Brain ischemia causes systemic Notch1 activity in endothelial cells to drive atherosclerosis.

Stroke leads to persistently high risk for recurrent vascular events caused by systemic atheroprogression that is driven by endothelial cell (EC) activation. However, whether and how stroke induces sustained pro-inflammatory and proatherogenic endothelial alterations in systemic vessels remain poorly understood. We showed that brain ischemia induces persistent activation, the upregulation of adhesion molecule VCAM1, and increased senescence in peripheral ECs until 4 weeks after stroke onset. This aberrant EC activity resulted from sustained Notch1 signaling, which was triggered by increased circulating Notch1 ligands DLL1 and Jagged1 after stroke in mice and humans. Consequently, this led to increased myeloid cell adhesion and atheroprogression by generating a senescent, pro-inflammatory endothelium. Notch1- or VCAM1-blocking antibodies and the genetic ablation of endothelial Notch1 reduced atheroprogression after stroke. Our findings revealed a systemic machinery that induces the persistent activation of peripheral ECs after stroke, which paves the way for therapeutic interventions or the prevention of recurrent vascular events following stroke.

Strain engineering and epitaxial stabilization of halide perovskites.

Strain engineering is a powerful tool with which to enhance semiconductor device performance1,2. Halide perovskites have shown great promise in device applications owing to their remarkable electronic and optoelectronic properties3-5. Although applying strain to halide perovskites has been frequently attempted, including using hydrostatic pressurization6-8, electrostriction9, annealing10-12, van der Waals force13, thermal expansion mismatch14, and heat-induced substrate phase transition15, the controllable and device-compatible strain engineering of halide perovskites by chemical epitaxy remains a challenge, owing to the absence of suitable lattice-mismatched epitaxial substrates. Here we report the strained epitaxial growth of halide perovskite single-crystal thin films on lattice-mismatched halide perovskite substrates. We investigated strain engineering of α-formamidinium lead iodide (α-FAPbI3) using both experimental techniques and theoretical calculations. By tailoring the substrate composition-and therefore its lattice parameter-a compressive strain as high as 2.4 per cent is applied to the epitaxial α-FAPbI3 thin film. We demonstrate that this strain effectively changes the crystal structure, reduces the bandgap and increases the hole mobility of α-FAPbI3. Strained epitaxy is also shown to have a substantial stabilization effect on the α-FAPbI3 phase owing to the synergistic effects of epitaxial stabilization and strain neutralization. As an example, strain engineering is applied to enhance the performance of an α-FAPbI3-based photodetector.

E3 ligase DECREASED GRAIN SIZE 1 promotes degradation of a G-protein subunit and positively regulates grain size in rice.

Grain size is one of the most important traits determining crop yield. However, the mechanism controlling grain size remains unclear. Here, we confirmed the E3 ligase activity of DECREASED GRAIN SIZE 1 (DGS1) in positive regulation of grain size in rice (Oryza sativa) suggested in a previous study. Rice G-protein subunit gamma 2 (RGG2), which negatively regulates grain size, was identified as an interacting protein of DGS1. Biochemical analysis suggested that DGS1 specifically interacts with canonical Gγ subunits (rice G-protein subunit gamma 1 [RGG1] and rice G-protein subunit gamma 2 [RGG2]) rather than non-canonical Gγ subunits (DENSE AND ERECT PANICLE 1 [DEP1], rice G-protein gamma subunit type C 2 [GCC2], GRAIN SIZE 3 [GS3]). We also identified the necessary domains for interaction between DGS1 and RGG2. As an E3 ligase, DGS1 ubiquitinated and degraded RGG2 via a proteasome pathway in several experiments. DGS1 also ubiquitinated RGG2 by its K140, K145 and S147 residues. Thus, this work identified a substrate of the E3 ligase DGS1 and elucidated the post transcriptional regulatory mechanism of the G-protein signalling pathway in the control of grain size.

Ultrathin Ternary FeCoNi Alloy Nanoarrays in BaTiO3 Matrix for Room-Temperature Multiferroic and Hyperbolic Metamaterial.

