Self-Assembly Growth of In-Rich InGaAs Core-Shell Structured Nanowires with Remarkable Near-Infrared Photoresponsivity.

Understanding the compositional distribution of ternary nanowires is essential to build the connection between nanowire structures and their potential applications. In this study, we grew epitaxial ternary InGaAs nanowires with high In concentration on GaAs {111}B substrates. Our detailed electron microscopy characterizations suggest that the grown ternary InGaAs nanowires have an extraordinary core-shell structure with In-rich cores and Ga-enriched shells, in which both nanowire cores and shells showed compositional gradient. It was found that In-rich nanowire cores are formed due to the Ga-limited growth environment, caused by the competition with the spontaneous InGaAs planar layer growth on the substrate that consumes more Ga than the nominal Ga concentration during the growth. Moreover, the composition gradient in the nanowires cores and shells is a result of strain relaxation between them. Our optoelectronic property measurements from prototype nanowire devices show a remarkable photoresponsivity under the near-infrared illumination. This study provides a new approach for designing and realizing complex nanowire heterostructures for high-efficiency nanowire-based systems and devices.

Multi-Dimensional and Objective Assessment of Motion Sickness Susceptibility Based on Machine Learning.

Background: As human transportation, recreation, and production methods change, the impact of motion sickness (MS) on humans is becoming more prominent. The susceptibility of people to MS can be accurately assessed, which will allow ordinary people to choose comfortable transportation and entertainment and prevent people susceptible to MS from entering provocative environments. This is valuable for maintaining public health and the safety of tasks. Objective: To develop an objective multi-dimensional MS susceptibility assessment model based on physiological indicators that objectively reflect the severity of MS and provide a reference for improving the existing MS susceptibility assessment methods. Methods: MS was induced in 51 participants using the Coriolis acceleration stimulation. Some portable equipment were used to digitize the typical clinical manifestations of MS and explore the correlations between them and Graybiel's diagnostic criteria. Based on significant objective parameters and selected machine learning (ML) algorithms, several MS susceptibility assessment models were developed, and their performances were compared. Results: Gastric electrical activity, facial skin color, skin temperature, and nystagmus are related to the severity of MS. Among the ML assessment models based on these variables, the support vector machine classifier had the best performance with an accuracy of 88.24%, sensitivity of 91.43%, and specificity of 81.25%. Conclusion: The severity of symptoms and signs of MS can be objectively quantified using some indicators. Multi-dimensional and objective assessment models for MS susceptibility based on ML can be successfully established.

Epitaxial GaAs/AlGaAs core-multishell nanowires with enhanced photoluminescence lifetime.

The modulation of complex GaAs/AlGaAs core-shell nanowire heterostructures by the process of embedding GaAs quantum wells or AlGaAs quantum dots is feasible due to their minor lattice mismatch. In this study, we have grown GaAs/AlGaAs core-multishell nanowire heterostructures by molecular beam epitaxy and investigated their structural and optical characteristics. Our advanced electron microscopy investigations confirmed that we have grown wurtzite-structured GaAs/AlGaAs core-multishell nanowires, in which the AlGaAs inner-shell with a high Al concentration acts as a quantum barrier for the GaAs nanowire core and AlGaAs outer-shell. Photoluminescence measurements show that this unique nanowire heterostructure has a significantly increased carrier lifetime compared to the conventional GaAs/AlGaAs core-shell nanowire heterostructures. The observed prolonged carrier lifetime can be attributed to the increased electron confinement at the core-inner-shell interface and thus the delayed recombination of photoexcited electron-hole pairs. This study provides a possible design of nanowire heterostructures for high-efficiency optoelectronic devices.

ING5 inhibits lung cancer invasion and epithelial-mesenchymal transition by inhibiting the WNT/ß-catenin pathway.

BACKGROUND: ING5 is the last member of the Inhibitor of Growth (ING) candidate tumor suppressor family that has been implicated in multiple cellular functions, including cell cycle regulation, apoptosis, and chromatin remodeling. Our previous study showed that ING5 overexpression inhibits lung cancer aggressiveness and epithelial-mesenchymal transition (EMT), with unknown mechanisms. METHODS: Western blotting was used to detect total and phosphorylated levels of ß-catenin and EMT-related proteins. Immunofluorescent staining was used to observe E-cadherin expression. Proliferation and colony formation, wound healing, and Transwell migration and invasion assays were performed to study the proliferative and invasive abilities of cancer cells. RESULTS: ING5 overexpression promotes phosphorylation of ß-catenin at Ser33/37, leading to a decreased ß-catenin protein level. Small hairpin RNA-mediated ING5 knockdown significantly increased the ß-catenin level and inhibited phosphorylation of ß-catenin S33/37. Treatment with the WNT/ß-catenin inhibitor XAV939 inhibited ING5-knockdown promoted proliferation, colony formation, migration, and invasion of lung cancer A549 cells, with increased phosphorylation of ß-catenin S33/37 and a decreased ß-catenin level. XAV939 also impaired ING5-knockdown-induced EMT, as indicated by upregulated expression of the EMT marker E-cadherin, an epithelial marker; and decreased expression of N-cadherin, a mesenchymal marker, and EMT-related transcription factors, including Snail, Slug, Twist, and Smad3. Furthermore, XAV939 could inhibit the activation of both IL-6/STAT3 and PI3K/Akt signaling pathways. CONCLUSION: ING5 inhibits lung cancer invasion and EMT by inhibiting the WNT/ß-catenin pathway.

