 and the inhibition of ERK1/2 activity. Overexpression of TRIM11 induced tumorigenesis of NSCLC in vitro, and the activation of ERK1/2 was significantly reversed by DUSP6 overexpression or additional dn-MEK1 treatment. Interestingly, we confirmed TRIM11 as a deubiquitinase that regulated DUSP6 accumulation, indicating that lung cancer progression is regulated via the DUSP6-ERK1/2 pathway. In conclusion, TRIM11 is an oncogene in NSCLC, likely through the DUSP6-mediated ERK1/2 signaling pathway.

Long non‑coding RNA Fer‑1‑like protein 4 (FER1L4) has been reported to play crucial regulatory roles in tumor progression and apoptosis. However, its clinical significance and biological role in non‑small cell lung cancer (NSCLC) are completely unknown. The purpose of this study was to investigate the expression of lncRNA FER1L4 in plasma and tissues of patients with NSCLC and study the mechanism of proliferation and apoptosis of lung cancer cells. The expression levels of FER1L4 in plasma and tissues of NSCLC patients and cell lines were analyzed via RT‑qPCR. The effects of FER1L4 on cell proliferation, migration and invasion were analyzed by CCK‑8, wound healing and Transwell assays, respectively. The expression levels of related proteins were detected by western blot assay, while cell apoptosis was determined by Hoechst staining and flow cytometry. The results revealed that FER1L4 was significantly downregulated in NSCLC plasma and tissues and lung cancer cell lines compared to corresponding controls. Moreover, a significant decrease of cell proliferation, migration and invasion were observed in FER1L4‑overexpressed cells. FER1L4 could promote phosphatase and tension homolog deleted on chromosome ten (PTEN) and p53 expression, inhibit AKT phosphorylation expression, thus increasing the proportion of apoptotic cells. The present study indicated that FER1L4 may inhibit cell proliferation and promote apoptosis of NSCLC cells via the PTEN/AKT/p53 pathway, which provides a better understanding of the pathogenesis of NSCLC and may provide a novel potential therapeutic target for clinical treatment.

Background: N6-methyladenosine modification has been involved in various biological processes. However, its role in non-small cell lung cancer has not been well studied. Here, we show that IGF2BP3, as an transcription factor, plays a critical oncogenic role in non-small-cell lung cancer carcinogenesis through activating FTO expression and inducing aberrant m6A modification. Methods: To evaluate the role of IGF2BP3 in non-small-cell lung cancer, we performed cell proliferation and cell cycle assays in three lung cancer cell lines. Lung cancer mouse model is used to examine the effects of IGF2BP3/FTO/N-myc on lung proliferation potentials in vivo. We analyzed the correlation between IGF2BP3 and FTO, IGF2BP3 and N-myc protein in colon cancer patients by Pearson correlation. To finally explore the relationship of IGF2BP3/FTO/N-myc, we used western blots, proliferation and cell cycle assays to confirm that IGF2BP3 may regulate lung cancer progression through FTO dependent m6A modification by stabilizing N-myc.Results: We first identified that IGF2BP3 overexpressed in non-small-cell lung cancer tissue and cells. Then, we showed that FTO was the dysregulated factor responsible for the abnormal N6-methyladenosine modification in non-small-cell lung cancer. The loss-of-function assay demonstrated that IGF2BP3 enhances FTO-mediated cell proliferation and promotes cell apoptosis, through regulating expression of target gene N-myc by reducing m6A level in mRNA transcript. Conclusion: Our study demonstrates the functional importance of IGF2BP3 and N6-methyladenosine methylation modification in the tumor progression of non-small-cell lung cancer, and provides profound insights into lung carcinogenesis and drug response.

