Compatible camouflage for dual-band guided-laser radar and infrared via a metamaterial perfect absorber.

Laser-guided detector and infrared detection have attracted increasing attention in a wide range of research fields, including multispectral detection, radiative cooling, and thermal management. Previously reported absorbers presented shortcomings of lacking either tunability or compatibility. In this study, a metamaterial perfect absorber based on a Helmholtz resonator and fractal structure is proposed, which realizes tunable perfect absorptivity (α 1.06µ m >0.99,α 10.6µ m >0.99) of guided-laser radar dual operating bands (1.06 µm and 10.6 µm) and a low infrared average emissivity (ε¯3-5µ m =0.03,ε¯8-14µ m =0.31) in two atmospheric windows for compatible camouflage. The proposed perfect absorber provides a dynamically tunable absorptivity without structural changes and can be applied to optical communication, military stealth or protection, and electromagnetic detection.

Real-time channel selection in multi-mode multiplexing optical interconnection implemented by hybrid algorithm and material system.

Multi-mode multiplexing optical interconnection (MMOI) has been widely used as a new technology that can significantly expand communication bandwidth. However, the constant-on state of each channel in the existing MMOI systems leads to serious interference for receivers when extracting and processing information, necessitating introducing real-time selective-on function for each channel in MMOI systems. To achieve this goal, combining several practical requirements, we propose a real-time selective mode switch based on phase-change materials, which can individually tune the passing/blocking of different modes in the bus waveguide. We utilize our proposed particle swarm optimization algorithm with embedded neural network surrogate models (NN-in-PSO) to design this mode switch. The proposed NN-in-PSO significantly reduces the optimization cost, enabling multi-dimensional simultaneous optimization. The resulting mode switch offers several advantages, including ultra-compactness, rapid tuning, nonvolatility, and large extinction ratio. Then, we demonstrate the real-time channel selection function by integrating the mode switch into the MMOI system. Finally, we prove the fabricating robustness of the proposed mode switch, which paves the way for its large-scale application.

Optimized wideband and compact multifunctional photonic device based on Sb2S3 phase change material.

In this paper, a 1 × 2 photonic switch is designed based on a silicon-on-insulator (SOI) platform combined with the phase change material (PCM), Sb2S3, assisted by the direct binary search (DBS) algorithm. The designed photonic switch exhibits an impressive operating bandwidth ranging from 1450 to 1650 nm. The device has an insertion loss (IL) from 0.44 dB to 0.70 dB (of less than 0.7 dB) and cross talk (CT) from -26 dB to -20 dB (of less than -20 dB) over an operating bandwidth of 200 nm, especially an IL of 0.52 dB and CT of -24 dB at 1550 nm. Notably, the device is highly compact, with footprints of merely 3 × 4 µm2. Furthermore, we have extended the device's functionality for multifunctional operation in the C-band that can serve as both a 1 × 2 photonic switch and a 3 dB photonic power splitter. In the photonic switch mode, the device demonstrates an IL of 0.7 dB and a CT of -13.5 dB. In addition, when operating as a 3 dB photonic power splitter, the IL is less than 0.5 dB.

Inverse-designed ultra-compact multi-channel and multi-mode waveguide crossings.

In this work, we use the inverse design method to design three-channel and four-channel dual-mode waveguide crossings with the design regions of 4.32 µm-wide regular hexagon and 6.68 µm-wide regular octagon, respectively. Based on the highly-symmetric structures, the fundamental transverse electric (TE0) and TE1 modes propagate through the waveguide crossings efficiently. Moreover, the devices are practically fabricated and experimentally characterized. The measured insertion losses and crosstalks of the three-channel and dual-mode waveguide crossing for both the TE0 and TE1 modes are less than 1.8 dB and lower than -18.4 dB from 1540 nm to 1560 nm, respectively. The measured insertion losses of the four-channel and dual-mode waveguide crossing for the TE0 and TE1 modes are less than 1.8 dB and 2.5 dB from 1540 nm to 1560 nm, respectively, and the measured crosstalks are lower than -17.0 dB. In principle, our proposed scheme can be extended to waveguide crossing with more channels and modes.

Three-dimensional mode-division multiplexing system.