Multifunctional vertically aligned nanocomposite (VAN) thin films exhibit considerable potential in diverse fields. Here, a BaTiO3-FeCoNi alloy (BTO-FCN) system featuring an ultrathin ternary FCN alloy nanopillar array embedded in the BTO matrix has been developed with tailorable nanopillar size and interpillar distance. The magnetic alloy nanopillars combined with a ferroelectric oxide matrix present intriguing multifunctionality and coupling properties. The room-temperature magnetic response proves the soft magnet nature of the BTO-FCN films with magnetic anisotropy has been demonstrated. Furthermore, the anisotropic nature of the dielectric-metal alloy VAN renders it an ideal candidate for hyperbolic metamaterial (HMM), and the epsilon-near-zero (ENZ) wavelength, where the real part of permittivity (ε') turns to negative, can be tailored from ∼700 nm to ∼1050 nm. Lastly, room-temperature multiferroicity has been demonstrated via interfacial coupling between the magnetic nanopillars and ferroelectric matrix.

Full-angle single-shot quantitative phase imaging based on Kramers-Kronig relations.

As a non-interference and non-iterative method, annular-illumination quantitative phase imaging based on Kramers-Kronig relations (AIKK) can realize phase measurement with full-angle resolution enhancement under multiple exposures. In order to completely record the object spectrum with a single shot, we proposed a colorful complementary illumination method in the recording process. The angle of this illumination mode is not symmetrical with each other, so the spectrum between the three channels can complement each other to avoid spectrum loss caused by spectrum conjugation. Meanwhile, the three spectral segments of full-angle information spectrum respectively carried by three wavelengths can be recorded. Additionally, the numerical filter is applied to correct the overlapped spectrum in the reconstruction process. Simulation and experimental results show that this method can achieve high spatiotemporal resolution quantitative phase measurement.

Verifying Quantum Advantage Experiments with Multiple Amplitude Tensor Network Contraction.

The quantum supremacy experiment, such as Google Sycamore [F. Arute et al., Nature (London) 574, 505 (2019).NATUAS0028-083610.1038/s41586-019-1666-5], poses a great challenge for classical verification due to the exponentially increasing compute cost. Using a new-generation Sunway supercomputer within 8.5 d, we provide a direct verification by computing 3×10^{6} exact amplitudes for the experimentally generated bitstrings, obtaining a cross-entropy benchmarking fidelity of 0.191% (the estimated value is 0.224%). The leap of simulation capability is built on a multiple-amplitude tensor network contraction algorithm which systematically exploits the "classical advantage" (the inherent "store-and-compute" operation mode of von Neumann machines) of current supercomputers, and a fused tensor network contraction algorithm which drastically increases the compute efficiency on heterogeneous architectures. Our method has a far-reaching impact in solving quantum many-body problems, statistical problems, as well as combinatorial optimization problems.

Effectiveness of CT radiomic features combined with clinical factors in predicting prognosis in patients with limited-stage small cell lung cancer.

BACKGROUND: The prognosis of SCLC is poor and difficult to predict. The aim of this study was to explore whether a model based on radiomics and clinical features could predict the prognosis of patients with limited-stage small cell lung cancer (LS-SCLC). METHODS: Simulated positioning CT images and clinical features were retrospectively collected from 200 patients with histological diagnosis of LS-SCLC admitted between 2013 and 2021, which were randomly divided into the training (n = 140) and testing (n = 60) groups. Radiomics features were extracted from simulated positioning CT images, and the t-test and the least absolute shrinkage and selection operator (LASSO) were used to screen radiomics features. We then constructed radiomic score (RadScore) based on the filtered radiomics features. Clinical factors were analyzed using the Kaplan-Meier method. The Cox proportional hazards model was used for further analyses of possible prognostic features and clinical factors to build three models including a radiomic model, a clinical model, and a combined model including clinical factors and RadScore. When a model has prognostic predictive value (AUC > 0.7) in both train and test groups, a nomogram will be created. The performance of three models was evaluated using area under the receiver operating characteristic curve (AUC) and Kaplan-Meier analysis. RESULTS: A total of 1037 features were extracted from simulated positioning CT images which were contrast enhanced CT of the chest. The combined model showed the best prediction, with very poor AUC for the radiomic model and the clinical model. The combined model of OS included 4 clinical features and RadScore, with AUCs of 0.71 and 0.70 in the training and test groups. The combined model of PFS included 4 clinical features and RadScore, with AUCs of 0.72 and 0.71 in the training and test groups. T stages, ProGRP and smoke status were the independent variables for OS in the combined model, whereas T stages, ProGRP and prophylactic cranial irradiation (PCI) were the independent factors for PFS. There was a statistically significant difference between the low- and high-risk groups in the combined model of OS (training group, p < 0.0001; testing group, p = 0.0269) and PFS (training group, p < 0.0001; testing group, p < 0.0001). CONCLUSION: Combined models involved RadScore and clinical factors can predict prognosis in LS-SCLC and show better performance than individual radiomics and clinical models.

