Preparation, Deformation Behavior and Irradiation Damage of Refractory Metal Single Crystals for Nuclear Applications: A Review.

Refractory metal single crystals have been applied in key high-temperature structural components of advanced nuclear reactor power systems, due to their excellent high-temperature properties and outstanding compatibility with nuclear fuels. Although electron beam floating zone melting and plasma arc melting techniques can prepare large-size oriented refractory metals and their alloy single crystals, both have difficulty producing perfect defect-free single crystals because of the high-temperature gradient. The mechanical properties of refractory metal single crystals under different loads all exhibit strong temperature and crystal orientation dependence. Slip and twinning are the two basic deformation mechanisms of refractory metal single crystals, in which low temperatures or high strain rates are more likely to induce twinning. Recrystallization is always induced by the combined action of deformation and annealing, exhibiting a strong crystal orientation dependence. The irradiation hardening and neutron embrittlement appear after exposure to irradiation damage and degrade the material properties, attributed to vacancies, dislocation loops, precipitates, and other irradiation defects, hindering dislocation motion. This paper reviews the research progress of refractory metal single crystals from three aspects, preparation technology, deformation behavior, and irradiation damage, and highlights key directions for future research. Finally, future research directions are prospected to provide a reference for the design and development of refractory metal single crystals for nuclear applications.

ZNF418 overexpression protects against gastric carcinoma and prompts a good prognosis.

BACKGROUND: This study aimed to investigate the prognostic power of zinc-finger protein 418 (ZNF418) in gastric cancer (GC) and its potential role in GC development and progression. PATIENTS AND METHODS: A total of 10 GC patients' individual plasmas were collected and screened for dysregulated mRNA using human microarray. Among these dysregulated mRNAs, ZNF418 was found to be significantly downregulated in IIIA-IV stage GC patients compared to IA-IIA stage GC patients. Subsequently, the ZNF418 levels were detected by quantitative reverse transcription-polymerase chain reaction in both GC plasmas and tissues in a larger sample, and the association between ZNF418 expression level and clinicopathological features as well as overall survival (OS) of GC patients was further analyzed. Finally, a network of ZNF418 interactions with other molecules was predicated in STRING and GEPIA databases. RESULTS: Human mRNA microarray was performed to screen for abnormally expressed mRNAs between five IIIA-IV stage GC patients' plasma and five IA-IIA stage GC patients' plasma. A total of 662 mRNAs were differentially expressed in the IIIA-IV stage GC plasma vs IA-IIA stage GC plasma among all the candidate mRNAs according to the Student's t-test. Results showed that a decrease in the ZNF418 expression level was associated with the presence of GC and also with higher tumor-node-metastasis stage and lower OS rates compared with that in adjacent noncancerous tissues. Cox regression analysis results demonstrated that the OS was independently correlated with ZNF418 expression. Finally, the prediction results showed that a total of eight mRNAs might have an interaction with ZNF418 in both STRING and GEPIA databases. CONCLUSION: ZNF418 was first identified to be significantly downregulated in GC. Our study indicated that ZNF418 might serve as a novel biomarker for GC and was involved in GC development.

TSPAN12 is overexpressed in NSCLC via p53 inhibition and promotes NSCLC cell growth in vitro and in vivo.

BACKGROUND: Tetraspanin 12 (TSPAN12), a member of the phylogenetically ancient tetraspanin family, is linked to impaired vascularization of the eye called familial exudative vitreoretinopathy, while the functional role of TSPAN12 in lung cancer has not been well characterized. RESULTS: In our study, TSPAN12 is able to regulate the growth of non-small-cell lung carcinoma (NSCLC) cells both in vitro and in vivo. TSPAN12 mRNA level was significantly increased in human NSCLC samples compared with their corresponding paracancerous histologic normal tissues. In addition, TSPAN12 expression, which is frequently upregulated in NSCLC, is inversely correlated with p53 expression. Furthermore, the expression levels of TSPAN12 were also increased in three human NSCLC cell lines compared to human bronchial epithelial (16HBE) cells. Then, we studied the effects of TSPAN12 silencing by short hairpin ribonucleic acid on NSCLC cell growth in vitro and tumorigenesis in vivo, along with the effect on the p53 pathway. Knockdown of TSPAN12 in NSCLC cells inhibited cell proliferation and colony formation. In addition, knockdown of TSPAN12 increased apoptosis in NSCLC cells. Mechanistically, TSPAN12 could modulate the expression of p53, p21, and p27 in NSCLC cells. In a tumor xenograft model, TSPAN12 silencing inhibits the tumor growth of H1299 cells. CONCLUSION: Taken together, our results reveal that TSPAN12 plays an important role in NSCLC and is a potential biomarker and a promising target in the treatment of NSCLC.