Background: Genome-wide association studies of lung cancer have shown a common variation at 15q24-25.1 as a determinant of risk, but the role of specific genes has not been proven. This study aims to explore the expression of mutations and the prognostic significance of 15q25 (CHRNA5 and PSMA4) mRNA in lung adenocarcinoma (LAC) based on immunohistochemistry, TCGA and bioinformatics. Methods: The expression of mutations on chromosome 15q25 of 576 primary LAC patients was selected and survival and gene expression data were extracted from TCGA. The relationship between expression of genes on 15q25 and clinical and prognostic Significance of LAC. An experiment with Beas-2b, A549 and H1299 cell lines was performed to further prove the difference in CHRNA5 and PSMA4 expression between lung cancer and normal cells. Immunohistochemistry data of CHRNA5 and PSMA4 were detected in LAC and normal tissues from 122 patients. Finally, Gene enrichment analysis (GSEA) was conducted to predict the regulatory genes of CHRNA5 and PSMA4. Results: CHRNA5 and PSMA4 are frequently mutated in TCGA (CHRNA5, 1.7%; PSMA4, 1.3%). Besides, the expression of CHRNA5 and PSMA4 was obviously higher in A549 and H1299 cells. And the immunohistochemical staining revealed that the levels of CHRNA5 and PSMA4 were considerably higher in the LAC group than in the normal group. Meanwhile, there was a significant association between high CHRNA5 expression and smoking history (P=0.011), smoking history pack year value (P=0.010). Furthermore, there was a significant correlation between CHRNA5 and PSMA4 expression levels and prognosis (P=0.003; P=0.008), and between higher expression and worse prognosis. GSEA results suggested that between samples with high CHRNA5 and PSMA4 expression were respectively enriched to cell cycle, base excision repair, oxidative phosphorylation, protein export, and aminoacyl tRNA biosynthesis, among others. Conclusions: CHRNA5 and PSMA4 mRNA expression has a significant impact on the clinical and survival of LAC, and they may be a potential target for treating patients with lung adenocarcinoma.

At present, in vitro cell experiments have confirmed that RaddeaninA can effectively inhibit the proliferation of some tumor cells, but the effect of RaddeaninA on lung cancer cells has not been observed. Therefore, this study explored its effect on lung cancer cells and its mechanism of action. Human lung cancer cell lines were treated with serum-free medium and varied concentrations of Raddeanin A. Cell proliferation and apoptosis were determined using MTT, and flow cytometric assays, respectively. The intracellular level of ROS was determined using DCFH-DA assay. Protein and mRNA expressions of bax, bcl-2 and cyt c were measured using Western blotting and qRT-PCR. RaddeaninA treatment can promote PC-9 cell apoptosis in a time and dose-dependent manner (p

Transforming growth factor-β1 (TGF-β1) is a potent stimulator of the epithelial-to-mesenchymal transition (EMT), which is a key event in the initiation of tumor cell metastasis. Aspirin-triggered resolvin D1 (AT-RvD1) is known to be involved in the resolution of inflammation; however, whether AT-RvD1 exerts effects on TGF-β1-induced EMT remains unclear. Thus, we first explored the effects of AT-RvD1 on the EMT of lung cancer cells. Treatment with TGF-β1 increased the level of reactive oxygen species (ROS) and reduced the expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2). The expression of E-cadherin in A549 lung cancer cells was reduced, and the expression of vimentin was enhanced. AT-RvD1 enhanced the expression of E-cadherin in a concentration‑dependent manner and suppressed the expression of Nrf2 and vimentin. AT-RvD1 did not affect the proliferation of A549 lung cancer cells whereas it suppressed the TGF-β1‑induced migration and invasion of A549 cells. The expression of pyruvate kinase M2 (Pkm2), which is associated with TGF-β-induced factor homeobox 2 (TGIF2), was significantly increased during the TGF-β1-induced EMT of A549 lung cancer cells. The mTOR pathway is known to regulate the expression of various glycolytic enzymes including Pkm2. We examined the involvement of the mTOR pathway in the suppressive effects of AT-RvD1 on Pkm2 expression in A549 cells. The mTOR activator restored the expression of Pkm2 and partially downregulated the expression of E-cadherin. However, the mTOR activator had no clear effect on the TGF-β1-induced EMT. These results suggest that AT-RvD1 is closely linked to oxidative stress and partially inhibits TGF-β1-induced EMT through the inhibition of the mTOR pathway by reducing the expression of Pkm2.

