From 1958 through 1992 a total of 3603 patients underwent surgery for esophageal squamous cell carcinoma in our department. Among these patients 3099 resections were performed, for an overall resectability of 86.0%. Of the resections, 2341 (75.5%) were classified as curative and 758 (24.5%) palliative. The overall morbidity and 30-day mortality rates were 23.4% and 3.8%, respectively. For resected cases the mortality was 4.0%. The more than 5-year follow-up rate of patients with resection was 97%. The actual 5-, 10-, and 15-year survival rates were 30.4%, 23.6%, and 17.9%, respectively. Recurrence or metastasis remained the cause of death in 60.9% and 25.5% of patients who lived longer than 5 years and 15 years, respectively, after operation. The TNM staging, lymph node metastasis, extra-esophageal invasion, tumor differentiation, tumor length, and category of operation were major determinants influencing long-term prognosis. The left thoracotomy approach was used exclusively in 2613 cases (84.3% of all resected cases) in which intrathoracic resections and anastomoses were performed. The stomach was used as a substitute for the esophagus in 98.8% of the resected cases compared with 1.2% colon transplants. The former procedure was far safer than the latter. Above-average results presented in this paper support the surgical policy we have pursued thus far: to resect the primary tumor by partial or subtotal esophagectomy and to remove all lymph nodes wherever they were found in all patients with disease earlier than stage III. Early detection and early treatment no doubt are the only ways to materially improve the long-term surgical results.

Abstract. Two events demonstrating periodic narrowband millisecond pulsations of radio emission both in intensity and polarization degree are analyzed. Large time delays between L-and R-polarization components are found. The radio emission is shown to be generated as unpolarized by a plasma mechanism at the second harmonic of the upper-hybrid frequency. Observed oscillations of the radiation polarization degree arise due to group delay between extraordinary and ordinary modes along the line of sight. The theoretically predicted dependence of the group delay on frequency (∼f −3 ) agrees excellently with the observed delay frequency dependence. Physical parameters of the emission source and "delay site" are determined within the proposed model.

Dihydroartemisinin (DHA) has been reported to possess anti-cancer activity against many cancers. However, the pharmacologic effect of DHA on HBV-positive hepatocellular carcinoma (HCC) remains unknown. Thus, the objective of the present study was to determine whether DHA could inhibit the proliferation of HepG2.2.15 cells and uncover the underlying mechanisms involved in the effect of DHA on HepG2.2.15 cells. We found that DHA effectively inhibited HepG2.2.15 HCC cell proliferation both in vivo and in vitro . DHA also reduced the migration and tumorigenicity capacity of HepG2.2.15 cells. Regarding the underlying mechanisms, results showed that DHA induced cellular senescence by up-regulating expression levels of proteins such as p-ATM, p-ATR, γ-H 2 AX, P53, and P21 involved in DNA damage response. DHA also induced autophagy (green LC3 puncta gathered together and LC3II/LC3I ratio increased through AKT-mTOR pathway suppression). Results also revealed that DHA-induced autophagy was not linked to senescence or cell death. TPP1 (telomere shelterin) overexpression could not rescue DHA-induced anticancer activity (cell proliferation). Moreover, DHA down-regulated TPP1 expression. Gene knockdown of TPP1 caused similar phenotypes and mechanisms as DHA induced phenotypes and mechanisms in HepG2.2.15 cells. These results demonstrate that DHA might inhibit HepG2.2.15 cells proliferation through inducing cellular senescence and autophagy.

