A Field Study on Safety Performance of Apron Controllers at a Large-Scale Airport Based on Digital Tower.

The innovative concept of digital tower provides a new solution for reducing the construction and operation costs of airports with adverse natural environments, poor intervisibility conditions, or sparse traffic. However, it leads to changes in the situational awareness of air traffic controllers and to challenges in safety performance. To research the safety performance of apron controllers at a large-scale airport applying a digital tower, a field study was conducted at Baiyun International Airport in Guangzhou, China. In this study, we established a comprehensive index system from the perspective of situational awareness, which provided measurements on the areas of interests, gaze and physiological features, and vigilance of controllers. Three modules were compared: a physical tower module, a digital tower module with a large panoramic screen, and a digital tower module with a small panoramic screen. The differences in the safety performances of apron controllers are discussed in two aspects: adaptability and reliability. The results indicated that the apron controllers at the three modules performed different cognition patterns, but similar cognition effort was paid toward maintaining performance. Furthermore, the significant vigilance decrement of controllers exists between after-duty and before-duty, but with no significant difference among the three modules. In conclusion, apron controllers at a large-scale airport could obtain effective safety performances based on a digital tower that were no less than those from a physical tower.

Enhancing the Performance of a Self-Standing Si/PCNF Anode by Optimizing the Porous Structure.

Embedding silicon nanoparticles into carbon nanofibers is one of the effective methods to fabricate a self-standing and binder-free Si-based anode material for lithium-ion batteries. However, the sluggish Li-ion transport limits the electrochemical performance in the regular strategies, especially under high rate conditions. Herein, a kind of silicon nanoparticle in porous carbon nanofiber structures (Si/PCNFs) has been fabricated through a facile electrospinning and subsequent thermal treatment. By adjusting the mass ratio to 0.4:1, a Si/PCNF anode material with an effective Li+-migration pathway and excellent structural stability can be obtained, resulting in an optimal electrochemical performance. Although increasing the mass ratio of PEG to PAN further can lead to a larger pore size and can be beneficial to Li+ migration, thus being profitable for the rate capacity, the structural stability will get worse at the same time as more defects will form and lead to a weaker C-C binding, thus decrease the cycling stability. Remarkably, the rate capacity reaches 1033.4 mA h g-1 at the current density of 5 A g-1, and the cycling capacity is 933.2 mA h g-1 at 0.5 A g-1 after 200 cycles, maintaining a retention rate of 80.9% with an initial coulombic efficiency of 83.37%.

Single high dose irradiation induces cell cycle arrest and apoptosis in human hepatocellular carcinoma cells through the Ras/Raf/MEK/ERK pathways.

Purpose: Stereotactic body radiation therapy (SBRT) is emerging as a new noninvasive treatment in patients with primary liver carcinoma or liver-confined metastatic cancer. However, the radiobiological targets remain a subject of debate. Here, we investigated the potential biological effects of the radiation on the human hepatocellular carcinoma HepG2 cells.Materials and methods: Firstly, HepG2 cells were divided into three groups: control group, 3.5 Gy*8f group (L group), and 15 Gy*1f group (H group). After treatment, cell proliferation was examined using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide and plate colony formation assays. Cell cycle and apoptosis were assessed using propidium iodide and Hoechst 33258 staining, respectively. Furthermore, the mechanisms underlying irradiation-induced cell cycle arrest and cell apoptosis were investigated by Western blot assay.Results: Irradiation could effectively inhibit the proliferation and colony formation of HepG2 cells, and the single high dose irradiation showed stronger inhibitory effects. Irradiation-induced cell cycle arrest at G2/M phase in HepG2 cell, during which the expression levels of cyclin B1, CDK1, and p-CDK1 proteins were downregulated, whereas expression of p21 was upregulated in the irradiated HepG2 cells. After irradiation, typical morphological changes of apoptosis in HepG2 cells were observed; the number of cell apoptosis and the expression of apoptosis associated proteins were significantly increased in HepG2 cells by high dose irradiation compared with low dose irradiation. Additionally, compared with low dose irradiation, high dose irradiation significantly downregulated the phosphorylated proteins in the Ras/Raf/MEK/ERK signaling pathway.Conclusions: Our results suggest that irradiation applied in SBRT, particularly single high dose irradiation, mediates its anti-tumor effects by inducing cell cycle arrest and apoptosis via modulation of the Ras/Raf/MEK/ERK signaling pathway.

