A high spatial resolution carbon dioxide (CO2) emission map of China is proving to be essential for China's carbon cycle research and carbon reduction strategies given the current low quality of CO2 emission data and the inconsistencies in data quality between different regions. Ten km resolution CO2 emission gridded data has been built up for China based on point emission sources and other supporting data. The predominance of emissions from industrial point sources (84% of total emissions) in China supports the use of bottom-up methodology. The resultant emission map is informative and proved to be more spatially accurate than the EDGAR data. Spatial distribution of CO2 emissions in China is highly unbalanced and has positive spatial autocorrelation. The spatial pattern is mainly influenced by key cities and key regions, i.e., the Jing-Jin-Ji region, the Yangtze River delta region, and the Pearl River delta region. The emission map indicated that the supervision of 1% of total land could enable the management of about 70% of emissions in China.

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The protein Dickkopf-1 (DKK1) is frequently overexpressed at the transcript level in hepatocellular carcinoma (HCC) and promotes metastatic progression through the induction of β-catenin, a Wnt signaling effector. We investigated how DKK1 expression is induced in HCC and found that activation of the epidermal growth factor receptor (EGFR) promoted parallel MEK-ERK and PI3K-Akt pathway signaling that converged to epigenetically stimulate DKK1 transcription. In HCC cell lines stimulated with EGF, EGFR-activated ERK phosphorylated the kinase PKM2 at Ser37, which promoted its nuclear translocation. Also in these cells, EGFR-activated Akt phosphorylated the acetyltransferase p300 at Ser1834. Subsequently, PKM2 and p300 mediated the phosphorylation and acetylation, respectively, of histone H3 at the DKK1 promoter, which synergistically enhanced DKK1 transcription. The mechanism was supported with mutational analyses in cells and in a chemically induced HCC model in rats. The findings suggest that dual inhibition of the MEK and PI3K pathways might suppress the expression of DKK1 and, consequently, tumor metastasis in patients with HCC.

Abnormal lipid metabolism has been commonly observed in various human cancers, including colorectal cancer (CRC). The mitochondrial citrate carrier SLC25A1 (also known as mitochondrial citrate/isocitrate carrier, CIC), has been shown to play an important role in lipid metabolism regulation. Our bioinformatics analysis indicated that SLC25A1 was markedly upregulated in CRC. However, the role of SLC25A1 in the pathogenesis and aberrant lipid metabolism in CRC remain unexplored. Here, we found that SLC25A1 expression was significantly increased in tumor samples of CRC as compared with paired normal samples, which is associated with poor survival in patients with CRC. Knockdown of SLC25A1 significantly inhibited the growth of CRC cells by suppressing the progression of the G1/S cell cycle and inducing cell apoptosis both in vitro and in vivo, whereas SLC25A1 overexpression suppressed the malignant phenotype. Additionally, we demonstrated that SLC25A1 reprogrammed energy metabolism to promote CRC progression through two mechanisms. Under normal conditions, SLC25A1 increased de novo lipid synthesis to promote CRC growth. During metabolic stress, SLC25A1 increased oxidative phosphorylation (OXPHOS) to protect protects CRC cells from energy stress-induced cell apoptosis. Collectively, SLC25A1 plays a pivotal role in the promotion of CRC growth and survival by reprogramming energy metabolism. It could be exploited as a novel diagnostic marker and therapeutic target in CRC.

