Identification of CD8+ T cell infiltration-related genes and their prognostic values in cervical cancer.

Cervical cancer is a female-specific cancer with relatively high morbidity and mortality. As known to all, immune cell infiltrations in the cancer microenvironment are closely related to the cancer diagnosis and prognosis. Here we revealed that the CD8+ T cell infiltration was significantly upregulated in cervical cancer versus normal cervix uteri samples. Through univariate and multivariate cox analyses, we discovered that the CD8+ T cell infiltration was the only independent beneficial factor for the prognosis of cervical cancer. To explore the genes associated with the CD8+ T cell infiltration in cervical cancer, we performed the WGCNA analysis on the differentially expressed genes (DEGs) of cervical cancer versus normal cervix uteri tissues. As a result, 231 DEGs were found to be associated with CD8+ T cell infiltration in cervical cancer. Subsequently, with the Cytoscape analysis, we identified 105 hub genes out of the 231 DEGs. To further explore the genes that might be responsible for the prognosis of cervical cancer, we performed a univariate cox analysis followed by a LASSO assay on the 105 hub genes and located four genes (IGSF6, TLR10, FCRL3, and IFI30) finally. The four genes could be applied to the prediction of the prognosis of cervical cancer, and relatively higher expression of these four genes predicted a better prognosis. These findings contributed to our understanding of the prognostic values of CD8+ T cell infiltration and its associated genes in cervical cancer and thus might benefit future immune-related therapies.

Hypoxia is fine-tuned by Hif-1α and regulates mesendoderm differentiation through the Wnt/ß-Catenin pathway.

BACKGROUND: Hypoxia naturally happens in embryogenesis and thus serves as an important environmental factor affecting embryo development. Hif-1α, an essential hypoxia response factor, was mostly considered to mediate or synergistically regulate the effect of hypoxia on stem cells. However, the function and relationship of hypoxia and Hif-1α in regulating mesendoderm differentiation remains controversial. RESULTS: We here discovered that hypoxia dramatically suppressed the mesendoderm differentiation and promoted the ectoderm differentiation of mouse embryonic stem cells (mESCs). However, hypoxia treatment after mesendoderm was established promoted the downstream differentiation of mesendoderm-derived lineages. These effects of hypoxia were mediated by the repression of the Wnt/ß-Catenin pathway and the Wnt/ß-Catenin pathway was at least partially regulated by the Akt/Gsk3ß axis. Blocking the Wnt/ß-Catenin pathway under normoxia using IWP2 mimicked the effects of hypoxia while activating the Wnt/ß-Catenin pathway with CHIR99021 fully rescued the mesendoderm differentiation suppression caused by hypoxia. Unexpectedly, Hif-1α overexpression, in contrast to hypoxia, promoted mesendoderm differentiation and suppressed ectoderm differentiation. Knockdown of Hif-1α under normoxia and hypoxia both inhibited the mesendoderm differentiation. Moreover, hypoxia even suppressed the mesendoderm differentiation of Hif-1α knockdown mESCs, further implying that the effects of hypoxia on the mesendoderm differentiation were Hif-1α independent. Consistently, the Wnt/ß-Catenin pathway was enhanced by Hif-1α overexpression and inhibited by Hif-1α knockdown. As shown by RNA-seq, unlike hypoxia, the effect of Hif-1α was relatively mild and selectively regulated part of hypoxia response genes, which fine-tuned the effect of hypoxia on mESC differentiation. CONCLUSIONS: This study revealed that hypoxia is fine-tuned by Hif-1α and regulates the mesendoderm and ectoderm differentiation by manipulating the Wnt/ß-Catenin pathway, which contributed to the understanding of hypoxia-mediated regulation of development.

Mutagenesis and Resistance Development of Bacteria Challenged by Silver Nanoparticles.