Ultrasensitive Fiber-Based ZnO Nanowire Network Ultraviolet Photodetector Enabled by the Synergism between Interface and Surface Gating Effects.

A flexible UV photodetector with a high on/off ratio is extremely important for environmental sensing, optical communication, and flexible optoelectronic devices. In this work, a flexible fiber-based UV photodetector with an ultrahigh on/off ratio is developed by utilizing the synergism between interface and surface gating effects on a ZnO nanowire network structure. The synergism between two gating effects is realized by the interplay between surface band bending and the Fermi level through the nanowire network structure, which is proved through the control experiments between the ZnO micro/nanowire photodetector and micro/nanowire junction photodetector, and the corresponding Kelvin probe force microscopy (KPFM) measurements. The on/off ratio of the fiber-based ZnO nanowire network UV photodetector reaches 1.98 × 108 when illuminated by 1.0 mW cm-2 UV light, which is 20 times larger than the largest reported result under the same UV illumination. This new UV sensor also has a high resolution to UV light intensity change in the nW cm-2 range. Furthermore, when the fiber-based photodetector is curved, it still shows excellent performance as above. This work gives a new effective route for the development of a high-performance UV photodetector or other optoelectronic detection devices.

Flexible Self-Powered ZnO Film UV Sensor with a High Response.

Response (on/off ratio) is one of the key parameters of ultraviolet (UV) sensors. In this paper, a kind of highly sensitive ZnO UV sensor with highly increased on/off current ratio was designed and developed. Under a weak UV intensity of 0.1 mW/cm2, this ultrathin ZnO film-based UV sensor has an on/off current ratio of 1.3 × 106 which is 3 times higher than the record value for ZnO-based UV sensors. In addition, it shows good flexibility and stable UV detection property during the bending process. When bending the sensor to a radius of curvature of about 18.5 mm, the sensor also shows high UV detection performance.

Loss of fatty acid synthase suppresses the malignant phenotype of colorectal cancer cells by down-regulating energy metabolism and mTOR signaling pathway.

PURPOSE: Altered cellular metabolism has received increased attention as an important hallmark of cancer. Activation of FASN has been found to be involved in many human tumors. Despite extensive research in FASN function on cancer, the underlying mechanism is not entirely understood yet. METHODS: Cerulenin was used to suppress the FASN expression in human colorectal cancer cell lines (HT29 and LoVo). Expression of PI3K, Akt, p-Akt, mTOR, p-mTOR, FASN, and AZGP1 was measured using western blotting and qPCR. ATP and lactic acid were assessed to investigate the activation of energy metabolism. Cell cytotoxicity assay was studied by cell counting kit-8 assay. The capacity of cell proliferation and migration was investigated by clonogenic and invasion assay. Analysis of apoptosis and the cell cycle was detected by flow cytometry. RESULTS: We found that the expression of FASN was down-regulated, while the expression of PI3K, p-Akt, p-mTOR, and AZGP1 was down-regulated in HT29 and LoVo cells treated with FASN inhibitor. Proliferation was reduced in FASN inhibitor-treated cells, which is consistent with an increased apoptosis rate. Furthermore, the migration of FASN inhibitor-treated cells was decreased and the content of ATP and lactic acid was also dropped. CONCLUSION: These findings suggest that inhibited FASN suppresses the malignant phenotype of colorectal cancer cells by down-regulating energy metabolism and mTOR signaling pathway. The results have paved the way to understand the relations of FASN, mTOR signaling pathway, and energy metabolism in colorectal cancer cells.