An interactive human-machine interface (iHMI), a platform for the two-way exchange of information between humans and computers for a variety of symbols and actions, has been the subject of extensive attention. [1,2] Traditionally, rigid sensors and actuators have been used for sensing in iHMI. However, rigid components are often poorly compatible with humans and uncomfortable to wear. Therefore, flexible, stretchable, and deformable actuators have been a focal point in recent studies. Soft actuators play an important role in a variety of fields such as haptic systems, [3,4] soft robots, [5,6] and rehabilitation devices [7,8] due to their low cost, easy deformation, high concealment, and good environmental adaptation. [9,10] Soft actuators can respond to a wide range of stimuli, including electrical [11] and magnetic fields, [12] light [13] and hydraulic pressure, [14] and so on. Based on the types of stimuli, soft actuators can be classified into electrothermal actuators (ETAs), magnetic response actuators, light thermal actuators, electrochemical actuator temperature response actuators, humidity response actuators, and so on. [15][16][17][18] Among them, the ETAs have attracted more interest due to their simple construction and ease of control. As a response to the input electrical signal, the ETAs can generate deformation because of the mismatch in the thermal expansion coefficient (TEC) between different materials/ layers of ETAs when heated. Compared with other electrically responsive actuators, the ETAs can respond to lower voltages rapidly and accurately, indicating these ETAs are more suitable for iHMI. [19] In addition, the highest level of national safety voltage is 6 V, which will not cause harm to human body. Thus, more studies have been carried out focusing on ETAs driven by lower voltage. The key to achieving fast low-voltage-driven ETAs is the acquisition of large, fast temperature increments, which depends on the Joule heat produced by the heating layer/conductive circuit. Thus, designing and fabricating suitable materials for the heating layer/conductive circuit is of significance for lower-voltage-driven ETAs.The conductive composite materials can be obtained by mixing conductive materials (such as carbon nanotubes, [20] silver nanowires, [21] and graphene [22] ) and flexible materials (such as polydimethylsiloxane (PDMS), [23] silicone rubber, and liquid crystal elastomer (LCE) [24] ). Ahn et al. proposed a new deformable ETA utilizing nonhomogeneous electrical conductivity. In the new ETA, carbon nanotubes/silver nanowires/PDMS composites are used as the heating layer, by which the temperature can be increased to up to 120 °C at a driving voltage of 10 V.

High‐mobility group protein A2 (HMGA2) is highly expressed in hepatocellular carcinoma (HCC) cells and contributes to tumor metastasis and poor patient survival. However, the molecular mechanism through which HMGA2 is transcriptionally regulated in HCC cells remains largely unclear. Here, we showed that the expression HMGA2 was upregulated in HCC, and that elevated HMGA2 could promote tumor metastasis. Incubation of HCC cells with epidermal growth factor (EGF) could promote the expression of HMGA2 mRNA and protein. Mechanistic studies suggested that EGF can phosphorylate p300 at Ser1834 residue through the PI3K/Akt signaling pathway in HCC cells. Knockdown of p300 can reverse EGF‐induced HMGA2 expression and histone H3‐K9 acetylation, whereas a phosphorylation‐mimic p300 S1834D mutant can stimulate HMGA2 expression as well as H3‐K9 acetylation in HCC cells. Furthermore, we identified that p300‐mediated H3‐K9 acetylation participates in EGF‐induced HMGA2 expression in HCC. In addition, the levels of H3‐K9 acetylation positively correlated with the expression levels of HMGA2 in a chemically induced HCC model in rats and human HCC specimens.

High expression of programmed death-ligand-1 (PD-L1) in hepatocellular carcinoma (HCC) cells usually inhibits the proliferation and functions of T cells, leading to immune suppression in tumor microenvironment. However, very little has been described regarding the mechanism of PD-L1 overexpression in HCC cells. In the present study, we found epidermal growth factor (EGF) stimulation promoted the expression of PD-L1 mRNA and protein in HCC cells. Inhibition of epidermal growth factor receptor (EGFR) could reverse EGF-induced the expression of PD-L1 mRNA and protein. Subsequently, we also observed that the phosphorylation level of Pyruvate kinase isoform M2 (PKM2) at Ser37 site was also increased in response to EGF stimulation. Expression of a phosphorylation-mimic PKM2 S37D mutant stimulated PD-L1 expression as well as H3-Thr11 phosphorylation in HCC cells, while inhibition of PKM2 significantly blocked EGF-induced PD-L1 expression and H3-Thr11 phosphorylation. Furthermore, mutation of Thr11 of histone H3 into alanine abrogated EGF-induced mRNA and protein expression of PD-L1, Chromatin immunoprecipitation (ChIP) assay also suggested that EGF treatment resulted in enhanced H3-Thr11 phosphorylation at the PD-L1 promoter. In a diethylnitrosamine (DEN)-induced rat model of HCC, we found that the expression of phosphorylated EGFR, PKM2 nuclear expression, H3-Thr11 phosphorylation as well as PD-L1 mRNA and protein was higher in the livers than that in normal rat livers. Taken together, our study suggested that PKM2-dependent histone H3-Thr11 phosphorylation was crucial for EGF-induced PD-L1 expression at transcriptional level in HCC. These findings may provide an alternative target for the treatment of hepatocellular carcinoma.