Predicting the prognosis of lung cancer patients treated with intensity-modulated radiotherapy based on radiomic features.

AIMS: This study aimed to develop a method for predicting short-term outcomes of lung cancer patients treated with intensity-modulated radiotherapy (IMRT) using radiomic features detected through computed tomography images. METHOD: A prediction model was developed based on a dataset of radiomic features obtained from 132 patients with lung cancer receiving IMRT. Dimension reduction was performed for the features using the maximum-relevance and minimum-redundancy (mRMR) algorithm, and the least absolute shrinkage and selection operator (LASSO) regression model was utilized to optimize feature selection for the IMRT-sensitivity prediction model. The model was constructed using binary logistic regression analysis and was evaluated using the concordance index (C-index), calibration plots, receiver operating characteristic curve, and decision curve analysis. RESULTS: Fifty features were selected from 1348 radiomic features using the mRMR method. Of these, three radiomic features were selected by LASSO logistic regression to construct the radiomics nomogram. The C-index of the model was 0.776 (95% confidence interval: 0.689-0.862) and 0.791 (95% confidence interval: 0.607-0.974) in the training and validation cohorts, respectively. Decision curve analysis showed that the radiomics nomogram was clinically useful. CONCLUSION: Radiomic features have the potential to be applied to predict the short-term efficacy of IMRT in patients with inoperable lung cancer.

Review on the Research and Applications of TLS in Ground Surface and Constructions Deformation Monitoring.

With the gradual maturity of the terrestrial laser scanners (TLS) technology, it is widely used in the field of deformation monitoring due to its fast, automated, and non-contact data acquisition capabilities. The TLS technology has changed the traditional deformation monitoring mode which relies on single-point monitoring. This paper analyzes the application of TLS in deformation monitoring, especially in the field of ground surface, dam, tunnel, and tall constructions. We divide the methods for obtaining ground surface deformation into two categories: the method based on point cloud distance and the method based on displacement field. The advantages and disadvantages of the four methods (M2M, C2C, C2M, M3C2) based on point cloud distance are analyzed and summarized. The deformation monitoring methods and precisions based on TLS for dams, tunnels, and tall constructions are summarized, as well as the various focuses of different monitoring objects. Additionally, their limitations and development directions in the corresponding fields are analyzed. The error sources of TLS point cloud data and error correction models are discussed. Finally, the limitations and future research directions of TLS in the field of deformation monitoring are presented in detail.

Quantitative analysis of the impact of COVID-19 on ship visiting behaviors to ports- A framework and a case study.

Corona Virus Disease 2019 (COVID-19) outbreak leads to a significant downturn in the global economy and supply chain. In the maritime sector, trade volume slumped by 3.8% in 2020 compared with 2019. To explore the impacts of COVID-19 on ship visiting behaviors, a framework is proposed to analyze the impact of COVID-19 on port traffic using Automatic Identification System (AIS) data. Firstly, a ship travel behavior-based model is proposed to identify the vessel anchoring and berthing. Then, the diversity in vessel anchoring and berthing time are analyzed, reflecting the impact of COVID-19. The port congestion caused by COVID-19 is quantified by accounting for the number of visiting ships and their residence time. Finally, a case study is carried out on vessels in the Beibu Gulf, China, operating from 2019 to 2020. The results show that the average anchoring time and berthing time increase by 62% and 11% for cargo ships and by 112% and 63% for oil tankers after the outbreak of COVID-19 compared with that before COVID-19. And the density of ships increases in the port area in 2020. Accordingly, the relevant improvements and countermeasures are proposed to reduce the adverse impact of the epidemic on the port navigation system. The paper has the potential to provide a reference for port management and improving port navigation efficiency in the post-pandemic era.

SCF promotes the production of IL-13 via the MEK-ERK-CREB signaling pathway in mast cells.

