Calculus bovis inhibits M2 tumor-associated macrophage polarization via Wnt/β-catenin pathway modulation to suppress liver cancer

BACKGROUND Calculus bovis(CB),used in traditional Chinese medicine,exhibits anti-tumor effects in various cancer models.It also constitutes an integral component of a compound formulation known as Pien Tze Huang,which is indicated for the treatment of liver cancer.However,its impact on the liver cancer tumor microenvironment,particularly on tumor-associated macrophages(TAMs),is not well understood.AIM To elucidate the anti-liver cancer effect of CB by inhibiting M2-TAM polarization via Wnt/β-catenin pathway modulation.METHODS This study identified the active components of CB using UPLC-Q-TOF-MS,evaluated its anti-neoplastic effects in a nude mouse model,and elucidated the underlying mechanisms via network pharmacology,transcriptomics,and molecular docking.In vitro assays were used to investigate the effects of CB-containing serum on HepG2 cells and M2-TAMs,and Wnt pathway modulation was validated by real-time reverse transcriptase-polymerase chain reaction and Western blot analysis.RESULTS This study identified 22 active components in CB,11 of which were detected in the bloodstream.Preclinical investigations have demonstrated the ability of CB to effectively inhibit liver tumor growth.An integrated approach employing network pharmacology,transcriptomics,and molecular docking implicated the Wnt signaling pathway as a target of the antineoplastic activity of CB by suppressing M2-TAM polarization.In vitro and in vivo experiments further confirmed that CB significantly hinders M2-TAM polarization and suppresses Wnt/β-catenin pathway activation.The inhibitory effect of CB on M2-TAMs was reversed when treated with the Wnt agonist SKL2001,confirming its pathway specificity.CONCLUSION This study demonstrated that CB mediates inhibition of M2-TAM polarization through the Wnt/β-catenin pathway,contributing to the suppression of liver cancer growth.

Myricetin induces M2 macrophage polarization to alleviate renal tubulointerstitial fibrosis in diabetic nephropathy via PI3K/Akt pathway

BACKGROUND Development of end-stage renal disease is predominantly attributed to diabetic nephropathy(DN).Previous studies have indicated that myricetin possesses the potential to mitigate the pathological alterations observed in renal tissue.Never-theless,the precise molecular mechanism through which myricetin influences the progression of DN remains uncertain.AIM To investigate the effects of myricetin on DN and explore its potential therapeutic mechanism.METHODS Db/db mice were administered myricetin intragastrically on a daily basis at doses of 50 mg/kg or 100 mg/kg for a duration of 12 wk.Subsequently,blood and urine indexes were assessed,along with examination of renal tissue pathology.Kidney morphology and fibrosis were evaluated using various staining techniques including hematoxylin and eosin,periodic acid–Schiff,Masson’s trichrome,and Sirius-red.Additionally,high-glucose culturing was conducted on the RAW 264.7 cell line,treated with 25 mM myricetin or co-administered with the PI3K/Akt inhibitor LY294002 for a period of 24 h.In both in vivo and in vitro settings,quantification of inflammation factor levels was conducted using western blotting,real-time qPCR and ELISA.RESULTS In db/db mice,administration of myricetin led to a mitigating effect on DN-induced renal dysfunction and fibrosis.Notably,we observed a significant reduction in expressions of the kidney injury markers kidney injury molecule-1 and neutrophil gelatinase associated lipocalin,along with a decrease in expressions of inflammatory cytokine-related factors.Furthermore,myricetin treatment effectively inhibited the up-regulation of tumor necrosis factor-alpha,interleukin-6,and interluekin-1βinduced by high glucose in RAW 264.7 cells.Additionally,myricetin modulated the M1-type polarization of the RAW 264.7 cells.Molecular docking and bioinformatic analyses revealed Akt as the target of myricetin.The protective effect of myricetin was nullified upon blocking the polarization of RAW 264.7 via inhibition of PI3K/Akt activation using LY294002.CONCLUSION This study demonstrated that myricetin effectively mitigates kidney injury in DN mice through the regulation of macrophage polarization via the PI3K/Akt signaling pathway.