Because of their extremely broad spectrum and strong biocidal power, nanoparticles of metals, especially silver (AgNPs), have been widely applied as effective antimicrobial agents against bacteria, fungi, and so on. However, the mutagenic effects of AgNPs and resistance mechanisms of target cells remain controversial. In this study, we discover that AgNPs do not speed up resistance mutation generation by accelerating genome-wide mutation rate of the target bacterium Escherichia coli. AgNPs-treated bacteria also show decreased expression in quorum sensing (QS), one of the major mechanisms leading to population-level drug resistance in microbes. Nonetheless, these nanomaterials are not immune to resistance development by bacteria. Gene expression analysis, experimental evolution in response to sublethal or bactericidal AgNPs treatments, and gene editing reveal that bacteria acquire resistance mainly through two-component regulatory systems, especially those involved in metal detoxification, osmoregulation, and energy metabolism. Although these findings imply low mutagenic risks of nanomaterial-based antimicrobial agents, they also highlight the capacity for bacteria to evolve resistance.

Theoretical Study on the High HER/OER Electrocatalytic Activities of 2D GeSi, SnSi, and SnGe Monolayers and Further Improvement by Imposing Biaxial Strain or Doping Heteroatoms.

Under the DFT calculations, two-dimensional (2D) GeSi, SnSi, and SnGe monolayers, considered as the structural analogues of famous graphene, are confirmed to be dynamically, mechanically and thermodynamically stable, and all of them can also possess good conductivity. Furthermore, we systematically investigate their electrocatalytic activities in overall water splitting. The SnSi monolayer can show good HER catalytic activity, while the SnGe monolayer can display remarkable OER catalytic activity. In particular, the GeSi monolayer can even exhibit excellent bifunctional HER/OER electrocatalytic activities. In addition, applying the biaxial strain or doping heteroatoms (especially P atom) can be regarded as the effective strategies to further improve the HER activities of these three 2D monolayers. The doped GeSi and SnSi systems can usually exhibit higher HER activity than the doped SnGe systems. The correlative catalytic mechanisms are also analyzed. This work could open up a new avenue for the development of non-noble-metal-based HER/OER electrocatalysts.

TNF Signaling Acts Downstream of MiR-322/-503 in Regulating DM1 Myogenesis.

Myotonic dystrophy type 1 (DM1) is caused by the expanded CUG repeats and usually displays defective myogenesis. Although we previously reported that ectopic miR-322/-503 expression improved myogenesis in DM1 by targeting the toxic RNA, the underlying pathways regulating myogenesis that were aberrantly altered in DM1 and rescued by miR-322/-503 were still unknown. Here, we constructed DM1 and miR-322/-503 overexpressing DM1 myoblast models, which were subjected to in vitro myoblast differentiation along with their corresponding controls. Agreeing with previous findings, DM1 myoblast showed remarkable myogenesis defects, while miR-322/-503 overexpression successfully rescued the defects. By RNA sequencing, we noticed that Tumor necrosis factor (TNF) signaling was the only pathway that was significantly and oppositely altered in these two experimental sets, with it upregulated in DM1 and inhibited by miR-322/-503 overexpression. Consistently, hyperactivity of TNF signaling was detected in two DM1 mouse models. Blocking TNF signaling significantly rescued the myogenesis defects in DM1. On the contrary, TNF-α treatment abolished the rescue effect of miR-322/-503 on DM1 myogenesis. Taking together, these results implied that TNF signaling mediated the myogenesis defects in DM1 and might act downstream of miR-322/-503 in regulating the myogenesis in DM1. Moreover, the inhibition of TNF signaling benefiting myogenesis in DM1 provided us with a novel therapeutic strategy for DM1.

Observation and control of pseudospin switching in a finite-width topological photonic crystal.