Hyperbaric Oxygen and Ginkgo Biloba Extract Ameliorate Cognitive and Memory Impairment via Nuclear Factor Kappa-B Pathway in Rat Model of Alzheimer's Disease.

BACKGROUND: Hyperbaric oxygen (HBO) and Ginkgo biloba extract (e.g., EGB 761) were shown to ameliorate cognitive and memory impairment in Alzheimer's disease (AD). However, the exact mechanism remains elusive. The aim of the present study was to investigate the possible mechanisms of HBO and EGB 761 via the function of nuclear factor kappa-B (NF-κB) pathway. METHODS: AD rats were induced by injecting ß-amyloid 25-35 into the hippocampus. All animals were divided into six groups: Normal, sham, AD model, HBO (2 atmosphere absolute; 60 min/d), EGB 761 (20 mg·kg-1·d-1 ), and HBO/EGB 761 groups. Morris water maze tests were used to assess cognitive, and memory capacities of rats; TdT-mediated dUTP Nick-End Labeling staining and Western blotting were used to analyze apoptosis and NF-κB pathway-related proteins in hippocampus tissues. RESULTS: Morris water maze tests revealed that EGB 761 and HBO significantly improved the cognitive and memory ability of AD rats. In addition, the protective effect of combinational therapy (HBO/EGB 761) was superior to either HBO or EGB 761 alone. In line, reduced apoptosis with NF-κB pathway activation was observed in hippocampus neurons treated by HBO and EGB 761. CONCLUSIONS: Our results suggested that HBO and EGB 761 improve cognitive and memory capacity in a rat model of AD. The protective effects are associated with the reduced apoptosis with NF-κB pathway activation in hippocampus neurons.

Expressions of fatty acid synthase and HER2 are correlated with poor prognosis of ovarian cancer.

The present study was designed to explore the cross talk between fatty acid synthase (FASN) and HER2 (ErbB2) in ovarian cancer. A total of 60 ovarian cancer patients and 15 normal ovarian tissues were enrolled. Tissue array was conducted by using a tissue microarray instrument. Immunohistochemistry was performed to quantify the expressions of HER2 and FASN. The FASN was detected to be distributed in the cell cytoplasm and was significantly correlated with cancer grade (p = 0.000) and FIGO staging (p = 0.000). Patients with FASN overexpression in ovarian cancer tend to have a worse overall survival rate (p = 0.000). HER2 was also stained to be distributed in the cell cytoplasm associated with higher expression in high-grade cancer. It was also disclosed that FASN expression level is not correlated with HER2 status in ovarian cancer. These results for the first time indicated that a cross talk in FASN and HER2 expressions might be associated with prognosis in malignant ovarian cancer.

Alpha-2-glycoprotein 1(AZGP1) regulates biological behaviors of LoVo cells by down-regulating mTOR signaling pathway and endogenous fatty acid synthesis.

AZGP1 is a multifaceted protein associated with lipid mobilization, a process that is regulated by FASN and other metabolic pathways such as mTOR signaling. The active mTOR signaling pathway has been found to be involved in a variety of tumors. However, it remains unclear whether it is involved in the regulation of AZGP1 and FASN. An AZGP1-expressing plasmid was transfected into a human colorectal cancer cell line (LoVo) with a low expression of AZGP1. The expression of AZGP1, FASN, eIF4E, p-mTOR, p-S6,and S6K1 were measured by Western blot analysis, and target genes were detected by RT-PCR. Cell proliferation was studied using the MTT and colony formation assays. The analysis of apoptosis and the cell cycle phase were assessed by flow cytometry. The capacity of cell migration was investigated using the transwell migration assay. We found that the expression of AZGP1 was up-regulated while the expression of FASN, eIF4E, p-mTOR, p-S6, and S6K1 were down-regulated in LoVo cells after AZGP1 was expressed. The proliferation of malignant cells was reduced in AZGP1-overexpression cells, which is consistent with an increased in the G2-arrest and apoptosis rate. Furthermore, the migration of AZGP1-overexpression cells was decreased. The overexpression of AZGP1 suppressed the activation of the mTOR pathway and endogenous FASN-regulated fatty acid synthesis, mitigating the malignant phenotype of LoVo cells. Herein, we provide evidence that AZGP1 may constitute a novel tumor suppressor for LoVo colorectal cancer cells.