ING5 knockdown enhances migration and invasion of lung cancer cells by inducing EMT via EGFR/PI3K/Akt and IL-6/STAT3 signaling pathways.

ING5 belongs to the Inhibitor of Growth (ING) candidate tumor suppressor family, whose functions have been involved in the regulation of chromatin remodeling, cell cycle progression, proliferation and apoptosis. Our previous study has shown that ING5 overexpression inhibits lung cancer aggressiveness via suppressing epithelial to mesenchymal transition (EMT). However, the mechanisms remain largely unknown. In the current study, by Phospho-Kinase array and western blot, we have defined significantly upregulated EGFR/PI3K/Akt and IL-6/STAT3 oncogenic signaling pathways in ING5 knockdown A549 cells, which could be downregulated by ING5 overexpression. PI3K inhibitor ZSTK474 or STAT3 inhibitor Niclosamide not only abolished ING5 knockdown-promoted proliferation, colony formation, migration and invasion of lung cancer A549 cells, but also impaired ING5 knockdown-stimulated metastasis of cancer cells in mouse xenograft models with tail vein injection of A549 cells. Furthermore, treatment with ZSTK474 or Niclosamide decreased protein level of EGFR, p-Akt, IL-6 and p-STAT3, and reversed ING5 knockdown-promoted EMT, as indicated by downregulated expression of EMT marker E-cadherin, an epithelial marker, increased expression of N-cadherin, a mesenchymal marker, and EMT-related transcription factors including Snail, Slug, Smad3 and Twist. Taken together, these results demonstrate that loss of ING5 enhances aggressiveness of lung cancer cells by promoting EMT via activation of EGFR/PI3K/Akt and IL-6/STAT3 signaling pathways.

WSTF promotes proliferation and invasion of lung cancer cells by inducing EMT via PI3K/Akt and IL-6/STAT3 signaling pathways.

Williams syndrome transcription factor (WSTF), which is encoded by the BAZ1B gene, was first identified as a hemizygously deleted gene in patients with Williams syndrome. WSTF protein has been reported to be involved in transcription, replication, chromatin remodeling and DNA damage response, and also functions as a tyrosine protein kinase. However, the function of WSTF in cancer is not known. Here, we show that WSTF overexpression promotes proliferation, colony formation, migration and invasion of lung cancer A549 and H1299 cells. WSTF overexpression also promotes tumor growth and invasive abilities of lung cancer cells in mouse xenograft models. cDNA microarray and subsequent qRT-PCR validation revealed that WSTF overexpression significantly upregulated the expression of EMT (epithelial to mesenchymal transition) marker fibronectin (FN1) and EMT-inducing genes Fos and CEACAM6. The changes of EMT markers including downregulated E-cadherin and upregulated N-cadherin and FN1 were further confirmed at both mRNA and protein levels upon WSTF overexpression, with typical morphological changes of EMT. Furthermore, WSTF activates both PI3K/Akt and IL-6/STAT3 oncogenic signaling pathways. Treatment with PI3K inhibitor ZSTK474 or STAT3 inhibitor niclosamide reversed the effects of WSTF overexpression by inhibiting cell proliferation, migration and invasion, with decreased level of p-Akt, p-STAT3 and IL-6. ZSTK474 and niclosamide also reversed EMT markers and EMT-inducing proteins including Snail, Slug, Twist and CEACAM6 in WSTF-overexpressing A549 cells. Taken together, these results demonstrate that WSTF may act as an oncoprotein in lung cancer to accelerate tumor aggressiveness by promoting EMT via activation of PI3K/Akt and IL-6/STAT3 pathways.

Ku70 is essential for histone deacetylase inhibitor trichostatin A-induced apoptosis.

It was previously reported that the histone deacetylase inhibitor (HDACI) trichostatin A (TSA) induced B cell lymphoma 2 (Bcl-2)-associated X protein (Bax)-dependent apoptosis in colorectal cancer (CRC) cells. In addition, Ku70 has been identified as a regulator of apoptosis, the mechanism of which proceeds via interacting with Bax. The aim of the present study was to investigate the role of Ku70 in TSA-induced apoptosis in the CRC cell lines HCT116 and HT29. The results showed that TSA induced the acetylation of Ku70, which was found to be associated with increased apoptosis. In addition, TSA treatment promoted the release of Bax from its complex with Ku70. Bax was then detected to have translocated from the cytoplasm into the mitochondria, while cytochrome c was detected to have translocated from the mitochondria into the cytoplasm. Furthermore, knockdown of Ku70 using small interfering RNA decreased TSA-induced apoptosis as well as downregulated the expression of Bax. These effects were rescued through pre-treatment of cells with the proteasome inhibitor MG132. In conclusion, the results of the present study suggested that Ku70 acetylation mediated TSA-induced apoptosis in CRC cells. In addition, Ku70 was found to be indispensable in TSA-induced apoptosis due to its role in protecting Bax from proteosomal degradation.