In this study, antioxidant and antibacterial packaging were developed by individually incorporating 1 wt% of flavones (chrysin, apigenin and luteolin) into chitosan (CS) and D-α-tocopheryl polyethylene glycol 1000 succinate (TPGS) composite films. The microstructures, physical properties, antioxidant and antibacterial activities of CS-TPGS films containing different flavones were compared. Microstructure observation showed that incorporation of flavones somewhat reduced the homogeneity of the films. Flavones formed hydrogen bonds with other film components and changed the crystallinity of the films. As compared with CS-TPGS film, the films containing different flavones exhibited reduced tensile strength but enhanced UV–vis light barrier property and antibacterial activity. Among the films containing different flavones, the film containing luteolin showed the highest water vapor, oxygen and UV light barrier properties, tensile strength and antioxidant activity. However, the film containing chrysin exhibited the lowest water vapor, oxygen and UV light barrier properties and tensile strength but the highest antibacterial activity against Escherichia coli, Salmonella typhimurium, Staphylococcus aureus and Listeria monocytogenes. Our results suggested CS-TPGS film containing luteolin could be used as antioxidant and antibacterial packaging in food industry.

Changjiang Sun,1 Xizhi Zhang,1 Yong Chen,1 Qingqing Jia,1 Jianqi Yang,1 Yusheng Shu2 1Department of Oncology, Subei People’s Hospital of Jiangsu Province, Yangzhou, Jiangsu, China; 2Department of Thoracic and Cardiovascular Surgery, Subei People’s Hospital of Jiangsu Province, Yangzhou, Jiangsu, China Background: A number of studies have indicated that expression of miRNA-365 (miR-365) is suppressed in various cancers, suggesting its cancer-suppressive role. In the present investigation, we evaluated the regulation and character of miR-365 in human esophageal squamous cell carcinoma (ESCC). Patients and methods: The tumor tissues and adjacent nontumor tissue samples were collected from 30 patients having ESCC, and the expression levels of miR-365 were studied by quantitative real-time polymerase chain reaction (PCR). MTT and cell invasion by Matrigel assay were done to study the effect of miR-365 on proliferation and metastasis of ESCC cells. An in vivo tumor model was generated by inoculating ESCC cells subcutaneously into BALB nude mice. A study of various biomarkers such as quantitative polymerase chain reaction (qPCR), luciferase activity assay, and Western blot was done to confirm the targets of miR-365. Results: In tumor tissues, a significant downregulation of miR-365 was observed versus the nontumor adjacent tissues and ESCC cells versus the selected esophageal endothelial cells. It was observed that higher expression levels of miR-365 inhibited the cell invasion, colony formation, growth in esophageal cancer cell lines in vitro, and tumor development in vivo. The study of biomarkers suggests involvement of phosphoserine aminotransferase 1 (PSAT1) as a favorable target for miR-365, and its abnormal expression inverted the miR-365-arbitrated suppression of invasion, viability, and epithelial–mesenchymal transition in esophageal cancer cells. A negative correlation existed with expression of miR-365 and PSAT1 in human esophageal cancer tissue samples. Conclusion: The study established that miR-365 exhibits tumor-suppressive action via regulating the levels of PSAT1 and leads to invasion and progressiveness of esophageal cancer. Keywords: esophageal cancer, miR-365, PSAT1, tumor