The protective effect of hyperbaric oxygen and Ginkgo biloba extract on Aß25-35-induced oxidative stress and neuronal apoptosis in rats.

Alzheimer's disease (AD) is characterized by accumulation and deposition of Aß peptides in human brains. The present study aimed to determine the protective effect of HBO and EGB761 on Aß25-35 peptides induced cognitive impairment and neuronal toxicity in rats. Characteristics of AD were induced in rats by the administration of Aß25-35 in hippocampus. Rats were treated with HBO (2ATA 60min/day), EGB761 (20mg/kg/day), and the combination of HBO+EGB761 (20mg/kg/day+2ATA). The Morris water maze was used to detect the protective effects of HBO and EGB761 against cognitive impairment. The activities of SOD and GSH, the apoptosis-related genes and proteins and the apoptosis rate of hippocampus were detected. Compared to the model group, EGB761 and HBO treatments synergistically improved the escape latency. Furthermore, the activities of SOD and GSH in rat hippocampal tissue were found to have increased with a concomitant reduction in MDA levels, Bax expression, cytochrome c release, and the activity of caspase-9/3. Accordingly, a significant reduction was observed in the apoptosis rate following the treatment with EGB761 and HBO in this model of AD. Our findings suggest that HBO and EGB761 reduce cell toxicity and oxidative stress by blocking mitochondria-mediated apoptosis signaling in AD, and the combined treatment of HBO and Ginkgo further enhances these effects.

Fatty acid synthase regulates proliferation and migration of colorectal cancer cells via HER2-PI3K/Akt signaling pathway.

Recent evidence suggests that fatty acid synthase mediating de novo fatty acid synthesis plays a crucial role in the carcinogenesis process of various cancers. Moreover, HER2 and related PI3K/Akt signaling pathway, which links intimately with cellular metabolism, influence cancer biological behavior. However, it remains unknown whether malignant phenotype of colorectal cancer cells is regulated by the HER2-PI3K/Akt-FASN signaling pathway. In this study, Caco-2 cells were selected for functional characterization, and treated with ZSTK474, followed by RT-qPCR and Western blot assays examining PI3K, Akt, HER2, and FASN expression. The MTT and colony formation assays were used to assess proliferation. The migration was investigated by transwell, apoptosis, and cell-cycle analysis. We found that the blockade of PI3K/Akt signaling pathway by ZSTK474 treatment led to downregulation of PI3K, Akt, HER2, and FASN expression. The proliferation was decreased upon treatment which was consistent with an increased percentage of G(1) arrested cells instead of apoptosis. The migration of Caco-2 cells was also impaired by ZSTK474 treatment. Inhibition of HER2-PI3K/Akt signaling pathway suppresses FASN expression of Caco-2 cells, and inhibition of FASN expression changes malignant phenotype of Caco-2 cells.

Hyperbaric oxygen and Ginkgo Biloba extract inhibit Aß25-35-induced toxicity and oxidative stress in vivo: a potential role in Alzheimer's disease.