Mast cells serve a key role in the occurrence and development of allergy. As an important growth factor of mast cells, stem cell factor (SCF) has an effect on the apoptosis, chemotaxis, adhesion, degranulation and other biological characteristics of mast cells. However, there are few studies regarding the effect of SCF signal on the production of cytokines from mast cells, particularly Th2 type cytokines. In the present study, the expression and secretion of IL-13 in P815 cells stimulated by SCF were detected by fluorescence quantitative PCR and ELISA, and western blotting and EMSA were used to detect ERK phosphorylation and activation of CREB in stimulated P815 cells. The results demonstrated that the production of IL-13 was significantly increased in P815 cells stimulated by SCF (1-100 ng/ml; P<0.01). There was an obvious phosphorylation of ERK and CREB activation in P815 cells stimulated by SCF (50 ng/ml). Compared with the SCF single stimulation group, the production of IL-13 was significantly reduced in P815 cells stimulated with U0126 (ERK-MEK/pathway inhibitor) or H-89 (CREB inhibitor) combined with SCF stimulation group (P<0.01). However, JSI-124 (JAK/STAT3 pathway inhibitor), Wortmannin (PI3K/Akt pathway inhibitor) and PDTC (NF-κB inhibitor) had no effect on the role of SCF promoting the P815 cells producing IL-13. Therefore, SCF signaling promotes mast cell P815 to produce IL-13, and this effect is associated with the MEK-ERK-CREB signaling pathway.

MicroRNA-20b promotes proliferation of H22 hepatocellular carcinoma cells by targeting PTEN.

MicroRNAs (miRNAs/miRs) are small, noncoding RNA molecules that are closely associated with the occurrence and development of tumors. miR-20b is overexpressed in hepatocellular carcinoma cell lines and tissues. However, it is not clear whether miR-20b can promote the proliferation of hepatocellular carcinoma cells. In the present study, the proliferation of H22 mouse hepatocellular carcinoma cells was detected using the Cell Counting Kit-8 assay. MiRanda software was used to predict the binding sites of miR-20b to the 3'-untranslated region (3'-UTR) of phosphatase and tensin homolog (PTEN). The 3'-UTR sequence of the PTEN gene was amplified using the polymerase chain reaction in H22 cells. The recombinant plasmid or empty plasmid was co-transfected with miR-20b mimics or miR-20b scramble into HeLa cells, and luciferase activity was assessed by Dual-Luciferase® Reporter Assay System 24 h post-transfection. In the present study, miR-20b knockdown significantly inhibited the proliferation of H22 mouse hepatocellular carcinoma cells. In addition, miR-20b inhibition upregulated the expression of PTEN, and it was revealed that miR-20b may directly target the 3'-untranslated region of the PTEN gene. Downregulation of PTEN partially reversed the anti-proliferative effect of miR-20b on H22 cells. In conclusion, miR-20b may promote H22 cell proliferation by targeting PTEN, providing a rationale for further study investigating novel therapeutic strategies for liver cancer.

IGF-1 Promotes Endocytosis of Alveolar Epithelial Cells through PI3K Signaling.

Airway inflammation can be mitigated when apoptotic cells are engulfed by pulmonary epithelial cells. Insulin-like growth factor 1 (IGF-1), a single chain polypeptide growth factor, is the main mediator of growth hormone activity in vivo. IGF-1 has many biological activities, such as the regulation of cell survival, proliferation, differentiation and metabolism. However, its effect on the engulfment of cells, especially by non-professional phagocytes such as alveolar epithelial cells (AECs), has not been fully elucidated. We report that IGF-1 increases endocytosis in a mouse alveolar epithelial cell line, MLE-12. The PI3K-Akt pathway is involved in this effect of IGF-1. Furthermore, IGF-1 can inhibit the production of interleukin-6 in lipopolysaccharide-stimulated AECs. We have found that IGF-1 can enhance endocytosis of AECs through the PI3K pathway and exhibit anti-inflammatory properties. These two observations suggest that IGF-1 is a potential mediator in the regulation of airway inflammation.

Upregulated IGF­1 in the lungs of asthmatic mice originates from alveolar macrophages.