Blindly increasing the channels of the mode (de)multiplexer on the single-layer chip can cause the device structure to be too complex to optimize. The three-dimensional (3D) mode division multiplexing (MDM) technology is a potential solution to extend the data capacity of the photonic integrated circuit by assembling the simple devices in the 3D space. In our work, we propose a 16 × 16 3D MDM system with a compact footprint of about 100 µm × 5.0 µm × 3.7 µm. It can realize 256 mode routes by converting the fundamental transverse electric (TE0) modes in arbitrary input waveguides into the expected modes in arbitrary output waveguides. To illustrate its mode-routing principle, the TE0 mode is launched in one of the sixteen input waveguides, and converted into corresponding modes in four output waveguides. The simulated results indicate that the ILs and CTs of the 16 × 16 3D MDM system are less than 3.5 dB and lower than -14.2 dB at 1550 nm, respectively. In principle, the 3D design architecture can be scaled to realize arbitrary network complexity levels.

Different-mode power splitters based on a multi-dimension direct-binary-search algorithm.

In this work, we design, fabricate, and characterize a different-mode (waveguide-connected) power splitter ((W)PS) by what we believe to be a novel multi-dimension direct-binary-search algorithm that can significantly balance the device performance, time cost, and fabrication robustness by searching the state-dimension, rotation-dimension, shape-dimension, and size-dimension parameters. The (W)PS can simultaneously generate the fundamental transverse electric (TE0) and TE1 mode with the 1:1 output balance. Compared with the PS, the WPS can greatly shorten the adiabatic taper length between the single-mode waveguide and the grating coupler. The measured results of the different-mode (W)PS indicate that the insertion loss and crosstalk are less than 0.9 (1.3) dB and lower than -17.8 (-14.9) dB from 1540 nm to 1560 nm. In addition, based on the tunable tap couplers, the different-mode (W)PS can be extended to multiple output ports with different modes and different transmittances.

Tailoring bound states in the continuum in symmetric photonic crystal slabs by coupling strengths.

In this work, we investigate polarization-insensitive dual bound states in the continuum (BICs) at Γ point in symmetric photonic crystal (PhC) slabs. Especially, BICs are tailored by tuning intra- and intercellular optical coupling strengths of PhC slabs. Based on four different approaches, we realize the transition from BIC to quasi-BIC resonances with various dispersion behaviors while maintaining the symmetry of slabs. Also, we show the two resonances are lowest-order even and odd eigenmodes that can match the symmetry of the incident plane wave, and their quality (Q) factors follow the inverse quadratic law except for cases with larger perturbations. Furthermore, multipolar decomposition reveals that even quasi-BICs are dominated by the toroidal dipole and magnetic quadrupole, while odd quasi-BICs are governed by the magnetic dipole and electric quadrupole. Interestingly, an anomalous increase of the Q factor is observed in one case, which is attributed to the mode transformation. Finally, anisotropic coupling adjustment is discussed, which enriches the degrees of freedom to manipulate BICs. This work introduces a novel perspective to tailor BICs at Γ point in PhC slabs and has potential planar photonic applications for nonlinear enhancement and sensing.

Tunable mid-infrared selective emitter based on inverse design metasurface for infrared stealth with thermal management.

Infrared (IR) stealth with thermal management is highly desirable in military applications and astronomy. However, developing selective IR emitters with properties suitable for IR stealth and thermal management is challenging. In this study, we present the theoretical framework for a selective emitter based on an inverse-designed metasurface for IR stealth with thermal management. The emitter comprises an inverse-designed gold grating, a Ge2Sb2Te5 (GST) dielectric layer, and a gold reflective layer. The hat-like function, which describes an ideal thermal selective emitter, is involved in the inverse design algorithm. The emitter exhibits high performance in IR stealth with thermal management, with the low emissivity (ɛ3-5 µm =0.17; ɛ8-14 µm =0.16) for dual-band atmospheric transmission windows and high emissivity (ɛ5-8 µm =0.85) for non-atmospheric windows. Moreover, the proposed selective emitter can realize tunable control of thermal radiation in the wavelength range of 3-14 µm by changing the crystallization fraction of GST. In addition, the polarization-insensitive structure supports strong selective emission at large angles (60°). Thus, the selective emitter has potential for IR stealth, thermal imaging, and mid-infrared multifunctional equipment.