Tissue calcification is a major cause of failure of bioprosthetic heart valves. Aim of this study was to examine whether surface heparin treatment of the decellularized porcine heart valve reduces tissue calcification. Fresh porcine aortic heart valves were dissected as tissue discs and divided into four groups. Group A: controls without treatment, Group B: decellularization only, Group C: decellularization and glutaraldehyde cross-linking, Group D: decellularization and glutaraldehyde cross-linking followed by surface heparin treatment. After implantation in New Zealand White rabbits for 60 days, the explanted heart valve discs from the different study groups underwent a series of histological examinations as well as determination of calcium content by the methyl thyme phenol blue colorimetric method. Results of the explanted heart valve discs for the Von Kossa staining demonstrated that in Group A the heart valve tissue was the most severely stained with black color, whereas in Group D there was hardly any area that was stained black after implantation indicating the least tissue calcification. Furthermore, the inflammatory cells identified by the Hematoxylin-eosin staining appeared to be the least in Group D. The average tissue calcium content was highest in Group A (0.197 ± 0.115 μmol mg-1 ), modest in Group B (0.113 ± 0.041 μmol mg-1 ), and Group C (0.089 ± 0.049 μmol mg-1 ), and the lowest in Group D (0.019 ± 0.019 μmol mg-1 , p

Esophagectomy through cervico-thoraco-abdominal approach is a useful surgical technique in treating patients with esophageal cancer. However, the cervical reconstruction is also known to have a high rate of anastomotic leakage, as well as anastomotic stricture, intrathoracic stomach syndrome, reflux esophagitis and other complications, thereby influencing postoperative recovery and quality of life.The objective of this study was to investigate whether tubular stomach is superior to whole stomach in reducing anastomotic leakage for esophageal reconstruction through the cervico-thoraco-abdominal (3-field) approach.A total of 850 patients undergoing the 3-field esophagectomy were retrospectively included in this study and divided into a tubular stomach reconstruction group (Group A, n=453) and a whole stomach reconstruction group (Group B, n=397). All patients underwent esophagectomy through right thorax, left cervical part, abdominal triple incisions and done in esophageal reconstruction by hand-sewn two-layer anastomosis.Results revealed that in comparison with whole stomach, esophageal reconstruction with tubular stomach had a lower incidence of anastomotic leakage (5.5 vs. 9.3%, P0.05), less manifestation of intrathoracic syndrome (3.3 vs. 9.8%, P0.001) and less occurence of reflux esophagitis (5.1 vs. 11.1%, P0.01). However, for the incidence of anastomotic stricture, there was no significant difference between the two groups (9.3 vs. 9.8%).This observation study suggests that for esophageal cancer patients undergoing the 3-field esophagectomy tubular stomach is better than whole stomach for esophageal reconstruction as reflected by a reduced postoperative anastomotic leakage, intrathoracic syndrome and reflux esophagitis.

Lung cancer is the most commonly diagnosed type of cancer worldwide. Although TRIM65 is an important protein involved in white matter lesion, the role of TRIM65 in human cancer remains less understood. Here, we reported that TRIM65 was significantly overexpressed in lung cancer tissues compared with adjacent normal lung tissues. Furthermore, TRIM65 expression was closely related to overall survival of patients with lung cancer. Knock down of TRIM65 in two lung cancer cell lines, SPC-A-1 and NCI-H358, resulted in a significant reduction in cell proliferation, migration, invasion and adhesion and a dramatic increase in G0-G1 phase arrest and apoptosis. In vivo tumorigenesis experiment also revealed that depletion of TRIM65 expression inhibited NCI-H358 cell growth. Moreover, based on gene set enrichment analysis (GSEA) with The Cancer Genome Atlas (TCGA) dataset, we found that TRIM65 was positive related to cell cycle, metastasis up and RHOA-REG pathways, which was further validated by RT-PCR and Western blot in TRIM65 knockdown lung cancer cells and indicated a possible mechanism underlying its effects on lung cancer. In summary, our study suggests that TRIM65 may work as an oncogene and a new effective therapeutic target for lung cancer treatment.