Base-mediated synthesis of aryl enol ethers from α-aryl allylic alcohols and arylsulfonium salts.

A concise synthesis of aryl enol ethers from allylic alcohols and arylsulfonium salts by simply using an inorganic base as a mediator is described. The reaction enabled the facile conversion of various α-aryl allylic alcohols into the corresponding aryl enol ethers in good yields with excellent selectivity. The results demonstrated that both symmetric triarylsulfonium triflate and 10-methyl-5-aryl-5,10-dihydrophenothiazin-5-ium salts were effective arylation reagents for the base-initiated selective O-arylation and isomerization of α-aryl allylic alcohols. This reaction represents the first use of arylsulfonium salts as arylation reagents to access aryl enol ethers directly from allylic alcohols.

MolCFL: A personalized and privacy-preserving drug discovery framework based on generative clustered federated learning.

In today's era of rapid development of large models, the traditional drug development process is undergoing a profound transformation. The vast demand for data and consumption of computational resources are making independent drug discovery increasingly difficult. By integrating federated learning technology into the drug discovery field, we have found a solution that both protects privacy and shares computational power. However, the differences in data held by various pharmaceutical institutions and the diversity in drug design objectives have exacerbated the issue of data heterogeneity, making traditional federated learning consensus models unable to meet the personalized needs of all parties. In this study, we introduce and evaluate an innovative drug discovery framework, MolCFL, which utilizes a multi-layer perceptron (MLP) as the generator and a graph convolutional network (GCN) as the discriminator in a generative adversarial network (GAN). By learning the graph structure of molecules, it generates new molecules in a highly personalized manner and then optimizes the learning process by clustering federated learning, grouping compound data with high similarity. MolCFL not only enhances the model's ability to protect privacy but also significantly improves the efficiency and personalization of molecular design. MolCFL exhibits superior performance when handling non-independently and identically distributed data compared to traditional models. Experimental results show that the framework demonstrates outstanding performance on two benchmark datasets, with the generated new molecules achieving over 90% in Uniqueness and close to 100% in Novelty. MolCFL not only improves the quality and efficiency of drug molecule design but also, through its highly customized clustered federated learning environment, promotes collaboration and specialization in the drug discovery process while ensuring data privacy. These features make MolCFL a powerful tool suitable for addressing the various challenges faced in the modern drug research and development field.

Self-Assembled Au Nanoelectrodes: Enabling Low-Threshold-Voltage HfO2-Based Artificial Neurons.

Filamentary-type resistive switching devices, such as conductive bridge random-access memory and valence change memory, have diverse applications in memory and neuromorphic computing. However, the randomness in filament formation poses challenges to device reliability and uniformity. To overcome this issue, various defect engineering methods have been explored, including doping, metal nanoparticle embedding, and extended defect utilization. In this study, we present a simple and effective approach using self-assembled uniform Au nanoelectrodes to controll filament formation in HfO2 resistive switching devices. By concentrating the electric field near the Au nanoelectrodes within the BaTiO3 matrix, we significantly enhanced the device stability and reduced the threshold voltage by up to 45% in HfO2-based artificial neurons compared to the control devices. The threshold voltage reduction is attributed to the uniformly distributed Au nanoelectrodes in the insulating matrix, as confirmed by COMSOL simulation. Our findings highlight the potential of nanostructure design for precise control of filamentary-type resistive switching devices.

PCSK9 involves in the high-fat diet-induced abnormal testicular function of male mice.