The Diagnostic Value of Routine Contrast Esophagram in Anastomotic Leaks After Esophagectomy.

BACKGROUND: Routine contrast esophagram has been shown to be increasingly limited in diagnosing anastomotic leaks after esophagectomy. METHODS: Patients undergoing esophagectomy from 2013 to 2014 at Huai'an First Peoples' Hospital were identified. We retrospectively analyzed patients who underwent routine contrast esophagram on postoperative day 7 (range 6-10) to preclude anastomotic leaks after esophagectomy. RESULTS: In 846 patients who underwent esophagectomy, a cervical anastomosis was performed in 286 patients and an intrathoracic anastomosis in 560 patients. There were 57 (6.73%) cases with anastomotic leaks, including cervical leaks in 36 and intrathoracic leaks in 21 patients. In the cervical anastomotic leak patients, 13 were diagnosed by early local clinical symptoms and 23 underwent routine contrast esophagram. There were 7 (30.4%) true-positive, 11 (47.8%) false-negative, and five (21.8%) equivocal cases. In the intrathoracic anastomotic leak patients, four (19%) were diagnosed by clinical symptoms, 16 (76.2%) were true positives, and one (4.8%) was a false negative. Aspiration occurred in five patients with cervical anastomoses and in eight patients with intrathoracic anastomoses; aspiration pneumonitis did not occur in these cases. CONCLUSIONS: Gastrografin and barium are safe contrast agents to use in post-esophagectomy contrast esophagram. Because of the low sensitivity in detecting cervical anastomotic leaks, routine contrast esophagram is not advised. For patients with intrathoracic anastomoses, it is still an effective method for detecting anastomotic leaks.

Epigenetic activation of SIN1 promotes NSCLC cell proliferation and metastasis by affecting the epithelial-mesenchymal transition.

Stress-activated protein kinase (SAPK) interacting protein 1 (SIN1) is an essential component of mTORC2. Previous studies have shown that SIN1 is a key regulator of Akt pathway which plays an important role in various pathological conditions including cancer. While its effects and mechanisms on the progression of NSCLC remain unknown. In this study, we report that SIN1 is able to promote the growth and migration of NSCLC cells both in vitro and in vivo. Overexpression of SIN1 promoted A549 and H1299 cells proliferation by both MTT and colony formation assays. Consistently, knockdown of SIN1 inhibited the proliferation of these cells. In transwell assay, overexpression of SIN1 increased the migration of A549 and H1299 cells, while SIN1 knockdown reduced their migration. In a tumor xenograft model, overexpression of SIN1 promoted tumor growth of A549 cells in vivo, while SIN1 knockdown suppresses the tumor growth. We also found a mechanistic link between SIN1 and H3K4me3, H3K4me3 is involved in SIN1 upregulation. Moreover, SIN1 can significantly promote the in vitro migration and invasion of NSCLC cells via induction epithelial mesenchymal transition (EMT) process, which subsequently leads to transcriptional downregulation of epithelial marker E-cadherin and upregulation of mesenchymal markers N-cadherin and Vimentin expression. Together, our results reveal that SIN1 plays an important role in NSCLC and SIN1 is a potential biomarker and a promising target in the treatment of NSCLC.

[Application of bundles of intervention in the treatment of esophageal carcinoma anastomotic leak].

