Application of a concrete thermal pile in cooling the warming permafrost under climate change

Permafrost degradation caused by climate warming is posing a serious threat to the stability of cast-in-place pile foundations in warm permafrost regions.Ambient cold energy can be effectively utilized by two-phase closed thermosyphons(TPCTs)to cool the permafrost.Therefore,we installed TPCTs in a cast-in-place pile foundation to create a unique structure called a thermal pile,which effectively utilizes the TPCTs to regulate ground temperature.And we conducted a case study and numerical simulation to exhibit the cooling performance,and optimize the structure of the thermal pile.The purpose of this study is to promote the application of thermal piles in unstable permafrost regions.Based on the findings,the thermal pile operated for approximately 53%of the entire year and effectively reduced the deep ground temperature at a rate of at least-0.1℃per year.Additionally,it successfully raised the permafrost table that is 0.35 m shallower than the natural ground level.These characteristics prove highly beneficial in mitigating the adverse effects of permafrost degradation and enhancing infrastructure safety.Expanding the length of the condenser section and the diameter of the TPCT in a suitable manner can effectively enhance the cooling capability of the thermal pile and ensure the long-term mechanical stability of the pile foundation even under climate warming.

Identification of a TGF-β/SMAD/lnc-UTGF positive feedback loop and its role in hepatoma metastasis

Aberrant activation of the TGF-β/SMAD signaling pathway is often observed in hepatocellular carcinoma(HCC).Whether lncRNA regulates the TGF-β/SMAD signaling remains largely unknown.Here,we identified an oncogenic lncRNA that was upregulated in HCC and was transcriptionally induced by TGF-β(named lnc-UTGF,lncRNA upregulated by TGF-β).Upon TGF-βstimulation,SMAD2/3 bound to the lnc-UTGF promoter and activated lnc-UTGF expression.In turn,the TGF-β/SMAD signaling was augmented by overexpressing lnc-UTGF,but was inhibited by silencing lnc-UTGF.Mechanism investigations revealed that lnc-UTGF interacted with the mRNAs of SMAD2 and SMAD4 via complementary base-pairing,resulting in enhanced stability of SMAD2/4 mRNAs.These data suggest a novel TGF-β/SMAD/lnc-UTGF positive feedback circuitry.Subsequent gain-and loss-of-function analyses disclosed that lnc-UTGF promoted the migration and invasion of hepatoma cells,and this effect of lnc-UTGF was attenuated by repressing SMAD2/4 expression or by mutating the SMAD2/4-binding sites in lnc-UTGF.Studies using mouse models further confirmed that in vivo metastasis of hepatoma xenografts was inhibited by silencing lnc-UTGF,but was enhanced by ectopic expression of lncUTGF.The lnc-UTGF level was positively correlated with the SMAD2/4 levels in xenografts.Consistently,we detected an association of lnc-UTGF upregulation with increase of SMAD2,SMAD4,and their metastasis effector SNAIL1 in human HCC.And high lnc-UTGF level was also significantly associated with enhanced metastasis potential,advanced TNM stages,and worse recurrence-free survival.Conclusion:there exists a lnc-UTGF-mediated positive feedback loop of the TGF-βsignaling and its deregulation promotes hepatoma metastasis.These findings may provide a new therapeutic target for HCC metastasis.

Correction: Identification of a TGF-β/SMAD/lnc-UTGF positive feedback loop and its role in hepatoma metastasis

Correction to:Signal Transduction and Targeted Therapy https://doi.org/10.1038/s41392-021-00781-3,published online 17 November 2021 In this article^(1) Jian-Hong Fang should have been denoted as a corresponding author along with Shi-Mei Zhuang,but was inadvertently removed during the production process.The original article has been corrected.