In brief: Impaired spermatogenesis resulting from disturbed cholesterol metabolism due to intake of high-fat diet (HFD) has been widely recognized, however, the role of preprotein invertase subtilin 9 (PCSK9), which is a negative regulator of cholesterol metabolism, has never been reported. This study aims to reveal the role of PCSK9 on spermatogenesis induced by HFD in mice. Abstract: Long-term consumption of a high-fat diet (HFD) is an important factor that leads to impaired spermatogenesis exhibiting poor sperm quantity and quality. However, the mechanism of this is yet to be elucidated. Disrupted cholesterol homeostasis is one of many crucial pathological factors which could contribute to impaired spermatogenesis. As a negative regulator of cholesterol metabolism, preprotein invertase subtilin 9 (PCSK9) mediates low density lipoprotein receptor (LDLR) degradation to the lysosome, thereby reducing the expression of LDLR on the cell membrane and increasing serum low-density lipoprotein cholesterol level, resulting in lipid metabolism disorders. Here, we aim to study whether PCSK9 is a pathological factor for impaired spermatogenesis induced by HFD and the underlying mechanism. To meet the purpose of our study, we utilized wild-type C57BL/6 male mice and PCSK9 knockout mice with same background as experimental subjects and alirocumab, a PCSK9 inhibitor, was used for treatment. Results indicated that HFD induced higher PCSK9 expression in serum, liver, and testes, and serum PCSK9 is negatively correlated with spermatogenesis, while both PCSK9 inhibitor treatment and PCSK9 knockout methodologies ameliorated impaired lipid metabolism and spermatogenesis in mice fed a HFD. This could be due to the overexpression of PCSK9 induced by HFD leading to dyslipidemia, resulting in testicular lipotoxicity, thus activating the Bcl-2-Bax-Caspase3 apoptosis signaling pathway in testes, particularly in Leydig cells. Our study demonstrates that PCSK9 is an important pathological factor in the dysfunction of spermatogenesis in mice induced by HFD. This finding could provide innovative ideas for the diagnosis and treatment of male infertility.

Polarization phase unwrapping by a dual-wavelength Mueller matrix imaging system.

In this Letter, we report a dual-wavelength Mueller matrix imaging system for polarization phase unwrapping, allowing simultaneous acquisition of the polarization images at 633 nm and 870 nm. After phase unwrapping, the relative error of linear retardance is controlled to be 3% and the absolute error of birefringence orientation is about 6°. We first show that polarization phase wrapping occurs when the samples are thick or present obvious birefringence effects, and further analyze the effect of phase wrapping on anisotropy parameters via Monte Carlo simulations. Then, experiments on porous alumina with different thicknesses and multilayer tapes are performed to verify the feasibility of phase unwrapping by a dual-wavelength Mueller matrix system. Finally, by comparing the temporal characteristics of linear retardance during tissue dehydration before and after phase unwrapping, we emphasize the significance of the dual-wavelength Mueller matrix imaging system not only for anisotropy analysis in static samples, but also for determining the trend in polarization properties of dynamic samples.

Local optimized Stokes polarimetry for specific polarization states.

In this Letter, we propose a locally optimized Stokes polarimetry. Focusing on the effect on polarization measurements by Poisson noise, the studies establish a new, to the best of our knowledge, optimization function combining the equally weighted variance with the condition number. This method considers both the stability and the precision of polarization measurements; by trading an increase in the condition number by 2.48%, we realize a decrease in equal-weighted variance by 19.1% near the north pole. The advantages of this local optimization method are demonstrated based on Monte Carlo (MC) simulations and experiments of continuous polarization state modulation. Finally, an imaging demonstration using a 4 µm pathological section implies the potential of this new local optimization method in improving polarization measurements and applying it to more biomedical research.

Age-related promoter-switch regulates Runx1 expression in adult rat hearts.

BACKGROUND: Runt-related transcription factor-1 (RUNX1), a key member of the core-binding factor family of transcription factors, has emerged as a novel therapeutic target for cardiovascular disease. There is an urgent need to fully understand the expression pattern of Runx1 in the heart and the mechanisms by which it is controlled under normal conditions and in response to disease. The expression of Runx1 is regulated at the transcriptional level by two promoters designated P1 and P2. Alternative usage of these two promoters creates differential mRNA transcripts diversified in distribution and translational potential. While the significance of P1/P2 promoter-switch in the transcriptional control of Runx1 has been highlighted in the embryogenic process, very little is known about the level of P1- and P2-specific transcripts in adult hearts, and the underlying mechanisms controlling the promoter-switch. METHODS: To amplify P1/P2 specific sequences in the heart, we used two different sense primers complementary to either P1 or P2 5'-regions to monitor the expression of P1/P2 transcripts. DNA methylation levels were assessed at the Runx1 promoter regions. Rats were grouped by age. RESULTS: The expression levels of both P1- and P2-derived Runx1 transcripts were decreased in older rats when compared with that in young adults, paralleled with an age-dependent decline in Runx1 protein level. Furthermore, older rats demonstrated a higher degree of DNA methylation at Runx1 promoter regions. Alternative promoter usage was observed in hearts with increased age, as reflected by altered P1:P2 mRNA ratio. CONCLUSION: Our data demonstrate that the expression of Runx1 in the heart is age-dependent and underscore the importance of gene methylation in the promoter-mediated transcriptional control of Runx1, thereby providing new insights to the role of epigenetic regulation in the heart.