Background Tripartite Motif Containing 11 (TRIM11), a member of TRIM proteins, is overexpressed in high-grade gliomas and plays an oncogenic function in glioma biology. However, little is known about the role of TRIM11 in lung cancer. Methods We analyzed TRIM11 mRNA expression in lung cancer tissues and adjacent non-neoplastic tissues by real-time PCR. We then explored the function of TRIM11 in lung cancer cells by small interfering RNA-mediated downregulation of this protein followed by analyses of cell proliferation, migration and invasion. Results TRIM11 was highly expressed in lung cancer tissues and lung cancer cell lines. The higher expression of TRIM11 was correlated with the poorer prognosis of patients. Suppressing of TRIM11 expression in lung cancer cells with higher expression of TRIM11 (A549 and NCI-H446 cells) significantly reduced cell growth, motility and invasiveness. We further demonstrated that knockdown of TRIM11 affected the expression of cell proliferation-related proteins (Cyclin D1 and PCNA), and epithelial-mesenchymal transformation-related proteins (VEGF, MMP-2, MMP-9, Twist1, Snail and E-cadherin). The activity of ERK and PI3K/AKT was also suppressed in TRIM11 knocked down cells. Further experiments in lung cells with lower expression of TRIM11 (NCI-H460 and NCI-H1975 cells) with AKT inhibitor suggested that TRIM11 may promote cell motility and invasiveness through AKT pathway. Conclusions Our results indicate that TRIM11 acts as an oncogene in lung cancer through promoting cell growth, migration and invasion. Our findings may have important implication for the detection and treatment of lung cancer.

Human vascular cells from saphenous veins have been used for cell seeding on the synthetic scaffolds for constructing tissue-engineered heart valve (TEHV). However, little is known about the seeding of human vascular cells on bovine pericardium, a potential natural scaffold for TEHV. This study was aimed to assess the basic in vitro and in vivo characteristics of the human vascular cells seeded on decellularized bovine pericardium. In vitro, bovine pericardium samples with cell seeding were inspected on day 7, 14, and 21 by histology, scanning electron microscopy, and immunohistochemistry. In vivo, experiments were performed in nude mice by bilateral dorsal incision for the implantation of decellularized bovine pericardium with and without cell seeding. Results demonstrated that a total of 810 x 10(6) cells were obtained within 45 wk by the primary co-culture, which were detected positive for von Willebrand factor, a-smooth muscle actin antibodies, and fibronectin, indicating the presence of endothelial cells, smooth muscle cells, and fibroblasts, respectively. In vitro, the seeded cells showed a steady increase of endothelial activity from day 1 to day 7 and remained stable until day 21. After 30 days of implantation in vivo, the cells on the decellularized bovine pericardium could differentiate directionally and show all the identities of human endothelial cells, smooth muscle cells, and fibroblasts. These results indicate that the human vascular cells from the saphenous vein are an optional cell source for seeding on decellularized bovine pericardium scaffold for constructing TEHV. (c) 2012 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 100B: 16541661, 2012.

Primary choriocarcinoma of the posterior mediastinum is considered to be extremely rare, and the majority of these tumors occur in the gonads and uterus. The current study presents the case of a 40-year-old male who presented to the Department of Thoracic Surgery (Medical College of Yangzhou University, Yangzhou, China) with left chest pain for two months. Computed tomography of the chest showed a 4.9×5.2-cm mass in the posterior mediastinum and enlargement of the mediastinal lymph nodes. Resection of the tumor and upper lobe of the left lung was performed and the patient received combination chemotherapy with six courses of etoposide plus cisplatin. The patient recovered and was discharged. One year post surgery and chemotherapy, the patient was followed up and evidence of a recurrent tumor in the cerebrum was observed.

Objective The aim of our study was to evaluate the clinical effect and the prospect of the three-incision (right thoracotomy, midline laparotomy and left cervical incisions) esophagectomy for the treatment of esophageal carcinoma.

