Cell polarization in ischemic stroke: molecular mechanisms and advances

Ischemic stroke is a cerebrovascular disease associated with high mortality and disability rates. Since the inflammation and immune response play a central role in driving ischemic damage, it becomes essential to modulate excessive inflammatory reactions to promote cell survival and facilitate tissue repair around the injury site. Various cell types are involved in the inflammatory response, including microglia, astrocytes, and neutrophils, each exhibiting distinct phenotypic profiles upon stimulation. They display either proinflammatory or anti-inflammatory states, a phenomenon known as ‘cell polarization.’ There are two cell polarization therapy strategies. The first involves inducing cells into a neuroprotective phenotype in vitro, then reintroducing them autologously. The second approach utilizes small molecular substances to directly affect cells in vivo. In this review, we elucidate the polarization dynamics of the three reactive cell populations(microglia, astrocytes, and neutrophils) in the context of ischemic stroke, and provide a comprehensive summary of the molecular mechanisms involved in their phenotypic switching. By unraveling the complexity of cell polarization, we hope to offer insights for future research on neuroinflammation and novel therapeutic strategies for ischemic stroke.

Defects‑Rich Heterostructures Trigger Strong Polarization Coupling in Sulfides/Carbon Composites with Robust Electromagnetic Wave Absorption

Defects-rich heterointerfaces integrated with adjustable crystalline phases and atom vacancies,as well as veiled dielectric-responsive character,are instrumental in electromagnetic dissipation.Conventional methods,however,constrain their delicate constructions.Herein,an innovative alternative is proposed:carrageenan-assistant cations-regulated(CACR)strategy,which induces a series of sulfides nanoparticles rooted in situ on the surface of carbon matrix.This unique configuration originates from strategic vacancy formation energy of sulfides and strong sulfides-carbon support interaction,benefiting the delicate construction of defects-rich heterostructures in M_(x)S_(y)/carbon composites(M-CAs).Impressively,these generated sulfur vacancies are firstly found to strengthen electron accumulation/consumption ability at heterointerfaces and,simultaneously,induct local asymmetry of electronic structure to evoke large dipole moment,ultimately leading to polarization coupling,i.e.,defect-type interfacial polarization.Such“Janus effect”(Janus effect means versatility,as in the Greek two-headed Janus)of interfacial sulfur vacancies is intuitively confirmed by both theoretical and experimental investigations for the first time.Consequently,the sulfur vacancies-rich heterostructured Co/Ni-CAs displays broad absorption bandwidth of 6.76 GHz at only 1.8 mm,compared to sulfur vacancies-free CAs without any dielectric response.Harnessing defects-rich heterostructures,this one-pot CACR strategy may steer the design and development of advanced nanomaterials,boosting functionality across diverse application domains beyond electromagnetic response.

Retrieving Jones matrix from an imperfect metasurface polarizer

Optical metasurfaces,which consist of subwavelength scale meta-atoms,represent a novel platform to manipulate the polarization and phase of light.The optical performance of metasurfaces heavily relies on the quality of nanofabrication.Retrieving the Jones matrix of an imperfect metasurface optical element is highly desirable.We show that this can be realized by decomposing the generalized Jones matrix of a meta-atom into two parallel ones,which correspond to the ideal matrix and a phase retardation.To experimentally verify this concept,we designed and fabricated metasurface polarizers,which consist of geometric phase-controlled dielectric meta-atoms.By scanning the polarization states of the incident and transmitted light,we are able to extract the coefficients of the two parallel matrices of a metasurface polarizer.Based on the results of the Jones matrix decomposition,we also demonstrated polarization image encryption and spin-selective optical holography.The proposed Jones matrix retrieval protocol may have important applications in computational imaging,optical computing,optical communications,and so on.