Series of ultra-low loss and ultra-compact multichannel silicon waveguide crossing.

Ultra-compact waveguide crossing (UC-WC) is a basic component in optoelectronic fusion chip solutions, as its footprint is smaller in the orders of magnitude than that of traditional photonic integrated circuits (PICs). However, a large loss of UC-WC (decibel level) becomes a barrier to scaling and practicality. Here, we propose a series of ultra-low loss UC-WC silicon devices using an advanced hybrid design that combines the adjoint method with the direct binary search (DBS) algorithm. Simulation results show that our 2 × 2 UC-WC has an insertion loss as low as 0.04 dB at 1550 nm, which is about ten times lower than the previous UC-WC results. In the valuable C-band (1530-1565 nm), the insertion loss of UC-WC is lower than -0.05 dB, and the channel crosstalk is lower than -34 dB. Furthermore, for the 3 × 3 UC-WC device, the highest insertion loss in the entire C-band is approximately -0.07 dB, and the highest channel crosstalk is lower than -33 dB. Additionally, the 4 × 4 and more complex 8 × 8 UC-WC devices were also analyzed. The highest insertion loss for 4 × 4 and 8 × 8 UC-WC in the C-band is only -0.19 dB and -0.20 dB, respectively, and the highest channel crosstalk is approximately -22dB and -28 dB, respectively. These results confirm that the designed devices possess two attractive features simultaneously: ultra-compactness and ultra-low insertion loss, which may be of great value in future large-scale optoelectronic fusion chips.

Collective topological corner modes in all-dielectric photonic crystal supercell arrays.

In this Letter, we propose collective topological corner modes in all-dielectric photonic crystal (PhC) supercell arrays, where each supercell is a second-order topological insulator. We show that coupled multipole corner modes are embedded in surrounding bulk modes at the Γ point even without the band gap, and individual or superposed dipole corner modes are selectively excited with collective behaviors by incident plane waves. These collective modes possess high-quality factors with an optimized thickness of the slab, and multipole decomposition reveals they are dominated by toroidal dipole and magnetic quadrupoles. Finally, we shrink the nontrivial region in each supercell to one unit-cell limit, where we show that collective corner modes still exist. Potential large-area topological applications are also discussed.

miR-H28 and miR-H29 expressed late in productive infection are exported and restrict HSV-1 replication and spread in recipient cells.

We report on the properties and function of two herpes simplex virus-1 (HSV-1) microRNAs (miRNAs) designated "miR-H28" and "miR-H29." Both miRNAs accumulate late in productive infection at a time when, for the most part, viral DNA and proteins have been made. Ectopic expression of miRNA mimics in human cells before infection reduced the accumulation of viral mRNAs and proteins, reduced plaque sizes, and at vey low multiplicities of infection reduced viral yields. The specificity of the miRNA mimics was tested in two ways. First, ectopic expression of mimics carrying mutations in the seed sequence was ineffective. Second, in similar tests two viral miRNAs made early in productive infection also had no effect. Both miR-H28 and miR-H29 are exported from infected cells in exosomes. A noteworthy finding is that both miR-H28 and miR-H29 were absent from murine ganglia harboring latent virus but accumulated in ganglia in which the virus was induced to reactivate. The significance of these findings rests on the principle that the transmission of HSV from person to person is by physical contact between the infected tissues of the donor and those of uninfected recipient. Diminished size of primary or recurrent lesions could be predicted to enhance person-to-person transmission. Reduction in the amount of reactivating latent virus would reduce the risk of retrograde transport to the CNS but would not interfere with anterograde transport to a site at or near the site of initial infection.

Role of activating transcription factor 3 in the synthesis of latency-associated transcript and maintenance of herpes simplex virus 1 in latent state in ganglia.

