Multi-spectral Mueller Matrix Imaging for Wheat Stripe Rust

Yang Feng,Tianyu He,Wenyi Ren,Dan Wu,Rui Zhang,Yingge Xie 한국광학회 2024 Current Optics and Photonics Vol.8 No.2

Hexadecylamine Modified Copper Nanowire Coated Superhydrophobic Cotton Fabric for Antifouling, Oil-water Separation, and Infrared Reflection Applications

Jiaojiao Zheng,Hong Zhang,Tianyu Cao,Yuanyuan Zhu,Lizhong He,Jianwei Li,Xudong Chen,Yinhu Qu 한국섬유공학회 2022 Fibers and polymers Vol.23 No.10

Superhydrophobic surfaces by creating surface roughness followed by coating with low-surface-energyfluorinated materials have been intensively developed on cotton fabrics. However, exploring superhydrophobic surfaces withnon-fluorine components and further improving their attachment with cotton fabrics is still challenging. Herein, wedeveloped a superhydrophobic surface on cotton fabric by dip coating with hexadecylamine (HDA) modified coppernanowires (Cu NWs) based on the coordination between Cu atoms and amine groups. The HDA modified Cu NWs not onlycreated surface roughness, but also decreased the surface energy, leading to a superhydrophobic cotton fabric with watercontact angle of 164 °±2.0 °. Furthermore, ultrasonic washing and tape peeling tests exhibited the Cu NWs were adheredtightly to the surface of cotton fibers, owing to the strong hydrogen bond between amine groups on HDA molecules andhydroxyl groups on cotton fibers. In addition, the superhydrophobic cotton fabric showed excellent antifouling, oil-waterseparation and infrared reflection properties. It is believed that this facile method provide promising industrial applicationsfor fabricating superhydrophobic surfaces on other substrates.

Effect of impurity components in stainless steel dust on the coloring properties of the prepared black ceramic pigments

Zhiqiao Li,Xiang Zhang,Guojun Ma,Dingli Zheng,Ruixiang He,Tianyu Du 한양대학교 청정에너지연구소 2023 Journal of Ceramic Processing Research Vol.24 No.1

Stainless steel dust (SSD) can be utilized as the primary raw material for the production of Fe-Cr-Ni-Mn system black ceramicpigments because it is high in transition metal elements. However, in addition to the ingredients required for the preparationof black pigments, it also contains some impurity elements like Ca, Mg, Si and Zn, and the influence of these impurity elementson the coloring performance of the pigments is unclear. In this paper, pure chemical reagents were used as raw materials tosimulate the main components of SSD for the solid-phase synthesis of black ceramic pigments doped with various impuritycomponents (CaO, MgO, SiO2 and ZnO). The results show that the doping of MgO can improve the purity of the preparedblack ceramic pigments, whereas CaO, SiO2 and ZnO can turn the pigments become reddish yellow. In the doped samples,ZnO and MgO mainly react with Fe2O3 to form ZnFe2O4 and MgFe2O4. In addition, CaO reacts with Fe2O3 to generateCaFe4O7. The reactions described above can increase the average crystallite size and distort the crystal lattice of the crystalsin the pigment samples. Moreover, SiO2 exists in amorphous form among spinel grains.

LGR5 Modulates Differentiated Phenotypes of Chondrocytes Through PI3K/AKT Signaling Pathway

Wu Xu,Fu Yaoyao,Ma Jing,Li Chenlong,He Aijuan,Zhang Tianyu 한국조직공학과 재생의학회 2024 조직공학과 재생의학 Vol.21 No.5

Background: Tissue engineering is increasingly viewed as a promising avenue for functional cartilage reconstruction. However, chondrocyte dedifferentiation during in vitro culture remains an obstacle for clinical translation of tissue engineered cartilage. Re-differentiated induction have been employed to induce dedifferentiated chondrocytes back to their original phenotype. Regrettably, these strategies have been proven to be only moderately effective. Methods: To explore underlying mechanism, RNA transcriptome sequencing was conducted on primary chondrocytes (P0), dedifferentiated chondrocytes (P5), and redifferentiated chondrocytes (redifferentiation-induction of P5, P5.R). Based on multiple bioinformatics analysis, LGR5 was identified as a target gene. Subsequently, stable cell lines with LGR5 knocking-down and overexpression were established using P0 chondrocytes. The phenotypic changes in P1 and P5 chondrocytes with either LGR5 knockdown or overexpression were assessed to ascertain the potential influence of LGR5 dysregulation on chondrocyte phenotypes. Regulatory mechanism was then investigated using bioinformatic analysis, protein–protein docking, immunofluorescence co-localization and immunoprecipitation. Results: The current study found that dysregulation of LGR5 can significantly impact the dedifferentiated phenotypes of chondrocytes (P5). Upregulation of LGR5 appears to activate the PI3K/AKT signal via increasing the phosphorylation levels of AKT (p-AKT1). Moreover, the increase of p-AKT1 may stabilize β-catenin and enhance the intensity of Wnt/β-catenin signal, and help to restore the dedifferentated phenotype of chondrocytes. Conclusion: LGR5 can modulate the phenotypes of chondrocytes in P5 passage through PI3K/AKT signaling pathway.