Finite-size effect plays a significant role in topology photonics not to mention in reality all experimental setups are in finite-size. A photonic bandgap is opened in the topological edge state dispersion if a topological photonic crystal with finite width is considered, and the bandgap size relies on the finite-size effect. Pseudospin-preserving and pseudospin-flipping processes can be realized when a selectively switch of the pseudospin of edge states are customized by our designs. Our microwave experiments also successfully demonstrate pseudospin switch-on and -off behaviors in a finite-width photonic crystal. By combining photonic crystals with finite widths, a multi-tunneling proposal of topological photonic crystals can also be achieved. Our study of the finite-size effect will provide new approaches and thoughts to improve the development of topological photonic devices in the future.

Phonon Thermal Transport in Silicene/Graphene Heterobilayer Nanostructures: Effect of Interlayer Interactions.

Heterostructuring, as a promising route to optimize the physical properties of 2D materials, has attracted great attention from the academic community. In this paper, we investigated the room-temperature in-plane and cross-plane phonon thermal transport in silicene/graphene van der Waals (vdW) heterostructures using molecular dynamics simulations. Our simulation results demonstrated that heat current along the graphene layer is remarkably larger than that along the silicene layer, which suggests that graphene dominates the thermal transport in silicene/graphene heterostructures. The in-plane phonon thermal conductivity of the silicene/graphene heterostructures could be a compromise between monolayer graphene and monolayer silicene. Heterostructuring can remarkably reduce the in-plane thermal conductivity of the graphene layer but increase the in-plane thermal conductivity of the silicene layer in heterobilayers compared with the freestanding monolayer counterparts because of their different structures. We also simulated the interlayer interaction strength effect on the in-plane phonon thermal conductivity and cross-plane interfacial thermal resistance of silicene/graphene heterostructures. Total in-plane phonon thermal conductivity and interfacial thermal resistance both decrease with the increase in the interlayer interaction strength in the silicene/graphene heterobilayers. In addition, the calculated interfacial thermal resistance shows the effect of the thermal transport direction across the interface. This study provides a useful reference for the thermal management regulation of 2D vdW heterostructures.

An integrated analysis of single-cell and bulk transcriptomics reveals EFNA1 as a novel prognostic biomarker for cervical cancer.

Cervical cancer is a serious threat to women's health and lives worldwide. The recovery and survival of cervical cancer can be improved by customizing therapy strategies based on individual-specific gene expression patterns. EFNA1 was reported to be dysregulated in many cancers and associated with their overall survivals, but its prognostic value in cervical cancer is still unclear. In this study, we performed analyses on the single-cell and bulk RNA sequencing data to study the role of EFNA1 in cervical cancer. EFNA1 was found to be significantly upregulated in cervical cancer tissue, especially the cancer cell subgroup within tumors, which was verified by immunohistochemistry. Through Cox regressions, we found that high EFNA1 expression is an independent risk factor for cervical cancer. Nomogram analysis indicated that EFNA1 could be a predicting factor for the survival probabilities of cervical cancer. Gene ontology and pathway analyses showed that EFNA1 was involved in many tumorigenesis pathways, protein, and virus productions. These findings suggested that EFNA1 could be a prognostic biomarker and potential therapeutic target for cervical cancer.

Material-structure integrated design for ultra-broadband all-dielectric metamaterial absorber.

Material and structure are the essential elements of all-dielectric metamaterials. Structure design for specific dielectric materials has been studied while the contribution of material and synergistic effect of material and structure have been overlooked in the past years. Herein, we propose a material-structure integrated design (MSID) methodology for all-dielectric metamaterials, increasing the degree of freedom in the metamaterial design, to comprehensively optimize microwave absorption performance and further investigate the contribution of material and structure to absorption. A dielectric metamaterial absorber with an ultra-broadband absorption from 5.3 to 18.0 GHz is realized. Theoretical calculation and numerical simulation demonstrate that the symphony of material and structure excites multiple resonance modes encompassing quarter-wavelength interference cancellation, spoof surface plasmon polariton mode, dielectric resonance mode and grating mode, which is essential to afford the desirable absorption performance. This work highlights the superiority of coupling of material and structure and provides an effective design and optimization strategy for all-dielectric metamaterial absorbers.