Objectives: Tetralogy of Fallot (TOF) with major aortopulmonary collaterals (MAPCA) is a well-known but always severe congenital heart disease. This study was designed to explore proper management after radical correction of TOF with MAPCA based on a hierarchical approach. Methods: The following data were collected from 39 patients planned to undergo radical correction of TOF: age, weight, number of aortopulmonary collaterals, total lumen diameter and collateral diameter-to-body weight ratio, transcatheter occlusion and cardiac catheterization findings, mechanical ventilation time, and ICU monitoring time. The patients were divided into 4 groups by collateral diameter-to-body weight ratio as follows: 0.500 mm/kg (group 3), and no MAPCA (group 4). Data analysis was performed using IBM SPSS Statistics software for Mac version 22.0 (SPSS Inc., Chicago, Ill., USA) with logistic regression and Fisher's exact test. Results: Most of the patients recovered well after radical correction; postoperative complications occurred in 12 patients and included bloody sputum, low cardiac output syndrome, and severe pulmonary infection that led to tracheotomy. By prolonging the mechanical ventilation time of the patients with postoperative complications, the conditions in 3 patients were improved. However, in the remaining patients, the condition worsened until transcatheter occlusions were performed. Transcatheter occlusion was performed in all 7 patients in group 3 (100%). Only 2 of the 8 patients in group 2 required transcatheter occlusion (25%), and none of the 9 patients in group 1 required transcatheter occlusion (0%). Only 1 patient (group 3) died after radical correction. The transcatheter occlusion results showed a strong association with the total lumen diameter and the collateral diameter-to-body weight ratio (p < 0.05) but no obvious association with age, weight, or the number of aortopulmonary collaterals (p > 0.05). Conclusions: Postoperative management of patients with TOF and MAPCA has great significance. To reduce the morbidity and mortality, transcatheter coil embolization or surgical ligation should be performed in patients with a collateral diameter-to-body weight ratio of at least 0.500 mm/kg. In patients with values between approximately 0.200 and 0.500 mm/kg, prolongation of mechanical ventilation should have priority over transcatheter occlusion, and for patients with values below 0.200 mm/kg no additional treatment is needed.

The endothelial-mesenchymal transition (EndMT) is known to be involved in the transformation of vascular endothelial cells to mesenchymal cells. EndMT has been confirmed that occur in various pathologic conditions. Transforming growth factor β1 (TGF-β1) is a potent stimulator of the vascular endothelial to mesenchymal transition (EMT). Aspirin-triggered resolvin D1 (ATRvD1) has been known to be involved in the resolution of inflammation, but whether it has effects on TGF-β1-induced EndMT is not yet clear. Therefore, we investigated the effects of AT-RvD1 on the EndMT of human umbilical vein vascular endothelial cells line (HUVECs). Treatment with TGF-β1 reduced the expression of Nrf2 and enhanced the level of F-actin, which is associated with paracellular permeability. The expression of endothelial marker VE-cadherin in HUVEC cells was reduced, and the expression of mesenchymal marker vimentin was enhanced. AT-RvD1 restored the expression of Nrf2 and vimentin and enhanced the expression of VE-cadherin. AT-RvD1 did also affect the migration of HUVEC cells. Inhibitory κB kinase 16 (IKK 16), which is known to inhibit the NF-κB pathway, had an ability to increase the expression of Nrf2 and was associated with the inhibition effect of AT-RvD1 on TGF-β1-induced EndMT, but it had no effect on TGF-β1-induced EndMT alone. Smad7, which is a key regulator of TGF-β/Smads signaling by negative feedback loops, was significantly increased with the treatment of AT-RvD1. These results suggest the possibility that AT-RvD1 suppresses the TGF-β1-induced EndMT through increasing the expression of Smad7 and is closely related to oxidative stress.

