Energy-absorption-based explanation of the photocatalytic activity enhancement mechanism of TiO2 nanofibers

As is reported, the photocatalytic activity will increase significantly when TiO₂ nanoparticles are agglomerated into TiO₂ nanofibers (NFs), but the photocatalytic activity enhancement mechanisms are still not fully understood. As is widely accepted, the optical absorption process plays a key role in photocatalysis, and it can even be said that the optical absorption capability of the photocatalyst directly determines its photocatalytic activity, while the influence of the structure on the optical absorption characteristics of TiO₂ has largely been ignored in the existing explanations. In this paper, optical simulations are introduced into analyzing optical characteristics of TiO₂ Nanofibers with which, the photocatalytic activity enhancement mechanism is further discussed, and a photocatalytic activity enhancement mechanism of TiO₂ Nanofibers is proposed.     

Megaprojects as complex adaptive systems: The Hinkley point C case

Megaprojects are complex projects which impact millions of people, involve public and private stakeholders, and present challenges related to decision making and performance shortfalls. They are relevant cases for studying faulty management thinking as well as performance evolutions and self-organizing dynamics. Our paper builds on the theory of Complex Adaptive Systems (CAS) to understand and model processes of evolution in the Hinkley Point C nuclear power plant megaproject. The results show that CAS properties apply to megaproject changes and provide a theoretical and practical framework for examining and modeling megaproject management dynamics. We designed a research methodology combining content analysis and historical research for its relevance in conducting organizational research in conditions of complexity and non-linearity. This original research design makes it possible to conduct causal analyses of relations between key megaproject events and thus build models of evolution dynamics in stakeholder success expectations, change mechanisms in the implementation of project outputs, and self-organizing patterns.     

一种纯方位跟踪中的自适应滤波算法

针对纯方位被动目标跟踪中扩展卡尔曼滤波算法易发散的不足，提出了一种自适应的改进算法。该算法利用极大后验噪声估计器Sage-Husa对虚拟观测噪声进行实时在线估计，动态补偿线性化带来的误差。算法的对比仿真分析结果表明，AEKF较之EKF滤波效果有所改善，增强了稳定性，提高了精度，为ST纯方位被动目标跟踪的实现提供一种新的方法。     

Friction and a Tribochemical Reaction between Ice and Hexagonal Boron Nitride: A Theoretical Study

Friction between ice-Ih and hexagonal boron nitride (h-BN) has been determined by periodic ab initio calculations. Surfaces of ice-Ih and h-BN were brought into sliding contact, and the interaction energies were calculated as a function of interplanar distance and lateral displacement of the surfaces. The friction between the surfaces was calculated from the interaction energies, producing a friction coefficient of 0.140. Friction is further influenced at high loads by a tribochemical reaction between ice-Ih and h-BN.     

浅谈汽车自适应前大灯

从自适应大灯的结构及工作原理,阐述了解决夜间行车的安全性问题,其优点在于保证汽车能在静态或动态行驶中,控制器一旦检测到加速或制动信号时,或者外界光的强度发生变化等不同工况时,都能自动改变照射光的位置,实现自我调节,减少交通事故率。     

Targeting DNA Methylation in Leukemia,Myelodysplastic Syndrome,and Lymphoma: A Potential Diagnostic,Prognostic, and Therapeutic Tool

DNA methylation represents a crucial mechanism of epigenetic regulation in hematologic malignancies. The methylation process is controlled by specific DNA methyl transferases and other regulators, which are often affected by genetic alterations. Global hypomethylation and hypermethylation of tumor suppressor genes are associated with hematologic cancer development and progression. Several epi-drugs have been successfully implicated in the treatment of hematologic malignancies, including the hypomethylating agents (HMAs) decitabine and azacytidine. However, combinations with other treatment modalities and the discovery of new molecules are still the subject of research to increase sensitivity to anti-cancer therapies and improve patient outcomes. In this review, we summarized the main functions of DNA methylation regulators and genetic events leading to changes in methylation landscapes. We provide current knowledge about target genes with aberrant methylation levels in leukemias, myelodysplastic syndromes, and malignant lymphomas. Moreover, we provide an overview of the clinical trials, focused mainly on the combined therapy of HMAs with other treatments and its impact on adverse events, treatment efficacy, and survival rates among hematologic cancer patients. In the era of precision medicine, a transition from genes to their regulation opens up the possibility of an epigenetic-based approach as a diagnostic, prognostic, and therapeutic tool.     