OBJECTIVE: To investigate the application of bundles of intervention in the treatment of esophageal carcinoma anastomotic leak. METHODS: From January 2014 to May 2015, 44 cases of esophageal carcinoma anastomotic fistula were treated by bundles of intervention (through the collection of a series of evidence-based treatment and care measures for the treatment of diseases) in Department of Thoracic Surgery, Huai'an First Hospital, Nanjing Medical University (bundles of intervention group), and 68 patients with esophageal carcinoma postoperative anastomotic leak from December 2013 to January 2012 receiving traditional therapy were selected as the control group. The clinical and nutritional indexes of both groups were compared. RESULTS: There were no significant differences in general data and proportion of anastomotic leak between the two groups. Eleven patients died during hospital stay, including 3 cases in bundles of intervention group(6.8%) and 8 cases in control group (11.8%) without significant difference(P = 0.390). In bundles of intervention group, 1 case died of type III( intrathoracic anastomotic leak, 2 died of type IIII( intrathoracic anastomotic leak. In control group, 2 cases died of type III( cervical anastomotic leak, 2 died of type III( intrathoracic anastomotic leak and 4 of type IIII( intrathoracic anastomotic leak. The mortality of bundles of intervention group was lower than that of control group. The duration of moderate fever [(4.1±2.4) days vs. (8.3±4.4) days, t=6.171, P=0.001], the time of antibiotic use [(8.2±3.8) days vs.(12.8±5.2) days, t=5.134, P = 0.001], the healing time [(21.5±12.7) days vs.(32.2±15.8) days, t=3.610, P=0.001] were shorter, and the average hospitalization expenses[(63±12) thousand yuan vs. (74±19) thansand yuan, t=3.564, P=0.001] was lower in bundles of intervention group than those in control group. Forty-eight hours after occurrence of anastomotic leak, the levels of hemoglobin, albumin and prealbumin were similar in both groups. However, at the time of fistula healing, the levels of hemoglobin [(110.6±10.5) g/L vs.(103.8±11.1) g/L, t=3.090, P=0.002], albumin [(39.2±5.2) g/L vs.(36.3±5.9) g/L, t=2.543, P=0.013] and prealbumin [(129.3±61.9) g/L vs.(94.1±66.4) g/L, t=2.688, P=0.008] were significantly higher in bundles of intervention group. CONCLUSION: In the treatment of postoperative esophageal carcinoma anastomotic leak, application of bundles of intervention concept can significantly improve the nutritional status and improve the clinical outcomes.

[Prognostic value of lymphangiogenesis and lymphatic vessel invasion in non-small cell lung cancer].

BACKGROUND AND OBJECTIVE: Studies have shown that tumor metastasis in a variety of tumors is associated with lymphangiogenesis and lymphatic vessel invasion (LVI). Tumor metastasis is an important factor that affects the prognosis of patients. The aim of this study is to determine the prognostic value of lymphangiogenesis and LVI in non-small cell lung cancer (NSCLC). METHODS: We marked the endothelial cells of lymph vessels in lymphangiogenesis with specific monoclonal antibody D2-40. Immunohistochemistry was used to detect the expression of lymphangiogenesis and LVI in 79 cases of stage I-III NSCLC. RESULTS: The intratumoral lymphatic vessel density (ITLVD) was significantly higher in patients with N2 disease than those with N0 disease (P=0.015). The ITLVD was significantly higher in patients with LVI+ than that in those with LVI- (P = 0.009). The ITLVD was also remarkably higher in poorly differentiated tumors than that in highly differentiated ones (P = 0.007). The ITLVD was remarkably higher in adenocarcinoma than that in squamous cell carcinomas (P = 0.025). Kaplan-Meier revealed that the survival rates of patients with higher ITLVD were remarkably poorer than those with lower ITLVD (P = 0.007). Thus, the ITLVD is an important prognostic factor of NSCLC. The peritumoral lymphatic vessel density is not correlated with the prognosis. CONCLUSIONS: The ITLVD level is an important prognostic factor of NSCLC.

[Study on the prognosis of the T1a non-small cell lung cancer].

BACKGROUND AND OBJECTIVE: The new edition of the TNM staging for lung and pleural tumours has been finished, which put weight on the extent of primary tumor as one of the important prognosises. But little study has performed on the primary tumor extent < or = 2 cm. The aim of this study is to explore the prognosis of patients with tumor extent < or = 2 cm in stage I of non-small cell lung cancer, which helps us to choose the best treatment for these patients. METHODS: Retrospective study on the clinical response and survival time of whom underwent complete surgical resection and diagnosed as T1a of stage I NSCLC from 1998 to 2004 was analyzed. Data was analyzed by SPSS 17.0 software. RESULTS: Overall survival rate was 80.8%. By the study, age (P = 0.241), gender (P = 0.175), history of smoking (P = 0.845), pathologic type ( P =0.265), and systematic mediastinal lymphadenectomy (SML )(P = 0.918) or not, postoperative adjuvant chemotherapy or not ( P = 0.616) and visceral pleural invasion (P = 0.827) were not the prognosises of these patients. Only the tumor differentiation such as poorly differentiated was the important prognosis ( P = 0.01). CONCLUSION: In the tumor extent < or = 2 cm of stage I non-small cell lung cancer, the visceral pleural invasion maybe not influence the patients survival. The tumor differentiation is one of the important prognostic factors.