Broadband and switchable terahertz polarization converter based on graphene metasurfaces.

In this work, we propose broadband and switchable terahertz (THz) polarization converters based on either graphene patch metasurface (GPMS) or its complementary structure (graphene hole metasurface, GHMS). The patch and hole are simply cross-shaped, composed of two orthogonal arms, along which plasmonic resonances mediated by Fabry-Perot cavity play a key role in polarization conversion (PC). An incidence of linear polarization will be converted to its cross-polarization (LTL) or circular polarization (LTC), as the reflected wave in the direction of two arms owning the same amplitude and π phase difference (LTL), or ±π/2 phase difference (LTC). Such requirements can be met by optimizing the width and length of two arms, thickness of dielectric layer, and Fermi level EF of graphene. By using GPMS, LTL PC of polarization conversion ratio (PCR) over 90% is achieved in the frequency range of 2.92 THz to 6.26 THz, and by using GHMS, LTC PC of ellipticity χ ≤ -0.9 at the frequencies from 4.45 THz to 6.47 THz. By varying the Fermi level, the operating frequency can be actively tuned, and the functionality can be switched without structural modulation; for instance, GPMS supports LTL PC as EF = 0.6 eV and LTC PC of χ ≥ 0.9 as EF = 1.0 eV, in the frequency range of 2.69 THz to 4.19 THz. Moreover, GHMS can be optimized to sustain LTL PC and LTC PC of |χ| ≥ 0.9, in the frequency range of 4.96 THz to 6.52 THz, which indicates that the handedness of circular polarization can be further specified. The proposed polarization converters of broad bandwidth, active tunability, and switchable functionality will essentially make a significant progress in THz technology and device applications, and can be widely utilized in THz communications, sensing and spectroscopy.

H19X-encoded miR-322(424)/miR-503 regulates muscle mass by targeting translation initiation factors.

BACKGROUND: Skeletal muscle atrophy is a debilitating complication of many chronic diseases, disuse conditions, and ageing. Genome-wide gene expression analyses have identified that elevated levels of microRNAs encoded by the H19X locus are among the most significant changes in skeletal muscles in a wide scope of human cachectic conditions. We have previously reported that the H19X locus is important for the establishment of striated muscle fate during embryogenesis. However, the role of H19X-encoded microRNAs in regulating skeletal mass in adults is unknown. METHODS: We have created a transgenic mouse strain in which ectopic expression of miR-322/miR-503 is driven by the skeletal muscle-specific muscle creatine kinase promoter. We also used an H19X mutant mouse strain in which transcription from the locus is interrupted by a gene trap. Animal phenotypes were analysed by standard histological methods. Underlying mechanisms were explored by using transcriptome profiling and validated in the two animal models and cultured myotubes. RESULTS: Our results demonstrate that the levels of H19X microRNAs are inversely related to postnatal skeletal muscle growth. Targeted overexpression of miR-322/miR-503 impeded skeletal muscle growth. The weight of gastrocnemius muscles of transgenic mice was only 54.5% of the counterparts of wild-type littermates. By contrast, interruption of transcription from the H19X locus stimulates postnatal muscle growth by 14.4-14.9% and attenuates the loss of skeletal muscle mass in response to starvation by 12.8-21.0%. Impeded muscle growth was not caused by impaired IGF1/AKT/mTOR signalling or a hyperactive ubiquitin-proteasome system, instead accompanied by markedly dropped abundance of translation initiation factors in transgenic mice. miR-322/miR-503 directly targets eIF4E, eIF4G1, eIF4B, eIF2B5, and eIF3M. CONCLUSIONS: Our study illustrates a novel pathway wherein H19X microRNAs regulate skeletal muscle growth and atrophy through regulating the abundance of translation initiation factors, thereby protein synthesis. The study highlights how translation initiation factors lie at the crux of multiple signalling pathways that control skeletal muscle mass.

