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As shield tunnels increase, managing shield muck strains construction and the environment. To mitigate this problem, shield muck replaced bentonite in silty clay to improve synchronous grouting slurry. Initially, the physical attributes and microstructural composition of shield muck were obtained, alongside an analysis of the effects of the muck content, particle size, and general influencing factors on the slurry properties through standardized tests and regression models. Subsequently, leveraging three-dimensional response surface methodology, admixture interactions and multiple factor impacts on the slurry were explored. Finally, utilizing the SQP optimization technique, an optimal slurry blend ratio tailored for actual project needs was derived for improved muck slurry. The findings reveal with the decreasing bleeding rates as the muck content rises, the particle size diminishes. An inverse relationship exists between the muck content and slurry fluidity. At soil–binder ratios below 0.6, a decrease in the soil–binder ratio intensifies the influence of the water–binder ratio on the slurry density, bleeding rate, and setting time. The fly flash–cement ratio inversely correlates with the slurry bleeding rate, while the ratio greater than 0.6 is positively correlated. For muck particle sizes under 0.2 mm, the fly flash–cement ratio inversely impacts the density, while over 0.2 mm, it correlates positively. The optimal proportion for silty clay stratum synchronous grouting slurry, substituting muck for bentonite, includes a water–binder ratio of 0.559, binder–sand ratio of 0.684, fly flash–cement ratio of 2.080, soil–binder ratio of 0.253, particle size under 0.075 mm, and water-reducing admixture of 0.06. [ABSTRACT FROM AUTHOR]

The effects of long non‐coding RNA TDRG1 have been established in several tumors; however, its roles in colorectal cancer (CRC) progression are never been found. Here, we found that TDRG1 level was upregulated in CRC cells compared to that in normal colon epithelial cells. Additionally, TDRG1 level was remarkably upregulated in 3D non‐adherent spheres derived from the parental CRC cells. Further in vitro and in vivo revealed that TDRG1 knockdown suppressed the stemness of CRC cells. What's more, combined with bioinformatics analysis, luciferase reporter and RNA pull down experiments showed that TDRG1 could bind to miR‐873‐5p, downregulated its level and thus increase the expression of PRKAR2. Finally, it was shown that TDRG1 functioned through the miR‐873‐5p/PRKAR2 axis. This study demonstrated a novel TDRG1/miR‐873‐5p/PRKAR2 signaling in CRC progression. [ABSTRACT FROM AUTHOR]

LIF maintains self-renewal growth in mouse embryonic stem cells (mESC) by activating STAT3, which translocates into nucleus for pluripotent gene induction. However, the ERK signaling pathway activated by LIF at large counteract with pluripotent gene induction during self-renewal growth. Here, it is reported that in mESC STAT3 undergoes multivesicular endosomes (MVEs) translocation and subsequent secretion, LIF-activated STAT3 is acetylated on K177/180 and phosphorylated on Y293 residues within the N-terminal coiled-coil domain, which is responsible for the interaction between STAT3 and Secl5b, an exocyst complex component 6B (EXOC6B). STAT3 translocation into MVEs resulted in the downregulation of T202/Y204-ERK1/2 phosphorylation and up-regulation of S9-GSK3β phosphorylation for maintaining mESC self-renewal growth. STAT3 with K177R/K180R or Y293F substitution fails to execute MVEs translocation and Secl5b-dependent secretion. Mice expressing K177RK180R substitution (STAT3 mut/mut ) are partially embryonic lethal. In STAT3 mut/mut embryos, gene expressions related to hematological system function changed significantly and those living ones carry a series of abnormalities in the hematopoietic system. Furthermore, mice with Secl5b knockout exhibit embryonic lethality. Thus, Secl5b mediated STAT3 MVEs translocation regulates the balance of ERK and GSK3β signaling pathways and maintain mESC self-renewal growth, which is involved in regulating the stability of hematopoietic system., (© 2024 The Author(s). Advanced Science published by Wiley‐VCH GmbH.)