The objective of this study is to investigate the feasibility and safety of single-port microthoracoscopic thoracic sympathicotomy for the treatment of palmar hyperhidrosis. Between January 2008 and March 2013, 56 patients (36 male, 20 female; mean age 25.6 years, age range 16–39 years) underwent single-port microthoracoscopic thoracic sympathicotomy for palmar hyperhidrosis. Nineteen patients (33.9 %) had moderate palmar hyperhidrosis that could thoroughly wet a handkerchief, and 37 (66.1 %) had severe palmar hyperhidrosis with sweat dripping from the palm. Eight patients (14.3 %) had a positive family history, 34 (60.7 %) had plantar hyperhidrosis, 22 (39.3 %) had axillary hyperhidrosis, and 20 (35.7 %) had both plantar and axillary hyperhidrosis. In addition, 21 patients (37.5 %) had palmar pompholyx, five (8.9 %) had keratolysis exfoliativa, 10 (17.9 %) had chilblains, and nine (16.1 %) had palmar rhagades. A single 10-mm skin incision was made in the third intercostal space at the anterior axillary line, posterior to the pectoralis muscle. A 5-mm microthoracoscope and a 3-mm microelectrocautery hook were inserted through a single port into the thoracic cavity. The third and fourth ribs were identified, and the sympathetic chain was cut using the microelectrocautery hook. The bypassing nerve fibers, such as the Kuntz nerve fiber bundle, were ablated for 2–3 cm along the surface of the rib. The palmar temperature was recorded before and after sympathicotomy. All 56 procedures were completed using single-port microthoracoscopy. No postoperative complications such as hemorrhage, wound infection, hemopneumothorax, bradycardia, or Horner’s syndrome were observed. Bilateral procedures were completed in 20–56 min (mean 30 min). The palmar temperature increased by 2.2 ± 0.3 °C after surgery. The postoperative hospital stay was 1–4 days (mean 2.5 days). Mild compensatory sweating of the back and thigh occurred in five patients (8.9 %) at 2–3 days after surgery and disappeared at 7–15 days. The patients were followed up for 28.5 months (range 1–62 months). Hyperhidrosis resolved in both hands after surgery, and the previously wet, cold hands became dry and warm. The efficacy rate was 100 %. Plantar hyperhidrosis was also significantly reduced in 33 of the 34 patients with this condition (remission rate 97.1 %), and axillary hyperhidrosis was significantly reduced in 19 of 22 patients (remission rate 86.4 %). Eighteen of the 20 patients (90.0 %) with both plantar and axillary hyperhidrosis experienced significant alleviation of their symptoms. Single-port microthoracoscopic thoracic sympathicotomy is a safe, convenient, and effective method of treating palmar hyperhidrosis. This procedure can accurately locate the sympathetic chain with a small incision, minimal invasiveness, and good cosmetic results. The procedure is suitable for extensive clinical use.