Long Non-coding RNA CASC15 Promotes Intrahepatic Cholangiocarcinoma Possibly through Inducing PRDX2/PI3K/AKT Axis

Yuan Zhang,Lufei Zhang,Sinan Lu,Yucheng Xiang,Cheng Zeng,Tianyu He,Yuan Ding,Weilin Wang 대한암학회 2021 Cancer Research and Treatment Vol.53 No.1

Purpose Intrahepatic cholangiocarcinoma (ICC) is one of the most common liver primary tumors but its treatments are limited. Bioinformatics showed that the expression level of long non-coding RNA cancer-associated susceptibility 15 gene (CASC15) is correlated with ICC progression, but its functional mechanism remains unclear. Materials and Methods Tissues from ICC patients, tumor and adjacent tissue, were used for detection of the expression of CASC15. Clinical data were also collected for clinicopathologic and survival analysis. Short interfering RNA and lentiviral short hairpin RNA were used to knock down CASC15 and PRDX2 expression in ICC cell lines, for the analysis of changes of cell function and xenografts. RNA-pulldown and RNA immunoprecipitation assays were used to detect RNA-binding protein, PRDX2. Male nude mice were used for ICC xenografts, and livers were collected after 4 weeks for immunohistochemistry. Results CASC15 is highly expressed in ICC tissues and is related to higher TNM stage. Knockdown of CASC15 in ICC cells reduced cell proliferation, migration, invasiveness and increased apoptosis, and G1/S block. PRDX2 bound to CASC15. Knockdown of CASC15 decreased PRDX2 expression which was rescued by the inhibition of proteasome formation. Downregulation of PRDX2 resulted in G1/S block, reduced ICC cell invasion. Downregulation of CASC15 inhibited phosphoinositide 3-kinase (PI3K)/AKT/c-Myc pathway through downregulating of PRDX2 and overexpressed PRDX2 rescued the block. CASC15 knockout in ICC xenografts suppressed tumor development in vivo, decreased the expression of PRDX2 and Ki67 and inhibited PI3K/AKT pathway. Conclusion CASC15 promotes ICC possibly by targeting PRDX2 via the PI3K/AKT pathway, indicating poor prognosis and high degree of malignancy of ICC.

YAP1 inhibits the senescence of alveolar epithelial cells by targeting Prdx3 to alleviate pulmonary fibrosis

Su Wei,Guo Yingying,Wang Qianqian,Ma Lu,Zhang Qing,Zhang Yuhan,Geng Yiding,Jin Tongzhu,Guo Jiayu,Yang Ruoxuan,Niu Zhihui,Ren Lingxue,Wang Yanjie,Ning Zhiwei,Li Wenyue,He Wenxin,Sun Jian,Li Tianyu,Li Z 생화학분자생물학회 2024 Experimental and molecular medicine Vol.56 No.-

The senescence of alveolar type II (AT2) cells impedes self-repair of the lung epithelium and contributes to lung injury in the setting of idiopathic pulmonary fibrosis (IPF). Yes-associated protein 1 (YAP1) is essential for cell growth and organ development; however, the role of YAP1 in AT2 cells during pulmonary fibrosis is still unclear. YAP1 expression was found to be downregulated in the AT2 cells of PF patients. Deletion of YAP1 in AT2 cells resulted in lung injury, exacerbated extracellular matrix (ECM) deposition, and worsened lung function. In contrast, overexpression of YAP1 in AT2 cells promoted alveolar regeneration, mitigated pulmonary fibrosis, and improved lung function. In addition, overexpression of YAP1 alleviated bleomycin (BLM) -induced senescence of alveolar epithelial cells both in vivo and in vitro. Moreover, YAP1 promoted the expression of peroxiredoxin 3 (Prdx3) by directly interacting with TEAD1. Forced expression of Prdx3 inhibited senescence and improved mitochondrial dysfunction in BLM-treated MLE-12 cells, whereas depletion of Prdx3 partially abrogated the protective effect of YAP1. Furthermore, overexpression of Prdx3 facilitated self-repair of the injured lung and reduced ECM deposition, while silencing Prdx3 attenuated the antifibrotic effect of YAP1. In conclusion, this study demonstrated that YAP1 alleviates lung injury and pulmonary fibrosis by regulating Prdx3 expression to improve mitochondrial dysfunction and block senescence in AT2 cells, revealing a potential novel therapeutic strategy for pulmonary fibrosis.