Atherosis-associated lnc_000048 activates PKR to enhance STAT1-mediated polarization of THP-1 macrophages to M1 phenotype

Our previous study has demonstrated that lnc_000048 is upregulated in large-artery atherosclerotic stroke and promotes atherosclerosis in ApoE^(-/-)mice.However,little is known about the role of lnc_000048 in classically activated macrophage(M1)polarization.In this study,we established THP-1-derived testing state macrophages(M0),M1 macrophages,and alternately activated macrophages(M2).Real-time fluorescence quantitative PCR was used to verify the expression of marker genes and the expression of lnc_000048 in macrophages.Flow cytometry was used to detect phenotypic proteins(CD11b,CD38,CD80).We generated cell lines with lentivirus-mediated upregulation or downregulation of lnc_000048.Flow cytometry,western blot,and real-time fluorescence quantitative PCR results showed that down-regulation of lnc_000048 reduced M1 macrophage polarization and the inflammation response,while over-expression of lnc_000048 led to the opposite effect.Western blot results indicated that lnc_000048 enhanced the activation of the STAT1 pathway and mediated the M1 macrophage polarization.Moreover,catRAPID prediction,RNA-pull down,and mass spectrometry were used to identify and screen the protein kinase RNA-activated(PKR),then catRAPID and RPIseq were used to predict the binding ability of lnc_000048 to PKR.Immunofluorescence(IF)-RNA fluorescence in situ hybridization(FISH)double labeling was performed to verify the subcellular colocalization of lnc_000048 and PKR in the cytoplasm of M1 macrophage.We speculate that lnc_000048 may form stem-loop structure-specific binding and activate PKR by inducing its phosphorylation,leading to activation of STAT1 phosphorylation and thereby enhancing STAT1 pathway-mediated polarization of THP-1 macrophages to M1 and inflammatory factor expression.Taken together,these results reveal that the lnc_000048/PKR/STAT1 axis plays a crucial role in the polarization of M1 macrophages and may be a novel therapeutic target for atherosclerosis alleviation in stroke.

Realizing optimized interfacial polarization and impedance matching with CNT-confined Co nanoparticles in hollow carbon microspheres for enhanced microwave absorption

The hollow porous structure with exceptional interfacial effect and customizable internal environment shows significant potential for application as electromagnetic shielding and absorption materials.However,designing hollow porous electromagnetic absorbers with both desirable impedance matching and high loss capability remains a challenge.Herein,3D hollow porous electromagnetic microspheres were constructed by assembling 0D Co magnetic nanoparticles,1D carbon nanotubes,and 2D carbon nanosheets.Due to the sufficient sites for Co^(2+)riveting,the high loading of magnetic carbon nanotubes(CoNC)and porous carbon spheres formed high-density interfaces,enhancing the interfacial polarization.Furthermore,high-density CoNC were grown in situ on the hollow porous carbon(HPC)microsphere,forming a highly dispersed 3D magnetic network that inhibited the aggregation of magnetic nanoparticles and enhanced magnetic coupling.Therefore,the asprepared CoNC/HPC microspheres exhibited excellent microwave absorption(MA)performance,with a minimum reflection loss of-33.2 dB and an effective bandwidth of 5.5 GHz at a thickness of only 1.8 mm.The interfacial polarization mechanism for enhanced MA performance was demonstrated by electron holography and density functional theory calculations.Magnetic holography and micromagnetic simulations also revealed magnetic confinement and coupling mechanism.This work provides a new approach for designing electromagnetic absorbers with optimized impedance matching and loss capability.

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.

Linear dichroism transition and polarization-sensitive photodetector of quasi-one-dimensional palladium bromide

Perpendicular optical reversal of the linear dichroism transition has promising applications in polarization-sensitive optoelectronic devices. We perform a systematical study on the in-plane optical anisotropy of quasi-one-dimensional PdBr_(2) by using combined measurements of the angle-resolved polarized Raman spectroscopy(ARPRS) and anisotropic optical absorption spectrum. The analyses of ARPRS data validate the anisotropic Raman properties of the PdBr_(2) flake.And anisotropic optical absorption spectrum of PdBr_(2) nanoflake demonstrates distinct optical linear dichroism reversal. Photodetector constructed by PdBr_(2) nanowire exhibits high responsivity of 747 A·W^(-1) and specific detectivity of 5.8×10^(12) Jones. And the photodetector demonstrates prominent polarization-sensitive photoresponsivity under 405-nm light irradiation with large photocurrent anisotropy ratio of 1.56, which is superior to those of most of previously reported quasi-one-dimensional counterparts. Our study offers fundamental insights into the strong optical anisotropy exhibited by PdBr_(2), establishing it as a promising candidate for miniaturization and integration trends of polarization-related applications.