Integration of Electrical Properties and Polarization Loss Modulation on Atomic Fe–N‑RGO for Boosting Electromagnetic Wave Absorption

Developing effective strategies to regulate graphene’s conduction loss and polarization has become a key to expanding its application in the electromagnetic wave absorption(EMWA)field.Based on the unique energy band structure of graphene,regulating its bandgap and electrical properties by introducing heteroatoms is considered a feasible solution.Herein,metal-nitrogen doping reduced graphene oxide(M–N-RGO)was prepared by embedding a series of single metal atoms M–N_(4) sites(M=Mn,Fe,Co,Ni,Cu,Zn,Nb,Cd,and Sn)in RGO using an N-coordination atom-assisted strategy.These composites had adjustable conductivity and polarization to optimize dielectric loss and impedance matching for efficient EMWA performance.The results showed that the minimum reflection loss(RL_(min))of Fe–N-RGO reaches−74.05 dB(2.0 mm)and the maximum effective absorption bandwidth(EAB_(max))is 7.05 GHz(1.89 mm)even with a low filler loading of only 1 wt%.Combined with X-ray absorption spectra(XAFS),atomic force microscopy,and density functional theory calculation analysis,the Fe–N_(4) can be used as the polarization center to increase dipole polarization,interface polarization and defect-induced polarization due to d-p orbital hybridization and structural distortion.Moreover,electron migration within the Fe further leads to conduction loss,thereby synergistically promoting energy attenuation.This study demonstrates the effectiveness of metal-nitrogen doping in regulating the graphene′s dielectric properties,which provides an important basis for further investigation of the loss mechanism.

Bioinspired Passive Tactile Sensors Enabled by Reversible Polarization of Conjugated Polymers

Tactile perception plays a vital role for the human body and is also highly desired for smart prosthesis and advanced robots.Compared to active sensing devices,passive piezoelectric and triboelectric tactile sensors consume less power,but lack the capability to resolve static stimuli.Here,we address this issue by utilizing the unique polarization chemistry of conjugated polymers for the first time and propose a new type of bioinspired,passive,and bio-friendly tactile sensors for resolving both static and dynamic stimuli.Specifically,to emulate the polarization process of natural sensory cells,conjugated polymers(including poly(3,4-ethylenedioxythiophen e):poly(styrenesulfonate),polyaniline,or polypyrrole)are controllably polarized into two opposite states to create artificial potential differences.The controllable and reversible polarization process of the conjugated polymers is fully in situ characterized.Then,a micro-structured ionic electrolyte is employed to imitate the natural ion channels and to encode external touch stimulations into the variation in potential difference outputs.Compared with the currently existing tactile sensing devices,the developed tactile sensors feature distinct characteristics including fully organic composition,high sensitivity(up to 773 mV N^(−1)),ultralow power consumption(nW),as well as superior bio-friendliness.As demonstrations,both single point tactile perception(surface texture perception and material property perception)and two-dimensional tactile recognitions(shape or profile perception)with high accuracy are successfully realized using self-defined machine learning algorithms.This tactile sensing concept innovation based on the polarization chemistry of conjugated polymers opens up a new path to create robotic tactile sensors and prosthetic electronic skins.

High-dose dexamethasone regulates microglial polarization via the GR/JAK1/STAT3 signaling pathway after traumatic brain injury