Loss of Interleukin-13-Receptor-Alpha-1 Induces Apoptosis and Promotes EMT in Pancreatic Cancer

In search of new therapies for pancreatic cancer, cytokine pathways have attracted increasing interest in recent years. Cytokines play a vital role in the crosstalk between tumour cells and the tumour microenvironment. The related inflammatory cytokines IL-4 and IL-13 can regularly be detected at increased levels in the microenvironment of pancreatic cancer. They share a receptor heterodimer consisting of IL-4Rα and IL-13Rα1. While IL-4Rα induces a more oncogenic phenotype, the role of IL-13Rα1 was yet to be determined. ShRNA-based knockdown of IL-13Rα1 was performed in Capan-1 and MIA PaCa-2. We assessed cell growth and migratory capacities under the influence of IL-13Rα1. Pathway alterations were detected by immunoblot analysis. We now have demonstrated that the loss of IL-13Rα1 induces apoptosis in pancreatic cancer cells. This was associated with an epithelial-to-mesenchymal transition. Loss of IL-13Rα1 also abolished the effects of exogenous IL-4 and IL-13 stimulation. Interestingly, in wild type cells, cytokine stimulation caused a similar increase in migratory capacities as after IL-13Rα1 knockdown. Overall, our results indicate the vital role of IL-13Rα1 in the progression of pancreatic cancer. The differential expression of IL-4Rα and IL-13Rα1 has to be taken into account when considering a cytokine-targeted therapy in pancreatic cancer.     

Role of the Ghrelin System in Colorectal Cancer

The ghrelin system contains several components (e.g., ghrelin with growing number of alternative peptides, growth hormone secretagogue receptors (GHS-Rs), and ghrelin-O-acyl-transferase (GOAT) and participates in regulation of a number of key processes of gastrointestinal (GI) tract cancer progression, including cell proliferation, migration, invasion, apoptosis, inflammation, and angiogenesis. However, its exact role in promoting or inhibiting cancer progression is still unclear. Colorectal cancer (CRC) is one of the most common human malignancies worldwide. Molecular studies suggest an autocrine/paracrine mechanism for the secretion of ghrelin in colorectal carcinogenesis and its contribution to its initial stages. However, the signalling pathways of CRC development involving the ghrelin system are poorly understood. Potential mechanisms of colon carcinogenesis involving components of the ghrelin system were previously described in an animal model and in in vitro studies. However, the diagnostic–prognostic role of serum ghrelin concentrations, tissue expression, or genetic changes of this system in various stages of CRC progression remains an open case. Thus, the aim of this study is to discuss the role of the ghrelin system in colon carcinogenesis, diagnostics and CRC prognostics, as well as the results of studies on the use of ghrelin and its analogues in the therapy of CRC-related syndromes (e.g., cachexia and sarcopenia).     

The Profile of MicroRNA Expression and Potential Role in the Regulation of Drug-Resistant Genes in Doxorubicin and Topotecan Resistant Ovarian Cancer Cell Lines

Epithelial ovarian cancer has the highest mortality among all gynecological malignancies. The main reasons for high mortality are late diagnosis and development of resistance to chemotherapy. Resistance to chemotherapeutic drugs can result from altered expression of drug-resistance genes regulated by miRNA. The main goal of our study was to detect differences in miRNA expression levels in two doxorubicin (DOX)- and two topotecan (TOP)-resistant variants of the A2780 drug-sensitive ovarian cancer cell line by miRNA microarray. The next aim was to recognize miRNAs as factors responsible for the regulation of drug-resistance genes. We observed altered expression of 28 miRNA that may be related to drug resistance. The upregulation of miR-125b-5p and miR-935 and downregulation of miR-218-5p was observed in both DOX-resistant cell lines. In both TOP-resistant cell lines, we noted the overexpression of miR-99a-5p, miR-100-5p, miR-125b-5p, and miR-125b-2-3p and decreased expression of miR-551b-3p, miR-551b-5p, and miR-383-5p. Analysis of the targets suggested that expression of important drug-resistant genes such as the collagen type I alpha 2 chain (COL1A2), protein Tyrosine Phosphatase Receptor Type K (PTPRK), receptor tyrosine kinase—EPHA7, Roundabout Guidance Receptor 2 (ROBO2), myristoylated alanine-rich C-kinase substrate (MARCK), and the ATP-binding cassette subfamily G member 2 (ABCG2) can be regulated by miRNA.     

Effect of Compressive Stress in Tumor Microenvironment on Malignant Tumor Spheroid Invasion Process

In this study, we proposed an in vitro tumor model to simulate the mechanical microenvironment and investigate the effect of compressive stress on the invasion process of malignant tumors. It has been pointed out that the biomechanical environment, as well as the biochemical environment, could affect the transformation of cancer cell migration, invasion, and metastasis. We hypothesized that the solid stress caused by the exclusion of surrounding tissue could transform tumor cells from noninvasive to invasive phenotypes. Colorectal cell spheroids were embedded and cultured in agarose gels of varying concentrations to simulate the earliest stages of tumor formation and invasion. The spheroids embedded in gels at higher concentrations showed peculiar growth after 72 h of culture, and the external compressive loading imposed on them caused peculiar growth even in the gels at lower concentrations. In conclusion, the mechanical microenvironment caused the transformation of tumor cell phenotypes, promoting the growth and invasion of tumor cell spheroids.