Asthma is characterized by inflammation and remodeling of the airways. Insulin­like growth factor-1 (IGF­1) serves an important role in the repair of lung tissue injury and airway remodeling by elevating collagen and elastin content, increasing the thickness of smooth muscle and promoting the proliferation of lung epithelial and interstitial cells, as well as fibroblasts; however, the content of IGF­1 and its cellular origin in the lungs of patients with asthma remain unknown. In the present study, a mouse model of asthma was constructed. Following isolation of alveolar macrophages (AMs), the content of IGF­1 in lung tissue and bronchoalveolar lavage fluid (BALF) was detected by ELISA. The proliferation and phagocytosis of alveolar epithelial cells (AECs) stimulated by IGF­1 were detected by Cell Counting Kit­8 method and flow cytometry, respectively. In the present study, IGF­1 was upregulated in the lung tissues of asthmatic mice, and the content of IGF­1 in BALF was also elevated. Depletion of AMs by treating mice with 2­chloroadenosine via nose dripping reversed the increase of IGF­1 by 80% in lung tissues and by ~100% in BALF of asthmatic mice, suggesting that elevated IGF­1 in asthmatic mice predominantly originated from AMs. As IGF­1 promotes the proliferation and phagocytosis of AECs, AM­derived IGF­1 may serve an important role in the regulation of airway inflammation and remodeling in asthmatic mice.

miR­20b negatively regulates VEGF expression by targeting STAT3 in H22 hepatocellular carcinoma cells.

Vascular endothelial growth factor (VEGF) promotes angiogenesis during tumor growth, and its expression involves multiple signaling pathways and transcription factors. In the present study, transforming growth factor (TGF)­ß1 promoted upregulation of VEGF and downregulation of microRNA (miR)­20b expression in mouse H22 hepatocellular carcinoma cells. miR­20b negatively regulated both constitutive VEGF expression and TGF­ß1­induced VEGF expression. The miRanda algorithm predicted that a binding site of the miR­20b GCAAUCUGGGCACUUU sequence was present in the signal transducer and activator of transcription (STAT)3 3'­untranslated region. Following transfection of miR­20b mimics into H22 cells, expression of STAT3 protein was downregulated. A dual­luciferase activity assay revealed that miR­20b directly targeted STAT3 to regulate its expression, and that interference with STAT3 expression significantly downregulated VEGF mRNA and protein expression. Interference with STAT3 expression resulted in increased VEGF expression in H22 cells overexpressing miR­20b, but expression was lower than that in quiescent H22 cells. This indicated that STAT3 was involved in the negative regulation of VEGF expression in H22 cells by miR­20b. The data demonstrated that miR­20b negatively regulated VEGF expression by directly targeting STAT3 in H22 cells.

Correlation between gamma passing rate and complexity of IMRT plan due to MLC position errors.

PURPOSE: This study evaluates the correlation between the susceptibility of the γ passing rate of IMRT plans to the multi-leaf collimator (MLC) position errors and a quantitative plan complexity metric. METHODS: Twenty patients were selected for this study. For each patient, two IMRT plans were generated using sliding window and step-&-shoot techniques, respectively. Modulation complexity score (MCS) was calculated for all IMRT plans, and symmetric MLC leaf bank errors, ranging from 0.3 mm to 1 mm, were introduced. Original and modified plans were delivered using Varian's Clinac iX. The obtained dose distribution using ArcCHECK was then compared with the TPS calculated dose distribution of the original plans. 3D gamma analysis was performed for each verification with passing criteria of 2%/2 mm. The γ passing rate decreasing gradient were calculated to evaluate relationship between variation of γ passing rate due to MLC errors and complexity. RESULTS: A linear regression analysis was applied between γ gradient and complexity, and the results showed a linear correlation (R2 = 0.81 and 0.82 for open and closed MLC error types, respectively) indicating the more complex plans are more susceptible to MLC leaf bank errors. Meanwhile, correlation of re-normalized γ passing rate and complexity for all errors scenarios also presented a strong correlation (r > 0.75). CONCLUSION: The statistics results revealed variation relationship of dosimetry robust of plans with various complexities to MLC errors. Our results also suggested that the observed susceptibility is independent of the delivery techniques.