A dynamic model for the ice-induced vibration (IIV) of structures is developed in

Esophageal squamous cell carcinoma (ESCC) is a malignancy that severely threatens human health and carries a high incidence rate and a low 5-year survival rate. MicroRNAs (miRNAs) are commonly accepted as a key regulatory function in human cancer, but the potential regulatory mechanisms of miRNA-mRNA related to ESCC remain poorly understood. The GSE55857, GSE43732, and GSE6188 miRNA microarray datasets and the gene expression microarray datasets GSE70409, GSE29001, and GSE20347 were downloaded from Gene Expression Omnibus databases. The differentially expressed miRNAs (DEMs) and differentially expressed genes (DEGs) were obtained using GEO2R. Gene ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis for DEGs were performed by Database for Annotation, Visualization and Integrated Discovery (DAVID). A protein–protein interaction (PPI) network and functional modules were established using the STRING database and were visualized by Cytoscape. Kaplan-Meier analysis was constructed based on The Cancer Genome Atlas (TCGA) database. In total, 26 DEMs and 280 DEGs that consisted of 96 upregulated and 184 downregulated genes were screened out. A functional enrichment analysis showed that the DEGs were mainly enriched in the ECM-receptor interaction and cytochrome P450 metabolic pathways. In addition, MMP9, PCNA, TOP2A, MMP1, AURKA, MCM2, IVL, CYP2E1, SPRR3, FOS, FLG, TGM1, and CYP2C9 were considered to be hub genes owing to high degrees in the PPI network. MiR-183-5p was with the highest connectivity target genes in hub genes. FOS was predicted to be a common target gene of the significant DEMs. Hsa-miR-9-3p, hsa-miR-34c-3p and FOS were related to patient prognosis and higher expression of the transcripts were associated with a poor OS in patients with ESCC. Our study revealed the miRNA-mediated hub genes regulatory network as a model for predicting the molecular mechanism of ESCC. This may provide novel insights for unraveling the pathogenesis of ESCC.

Group delay between two magnetoionic modes is discovered and spectrally confirmed ( deltat(g) proportional, variantf(-3)) for the first time for quasiperiodic narrow band millisecond solar radio pulsations. Analysis of cross delays and autodelays proves that both X and O modes originate at the same source, so the radiation is weakly polarized originally. This finding allows one to specify the emission mechanism of the pulsations to be a nonlinear plasma mechanism operating at the second harmonics. Physical parameters of the solar corona are determined by the use of the theory of the nonlinear plasma mechanism; they agree well with independent observations of solar millisecond pulsations.

Background: Dihydroartemisinin (DHA), a derivate of artemisinin, is an effective antimalarial agent. DHA has been shown to exert anticancer activities to numerous cancer cells in the past few years, while the exact molecular mechanisms remain to be elucidated, especially in esophageal cancer. Methods: Crystal violet assay was conducted to determine the cell viability of human esophageal cancer cell line Eca109 treated with DHA. Tumor-bearing nude mice were employed to evaluate the anticancer effect of DHA in vivo. Soft agar and crystal violet assays were used to measure the tumorigenicity of Eca109 cells. Flow cytometry was performed to evaluate ROS or cell cycle distribution. GFP-LC3 plasmids were delivered into Eca109 cells to visualize autophagy induced by DHA under a fluorescence microscope. The mRNA and protein levels of each gene were tested by qRT-PCR and western blot, respectively. Results: Our results proved that DHA significantly reduced the viability of Eca109 cells in a dose-and time-dependent manner. Further investigation showed that DHA evidently induced cell cycle arrest at the G2/M phase in Eca109 cells. Mechanistically, DHA induced intracellular ROS generation and autophagy in Eca109 cells, while blocking ROS by an antioxidant NAC obviously inhibited autophagy. Furthermore, we found that telomere shelterin component TRF2 was down-regulated in Eca109 cells exposed to DHA through autophagy-dependent degradation, which could be rescued after autophagy was blocked by ROS inhibition. Moreover, the DNA damage response (DDR) was induced obviously in DHA treated cells. To further explore whether ROS or autophagy played a vital role in DHA induced cell cycle arrest, the cell cycle distribution of Eca109 cells was evaluated after ROS or autophagy blocking, and the results showed that autophagy, but not ROS, was essential for cell cycle arrest in DHA treated cells. Conclusion: Taken together, DHA showed anticancer effect on esophageal cancer cells through autophagy-dependent cell cycle arrest at the G2/M phase, which unveiled a novel mechanism of DHA as a chemotherapeutic agent, and the degradation of TRF2 followed by DDR might be responsible for this cell phenotype.

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