Alzheimer's disease is characterized by the accumulation and deposition of Aß peptides in human brains and Aß induced free radical-mediated damage is one of the hypotheses. In the present study, we explored the protective effects of hyperbaric oxygen (HBO) and Ginkgo Biloba extract (EGB761) on Aß25-35-induced brain toxicity. Our results demonstrated that EGB761, HBO, and the combination HBO and EGB761, could significantly improve the cognitive function in AD rats' model, especially the combination group. What's more, the activities of superoxide dismutase (SOD) in rat hippocampal tissue were obviously enhanced followed by evidently reduced malondialdehyde (MDA) levels in the same treatment groups mentioned earlier. There were no differences of nitric oxide (NO) productions in the group of EGB761, HBO, and HBO and EGB761, but they were all lower than that of model group. These findings suggest that both HBO and EGB761 may relieve cell toxicity and oxidative stress in AD and thus play a potential protective role in AD. Furthermore, the combination could have better effects compared with single one.

Suppression of mucin 2 enhances the proliferation and invasion of LS174T human colorectal cancer cells.

Altered expression of MUC2 (mucin 2) is related to tumour development in colorectal cancer. Colorectal mucinous carcinomas are positive for MUC2 expression, whereas MUC2 is down-regulated in non-mucinous adenocarcinomas. In the present study, we down-regulated MUC2 expression by RNAi (RNA interference) and investigated the in vitro and in vivo effects on the proliferation and invasion/migration potential of the LS174T human colorectal cancer cells. The LS174T cell line is a goblet-cell-like colorectal cancer cell line that continuously produces high levels of MUC2. Inhibition of MUC2 expression in vitro by transfection of LS174T cells with the recombinant plasmid pcDNA6.2-GW/EmGFP-miR-MUC2 led to the production of a stably transfected MUC2-RNAi LS174T cell line. The proliferation and invasion/migration of MUC2-RNAi cells in vitro were significantly higher than those in control cells, as assessed by MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide], colony formation and transwell assays. Subcutaneous injection of MUC2-RNAi LS174T cells into nude mice resulted in the development of subcutaneous tumours visible to the naked eye after 1 week. The growth rate of tumours derived from MUC2-RNAi LS174T cells was greater than that of tumours derived from control cells. Ki67 and matrix metalloproteinase-9 proteins were detected by immunohistochemistry in the xenografts. The expression levels of these proteins were higher in the MUC2-RNAi-derived xenografts than in xenografts derived from control cells. Although the role of MUC2 in colorectal tumorigenesis is not fully understood, these results strongly suggest a relationship between the proliferation and invasion of LS174T cells and the expression of MUC2.

Caco-2 and LS174T cell lines provide different models for studying mucin expression in colon cancer.

To compare the differences in MUC2 and MUC5AC mRNA among four colon cancer cell lines and to identify the best in vitro models for studying mucin expression, quantitative real-time polymerase chain reaction was used to measure the expression of MUC2 and MUC5AC mRNA in Caco-2, HT29, LoVo, and LS174T cell lines. The levels of MUC2 mRNA expression in the four colon cancer cell lines ranked in order of mRNA abundance were: LS174T>LoVo>HT-29>Caco-2. In contrast to MUC2, the abundances of MUC5AC mRNA were in the order: Caco-2>HT-29>LS174T>LoVo. Caco-2 (highest level of MUC5AC mRNA) and LS174T (highest level of MUC2 mRNA) were used to investigate the phenotypes. Morphologically, Caco-2 cells were larger with low electron density mucus-storing vacuoles, many cell surface microvilli, and no obvious intercellular spaces between cells, compared to LS174T cells. The proliferative and invasive capacities of LS174T cells were significantly higher than those of Caco-2 cells. Caco-2 and LS174T cells provide excellent in vitro models for studying mucin expression in colon cancer.

Expression of p53, Ki-67 and c-Myc proteins is predictive of the surgical molecular margin in colorectal carcinoma.

