Enhancement of Hydration Activity and Microstructure Analysis of γ-C2S.

This paper investigated the combined effect of chemical activators and nano-SiO2 on the hydration reaction and the microstructure of γ-C2S. The hydration reaction of γ-C2S slurry activated with chemical activators (NaHCO3, NaOH, K2CO3, and KOH at 1 mol/L) was enhanced by 1% nano-SiO2. The hydrate reaction rate was determined by isothermal calorimetry, and the hydrated samples were characterized by XRD, TGA/DTG, SEM-EDS, and 29Si MAS/NMR. The results revealed a substantial enhancement in the hydration activity of γ-C2S due to the presence of the alkaline activator. Furthermore, nano-SiO2 did not alter the composition of γ-C2S hydration products, instead providing nucleation sites for the growth of hydration products. Incorporating nano-SiO2 promoted the formation of C-(R)-S-H gel with a low calcium-to-silica ratio and increased its polymerization levels, resulting in more favorable structures. Among all the activators used in this study, potassium salts had a better activation effect than sodium salts. After 28 days of curing, the degree of hydration reaction in the KC+Si group was 48% and about 37% for the NHC+Si group. Whereas, the KH+Si and NH+Si groups only reached approximately 20% after the same hydration duration.

LncRNA FAM138B inhibits the progression of non-small cell lung cancer through miR-105-5p.

As a type of lung cancer, non-small cell lung cancer (NSCLC) has the characteristics of high mortality and high recurrence rate, which poses a great threat to human life and health. Due to the high risk of surgical treatment and the slow recovery of wounds, non-coding RNAs, especially lncRNAs are used as new potential clinical prognostic markers to prevent and treat cancer in advance. This study aims to explore the role of FAM138B in NSCLC and its possibility as a prognostic biomarker. Real-timequantitative polymerase chain reaction (RT-qPCR) was used to detect the expression and overexpression level of lncRNA FAM138B (FAM138B) in cells and tissues. The CCK-8, Transwell migration and invasion methods were performed to observe the cell transfection.The interaction between FAM138B and miR-105-5p was predicted by the bioinformatics tool starBase v2.0, and verified by the luciferase reporter gene experiment. Kaplan-Meier and Cox regression analyses were used to determine the prognostic significance of FAM138B in NSCLC. The expression of FAM138B is down-regulated in NSCLC cells and tissues. Overexpression of FAM138B can inhibit the expression level of miR-105-5p in NSCLC cells, and the ability of NSCLC cells to proliferate, migrate and invade is downregulated. FAM138B targets miR-105-5p, and there is a negative correlation between FAM138B and miR-105-5p. It is confirmed that FAM138B inhibits the progression of NSCLC by targeting miR-105-5p and can be a potential prognostic biomarker for NSCLC.

Long Non-Coding RNA LINC01929 Facilitates Cell Proliferation and Metastasis as a Competing Endogenous RNA Against MicroRNA miR-1179 in Non-Small Cell Lung Carcinoma.

Introduction: Non-small cell lung carcinoma (NSCLC) constitutes most lung cancers and has a poor prognosis. LncRNAs are a potential repository for the discovery of cancer prognostic markers. This study explored the role of LINC01929 in NSCLC, both the clinical prognostic significance and the mechanism of its influence on cells. Materials and Methods: LINC01929 levels in 143 pairs of NSCLC tissues and non-cancerous tissues were detected by RT-qPCR. Kaplan-Meier curves and multivariate Cox regression assays were generated for evaluating the prognostic values of LINC01929. To evaluate the cellular function, an XTT assay and transwell invasion assays were performed. Results: LINC01929 was up-regulated in NSCLC tissues compared with healthy tissues. A positive correlation was observed between LINC01929 expression level and tumor T (p = 0.002) or N stage (p = 0.010). Patients with higher LINC01929 levels had shorter overall survival (p = 0.009). Compared with other factors, high LINC01929 expression was significantly associated with poor survival in univariate Cox analysis (HR: 2.485, 95%CI: 1.220-5.060, p = 0.012). After multivariate Cox regression assays, LINC01929 was a independent prognostic factor (HR: 3.021, 95%CI: 1.377-6.628, p = 0.006). miR-1179 was a target miRNA of LINC01929. Inhibited expression of LINC01929 significantly reduced the proliferation, migration, and invasion of NSCLC cells by targeting miR-1179. Discussion: This study revealed the upregulation of LINC01929 in NSCLC. This study supports previous studies showing LINC01929 as a potential prognostic factor for NSCLC.