Although microglial polarization and neuroinflammation are crucial cellular responses after traumatic brain injury,the fundamental regulatory and functional mechanisms remain insufficiently understood.As potent anti-inflammato ry agents,the use of glucoco rticoids in traumatic brain injury is still controversial,and their regulatory effects on microglial polarization are not yet known.In the present study,we sought to determine whether exacerbation of traumatic brain injury caused by high-dose dexamethasone is related to its regulatory effects on microglial polarization and its mechanisms of action.In vitro cultured BV2 cells and primary microglia and a controlled cortical impact mouse model were used to investigate the effects of dexamethasone on microglial polarization.Lipopolysaccharide,dexamethasone,RU486(a glucocorticoid receptor antagonist),and ruxolitinib(a Janus kinase 1 antagonist)were administered.RNA-sequencing data obtained from a C57BL/6 mouse model of traumatic brain injury were used to identify potential targets of dexamethasone.The Morris water maze,quantitative reverse transcription-polymerase chain reaction,western blotting,immunofluorescence and confocal microscopy analysis,and TUNEL,Nissl,and Golgi staining were performed to investigate our hypothesis.High-throughput sequencing results showed that arginase 1,a marker of M2 microglia,was significantly downregulated in the dexamethasone group compared with the traumatic brain injury group at3 days post-traumatic brain injury.Thus dexamethasone inhibited M1 and M2 microglia,with a more pronounced inhibitory effect on M2microglia in vitro and in vivo.Glucocorticoid receptor plays an indispensable role in microglial polarization after dexamethasone treatment following traumatic brain injury.Additionally,glucocorticoid receptor activation increased the number of apoptotic cells and neuronal death,and also decreased the density of dendritic spines.A possible downstream receptor signaling mechanism is the GR/JAK1/STAT3 pathway.Overactivation of glucocorticoid receptor by high-dose dexamethasone reduced the expression of M2 microglia,which plays an antiinflammatory role.In contrast,inhibiting the activation of glucocorticoid receptor reduced the number of apoptotic glia and neurons and decreased the loss of dendritic spines after traumatic brain injury.Dexamethasone may exe rt its neurotoxic effects by inhibiting M2 microglia through the GR/JAK1/STAT3 signaling pathway.

Pharmacological targeting cGAS/STING/NF-κB axis by tryptanthrin induces microglia polarization toward M2 phenotype and promotes functional recovery in a mouse model of spinal cord injury

The M1/M2 phenotypic shift of microglia after spinal cord injury plays an important role in the regulation of neuroinflammation during the secondary injury phase of spinal cord injury.Regulation of shifting microglia polarization from M1(neurotoxic and proinflammatory type)to M2(neuroprotective and anti-inflammatory type)after spinal cord injury appears to be crucial.Tryptanthrin possesses an anti-inflammatory biological function.However,its roles and the underlying molecular mechanisms in spinal cord injury remain unknown.In this study,we found that tryptanthrin inhibited microglia-derived inflammation by promoting polarization to the M2 phenotype in vitro.Tryptanthrin promoted M2 polarization through inactivating the cGAS/STING/NF-κB pathway.Additionally,we found that targeting the cGAS/STING/NF-κB pathway with tryptanthrin shifted microglia from the M1 to M2 phenotype after spinal cord injury,inhibited neuronal loss,and promoted tissue repair and functional recovery in a mouse model of spinal cord injury.Finally,using a conditional co-culture system,we found that microglia treated with tryptanthrin suppressed endoplasmic reticulum stress-related neuronal apoptosis.Taken together,these results suggest that by targeting the cGAS/STING/NF-κB axis,tryptanthrin attenuates microglia-derived neuroinflammation and promotes functional recovery after spinal cord injury through shifting microglia polarization to the M2 phenotype.

Overexpression of low-density lipoprotein receptor prevents neurotoxic polarization of astrocytes via inhibiting NLRP3 inflammasome activation in experimental ischemic stroke

Neurotoxic astrocytes are a promising therapeutic target for the attenuation of cerebral ischemia/reperfusion injury.Low-density lipoprotein receptor,a classic cholesterol regulatory receptor,has been found to inhibit NLR family pyrin domain containing protein 3(NLRP3)inflammasome activation in neurons following ischemic stroke and to suppress the activation of microglia and astrocytes in individuals with Alzheimer’s disease.However,little is known about the effects of low-density lipoprotein receptor on astrocytic activation in ischemic stroke.To address this issue in the present study,we examined the mechanisms by which low-density lipoprotein receptor regulates astrocytic polarization in ischemic stroke models.First,we examined low-density lipoprotein receptor expression in astrocytes via immunofluorescence staining and western blotting analysis.We observed significant downregulation of low-density lipoprotein receptor following middle cerebral artery occlusion reperfusion and oxygen-glucose deprivation/reoxygenation.Second,we induced the astrocyte-specific overexpression of low-density lipoprotein receptor using astrocyte-specific adeno-associated virus.Low-density lipoprotein receptor overexpression in astrocytes improved neurological outcomes in middle cerebral artery occlusion mice and reversed neurotoxic astrocytes to create a neuroprotective phenotype.Finally,we found that the overexpression of low-density lipoprotein receptor inhibited NLRP3 inflammasome activation in oxygen-glucose deprivation/reoxygenation injured astrocytes and that the addition of nigericin,an NLRP3 agonist,restored the neurotoxic astrocyte phenotype.These findings suggest that low-density lipoprotein receptor could inhibit the NLRP3-meidiated neurotoxic polarization of astrocytes and that increasing low-density lipoprotein receptor in astrocytes might represent a novel strategy for treating cerebral ischemic stroke.