Inhibition of Postn Rescues Myogenesis Defects in Myotonic Dystrophy Type 1 Myoblast Model.

Myotonic dystrophy type 1 (DM1) is an inherited neuromuscular disease caused by expanded CTG repeats in the 3' untranslated region (3'UTR) of the DMPK gene. The myogenesis process is defective in DM1, which is closely associated with progressive muscle weakness and wasting. Despite many proposed explanations for the myogenesis defects in DM1, the underlying mechanism and the involvement of the extracellular microenvironment remained unknown. Here, we constructed a DM1 myoblast cell model and reproduced the myogenesis defects. By RNA sequencing (RNA-seq), we discovered that periostin (Postn) was the most significantly upregulated gene in DM1 myogenesis compared with normal controls. This difference in Postn was confirmed by real-time quantitative PCR (RT-qPCR) and western blotting. Moreover, Postn was found to be significantly upregulated in skeletal muscle and myoblasts of DM1 patients. Next, we knocked down Postn using a short hairpin RNA (shRNA) in DM1 myoblast cells and found that the myogenesis defects in the DM1 group were successfully rescued, as evidenced by increases in the myotube area, the fusion index, and the expression of myogenesis regulatory genes. Similarly, Postn knockdown in normal myoblast cells enhanced myogenesis. As POSTN is a secreted protein, we treated the DM1 myoblast cells with a POSTN-neutralizing antibody and found that DM1 myogenesis defects were successfully rescued by POSTN neutralization. We also tested the myogenic ability of myoblasts in the skeletal muscle injury mouse model and found that Postn knockdown improved the myogenic ability of DM1 myoblasts. The activity of the TGF-ß/Smad3 pathway was upregulated during DM1 myogenesis but repressed when inhibiting Postn with a Postn shRNA or a POSTN-neutralizing antibody, which suggested that the TGF-ß/Smad3 pathway might mediate the function of Postn in DM1 myogenesis. These results suggest that Postn is a potential therapeutical target for the treatment of myogenesis defects in DM1.

A Deep Learning Framework About Traffic Flow Forecasting for Urban Traffic Emission Monitoring System.

As urban traffic pollution continues to increase, there is an urgent need to build traffic emission monitoring and forecasting system for the urban traffic construction. The traffic emission monitoring and forecasting system's core is the prediction of traffic emission's evolution. And the traffic flow prediction on the urban road network contributes greatly to the prediction of traffic emission's evolution. Due to the complex non-Euclidean topological structure of traffic networks and dynamic heterogeneous spatial-temporal correlations of traffic conditions, it is difficult to obtain satisfactory prediction results with less computation cost. To figure these issues out, a novel deep learning traffic flow forecasting framework is proposed in this paper, termed as Ensemble Attention based Graph Time Convolutional Networks (EAGTCN). More specifically, each component of our model contains two major blocks: (1) the global spatial patterns are captured by the spatial blocks which are fused by the Graph Convolution Network (GCN) and spatial ensemble attention layer; (2) the temporal patterns are captured by the temporal blocks which are composed by the Time Convolution Net (TCN) and temporal ensemble attention layers. Experiments on two real-world datasets demonstrate that our model obtains more accurate prediction results than the state-of-the-art baselines at less computation expense especially in the long-term prediction situation.

miR-322/-503 rescues myoblast defects in myotonic dystrophy type 1 cell model by targeting CUG repeats.