Polydatin ameliorates hepatic ischemia-reperfusion injury by modulating macrophage polarization

Background:Polydatin,a glucoside of resveratrol,has shown protective effects against various diseases.However,little is known about its effect on hepatic ischemia-reperfusion(I/R)injury.This study aimed to elucidate whether polydatin protects liver against I/R-induced injury and to explore the underlying mechanism.Methods:After gavage feeding polydatin once daily for a week,mice underwent a partial hepatic I/R procedure.Serum alanine aminotransferase(ALT)/aspartate aminotransferase(AST),hematoxylin-eosin(H&E)and TdT-mediated dUTP nick-end labeling(TUNEL)staining were used to evaluate liver injury.The severity related to the inflammatory response and reactive oxygen species(ROS)production was also investigated.Furthermore,immunofluorescence and Western blotting were used to detect macrophage polarization and the NF-κB signaling pathway in macrophages.Results:Compared with the I/R group,polydatin pretreatment significantly attenuated I/R-induced liver damage and apoptosis.The oxidative stress marker(dihydroethidium fluorescence,malondialdehyde,superoxide dismutase and glutathione peroxidase)and I/R related inflammatory cytokines(interleukin1β,interleukin-10 and tumor necrosis factor-α)were significantly suppressed after polydatin treatment.In addition,the result of immunofluorescence indicated that polydatin reduced the polarization of macrophages toward M1 macrophages both in vivo and in vitro.Western blotting showed that polydatin inhibited the pro-inflammatory function of RAW264.7 via down-regulating the NF-κB signaling pathway.Conclusions:Polydatin protects the liver from I/R injury by remodeling macrophage polarization via NFκB signaling.

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.

Ultra-broadband and wide-angle reflective terahertz polarization conversion metasurface based on topological optimization

Terahertz polarization conversion devices have significant potential applications in various fields such as terahertzimaging and spectroscopy.In this paper,we utilize genetic algorithms to topologically optimize the metasurface unit cellsand design a reflective linear polarization conversion metasurface with ultra-broadband and wide-angle characteristics.By partitioning the metallic pattern layer into quadrants,the encoding length is effectively reduced,resulting in a shorteroptimization time.The research results indicate that the converter possesses a polarization conversion efficiency ratio higherthan 90%and a relative bandwidth ratio of 125%in a range of 0.231-0.995 THz.Meanwhile,it can maintain excellentpolarization conversion properties when the incident angle of terahertz waves is less than 45°and the polarization angle isless than 15°,demonstrating excellent practicality.New insights are provided for the design of terahertz wide-angle ultrawidebandpolarization conversion devices,and the proposed metasurfce has potential applications in terahertz polarizationimaging,spectroscopy and communication fields.

Effect of electron-electron interaction on polarization process of exciton and biexciton in conjugated polymer

By using one-dimensional tight-binding model modified to include electron-electric field interaction and electron-electron interaction,we theoretically explore the polarization process of exciton and biexciton in cis-polyacetylene.The dynamical simulation is performed by adopting the non-adiabatic evolution approach.The results show that under the effect of moderate electric field,when the strength of electron-electron interaction is weak,the singlet exciton is stable but its polarization presents obvious oscillation.With the enhancement of interaction,it is dissociated into polaron pairs,the spin-flip of which can be observed through modulating the interaction strength.For the triplet exciton,the strong electron-electron interaction restrains its normal polarization,but it is still stable.In the case of biexciton,the strong electron-electron interaction not only dissociate it,but also flip its charge distribution.The yield of the possible states formed after the dissociation of exciton and biexciton is also calculated.

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.

A 1-bit electronically reconfigurable beam steerable metasurface reflectarray with multiple polarization manipulations

A 1-bit electronically controlled metasurface reflectarray is presented to achieve beam steering with multiple polarization manipulations. A metsurface unit cell loaded by two PIN diodes is designed. By switching the two PIN diodes between ON and OFF states, the isotropic and anisotropic reflections can be flexibly achieved. For either the isotropic reflection or the anisotropic reflection, the two operation states achieve the reflection coefficients with approximately equal magnitude and 180°out of phase, thus giving rise to the isotropic/anisotropic 1-bit metasurface unit cells. With the 1-bit unit cells, a 12-by-12 metasurface reflectarray is optimally designed and fabricated. Under either y-or x-polarized incident wave illumination, the reflectarray can achieve the co-polarized and cross-polarized beam scanning, respectively, with the peak gains of 20.08 d Bi and 17.26 d Bi within the scan range of about ±50°. With the right-handed circular polarization(RHCP) excitation, the left-handed circular polarization(LHCP) radiation with the peak gain of 16.98 d Bic can be achieved within the scan range of ±50°. Good agreement between the experimental results and the simulation results are observed for 2D beam steering and polarization manipulation capabilities.