Inhibiting SHP2 reduces glycolysis, promotes microglial M1 polarization, and alleviates secondary inflammation following spinal cord injury in a mouse model

Reducing the secondary inflammatory response, which is partly mediated by microglia, is a key focus in the treatment of spinal cord injury. Src homology 2-containing protein tyrosine phosphatase 2(SHP2), encoded by PTPN11, is widely expressed in the human body and plays a role in inflammation through various mechanisms. Therefore, SHP2 is considered a potential target for the treatment of inflammation-related diseases. However, its role in secondary inflammation after spinal cord injury remains unclear. In this study, SHP2 was found to be abundantly expressed in microglia at the site of spinal cord injury. Inhibition of SHP2 expression using siRNA and SHP2 inhibitors attenuated the microglial inflammatory response in an in vitro lipopolysaccharide-induced model of inflammation. Notably, after treatment with SHP2 inhibitors, mice with spinal cord injury exhibited significantly improved hind limb locomotor function and reduced residual urine volume in the bladder. Subsequent in vitro experiments showed that, in microglia stimulated with lipopolysaccharide, inhibiting SHP2 expression promoted M2 polarization and inhibited M1 polarization. Finally, a co-culture experiment was conducted to assess the effect of microglia treated with SHP2 inhibitors on neuronal cells. The results demonstrated that inflammatory factors produced by microglia promoted neuronal apoptosis, while inhibiting SHP2 expression mitigated these effects. Collectively, our findings suggest that SHP2 enhances secondary inflammation and neuronal damage subsequent to spinal cord injury by modulating microglial phenotype. Therefore, inhibiting SHP2 alleviates the inflammatory response in mice with spinal cord injury and promotes functional recovery postinjury.

Design of Serially Concatenated Two-Level Polar Coded Modulation System with Low-Complexity

Multilevel coding(MLC)is a commonly used polar coded modulation scheme,but challenging to implement in engineering due to its high complexity and long decoding delay for high-order modulations.To address these limitations,a novel two-level serially concatenated MLC scheme,in which the bitlevels with similar reliability are bundled and transmitted together,is proposed.The proposed scheme hierarchically protects the two bit-level sets:the bitlevel sets at the higher level are sufficiently reliable and do not require excessive resources for protection,whereas only the bit-level sets at the lower level are encoded by polar codes.The proposed scheme has the advantages of low power consumption,low delay and high reliability.Moreover,an optimized constellation signal labeling rule that can enhance the performance is proposed.Finally,the superiority of the proposed scheme is validated through the theoretical analysis and simulation results.Compared with the bit interleaving coding modulation(BICM)scheme,under 256-quadrature amplitude modulation(QAM),the proposed scheme attains a performance gain of 1.0 dB while reducing the decoding complexity by 54.55%.