A key property of herpes simplex viruses (HSVs) is their ability to establish latent infection in sensory or autonomic ganglia and to reactivate on physical, hormonal, or emotional stress. In latently infected ganglia, HSVs express a long noncoding RNA, a latency-associated transcript (LAT), which plays a key role in maintaining latently infected neurons, but not viral proteins. To investigate the events leading to reactivation, we examined the use of ganglionic organ cultures that enable rapid reactivation in medium containing antibody to nerve growth factor (NGF) or delayed reactivation in medium containing NGF and epidermal growth factor (EGF). Here we report the discovery that activating transcription factor 3 (ATF3), a stress response protein, profoundly affects the interaction of HSV with its host. Specifically, (i) ATF3 is induced by stress, such as inhibition of protein synthesis or infection; (ii) in infected cells, ATF3 enhances the accumulation of LAT by acting on the response elements in the promoter of the LAT precursor RNA; (iii) ATF3 is induced nearly 100-fold in ganglionic organ cultures; and (iv) ATF3 plays a key role in the maintenance of the latent state, inasmuch as expression of ATF3 bereft of the C-terminal activation domain acts as a dominant negative factor, inducing HSV gene expression in ganglionic organ cultures harboring latent virus and incubated in medium containing NGF and EGF. Thus, ATF3 is a component of a cluster of cellular proteins that together with LAT maintain the integrity of the neurons harboring latent virus.

Patterns of accumulation of miRNAs encoded by herpes simplex virus during productive infection, latency, and on reactivation.

The key events in herpes simplex virus (HSV) infections are (i) replication at a portal of entry into the body modeled by infection of cultured cells; (ii) establishment of a latent state characterized by a sole latency-associated transcript and microRNAs (miRNAs) modeled in murine peripheral ganglia 30 d after inoculation; and (iii) reactivation from the latent state modeled by excision and incubation of ganglia in medium containing anti-NGF antibody for a timespan of a single viral replicative cycle. In this report, we examine the pattern of synthesis and accumulation of 18 HSV-1 miRNAs in the three models. We report the following: (i) H2-3P, H3-3P, H4-3P, H5-3P, H6-3P, and H7-5P accumulated in ganglia harboring latent virus. All but H4-3P were readily detected in productively infected cells, and most likely they originate from three transcriptional units. (ii) H8-5P, H15, H17, H18, H26, and H27 accumulated during reactivation. Of this group, only H26 and H27 could be detected in productively infected cells. (iii) Of the 18 we have examined, only 10 miRNAs were found to accumulate above background levels in productively infected cells. The disparity in the accumulation of miRNAs in cell culture and during reactivation may reflect differences in the patterns of regulation of viral gene expression during productive infection and during reactivation from the latent state.

Cells infected with herpes simplex virus 1 export to uninfected cells exosomes containing STING, viral mRNAs, and microRNAs.

STING (stimulator of IFN genes) activates the IFN-dependent innate immune response to infection on sensing the presence of DNA in cytosol. The quantity of STING accumulating in cultured cells varies; it is relatively high in some cell lines [e.g., HEp-2, human embryonic lung fibroblasts (HEL), and HeLa] and low in others (e.g., Vero cells). In a preceding publication we reported that STING was stable in four cell lines infected with herpes simplex virus 1 and that it was actively stabilized in at least two cell lines derived from human cancers. In this report we show that STING is exported from HEp-2 cells to Vero cells along with virions, viral mRNAs, microRNAs, and the exosome marker protein CD9. The virions and exosomes copurified. The quantity of STING and CD9 exported from one cell line to another was inoculum-size-dependent and reflected the levels of STING and CD9 accumulating in the cells in which the virus inoculum was made. The export of STING, an innate immune sensor, and of viral mRNAs whose major role may be in silencing viral genes in latently infected neurons, suggests that the virus has evolved mechanisms that curtail rather than foster the spread of infection under certain conditions.

HSV carrying WT REST establishes latency but reactivates only if the synthesis of REST is suppressed.