Surgical resection is the mainstay of treatment for colorectal carcinoma, however, the overall survival is modest due to frequent local recurrence from residual cancer cells after "curative" resection. Therefore, the status of surgical margin (tumor free or positive) has a significant influence on patient's survival. The difference in molecular profile between mucosa neighboring tumor lesions and remote area (surgical margin) may aid in evaluating resection status. 44 colorectal tumor tissues with corresponding adjacent non-neoplastic mucosa (within 3 cm from tumor tissues), and 110 tumor tissues with corresponding surgical margin mucosa (5 cm from tumor tissues) were randomly collected, fixed in 10% formalin and followed by embedding in paraffin. And the expression of p53, Ki-67 and c-Myc were investigated by tissue microarray (TMA) and immunohistochmistry. The expression of p53, Ki-67 and c-Myc were decreased in both adjacent non-neoplastic mucosa and mucosa of surgical margin, comparing to their expression in corresponding cancer cells. Furthermore, the expression of these proteins in mucosa of remote area (surgical margin) was significantly lower than those adjacent to tumor lesions. The expression of p53, Ki-67 and c-Myc in mucosa can be used as molecular marker for assessing surgical margin status in colorectal carcinoma.

Altered expression of MUC2 and MUC5AC in progression of colorectal carcinoma.

AIM: To study the expression profiles of MUC2 and MUC5AC in tumorigenesis of colorectal carcinoma and in its different pathologic types. METHODS: Formalin-fixed, paraffin-embedded human colorectal tissue specimens were immunostained with antibodies against MUC2 and MUC5AC. Six samples of normal mucosa (NM), 12 samples of hyperplastic polyp (HP), 15 samples of tubular adenoma with low-grade dysplasia (LGD), 14 samples of tubular adenoma with high-grade dysplasia (HGD), 26 samples of conventional colorectal adenocarcinoma (CCA), 15 samples of mucinous carcinoma (MC), and 8 samples of signet-ring cell carcinoma (SRCC) were collected. RESULTS: MUC2 was the most widely expressed protein in each study group, although the number of MUC2-positive cases was less in CCA group than in other groups (P < 0.05). The staining score for MUC2 was significantly decreased in the HP-LGD-HGD-CCA sequence (r = -0.73436, P < 0.0001). Among the neoplasms, MC and SRCC were more frequently associated with the high expression of MUC2 (P < 0.05) than with that of CCA. MUC5AC expression was detected in all groups but not in NM group. Furthermore, the staining score for MUC5AC was higher in HP, LGD, HGD, MC and SRCC groups than in NM and CCA groups (P < 0.05). The frequency of simultaneous expression of MUC proteins was significantly higher in MC and SRCC groups than in CCA group (P < 0.05). CONCLUSION: Alterations in MUC expression occur during colorectal tumorigenesis. The transformation process in MC and SRCC may be different from that in the traditional adenoma-carcinoma sequence.

Inhibition of DLC-1 gene expression by RNA interference in the colon cancer LoVo cell line.

DLC-1 (deleted in liver cancer-1) is a potential tumor suppressor gene, which is inactive in liver carcinogenesis. To observe the effects of DLC-1 gene expression on cell proliferation and migration in the human colon cancer cell line, RNAi Lipo-recombinant of the DLC-1 gene (pGCsil-DLC-1) was constructed and transduced into LoVo cells which are positive for DLC-1 gene expression. Results showed that the RNAi recombinant effectively inhibited the expression of the DLC-1 gene in LoVo cells. Additionally, our data showed decreased DLC-1 gene expression which resulted in the promotion of LoVo cell proliferation. Flow cytometry in cell cycle detection further indicated that the DLC-1 gene induced cell cycle arrest at G2/M and a cell migration assay confirmed that the knocking down of DLC-1 gene expression promotes LoVo cell migration. Our observations suggest that the DLC-1 gene is associated with LoVo cell proliferation, migration and cell cycle distribution. DLC-1 is a potential suppressor gene in the colon cancer LoVo cell line and may play an important role in colon cancer mechanisms.