Macrophage polarization in cardiac transplantation:Insights into immune modulation and therapeutic approaches

The role and regulatory mechanisms of macrophage polarization in cardiac transplantation have gained significant attention.Macrophages can polarize into either the M1(pro-inflammatory)or M2(anti-inflammatory)phenotype in response to environmental cues.M1 macrophages facilitate transplant rejection by releasing inflammatory mediators and activating T cells,whereas M2 macrophages support graft survival by secreting antiinflammatory factors and promoting tissue repair.Mitochondrial quality control regulation plays a crucial role in macrophage polarization,which may influence graft survival and immune responses.This review provides an overview of the current understanding of mitochondrial quality control-regulated macrophage polarization in cardiac transplantation,its effects on graft outcomes,and potential therapeutic strategies to modulate this process to enhance transplant success rates.The review was conducted by systematically analyzing recent studies and integrating findings from key research articles to synthesize a comprehensive understanding of this emerging field.

O-linked β-N-acetylglucosamine transferase regulates macrophage polarization in diabetic periodontitis: In vivo and in vitro study

BACKGROUND Periodontitis,when exacerbated by diabetes,is characterized by increased M1 macrophage polarization and decreased M2 polarization.O-linkedβ-N-acetylglucosamine(O-GlcNAcylation),catalyzed by O-GlcNAc transferase(OGT),promotes inflammatory responses in diabetic periodontitis(DP).Additionally,p38 mitogen-activated protein kinase regulates macrophage polarization.However,the interplay between OGT,macrophage polarization,and p38 signaling in the progression of DP remains unexplored.AIM To investigate the effect of OGT on macrophage polarization in DP and its role in mediating O-GlcNAcylation of p38.METHODS For in vivo experiments,mice were divided into four groups:Control,DP model,model+short hairpin(sh)RNAnegative control,and model+sh-OGT.Diabetes was induced by streptozotocin,followed by ligation and lipopolysaccharide(LPS)administration to induce periodontitis.The impact of OGT was assessed by injecting sh-OGT lentivirus.Maxillary bone destruction was evaluated using micro-computed tomography analysis and tartrateresistant acid phosphatase staining,while macrophage polarization was determined through quantitative real-time polymerase chain reaction(qPCR)and immunohistochemistry.For in vitro experiments,RAW264.7 cells were treated with LPS and high glucose(HG)(25 mmol/L D-glucose)to establish a cell model of DP.OGT was inhibited by OGT inhibitor(OSMI4)treatment and knocked down by sh-OGT transfection.M1/M2 polarization was analyzed using qPCR,immunofluorescence,and flow cytometry.Levels of O-GlcNAcylation were measured using immunoprecipitation and western blotting.RESULTS Our results demonstrated that M1 macrophage polarization led to maxillary bone loss in DP mice,associated with elevated O-GlcNAcylation and OGT levels.Knockdown of OGT promoted the shift from M1 to M2 macrophage polarization in both mouse periodontal tissues and LPS+HG-induced RAW264.7 cells.Furthermore,LPS+HG enhanced the O-GlcNAcylation of p38 in RAW264.7 cells.OGT interacted with p38 to promote its O-GlcNAcylation at residues A28,T241,and T347,as well as its phosphorylation at residue Y221.CONCLUSION Inhibition of OGT-mediated p38 O-GlcNAcylation deactivates the p38 pathway by suppressing its self-phosphorylation,thereby promoting M1 to M2 macrophage polarization and mitigating DP.These findings suggested that modulating macrophage polarization through regulation of O-GlcNAcylation may represent a novel therapeutic strategy for treating DP.

Dapagliflozin exerts anti-apoptotic effects by mitigating macrophage polarization via modulation of the phosphoinositide 3-kinase/protein kinase B signaling pathway

