Failure evolution and instability prediction of fiber-reinforced polymer-confined cement mortar specimens under axial compression.

In geotechnical engineering, a large number of pillars are often left in underground space to support the overlying strata and protect the surface environment. To enhance pillar stability and prevent instability, this study proposes an innovative technology for pillar reinforcement. Specifically, local confinement of the pillar is achieved through fiber-reinforced polymer (FRP) strips, resulting in the formation of a more stable composite structure. In order to validate the effectiveness of this structural approach, acoustic emission characteristics and surface strain field characteristics were monitored during failure processes, while mathematical models were employed to predict specimen instability. The test results revealed that increasing FRP strip confinement width led to heightened activity in acoustic emission events during failure processes, accompanied by a decrease in shear cracks but an increase in tensile cracks. Moreover, ductility was improved and deformation resistance capacity was enhanced within specimens. Notably, initial crack generation occurred within unconfined regions of specimens during failures; however, both length and width as well as overall numbers of cracks significantly decreased due to implementation of FRP strips. Consequently, specimen failure speed was slowed down accordingly. Finally, the instability of the partial FRP-confined cement mortar could be more accurately predicted based on the model of FRP-confined concrete. It was verified by the test results.

MicroRNA-135b regulates apoptosis and chemoresistance in colorectal cancer by targeting large tumor suppressor kinase 2.

Colorectal cancer remains the third most common cause of death from cancer worldwide. MicroRNA emerges as a good area of research for current cancer therapy. Here, we identified miR-135b to be a contributor to anti-apoptosis and chemoresistance in colorectal cancer. We observed high levels of miR-135b in colorectal cancer cell lines and clinical tissues, compared to colorectal epithelium cell line and noncancerous tissues. Furthermore, enforced expression of miR-135b attenuated doxorubicin-induced apoptosis in colorectal cells. (Doxorubicin alone can trigger significant apoptosis). In elucidating the molecular mechanism by which miR-135b participate in the regulation of apoptosis and chemoresistance in colorectal cancer, we discovered that large tumor suppressor kinase 2 (LATS2) is a direct target of miR-135b. The role of miR-135b was confirmed in colorectal tumor xenograft models. The growth of established tumors was suppressed by an inhibition of miR-135b expression and enhanced apoptosis was further assessed by TUNEL assay. Taken together, our results reveal that miR-135b and LATS2 axis may be a novel therapeutic target for colorectal cancer.