Myotonic dystrophy type 1 (DM1) is the most common type of adult muscular dystrophy caused by the expanded triple-nucleotides (CUG) repeats. Myoblast in DM1 displayed many defects, including defective myoblast differentiation, ribonuclear foci, and aberrant alternative splicing. Despite many were revealed to function in DM1, microRNAs that regulated DM1 via directly targeting the expanded CUG repeats were rarely reported. Here we discovered that miR-322/-503 rescued myoblast defects in DM1 cell model by targeting the expanded CUG repeats. First, we studied the function of miR-322/-503 in normal C2C12 myoblast cells. Downregulation of miR-322/-503 significantly hindered the myoblast differentiation, while miR-322/-503 overexpression promoted the process. Next, we examined the role of miR-322/-503 in the DM1 C2C12 cell model. miR-322/-503 was downregulated in the differentiation of DM1 C2C12 cells. When we introduced ectopic miR-322/-503 expression into DM1 C2C12 cells, myoblast defects were almost fully rescued, marked by significant improvements of myoblast differentiation and repressions of ribonuclear foci formation and aberrant alternative splicing. Then we investigated the downstream mechanism of miR-322/-503 in DM1. Agreeing with our previous work, Celf1 was proven to be miR-322/-503's target. Celf1 knockdown partially reproduced miR-322/-503's function in rescuing DM1 C2C12 differentiation but was unable to repress ribonuclear foci, suggesting other targets of miR-322/-503 existed in the DM1 C2C12 cells. As the seed regions of miR-322 and miR-503 were complementary to the CUG repeats, we hypothesized that the CUG repeats were the target of miR-322/-503. Through expression tests, reporter assays, and colocalization staining, miR-322/-503 was proved to directly and specifically target the expanded CUG repeats in the DM1 cell model rather than the shorter ones in normal cells. Those results implied a potential therapeutic function of miR-322/-503 on DM1, which needed further investigations in the future.

Wild­type IDH1 affects cell migration by modulating the PI3K/AKT/mTOR pathway in primary glioblastoma cells.

Glioblastoma (GBM) is the most common type of brain cancer and has the highest mortality. Dysregulated expression of wild­type isocitrate dehydrogenase 1 (IDH1) has been demonstrated to promote the progression of primary GBM without accumulating D­2­hydroxyglutarate, which differs from IDH1 mutation­related mechanisms of tumorigenesis. Previous studies have revealed several roles of wild­type IDH1 in primary GBM, involving proliferation and apoptosis. However, the function of IDH1 in cell migration has not been investigated. In the current study, the results of bioinformatics analysis revealed that IDH1 expression was significantly upregulated in patients with primary GBM. Wound healing and Transwell assays demonstrated that IDH1 overexpression promoted cell migration in primary GBM cells and that IDH1 knockdown hindered this process. Furthermore, α­ketoglutarate (α­KG), which is the main product of IDH1­catalyzed reactions, was significantly decreased by IDH1 knockdown and upregulated by IDH1 overexpression. α­KG treatment significantly increased the migration of primary GBM cells. Additionally, RNA sequence analysis of patients with primary GBM reported significant alterations in the expression of phosphoinositide 3­kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway­regulated genes, including Myc, Snail family transcriptional repressor 2 and Twist­related protein 1, which are primarily cell migration regulatory factors. Western blotting revealed that the overexpression or knockdown of IDH1 promoted or inhibited the PI3K/AKT/mTOR pathway, respectively. α­KG treatment of primary GBM cells also promoted the PI3K/AKT/mTOR pathway. Furthermore, IDH1­overexpressing and α­KG­treated U87 cells were incubated with rapamycin, an mTOR­specific inhibitor, and the results revealed that rapamycin treatment reversed the increased cell migration caused by IDH1 overexpression and α­KG treatment. The results indicated that IDH1 regulated the migration of primary GBM cells by altering α­KG levels and that the function of the IDH1/α­KG axis may rely on PI3K/AKT/mTOR pathway regulation.

A Band-Pass Filter Based on Half-Mode Substrate Integrated Waveguide and Spoof Surface Plasmon Polaritons.