MicroRNA-122-5p promotes renal fibrosis and injury in spontaneously hypertensive rats by targeting FOXO3.

Hypertensive renal injury is accompanied by tubular interstitial fibrosis leading to increased risk for renal failure. This study aimed to explore the influences of miR-122-5p in hypertension-mediated renal fibrosis and damage. 14-week-old male SHR and WKY rats were randomly assigned to treat with rAAV-miR-122-5p or rAAV-GFP for 8 weeks. There were marked increases in miR-122-5p and Kim-1 levels and decreases in FOXO3 and SIRT6 levels in hypertensive rats. Transfection with rAAV-miR-122-5p triggered exacerbation of renal fibrosis, apoptosis and inflammatory injury in SHR, associated with downregulated levels of FOXO3, SIRT6, ATG5 and BNIP3 as well as upregulated expression of Kim-1, NOX4, CTGF, and TGF-ß1. In cultured primary mouse renal tubular interstitial fibroblasts, exposure to angiotensin II resulted in obvious downregulation of FOXO3, SIRT6, ATG5, BNIP3 and nitric oxide levels as well as augmented cellular migration, oxidative stress, and inflammation, which were exacerbated by miR-122-5p mimic while rescued by miR-122-5p inhibitor and rhFOXO3, respectively. Notably, knockdown of FOXO3 strikingly blunted cellular protective effects of miR-122-5p inhibitor. In summary, miR-122-5p augments renal fibrosis, inflammatory and oxidant injury in hypertensive rats by suppressing the expression of FOXO3. Pharmacological inhibition of miR-122-5p has potential therapeutic significance for hypertensive renal injury and fibrosis-related kidney diseases.

Expression profile and the G63A mutation of IGF2 gene associated with growth traits in Zhedong-White goose.

Insulin-like growth factors 2 (IGF2) is an insulin-like growth factor that plays a major role in animal growth, cell proliferation and differentiation, as well as reproduction. IGF2 is well-known to be a candidate gene of growth and reproductive traits in many agricultural animals. Our previous study revealed that the G63A (Chr2: G26541617A) mutation within IGF2 exon 1 showed a significant association with egg numbers (E180d) of Sanhua goose population (p < 0.05). However, little work focus on the correlation between the IGF2 mutations and goose growth traits. In this study, qPCR indicated that the IGF2 mRNA highly expressed in leg muscle, liver, ovary and pituitary gland. Meanwhile, association analysis showed that the G63A mutation was significantly associated with the body weight of first-hatched Zhedong-White geese (BW0, p < 0.05), and strongly significantly associated with the BW2, BW4, BW6, BW8 and BW10 (p < 0.01). The GG homozygous had the lowest BW (from 4 weeks to 10 weeks) than those of AA and AG genotypes (p < 0.01), and the allele A was also positively correlated with the BW of the Zhedong-White goose population. Therefore, the G63A mutation in IGF2 may be an important genetic marker for goose breeding.

Research on the Surface Deformation, Fault Rupture, and Coseismic Geohazard of the 2022 Luding Mw 6.8 Earthquake.

An Mw 6.8 earthquake occurred in Luding County, Ganzi Tibetan Autonomous Prefecture, Sichuan Province, on 5 September 2022. This seismic event triggered numerous coseismic geohazards in the seismic zone. In this study, the ascending- and descending-track synthetic aperture radar (SAR) images observed by the Sentinel-1A satellite are utilized to extract the coseismic surface deformation of the Luding earthquake. Subsequently, a faulting model is estimated based on the elastic dislocation theory, under the constraint of the InSAR observation. Additionally, the POT technique was employed to detect coseismic geohazards. High-spatial-resolution optical remote sensing images served to validate the reliability of the detection results. The coseismic interferometric synthetic aperture radar (InSAR) deformation field indicated a maximum deformation of ~190 mm and ~140 mm along the ascending and descending tracks, respectively. The estimated best-fitting faulting model suggests that the optimal seismogenic fault strike and dip angles are 169.3° and 70°, respectively. The fault slip predominantly exhibits left-lateral strike-slip characteristics and is concentrated at depths of 3-12 km. The estimated maximum fault slip was 2.67 m, occurring at a depth of 7 km. The pixel offset tracking (POT) result derived from the pre- and post-earthquake SAR images found a total of 245 medium- to large-scale coseismic geohazards, with a verification rate from optical images exceeding 64%. The distribution of these geohazards is notably dense within the significant fault rupture segment. Geohazards on the fault hanging wall are densely packed, whereas landslides along the Dadu River's fault footwall are also notably frequent.