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.

Internal Polarization Field Induced Hydroxyl Spillover Effect for Industrial Water Splitting Electrolyzers

The formation of multiple oxygen intermediates supporting efficient oxygen evolution reaction(OER)are affinitive with hydroxyl adsorption.However,ability of the catalyst to capture hydroxyl and maintain the continuous supply at active sits remains a tremendous challenge.Herein,an affordable Ni2P/FeP2 heterostructure is presented to form the internal polarization field(IPF),arising hydroxyl spillover(HOSo)during OER.Facilitated by IPF,the oriented HOSo from FeP2 to Ni2P can activate the Ni site with a new hydroxyl transmission channel and build the optimized reaction path of oxygen intermediates for lower adsorption energy,boosting the OER activity(242 mV vs.RHE at 100 mA cm-2)for least 100 h.More interestingly,for the anion exchange membrane water electrolyzer(AEMWE)with low concentration electrolyte,the advantage of HOSo effect is significantly amplified,delivering 1 A cm^(-2)at a low cell voltage of 1.88 V with excellent stability for over 50 h.

The First Ground-based White Light Lunar Polarization Imaging:A New Kind of FeO Observation on the Near Side of the Moon

Lunar optical polarization is a fascinating phenomenon that occurs when sunlight reflects off the surface of the Moon and becomes polarized.This study employs a novel split-focus plane polarimetric camera to conduct the initial white light polarimetric observations on the near side of the Moon.We obtained the linear degree of polarization(DOP)parameters of white light by observation from the eastern and western hemispheres of the Moon.The findings indicate that the white light polarization is lower in the lunar highland than in the lunar maria overall.Combining the analysis of lunar soil samples,we noticed and determined that the DOP parameters of white light demonstrate high consistency with iron oxide on the Moon.This study may serve as a new diagnostic tool for the Moon.

Enhancing Defect-Induced Dipole Polarization Strategy of SiC@MoO_(3)Nanocomposite Towards Electromagnetic Wave Absorption

Defect engineering in transition metal oxides semiconductors(TMOs)is attracting considerable interest due to its potential to enhance conductivity by intentionally introducing defects that modulate the electronic structures of the materials.However,achieving a comprehensive understanding of the relationship between micro-structures and electromagnetic wave absorption capabilities remains elusive,posing a substantial challenge to the advancement of TMOs absorbers.The current research describes a process for the deposition of a MoO_(3)layer onto SiC nanowires,achieved via electro-deposition followed by high-temperature calcination.Subsequently,intentional creation of oxygen vacancies within the MoO_(3)layer was carried out,facilitating the precise adjustment of electromagnetic properties to enhance the microwave absorption performance of the material.Remarkably,the SiC@MO-t4 sample exhibited an excellent minimum reflection loss of-50.49 dB at a matching thickness of 1.27 mm.Furthermore,the SiC@MO-t6 sample exhibited an effective absorption bandwidth of 8.72 GHz with a thickness of 2.81 mm,comprehensively covering the entire Ku band.These results not only highlight the pivotal role of defect engineering in the nuanced adjustment of electromagnetic properties but also provide valuable insight for the application of defect engineering methods in broadening the spectrum of electromagnetic wave absor ption effectiveness.SiC@MO-t samples with varying concentrations of oxygen vacancies were prepared through in-situ etching of the SiC@MoO_(3)nanocomposite.The presence of oxygen vacancies plays a crucial role in adjusting the band gap and local electron distribution,which in turn enhances conductivity loss and induced polarization loss capacity.This finding reveals a novel strategy for improving the absorption properties of electromagnetic waves through defect engineering.