BACKGROUND Macrophages are central to the orchestration of immune responses,inflammatory processes,and the pathogenesis of diabetic complications.The dynamic polarization of macrophages into M1 and M2 phenotypes critically modulates inflammation and contributes to the progression of diabetic nephropathy.Sodiumglucose cotransporter 2 inhibitors such as dapagliflozin,which are acclaimed for their efficacy in diabetes management,may influence macrophage polarization,thereby ameliorating diabetic nephropathy.This investigation delves into these mechanistic pathways,aiming to elucidate novel therapeutic strategies for diabetes.AIM To investigate the inhibitory effect of dapagliflozin on macrophage M1 polarization and apoptosis and to explore its mechanism of action.METHODS We established a murine model of type 2 diabetes mellitus and harvested peritoneal macrophages following treatment with dapagliflozin.Concurrently,the human monocyte cell line cells were used for in vitro studies.Macrophage viability was assessed in a cell counting kit 8 assay,whereas apoptosis was evaluated by Annexin V/propidium iodide staining.Protein expression was examined through western blotting,and the expression levels of macrophage M1 surface immunosorbent assay,and quantitative real-time polymerase chain reaction analyses.RESULTS Dapagliflozin attenuated M1 macrophage polarization and mitigated apoptosis in the abdominal macrophages of diabetic mice,evidenced by the downregulation of proapoptotic genes(Caspase 3),inflammatory cytokines[interleukin(IL)-6,tumor necrosis factor-α,and IL-1β],and M1 surface markers(inducible nitric oxide synthase,and cluster of differentiation 86),as well as the upregulation of the antiapoptotic gene BCL2.Moreover,dapagliflozin suppressed the expression of proteins associated with the phosphoinositide 3-kinase(PI3K)/protein kinase B(AKT)signaling pathway(PI3K,AKT,phosphorylated protein kinase B).These observations were corroborated in vitro,where we found that the modulatory effects of dapagliflozin were abrogated by 740Y-P,an activator of the PI3K/AKT signaling pathway.CONCLUSION Dapagliflozin attenuates the polarization of macrophages toward the M1 phenotype,thereby mitigating inflammation and promoting macrophage apoptosis.These effects are likely mediated through the inhibition of the PI3K/AKT signaling pathway.

一种基于Polar译码度量选择的第三方高效PDCCH盲检方法

为研究和设计面向第三方场景的高效盲检方法,提出了一种基于Polar译码度量选择的第三方高效PDCCH盲检方法,其技术路线包括Polar译码算法与物理的下行控制信道(PDCCH)盲检算法2个板块.基于Polar译码盲检算法,引入一种基于下行控制信息(DCI)长度的Polar译码度量,提出了改进的基于Polar译码度量选择的第三方盲检方法.基于PDCCH盲检算法,引入一种重排序盲检算法.将改进的Polar译码算法与重排序盲检算法有机结合,提出面向第三方场景的高效PDCCH盲检方法.基于MATLAB平台搭建5G PDCCH盲检仿真链路,对所提方法进行验证与分析.结果表明,该方法能够同时有效减小PDCCH盲检次数与DCI候选长度数量,在保证目标捕获准确率的前提下提高盲检效率.

Ellipsometric configurations using a phase retarder and a rotating polarizer and analyzer at any speed ratio

In this paper, we propose an ellipsometer using a phase retarder and rotating polarizer and analyzer at a speed ratio I：N. Different ellipsometric configurations are presented by assuming N = 1, 2, and 3. Moreover, two values of the offset angle of the retarder are considered for each ellipsometric configuration. The Mueller formalism is employed to extract the Stokes parameters, from which the intensity received by the detector is obtained. The optical properties of c-Si are calculated using all configurations. A comparison between different configurations is carried out considering the effect of the noise on the results and the uncertainties in the ellipsometric parameters as functions of the uncertainties of the Fourier coefficients. It is found that the alignment of the phase retarder has a crucial impact on the results and the ellipsometric configuration with speed ratio 1：1 is preferred over the other configurations.

Compact TE-pass polarizer based on lithium-niobate-on-insulator assisted by indium tin oxide and silicon nitride

An indium tin oxide(ITO) and silicon nitride(Si_(3)N_(4)) assisted compact TE-pass waveguide polarizer based on lithiumniobate-on-insulator is proposed and numerically analyzed.By properly designing the ITO and Si_(3)N_(4) assisted structure and utilizing the epsilon-near-zero effect of ITO,the TM mode is strongly confined in the ITO layer with extremely high loss,while the TE mode is hardly affected and passes through the waveguide with low loss.The simulation results show that the polarizer has an extinction ratio of 22.5 dB and an insertion loss of 0.8 dB at the wavelength of 1.55 μm,and has an operating bandwidth of about 125 nm(from 1540 nm to 1665 nm) for an extinction ratio of>20 dB and an insertion loss of<0.95 dB.Moreover,the proposed device exhibits large fabrication tolerances.More notably,the device is compact,with a length of only 7.5 μm,and is appropriate for on-chip applications.