Genetic deletion of CMG2 exacerbates systemic-to-pulmonary shunt-induced pulmonary arterial hypertension.

Pulmonary arterial hypertension (PAH) secondary to congenital heart disease (CHD-PAH) with systemic-to-pulmonary shunt (SPS) is characterized by proliferative vascular remodeling. Capillary morphogenesis gene-2 (CMG2) plays a key role in cell proliferation and apoptosis. This study aimed to determine the role of CMG2 in the pathogenesis of SPS-induced PAH. CMG2 levels were significantly downregulated in pulmonary arterioles from patients with Eisenmenger syndrome and rats with SPS-induced PAH. CMG2 was highly expressed in several cells including human pulmonary arterial smooth muscle cells (HPASMCs). CMG2-/- rats exhibited more severe PAH and pulmonary vascular remodeling than wild-type rats when exposed to SPS for 8 weeks. Overexpression of CMG2 significantly inhibited proliferation and promoted apoptosis of HPASMCs, while knockdown of CMG2 promoted cell proliferation and inhibited cell apoptosis. Next-generation sequencing and subsequent validation results suggested that PI3K-AKT was the most prominent signaling pathway regulated by differentially expressed genes (DEGs) in CMG2-/- rat lungs. Our work identified a novel role for CMG2 in SPS-induced PAH based on the findings that CMG2 deficiency exacerbates SPS-induced vascular remodeling in the development of PAH, indicating that CMG2 might act as a potential target for the treatment of CHD-PAH.

Association of plasma bone morphogenetic protein-4 levels with arterial stiffness in hypertensive patients.

BACKGROUND: Arterial stiffness interacts with hypertension, becoming an early marker of hypertension-mediated target organ damage. This study aimed to assess the association between plasma concentrations of bone morphogenetic protein-4 (BMP-4) and arterial stiffness during hypertension. METHODS: Using cardio-ankle vascular index (CAVI) to determine arterial stiffness status, 204 individuals with essential hypertension were classified into two groups, high CAVI (abnormal) group (n = 94) and low (normal) CAVI group (n = 110). Data were collected including clinical characteristics and laboratory measurements. Plasma levels of BMP-4 were tested by using ELISA analysis. RESULTS: Plasma levels of BMP-4 were substantially greater in high CAVI group than that in low CAVI group [38.51 (31.79-50.83) pg/mL vs. 31.15 (29.38-32.37) pg/mL; p < 0.001]. As shown by spearman correlation analysis, BMP-4 concentrations were correlated with CAVI values in hypertensive individuals (r = 0.406, p < 0.001). After adjustment for potential confounders, elevated BMP-4 levels were related with high CAVI (OR, 1.070; 95% CI, 1.003-1.108; p < 0.001). The best BMP-4 cutoff value for identifying high CAVI, as determined by ROC curve analysis, was 33.34 pg/mL (AUC, 0.751; 95% CI, 0.683-0.818; p < 0.001). CONCLUSION: Plasma levels of BMP-4 are increased in hypertensive individuals with high CAVI. Elevated BMP-4 levels are strongly correlated with higher CAVI values, implying a predictive value of BMP-4 in arterial stiffness during hypertension.

Transcending conventional snapshot polarimeter performance via neuromorphically adaptive filters.

A channeled Stokes polarimeter that recovers polarimetric signatures across the scene from the modulation induced channels is preferrable for many polarimetric sensing applications. Conventional channeled systems that isolate the intended channels with low-pass filters are sensitive to channel crosstalk effects, and the filters have to be optimized based on the bandwidth profile of scene of interest before applying to each particular scenes to be measured. Here, we introduce a machine learning based channel filtering framework for channeled polarimeters. The machines are trained to predict anti-aliasing filters according to the distribution of the measured data adaptively. A conventional snapshot Stokes polarimeter is simulated to present our machine learning based channel filtering framework. Finally, we demonstrate the advantage of our filtering framework through the comparison of reconstructed polarimetric images with the conventional image reconstruction procedure.