Multidrug resistance (MDR) is closely correlated to an unfavorable prognosis in various human cancers. However, the clinical significance of the expression of MDR-related proteins p-glycoprotein (PGP), glutathione-s-transferases (GST-pi), topoisomerase-II (Topo-II) and lung resistance protein (LRP) in primary gastric cardiac adenocarcinoma (PGCA) remains unclear. In this present study, the total of the four kinds of MDR-related proteins mentioned above were detected by using immunohistochemistry, and their clinical significance in chemoresistance were also investigated.This retrospective study included 69 resected specimens from patients with PGCA. The expression of PGP, GST-pi, Topo-II and LRP in formalin-fixed paraffin-embedded tissue sections was determined by a labelled streptavidin-biotin immunohistochemical technique, and the results were analyzed in correlation with clinicopathological data. None of these patients received chemotherapy prior to surgery.The positive rates of expression of PGP, GST-pi, Topo-II and LRP in malignant tissues (49.2%, 75.4%, 68.1% and 58%, respectively) were all higher than that of the normal tissues(0, 30%, 20% and 0, respectively, P0.01). PGP expression in tumors that had metastasized was significantly more frequent than in tumors that had not metastasized (67.5% vs 24.1%, P0.01). The expression of PGP was closely related with clinicopathologic staging (staging 1/2 vs 3/4, 28.6% vs 58.3%, P0.05). No significant correlation was shown between PGP and increasing differentiated degree (40%, 42.4% and 61.5%, P0.05). GST-pi expression status progressively increased with increasing differentiated degree (40%, 75.8% and 88.5%, P0.05) and clinicopathologic stage (staging 1/2 vs 3/4, 57.1% vs 83.3%, P0.05). In addition, a significant positive correlation was also observed between GST-pi and lymphatic metastasis (with vs. without metastasis, 87.5% vs 58.6%, P0.05). The expression of Topo-II was associated with increasing differentiated degree (33.3%, 69.7 and 80.7%, P0.01). No significant differences with Topo-II expression were found in relation to the clinicopathologic stage (staging 1/2 vs 3/4, 57.1% vs 72.9%, P0.05) and lymphatic metastasis (with vs. without metastasis, 65.0% vs 72.4%, P0.05). Moreover, a significant difference with the expression of LRP was found in relation to the clinicopathologic stage (staging 1/2 vs 3/4, 38% vs 66.6%, P0.05), and lymphatic metastasis (with vs without metastasis, 70.0% vs 41.4%, P0.05). Comparing the well, moderately and poorly differentiated cohort, a non-statistical increasing trend towards LRP expression status was noted (50.0%, 54.5% and 65.3%, respectively, P0.05). Besides, the co-expression of all four tested MDR-related proteins also existed. The positive rates of co-expression of PGP and GST-pi, PGP and Topo-II, PGP and LRP, GST-pi and Topo-II, LRP and GST-pi, LRP and Topo-II, PGP, GST-pi, Topo-II and LRP in malignant cells were 23.2%, 15.9%, 11.6%, 13.0, 26.1, 7.24, 5.8, respectively.MDR-related proteins PGP, GST-pi, Topo-II alpha and LRP are involved in multiple mechanisms of drug resistance in PGCA. Combined determination of PGP, GST-pi, Topo-II and LRP may be prospectively valuable for optimizing the chemotherapy regimes, developing high quality anti-cancer drugs, and further predicting the outcomes of those patients with PGCA.

The present study describes the case of an asymptomatic 65‑year‑old male who presented with a Solitary Fibrous Tumor (SFT) in the lung during a physical examination. Enhanced computed tomography revealed a 1.5x1.5-cm mass in the lung; however, further physical examinations were normal. The patient underwent surgery due to the uncertain diagnosis and the possibility that the mass was malignant. Histopathological analyses of the tumor demonstrated the typical histological characteristics of an SFT. Immunohistochemical staining for B-cell lymphoma-2 and cluster of differentiation 34 were positive. The patient recovered and was discharged successfully. At the six-month post-surgery follow-up, no recurrence or metastasis were observed.

AIM: To retrospectively evaluate our experience with the diagnosis and surgical resection of esophageal gastrointestinal stromal tumors (GISTs). METHODS: Between January 2003 and August 2014, five esophageal GIST cases were admitted to our hospital. In this study, the hospital records, surgery outcomes, tumor recurrence and survival of these patients were retrospectively reviewed. RESULTS: The median age of the patients was 45.6 years (range: 12-62 years). Three patients presented with dysphagia, and one patient presented with chest discomfort. The remaining patient was asymptomatic. Four patients were diagnosed with esophageal GISTs by a preoperative endoscopic biopsy. Three patients underwent esophagectomy, and two patients underwent video-assisted thoracoscopic surgery. The mean operating time was 116 min (range: 95-148 min), and the mean blood loss was 176 mL (range: 30-300 mL). All tumors were completely resected. The mean length of postoperative hospital stay was 8.4 d (range: 6-12 d). All patients recovered and were discharged successfully. The median postoperative follow-up duration was 48 mo (range: 29-72 mo). One patient was diagnosed with recurrence, one patient was lost to follow-up, and three patients were asymptomatic and are currently being managed with close radiologic and clinical follow-up. CONCLUSION: Surgery is the standard, effective and successful treatment for esophageal GISTs. Long-term follow-up is required to monitor recurrence and metastasis.