Search

Plasmonic hot spots located between metallic dimer nanostructures have been utilized comprehensively to achieve efficient light emission. However, different from the enhancement occurred in the plasmonic hot spot, the investigation of light emission off the hot spot on submicron scale remains challenge. In this work, we have constructed a plasmonic nanowire dimer (NWD) system to brighten the light emission of the surface defects of silicon off the hot spot on the submicron scale. The NWD can trap light through plasmonic gap, then, the excited emitter on the submicron scale can radiate light efficiently by coupling with the dipole gap plasmonic mode. Furthermore, the coupling of dipole plasmonic mode with the emitters can be tuned by changing the gap size, and then photoluminescence emission was drastically enhanced up to 126 folds. Theoretical simulations reveal the photoluminescence enhancement arises from the combination of the NWD’s high radiation efficiency, Purcell enhancement, efficient redirection of the emitted photoluminescence and the excitation enhancement. In this study, the photoluminescence signal can be effectively enhanced by placing nano-antenna patch on the detected low-quantum-efficiency emitters, which may open up a pathway toward controlling plasmonic gap mode enhanced light emission off the hot spot on submicron scale.

The effective reservoir sediment regulation measure is extremely significant for the sedimentladen river. It should not only extend the reservoir life, but also pose favorable conditions for the management of the river-reservoir system. Especially, the remarkable changes in the hydrological processes challenge to the system in some respects, like flood control, rive training, ecological environment improvement and so on. This paper gives a brief discussion on the representative existing problems in Ningxia-Inner Mongolia reach of the Yellow River. The water-sediment parameters and artificial regulation factors are then summed through a comprehensive literature review. Then we investigate the response to the different scales of floods in the Inner Mongolia reach through a three-dimensional model, in which the simulation region is from Bayangaole gauging station to Toudaoguai gauging station. With respect to the riverbed deformation, it is effective to control the relationship between the incoming water and sediment to restrain the shrinkage of the main channel; and surely that there exists a nonlinear relationship between channel scouring and incoming water-sediment conditions. Through data analysis and simulation results, the response characteristics of different watersediment regulation boundary conditions can be obtained, such as the ratio between sediment concentration and discharge, the discharge duration and the discharge, which is favorable to further water-sediment regulation of the reservoir and the management in Ningxia-Inner Mongolia reach of the Yellow River.

Abstract Background Hepatocellular carcinoma (HCC) presents one of the major health threats in China today. A better understanding of the molecular genetics underlying malignant transformation of hepatocytes is critical to success in the battle against this disease. The methylation state of C5 of the cytosine in the CpG di-nucleotide that is enriched within or near the promoter region of over 50 % of the polymerase II genes has a drastic effect on transcription of these genes. Changes in the methylation profile of the promoters represent an alternative to genetic lesions as causative factors for the tumor-specific aberrant expression of the genes. Methods We have used the methylation specific PCR method in conjunction with DNA sequencing to assess the methylation state of the promoter CpG islands of twenty genes. Aberrant expression of these genes have been attributed to the abnormal methylation profile of the corresponding promoter CpG islands in human tumors. Results While the following sixteen genes remained the unmethylated in all tumor and normal tissues: CDH1, APAF1, hMLH1, BRCA1, hTERC, VHL, RARβ, TIMP3, DAPK1, SURVIVIN, p14ARF, RB1, p15INK4b, APC, RASSF1c and PTEN, varying degrees of tumor specific hypermethylation were associated with the p16INK4a , RASSF1a, CASP8 and CDH13 genes. For instance, the p16INK4a was highly methylated in HCC (17/29, 58.6%) and less significantly methylated in non-cancerous tissue (4/29. 13.79%). The RASSF1a was fully methylated in all tumor tissues (29/29, 100%), and less frequently methylated in corresponding non-cancerous tissue (24/29, 82.75%). Conclusions Furthermore, co-existence of methylated with unmethylated DNA in some cases suggested that both genetic and epigenetic (CpG methylation) mechanisms may act in concert to inactivate the p16INK4a and RASSF1a in HCC. Finally, we found a significant association of cirrhosis with hypermethylation of the p16INK4a and hypomethylation of the CDH13 genes. For the first time, the survey was carried out on such an extent that it would not only provide new insights into the molecular mechanisms underscoring the aberrant expression of the genes in this study in HCC, but also offer essential information required for a good methylation-based diagnosis of HCC.

The issues of health assessment and lifespan prediction have always been prominent challenges in the large‐scale application of lithium‐ion batteries (LIBs). This paper reviews the multiscale modeling techniques and their applications in battery health analysis, including atomic scale computational chemistry, particle scale reaction simulations, electrode scale structural models, macroscale electrochemical models, and data‐driven models at the system level. Multiscale modeling offers a profound insight into material behavior and the aging process of batteries, thereby providing a valuable reference for both estimation and management strategies of battery state of health. To extend the battery lifespan, the utilization of artificial intelligence for material discovery and manufacturing process optimization, the implementation of end‐cloud collaborative battery management systems, and the design of a multiscale simulation integration platform are considered. A management framework aimed at extending battery life is further proposed. This framework offers a promising roadmap for addressing health analysis challenges in LIBs, ultimately leading to more reliable, efficient, and durable solutions for next‐generation batteries. [ABSTRACT FROM AUTHOR]

The activation of hepatic stellate cells (HSCs) is the main cause of liver fibrogenesis in response to different etiologies of chronic liver injuries. HSCs are heterogeneous, but the lack of specific markers to distinguish different HSC subset hinders the development of targeted therapy for liver fibrosis. In this study, we aim to reveal new HSC subsets by cell fate tracking. We constructed a novel ReelinCreERT2 transgenic mouse model to track the fate of cells expressing Reelin and their progeny (Reelin+ cells). And we investigated the property of Reelin+ cells, such as differentiation and proliferation, in hepatotoxic (carbon tetrachloride; CCl4) or cholestatic (bile duct ligation; BDL) liver injury models by immunohistochemistry. Our study revealed that Reelin+ cells were a new HSC subset. In terms of activation, migration, and proliferation, Reelin+ HSCs displayed different properties from Desmin+ HSCs (total HSCs) in cholestatic liver injury model but shared similar properties to total HSCs in hepatotoxic liver injury model. Besides, we did not find evidence that Reelin+ HSCs transdifferentiated into hepatocytes or cholangiocytes through mesenchymal‐epithelial transition (MET). In this study, our genetic cell fate tracking data reveal that ReelinCreERT2‐labelled cells are a new HSC subset, which provides new insights into targeted therapy for liver fibrosis. [ABSTRACT FROM AUTHOR]