HSVs transit from vigorous replication at the portal of entry into the body to a latent state in sensory neurons in which only noncoding (e.g., latency-associated transcript) and micro-RNAs are expressed. In productive infection, viral genes must be sequentially derepressed at two checkpoints. A leading role in the repression of viral genes is carried out by histone deacetylase (HDAC)/corepressor element-1 silencing transcription factor (CoREST)/lysinespecific demethylase1(LSD1)/RE1-silencing transcription factor (REST) repressor complex (HCLR). Previously, we reported that to define the role of the components of the HCLR complex in the establishment of latency, we constructed recombinant virus (R112) carrying a dominant-negative REST that bound response elements in DNA but could not recruit repressive proteins. This recombinant virus was unable to establish latency. In the current studies, we constructed a virus (R111) carrying WT REST with a WT genome. We report the following findings: (a) R111 readily established latent infection in trigeminal ganglia; however, although the amounts of viral DNAs in latently infected neurons were similar to those of WT virus, the levels of latency-associated transcript and micro-RNAs were 50- to 100-fold lower; (b) R111 did not spontaneously reactivate in ganglionic organ cultures; however, viral genes were expressed if the synthesis of REST was blocked by cycloheximide; and (c) histone deacetylase inhibitors reactivated the WT parent but not the R111 recombinant virus. The results suggest that REST plays a transient role in the establishment of latency but not in reactivation and suggest the existence of at least two phases at both establishment and reactivation.

Modulation of reactivation of latent herpes simplex virus 1 in ganglionic organ cultures by p300/CBP and STAT3.

A key property of herpes simplex viruses (HSVs) is their ability to establish latent infection in sensory or autonomic ganglia and to reactivate on physical, hormonal, or emotional stress. In latently infected ganglia, HSV expresses a long noncoding RNA and a set of microRNAs, but viral proteins are not expressed. The mechanism by which latent HSV reactivates is unknown. A key question is, what is the mechanism of reactivation in the absence of tegument proteins that enable gene expression in productive infection? Elsewhere we have reported the use of ganglionic organ cultures that enable rapid reactivation in medium containing antibody to NGF or delayed reactivation in medium containing NGF and EGF. We also reported that in the ganglionic organ cultures incubated in medium containing antibody to NGF, all viral genes are derepressed at once without requiring de novo protein synthesis within the time frame of a single replicative cycle. Here we report that latent HSV in ganglia immersed in medium containing NGF and EGF is reactivated by (i) broad spectrum as well as specific histone deacetylase 1 or histone deacetylase 4 inhibitors, (ii) activation of p300/CBP, and (iii) either STAT3 carrying the substitution of tyrosine 705 to phenylalanine or an inhibitor of STAT3. Conversely, reactivation of latent HSV was blocked by p300/CBP inhibitor in medium containing antibody to NGF. The results suggest that (i) STAT3 is required for the maintenance of the latent state and interference with its functions leads to reactivation and (ii) p300/CBP is essential for HSV reactivation.

The stability of herpes simplex virus 1 ICP0 early after infection is defined by the RING finger and the UL13 protein kinase.

UNLABELLED: Herpes simplex virus 1 (HSV-1)-infected cell protein 0 (ICP0) is a multifunctional protein that plays a key role in overcoming numerous facets of host innate immunity. A key function of ICP0 that requires an intact RING finger domain is that of an ubiquitin E3 ligase: ICP0 interacts with at least three ubiquitin-conjugating enzymes of which one, UbcH5a, is required for degradation of PML and SP100. A preceding report showed that ICP0 is highly unstable at very early times after infection but becomes stable at later times. We report here that (i) the degradation of ICP0 is not infected cell specific, (ii) the degradation does not require the interaction of ICP0 with either UbcH5a, UbcH6, or UbcH9, (iii) ICP0 is degraded both early and late in cells infected with a mutant lacking the UL13 protein kinase, (iv) ICP0 encoded by wild-type virus or the ΔUL13 mutant is stable in cells transfected with a plasmid encoding UL13 before infection, (v) ICP0 carrying mutations in the RING finger domain is stable both early and late in infection, and, finally, (vi) in cells infected with both wild type and RING finger mutant only the wild-type ICP0 is rapidly degraded at early times. The results suggest that the stability of ICP0 is mediated by the UL13 protein kinase and that the target of proteolysis is a site at or near the RING domain of ICP0. IMPORTANCE: ICP0, a major regulatory protein of HSV-1, turns over rapidly early in infection but becomes stable at late times. We report that stabilization requires the presence of UL13 protein kinase and that an ICP0 with mutations in RING finger is stable. In mixed infections mutant ICP0 is stable, whereas the wild-type ICP0 is degraded. Our findings suggest that the lifestyle of HSV-1 requires an ICP0 that turns over rapidly if late proteins are absent.