The Synergistic Effect of Ester-Ether Copolymerization Thixo-Tropic Superplasticizer and Nano-Clay on the Buildability of 3D Printable Cementitious Materials.

The shape retention ability of materials deposited layer by layer is called buildability, which is an indispensable performance parameter for successful 3D printable cementitious materials (3DPC). This study investigated the synergistic effect of nano-clay (NC) and thixotropic superplasticizer (TP) on the buildability of 3DPC. The rheological parameters and static yield stress are characterized by the rheology testing, the green strength is measured by a self-made pressure tester, and the fluidity is tested by flow table. Results indicate that NC significantly increases the growth rate of static yield stress and green strength and TP can improve the initial rheological parameters and fluidity, which ensures the initial stiffness and workability of printed materials. The mixture with 7‰ (by mass of cementitious materials) NC and 3‰ TP obtains excellent extrudability and buildability, due to the synergistic effect of NC and TP. Based on the rheology testing and specific printing experiments, a printable window with 1.0 Pa/s~2.0 Pa/s of the rate of static yield stress evolution over time (RST) or 170 mm~200 mm of fluidity is established. This work provides theorical support for the control and evaluation of rheological properties in 3DPC.

Effect of Structural Build-Up on Interlayer Bond Strength of 3D Printed Cement Mortars.

Understanding the relationship between the intrinsic characteristics of materials (such as rheological properties and structural build-up) and printability and controlling intrinsic characteristics of materials through additives to achieve excellent printability is vital in digital concrete additive manufacturing. This paper aims at studying the effects of material's structural build-up on the interlayer bond strength of 3DPC with different time gaps. Structural build-up can indirectly affect the interlayer bond strength by affecting the surface moisture of concrete. Based on the structural build-up of 3DPC, a new parameter, maximum operational time (MOT), is proposed, which can be considered as the limit of time gap to ensure high interlayer bond strength. Slump-retaining polycarboxylate superplasticizer (TS) slightly slows down the physical flocculation rate, but increases the maximum operational time of the cement paste. Nano clay significantly increases the sort-term structural build-up rate and has the function of internal curing and water retaining. Composite with nano-clay and TS can reduce the loss of surface moisture of 3D printed layers, prevent the formation of interface weak layer, and increase the interlayer bond strength between printed layers. This contribution can provide new insight into the design of 3D-printed ink with good extrudability, outstanding buildability, and excellent interlayer bond strength.

HCG18/miR-34a-5p/HMMR axis accelerates the progression of lung adenocarcinoma.

As the most common subtype of lung cancer, lung adenocarcinoma (LUAD) is the frequently occurred cancers in human. Therefore, thorough investigation is necessary for understanding the progression of LUAD. HMMR has functioned as a regulator in some cancers, whereas its biological role still needs to be investigated in LUAD. By bioinformatics analysis, we found that HMMR was highly expressed in LUAD tissues and associated with patients' poor prognosis. Further, qRT-PCR demonstrated that HMMR was up-regulated in LUAD tissues and cells. Loss-of-function assays manifested that HMMR knockdown refrained cell proliferation, migration and invasion and enhanced cell apoptosis in LUAD. Later, HMMR was identified as a target gene of miR-34a-5p, which expressed at a low level in LUAD cell and played an anti-oncogenic role in LUAD. Simultaneously, we discovered that miR-34a-5p could directly bind to HCG18. Subsequent assays revealed that HCG18 mediated HMMR expression by sequestering miR-34a-5p. At last, rescue assays proved the carcinogenic role of HCG18/miR-34a-5p/HMMR axis in LUAD cells growth. Importantly, HCG18 was found to facilitate tumor growth in LUAD. Conclusively, HCG18 acted an oncogene in LUAD and enhanced LUAD progression by targeting miR-34a-5p/HMMR axis.