In this paper, a band-pass filter based on half-mode substrate integrated waveguide (HMSIW) and double-layer spoof surface plasmon polaritons (SSPPs) consisting of two corrugated metal strips is proposed, which can realize band-pass transmission by etching periodic grooves at the top and bottom metal layers of the HMSIW. Moreover, the influences of important parameters on the performance of the proposed band-pass filter are analyzed by parametric study. By changing the key parameters, the low and high cut-off frequency can be controlled independently. The corresponding equivalent circuit of the proposed band-pass filter is put forward to explain the physical mechanism. Compared with the previous structures, this structure features smaller size, wider bandwidth and lower loss. Simulated results show that the proposed band-pass filter achieves a bandwidth (for |S11| < -10 dB and |S21| > -0.8 dB) of about 69.77% (15.6-32.1 GHz). The measured results have good agreements with the simulated ones, which verify that the proposed band-pass filter has good performances and potential applications at the microwave frequencies.

Visualization of Higher-Order Topological Insulating Phases in Two-Dimensional Dielectric Photonic Crystals.

The studies of topological phases of matter have been developed from condensed matter physics to photonic systems, resulting in fascinating designs of robust photonic devices. Recently, higher-order topological insulators have been investigated as a novel topological phase of matter beyond the conventional bulk-boundary correspondence. Previous studies of higher-order topological insulators have been mainly focused on the topological multipole systems with negative coupling between lattice sites. Here we experimentally demonstrate that second-order topological insulating phases without negative coupling can be realized in two-dimensional dielectric photonic crystals. We visualize both one-dimensional topological edge states and zero-dimensional topological corner states by using the near-field scanning technique. Our findings open new research frontiers for photonic topological phases and provide a new mechanism for light manipulating in a hierarchical way.

Splitting spoof surface plasmon polaritons to different directions with high efficiency in ultra-wideband frequencies.

An efficient method to split spoof surface plasmon polaritons (SSPPs) to different directions is proposed by designing a low-loss SSPP waveguide in an ultrawide frequency band. For this purpose, a coplanar-waveguide-based SSPP structure with double-row hole arrays etched on its middle line is first studied, which can be easily used to split the SSPP waves. Based on this method, a Y-shaped -3 dB SSPP power divider and its application on a Mach-Zehnder interferometer are presented. The experiment demonstrates that the proposed method splits the SSPP waves to different directions effectively in ultrawide frequencies (2.5-39.7 GHz) with good isolations, indicating that the proposed SSPP power divider can have good application on a Mach-Zehnder interferometer and plasmonic integrated circuits.

Magnetoplasmon excitation and hybridization in gyroelectric cylinders.

We investigate magnetoplasmon resonances and their coupling effects in gyroelectric cylinders. In individual cylinders, the dipole plasmon can be excited by plane wave illumination, and the dipole plasmon splits into lower energy and higher energy rotational magnetoplasmons in the presence of an external magnetic field. With respect to the external magnetic field, the two magnetoplasmons carry either right-handed chirality or left-handed chirality. In addition, originally dark plasmons can also be excited as the magnetic field increases. They are lower-order bulk plasmons (such as the radial breathing mode). In cylindrical dimers, the optically bright modes are combinations of magnetoplasmons with the same chirality. If the magnetic fields are antiparallel, the absorption spectra will be different for light incident from two opposite directions. This asymmetry can be well understood by carrying out eigenstate analysis, where the eigenstate does not possess mirror symmetry respecting the dimer axis. The dark modes engineering and asymmetrical optical behavior could have potential for terahertz device applications.

An Improved Staining Method for Low Signal LacZ Reporter Detection in Mouse Embryos.

In many fields of biology, especially in the field of developmental biology, LacZ reporter staining is an approach used to monitor gene expression patterns. In the LacZ reporter system, the LacZ gene is inserted in the endogenous location of the target gene via gene knock-in or by constructing a transgenic cassette in which LacZ is placed downstream of the promoter of the target gene being examined. Currently, the most common LacZ staining methods used are X-gal/FeCN staining and S-gal/TNBT staining. A serious limitation of both of these methods is that they are not effective when the LacZ gene is expressed at a low level. In an attempt to remedy this problem, we have established a new staining protocol which combines both methods. When compared to them, the method described here is better for visualizing lowly expressed genes and it has low background with high sensitivity.