Sp-1 Negatively Regulates miR-20b Expression in Macrophages.

miR-20b is a member of the miR-106a-363 gene cluster, located on the X chromosome. miR-20b regulates the expression of multiple genes in vivo and it is closely related to the occurrence and development of many diseases. These diseases include inflammatory diseases and tumor development, amongst others. However, few studies have focused on the regulation of the miR-20b gene itself. In this study, we are using the miRBase database to obtain the upstream 2000 bp sequence of the miR-20b precursor. Bio-informatics software P-MATCH 1.0 and AliBaba2 werethen used to predict transcription factor binding in the upstream region. Sp-1 was identified as one of the most probable transcription factors regulating miR-20b gene expression. After treatment with a Sp-1 siRNA, the expression of miR-20b was significantly increased in RAW264.7 cells, as well as peritoneal and alveolar macrophages. In addition, the interference with Sp-1 gene expression also reversed the decrease in miR-20b expression in RAW264.7 cells induced by TNF-α. These results indicate that Sp-1 negatively regulates the expression of miR-20b in macrophages. This finding suggests the potential of Sp-1 as a target for therapies in diseases that are associated with miR-20b overexpression.

MicroRNA-20b promotes the accumulation of CD11b+Ly6G+Ly6Clow myeloid-derived suppressor cells in asthmatic mice.

miR-20b is a member of the miR-106a-363 gene cluster, which has been shown to play an important role in a variety of diseases, including cancer, inflammation, and autoimmune diseases. Our previous study indicated that miR-20b has an inhibitory effect on airway inflammation in asthmatic mice, but the exact mechanism is unclear. In this study, we report that the ratio of CD11b+Ly6G+Ly6Clow cells, but not the amount of CD11b+Ly6C+Ly6G- cells, was increased in the lung tissue of asthmatic mice after intranasal instillation with miR-20b mimics, while Th2-type cytokines (interleukin (IL)-4 and IL-13) were significantly decreased in the bronchoalveolar lavage fluid. In addition, the transcription factor CREB regulated the expression of miR-20b. Our findings suggest that miR-20b can induce the accumulation of myeloid-derived suppressor cells in the lungs of asthmatic mice, which may be a mechanism by which miR-20b inhibits airway inflammation in asthmatic mice. Thus, miR-20b may be used as a target for the effective treatment of asthma in the future.

Mir-20b-Induced Increase in Myeloid-Derived Suppressor Cells in the Lungs of Mice with Chronic Asthma.

Bronchial asthma is a common chronic airway inflammatory disease. MicroRNAs (miRNAs) play an important role in the pathogenesis of asthma. We have previously shown that miR-20b can inhibit airway inflammation in asthmatic mice, but the exact mechanism is unknown. In the present study, we show that administration of nasal drops containing miR-20b induced an increase in the percentage of Gr1+CD11b+ myeloid-derived suppressor cells (MDSCs) in lung tissue from asthmatic mice, and the content of TGF-ß in lung tissues also increased after treatment. However, there was no significant change in the number of Gr1+CD11b+ MDSCs in bone marrow, peripheral blood, or spleens of asthmatic mice receiving the miR-20b nasal drip compared with untreated asthmatic mice. Since MDSCs originate in the bone marrow, these results suggest that miR-20b nasal drops may promote the increase of Gr1+CD11b+ MDSCs in the lungs of asthmatic mice by the mechanism of inducing expansion.

ARCH: Adaptive recurrent-convolutional hybrid networks for long-term action recognition.

Recognition of human actions from digital video is a challenging task due to complex interfering factors in uncontrolled realistic environments. In this paper, we propose a learning framework using static, dynamic and sequential mixed features to solve three fundamental problems: spatial domain variation, temporal domain polytrope, and intra- and inter-class diversities. Utilizing a cognitive-based data reduction method and a hybrid "network upon networks" architecture, we extract human action representations which are robust against spatial and temporal interferences and adaptive to variations in both action speed and duration. We evaluated our method on the UCF101 and other three challenging datasets. Our results demonstrated a superior performance of the proposed algorithm in human action recognition.