Precision integration of grating-based polarizers onto focal plane arrays of near-infrared photovoltaic detectors for enhanced contrast polarimetric imaging

Polarimetric imaging enhances the ability to distinguish objects from a bright background by detecting their particular polarization status,which offers another degree of freedom in infrared remote sensing.However,to scale up by monolithically integrating grating-based polarizers onto a focal plane array(FPA)of infrared detectors,fundamental technical obstacles must be overcome,including reductions of the extinction ratio by the misalignment between the polarizer and the detector,grating line width fluctuations,the line edge roughness,etc.This paper reports the authors’latest achievements in overcoming those problems by solving key technical issues regarding the integration of large-scale polarizers onto the chips of FPAs with individual indium gallium arsenide/indium phosphide(In Ga As/In P)sensors as the basic building blocks.Polarimetric and photovoltaic chips with divisions of the focal plane of 540×4 pixels and 320×256 superpixels have been successfully manufactured.Polarimetric imaging with enhanced contrast has been demonstrated.The progress made in this work has opened up a broad avenue toward industrialization of high quality polarimetric imaging in infrared wavelengths.

融合路径度量值和行重特性的Polar码SCL译码算法

首先提出基于初始对数似然比(Log-Likelihood Ratio,LR)与路径度量值(Path Metric,PM)的PM-LLR-SCL译码算法,在接收端初始LLR和PM值之间建立映射关系,并通过重排PM值完成翻转功能。其次,提出基于极化码生成矩阵的行重特性和PM值的PM-RW-SCL译码算法,不仅考虑了Polar码的最小码距和极化子信道可靠度,同时将路径分裂每一层的PM值引入到译码策略中,从而提高了译码性能。仿真结果显示,与串行抵消列表比特翻转(Successive Cancellation List Bit-flip,SCLF)相比,提出的PM-LLR-SCL算法最大可获得约0.23 dB的性能增益,而基于路径数量的复杂度降低了约62%;与基于行权重的串行抵消列表翻转译码算法相比,PM-RW-SCL算法最大可获得约1.5 dB的性能增益,而复杂度降低了约39%。

动态扰动辅助的串行抵消双比特翻转Polar译码算法

针对串行抵消翻转译码算法(Successive Cancellation Flip,SCF)受限于单比特翻转而性能提升有限问题,提出了一种双比特翻转译码算法(Successive Cancellation Flip with 2 Bits,SCF2)。针对SCP算法扰动方差初始值固定的问题,设计了一种扰动方差可随码长和码率变化的改进SCP算法。在此基础上,结合翻转和扰动机制,提出了一种动态扰动辅助的串行抵消双比特翻转(Dynamic Perturbation-Aided SCF2,DPA-SCF2)译码算法,并对其译码复杂度和性能进行了分析。仿真结果显示,相比于列表长度为4的循环冗余校验辅助串行抵消列表(Cyclic Redundancy Check Aided Successive Cancellation List,CA-SCL)译码算法,所提算法最大可获得约0.5 dB的性能增益。

A Transmission-Type Electrically Tunable Polarizer Based on Graphene Ribbons at Terahertz Wave Band

We theoretically and numerically demonstrate that a transmission-type electrically tunable polarizer can be realized by using graphene ribbons supported on a dielectric film with a graphene sheet behind. The polarization mechanism originates from the antenna plasmon resonance of graphene stripes. The results of full-wave numerical simulations reveal that transmittance of 0.70 for one polarization and 0.0073 for another polarization can be obtained at normal incidence. The transmission-type electrically tunable polarizer provides and facilitates a variety of applications, including filtering, detecting, and imaging.