Simultaneous fluorescence and Compton scattering computed tomography based on linear polarization X-ray

Purpose To propose a method for simultaneous fluorescence and Compton scattering computed tomography by using linearly polarized X-rays.Methods Monte Carlo simulations were adopted to demonstrate the feasibility of the proposed method.In the simulations,the phantom is a polytetrafluoroethylene cylinder inside which are cylindrical columns containing aluminum,water,and gold(Au)-loaded water solutions with Au concentrations ranging between 0.5 and 4.0 wt%,and a parallel-hole collimator imaging geometry was adopted.The light source was modeled based on a Thomson scattering X-ray source.The phantom images for both imaging modalities were reconstructed using a maximumlikelihood expectation maximization algorithm.Results Both the X-ray fluorescence computed tomography(XFCT)and Compton scattering computed tomography(CSCT)images of the phantom were accurately reconstructed.A similar attenuation contrast problem for the different cylindrical columns in the phantom can be resolved in the XFCT and CSCT images.The interplay between XFCT and CSCT was analyzed,and the contrast-to-noise ratio(CNR)of the reconstruction was improved by correcting for the mutual influence between the two imaging modalities.Compared with K-edge subtraction imaging,XFCT exhibits a CNR advantage for the phantom.Conclusion Simultaneous XFCT and CSCT can be realized by using linearly polarized X-rays.The synergy between the two imaging modalities would have an important application in cancer radiation therapy.

Breaking the optical efficiency limit of virtual reality with a nonreciprocal polarization rotator

A catadioptric lens structure,also known as pancake lens,has been widely used in virtual reality(VR)displays to reduce the formfactor.However,the utilization of a half mirror(HM)to fold the optical path thrice leads to a significant optical loss.The theoretical maximum optical efficiency is merely 25%.To transcend this optical efficiency constraint while retaining the foldable characteristic inherent to traditional pancake optics,in this paper,we propose a theoretically lossless folded optical system to replace the HM with a nonreciprocal polarization rotator.In our feasibility demonstration experiment,we used a commercial Faraday rotator(FR)and reflective polarizers to replace the lossy HM.The theoretically predicted 100%efficiency can be achieved approximately by using two high-extinction-ratio reflective polarizers.In addition,we evaluated the ghost images using a micro-OLED panel in our imaging system.Indeed,the ghost images can be suppressed to undetectable level if the optics are with antireflection coating.Our novel pancake optical system holds great potential for revolutionizing next-generation VR displays with lightweight,compact formfactor,and low power consumption.

Knockout of C6orf120 in Rats Alleviates Concanavalin A-induced Autoimmune Hepatitis by Regulating Macrophage Polarization

Objective The effect of the functionally unknown gene C6orf120 on autoimmune hepatitis was investigated on C6orf120 knockout rats(C6orf120^(-/-))and THP-1 cells.Method Six–eight-week-old C6orf120^(-/-)and wild-type(WT)SD rats were injected with Con A(16 mg/kg),and euthanized after 24 h.The sera,livers,and spleens were collected.THP-1 cells and the recombinant protein(rC6ORF120)were used to explore the mechanism in vitro.The frequency of M1 and M2 macrophages was analyzed using flow cytometry.Western blotting and PCR were used to detect macrophage polarization-associated factors.Results C6orf120 knockout attenuated Con A-induced autoimmune hepatitis.Flow cytometry indicated that the proportion of CD68^(+)CD86^(+)M1 macrophages from the liver and spleen in the C6orf120^(-/-)rats decreased.C6orf120 knockout induced downregulation of CD86 protein and the mRNA levels of related inflammatory factors TNF-α,IL-1β,and IL-6 in the liver.C6orf120 knockout did not affect the polarization of THP-1 cells.However,rC6ORF120 promoted the THP-1 cells toward CD68^(+)CD80^(+)M1 macrophages and inhibited the CD68^(+)CD206^(+)M2 phenotype.Conclusion C6orf120 knockout alleviates Con A-induced autoimmune hepatitis by inhibiting macrophage polarization toward M1 macrophages and reducing the expression of related inflammatory factors in C6orf120^(-/-)rats.

High-Power Raman Soliton Generation at 1.7 μm in All-Fiber Polarization-Maintaining Erbium-Doped Amplifier

An all-fiber polarization maintaining high-power laser system operating at 1.7 μm based on the Ramaninduced soliton self-frequency shifting effect is demonstrated. The entirely fiberized system is built by erbiumdoped oscillator and two-stage amplifiers with polarization maintaining commercial silica fibers and devices, which can provide robust and stable soliton generation. High-power soliton laser with the average power of 0.28 W,the repetition rate of 42.7 MHz, and pulse duration of 515 fs is generated directly from the main amplifier.Our experiment provides a feasible method for high-power all-fiber polarization maintaining femtosecond laser generation working at 1.7 μm.