Achieving larger electromagnetic enhancement using a nanogap between neighboring metallic nanostructures has been long pursued for boosting light–matter interactions. However, the quantitative probing of this enhancement is hindered by the lack of a reliable experimental method for measuring the local fields within a subnanometer gap. Here, we use layered MoS2 as a two-dimensional atomic crystal probe in nanoparticle-on-mirror nanoantennas to measure the plasmonic enhancement in the gap by quantitative surface-enhanced Raman scattering. Our designs ensure that the probe filled in the gap has a well-defined lattice orientation and thickness, enabling independent extraction of the anisotropic field enhancements. We find that the field enhancement can be safely described by pure classical electromagnetic theory when the gap distance is no <1.24 nm. For a 0.62 nm gap, the probable emergence of quantum mechanical effects renders an average electric field enhancement of 114-fold, 38.4% lower than classical predictions.

The fact that metallic nanostructures are an excellent light receiver and transmitter connects the underlying principles of two widely applied optical processes: surface-enhanced Raman scattering (SERS) and surface-enhanced fluorescence (SEF). A comparative study of SERS and SEF can eliminate the typical unknown quantities of the system and reveal important parameters that cannot be accessed by conventional techniques. Here, we use this simultaneous SERS and SEF technique in a monolayer MoSe 2 coupled plasmonic nanocavity. After optimizing the spatial and the spectral overlaps between excitonic and plasmonic resonances, the SERS and SEF enhancement factors can exceed 10 7 and 6000, respectively, at the same time on the same nanocube. The comparison of the SERS and SEF enhancements allows the estimation of the ultrafast total decay rate of the bright exciton in monolayer MoSe 2 in the nanocavity down to tens of femtoseconds, which is otherwise hard to realize using time-resolved techniques.

BackgroundHemorrhagic fever with renal syndrome (HFRS) is caused by different hantaviruses within the Bunyaviridae family. HFRS is a fulminant, infectious disease that occurs worldwide and is endemic in all 31 provinces of China. Since the first HFRS case in Hubei Province was reported in 1957, the disease has spread across the province and Hubei has become one of the seriously affected areas in China with the greatest number of reported HFRS cases in the 1980's. However, the epidemic characteristics of HFRS in Hubei are still not entirely clear and long-term, systematic investigations of this epidemic area have been very limited.MethodsThe spatiotemporal distribution of HFRS was investigated using data spanning the years 1980 to 2009. The annual HFRS incidence, fatality rate and seasonal incidence between 1980 and 2009 were calculated and plotted. GIS-based spatial analyses were conducted to detect the spatial distribution and seasonal pattern of HFRS. A spatial statistical analysis, using Kulldorff's spatial scan statistic, was performed to identify clustering of HFRS.ResultsA total of 104,467 HFRS cases were reported in Hubei Province between 1980 and 2009. Incidence of and mortality due to HFRS declined after the outbreak in 1980s and HFRS cases have been sporadic in recent years. The locations and scale of disease clusters have changed during the three decades. The seasonal epidemic pattern of HFRS was characterized by the shift from the unimodal type (autumn/winter peak) to the bimodal type.ConclusionsSocioeconomic development has great influence on the transmission of hantaviruses to humans and new epidemic characteristics have emerged in Hubei Province. It is necessary to reinforce preventative measures against HFRS according to the newly-presented seasonal variation and to intensify these efforts especially in the urban areas of Hubei Province.

Achieving strong coupling between emitters and photons in cavities holds an important position in the light-matter interaction due to the enabled applications such as polariton lasing, all-optical switches, and quantum...

Bladder cancer-associated protein (BLCAP) gene is a highly conserved gene with tumor-suppressor function in different carcinomas. It is also a novel ADAR-mediated editing substrate undergoes multiple A-to-I RNA editing events. Although the anti-tumorigenic role of BLCAP has been examined in preliminarily studies, the relationship between BLCAP function and A-to-I RNA editing in cervical carcinogenesis still require further exploration. Herein, we analyzed the coding sequence of BLCAP transcripts in 35 paired cervical cancer samples using high-throughput sequencing. Of note, editing levels of three novel editing sites were statistically different between cancerous and adjacent cervical tissues, and editing of these three sites was closely correlated. Moreover, two editing sites of BLCAP coding region were mapped-in the key YXXQ motif which can bind to SH2 domain of STAT3. Further studies revealed that BLCAP interacted with signal transducer and activator of transcription 3 (STAT3) and inhibited its phosphorylation, while A-to-I RNA editing of BLCAP lost the inhibition to STAT3 activation in cervical cancer cell lines. Our findings reveal that A-to-I RNA editing events alter the genetically coded amino acid in BLCAP YXXQ motif, which drive the progression of cervical carcinogenesis through regulating STAT3 signaling pathway.

The miniaturization in energy devices and their critical needs for heat dissipation have facilitated research on exceptional thermal properties of novel low-dimensional materials. Current studies demonstrated the main challenge for solving thermal transport issues is the large thermal contact resistance across these low-dimensional material interfaces when they are either bundled together or supported by a substrate. A clear understanding of thermal transport across these atomic interfaces through experimental characterization or numerical simulation is important, but nontrivial. Due to instrumentation limit, only a few thermal characterization methods are applicable. Accordingly, many studies have been conducted by theoretical analysis and molecular dynamics to understand the physical process during this ultra-fast and ultra-small thermal transport. In this review, both experimental work and molecular dynamics studies on atomic-scale thermal contact resistance of low-dimensional materials (from zero-to two-dimensional) are reviewed. Challenges as well as opportunities in the study of thermal transport in atomic-layer structures are outlined. Considering the remarkable complexity of physical/chemical conditions, there is still a large room in understanding fundamentals of energy coupling across these atomic-layer interfaces.

BackgroundChronic hepatitis C virus (HCV) infection is an important cause of hepatocellular carcinoma (HCC). Epithelial to mesenchymal transition (EMT) is a key process associated with tumor metastasis and poor prognosis. HCV infection, HCV core and NS5A protein could induce EMT process, but the role of NS4B on EMT remains poorly understood.MethodsWe overexpressed HCV NS4B protein in HepG2 cells or Huh7.5.1 cells infected by HCVcc, the E-cadherin expression, N-cadherin expression and the EMT-associated transcriptional factor Snail were determined. The migration and invasion capabilities of the transfected cells were evaluated using wound-healing assay. Additionally, we used Snail siRNA interference to confirm the relation of HCV NS4B and Snail on EMT promotion.ResultsHCV NS4B increased the expression of EMT related markers and promoted cell migration and invasion. Snail knock-down almost completely eliminated the function of NS4B protein in EMT changes and reversed cell migration capacity to lower level. HCV NS4B protein could reduce the expression of Scribble and Hippo signal pathway were subsequently inactivated, resulting in the activation of PI3K/AKT pathway, which may be the reason for the up-regulation of Snail.ConclusionsThis study demonstrates that HCV NS4B protein induces EMT progression via the upregulation of Snail in HCC, which may be a novel underlying mechanism for HCV-associated HCC development, invasion and metastasis.

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