Induction of apoptosis accelerates reactivation of latent HSV-1 in ganglionic organ cultures and replication in cell cultures.

Herpes simplex viruses replicate at the portal of entry into the body and are transported retrograde to sensory neurons in which they can establish a silent, latent infection characterized by the expression of a noncoding latency-associated transcript and a set of microRNAs. At the portal of entry into the body and in cell culture a viral protein, VP16, recruits cellular proteins that initiate a sequential derepression of several kinetic classes of viral genes. Earlier studies have shown that upon reactivation of latent virus in ganglionic organ cultures all genes are derepressed at once, thus obviating the need for VP16 to initiate sequential derepression of viral genes. One hypothesis that could explain the data is that the massive reactivation of all classes of viral genes is the consequence of activation of an apoptotic pathway. Here we show that two proapoptotic drugs, dexamethasone and 2[[3-(2,3-dichlorophenoxy)propyl]amino]-ethanol, each accelerates viral gene expression in ganglionic organ cultures. We also show that in cultured cells apoptosis induced by dexamethasone accelerates viral gene expression and accumulation of infectious virus. The results are surprising in light of the relatively large number of viral proteins that independently block apoptosis induced by viral gene products or exogenous agents. The results suggest that the virus may rely on apoptosis to exit from latency but that apoptosis may be detrimental for virus replication or spread at the portal of entry into the body.

HSV-1 gene expression from reactivated ganglia is disordered and concurrent with suppression of latency-associated transcript and miRNAs.

In cell cultures, HSV-1 replication is initiated by recruitment by virion protein 16 of transcriptional factors and histone-modifying enzymes to immediate early (α) gene promoters. HSV establishes latent infections characterized by suppression of viral gene expression except for latency-associated transcripts (LATs) and miRNAs. The latent virus reactivates in stressed neurons. A fundamental question is how reactivation initiates in the absence of virion protein 16. We report the following findings in the ganglion explant model. (i) Anti-nerve growth factor antibody accelerated the reactivation of latent virus. Viral mRNAs were detected as early as 9 h after explantation. (ii) After explantation the amounts of viral mRNAs increased whereas amounts of miRNAs and LATs decreased. The decrease in miRNAs and LATs required ongoing protein synthesis, raising the possibility that LAT and miRNAs were degraded by a viral gene product. (iii) The expression of viral genes in explanted ganglia was disordered rather than sequentially ordered as in infected cells in culture. These findings suggest that in reactivating ganglia gene expression is totally derepressed and challenge the current models in that establishment of or exit from latency could not be dependent on the suppression or activation of single or small clusters of viral genes. Finally, miRNAs and LATs reached peak levels 9-11 d after corneal inoculation, thus approximating the pattern of virus replication in these ganglia. These findings suggest that the patterns of accumulation of LATs and miRNAs reflect many different stages in the infection of neurons.

Targeted genomic sequencing identifies PRRT2 mutations as a cause of paroxysmal kinesigenic choreoathetosis.

BACKGROUND: Paroxysmal kinesigenic choreoathetosis (PKC) is characterised by recurrent and brief attacks of involuntary movement, inherited as an autosomal dominant trait with incomplete penetrance. A PKC locus has been previously mapped to the pericentromeric region of chromosome 16 (16p11.2-q12.1), but the causative gene remains unidentified. METHODS/RESULTS: Deep sequencing of this 30 Mb region enriched with array capture in five affected individuals from four Chinese PKC families detected two heterozygous PRRT2 insertions (c.369dupG and c.649dupC), producing frameshifts and premature stop codons (p.S124VfsX10 and p.R217PfsX8, respectively) in two different families. Sanger sequencing confirmed these two mutations and revealed a missense PRRT2 mutation (c.859G→A, p.A287T) in one of the two remaining families. This study also sequenced PRRT2 in 29 sporadic cases affected with PKC and identified mutations in 10 cases, including six with the c.649dupC mutation. Most variants were truncating mutations, consistent with loss-of-function and haploinsufficiency. CONCLUSION: The present study identifies PRRT2 as the gene mutated in a subset of PKC, and suggests that PKC is genetically heterogeneous.