Regulation of Hot Electrons Transport Achieved through Controlled Electron-Phonon Coupling in Metallic Heterostructures.

The electron-phonon (e-ph) interactions are pivotal in shaping the electrical and thermal properties, and in particular, determining the carrier dynamics and transport behaviors in optoelectronic devices. By employing pump-probe spectroscopy and ultrafast microscopy, the consequential role of e-ph coupling strength in the spatiotemporal evolution of hot electrons is elucidated. Thermal transport across the metallic interface is controlled to regulate effective e-ph coupling factor Geff in Au and Au/Cr heterostructure, and their impact on nonequilibrium transport of hot electrons is examined. Via the modulation of buried Cr thickness, a strong correlation between Geff and the diffusive behavior of hot electrons is found. By enhancing Geff through the regulation of thermal transport across interface, there is a significant reduction in e-ph thermalization time, the maximum diffusion length of hot electrons, and lattice heated area which are extracted from the spatiotemporal evolution profiles. Therefore, the increased Geff significantly weakens the diffusion of hot electrons and promotes heat relaxation of electron subsystems in both time and space. These insights propose a robust framework for spatiotemporal investigations of G impact on hot electron diffusion, underscoring its significance in the rational design of advanced optoelectronic devices with high efficiency.

Prediction of esophageal cancer risk based on genetic variants and environmental risk factors in Chinese population.

BACKGROUND: Results regarding whether it is essential to incorporate genetic variants into risk prediction models for esophageal cancer (EC) are inconsistent due to the different genetic backgrounds of the populations studied. We aimed to identify single-nucleotide polymorphisms (SNPs) associated with EC among the Chinese population and to evaluate the performance of genetic and non-genetic factors in a risk model for developing EC. METHODS: A meta-analysis was performed to systematically identify potential SNPs, which were further verified by a case-control study. Three risk models were developed: a genetic model with weighted genetic risk score (wGRS) based on promising SNPs, a non-genetic model with environmental risk factors, and a combined model including both genetic and non-genetic factors. The discrimination ability of the models was compared using the area under the receiver operating characteristic curve (AUC) and the net reclassification index (NRI). The Akaike information criterion (AIC) and Bayesian information criterion (BIC) were used to assess the goodness-of-fit of the models. RESULTS: Five promising SNPs were ultimately utilized to calculate the wGRS. Individuals in the highest quartile of the wGRS had a 4.93-fold (95% confidence interval [CI]: 2.59 to 9.38) increased risk of EC compared with those in the lowest quartile. The genetic or non-genetic model identified EC patients with AUCs ranging from 0.618 to 0.650. The combined model had an AUC of 0.707 (95% CI: 0.669 to 0.743) and was the best-fitting model (AIC = 750.55, BIC = 759.34). The NRI improved when the wGRS was added to the risk model with non-genetic factors only (NRI = 0.082, P = 0.037). CONCLUSIONS: Among the three risk models for EC, the combined model showed optimal predictive performance and can help to identify individuals at risk of EC for tailored preventive measures.

Visible light to the second near-infrared light-harvesting donor-acceptor1-donor-acceptor2-type terpolymers for boosted photocatalytic hydrogen evolution via dual-sulfone-acceptor engineering.

Developing visible to near-infrared light-absorbing conjugated polymer photocatalysts is crucial for enhancing solar energy utilization efficiency, as most conjugated organic polymers only absorb light in the visible range. In this work, we firstly developed a novel thiophene S,S-dioxide (TDO) monomer with the stronger electron-withdrawing character, and then prepared a series of donor-acceptor1-donor-acceptor2-type (D-A1-D-A2-type) conjugated terpolymers (THTDB-1-THTDB-5) by statistically adjusting the molar ratio of two sulfone-based acceptor monomers, dibenzothiophene-S,S-dioxide (BTDO, A1) and TDO (A2). These terpolymers demonstrate a gradually expanding absorption range from visible light to the second near-infrared (Vis-to-NIR-II) region with the gradual increase of the TDO contents in the polymer skeleton, showcasing excellent absorption properties and efficient light-capturing capabilities. The optimized D-A1-D-A2 polymer photocatalyst THTDB-4 exhibits a high hydrogen evolution rate of 21.27 mmol g-1 h-1 under visible light without any co-catalyst. The dual-sulfone-acceptor engineering offers a viable approach for developing efficient the longer Vis-to-NIR-II light-harvesting polymer photocatalysts.

Cell mechanics regulate the migration and invasion of hepatocellular carcinoma cells via JNK signaling.

Hepatocellular carcinoma (HCC) cells, especially those with metastatic competence, show reduced stiffness compared to the non-malignant counterparts. However, it is still unclear whether and how the mechanics of HCC cells influence their migration and invasion. This study reports that HCC cells with enhanced motility show reduced mechanical stiffness and cytoskeleton, suggesting the inverse correlation between cellular stiffness and motility. Through pharmacologic and genetic approaches, inhibiting actomyosin activity reduces HCC cellular stiffness but promotes their migration and invasion, while activating it increases cell stiffness but impairs cell motility. Actomyosin regulates cell motility through the influence on cellular stiffness. Mechanistically, weakening/strengthening cells inhibits/promotes c-Jun N terminal kinase (JNK) phosphorylation, activation/inhibition of which rescues the effects of cell mechanics on their migration and invasion. Further, HCC cancer stem cells (CSCs) exhibit higher motility but lower stiffness than control cells. Increasing CSC stiffness weakens migration and invasion through the activation of JNK signaling. In conclusion, our findings unveil a new regulatory role of actomyosin-mediated cellular mechanics in tumor cell motility and present new evidence to support that tumor cell softening may be one driving force for HCC metastasis. STATEMENT OF SIGNIFICANCE: Tumor cells progressively become softened during metastasis and low cell stiffness is associated with high metastatic potential. However, it remains unclear whether tumor cell softening is a by-product of or a driving force for tumor progression. This work reports that the stiffness of hepatocellular carcinoma cells is linked to their migration and invasion. Importantly, tumor cell softening promotes migration and invasion, while cell stiffening impairs the mobility. Weakening/strengthening cells inhibits/promotes JNK phosphorylation, activation/inhibition of which rescues the effects of cell mechanics on their migration and invasion ability. Further, stiffening liver cancer stem cells attenuates their motility through activating JNK signaling. In summary, our study uncovers a previously unappreciated role of tumor cell mechanics in migration and invasion and implicates the therapeutic potential of cell mechanics in the mechanotargeting of metastasis.

Circulating tumor cells with metastasis-initiating competence survive fluid shear stress during hematogenous dissemination through CXCR4-PI3K/AKT signaling.

To seed lethal secondary lesions, circulating tumor cells (CTCs) must survive all rate-limiting factors during hematogenous dissemination, including fluid shear stress (FSS) that poses a grand challenge to their survival. We thus hypothesized that CTCs with the ability to survive FSS in vasculature might hold metastasis-initiating competence. This study reported that FSS of physiologic magnitude selected a small subpopulation of suspended tumor cells in vitro with the traits of metastasis-initiating cells, including stemness, migration/invasion potential, cellular plasticity, and biophysical properties. These shear-selected cells generated local and metastatic tumors at the primary and distal sites efficiently, implicating their metastasis competence. Mechanistically, FSS activated the mechanosensitive protein CXCR4 and the downstream PI3K/AKT signaling, which were essential in shear-mediated selection of metastasis-competent CTCs. In summary, these findings conclude that CTCs with metastasis-initiating competence survive FSS during hematogenous dissemination through CXCR4-PI3K/AKT signaling, which may provide new therapeutic targets for the early prevention of tumor metastasis.