Channeled Mueller matrix spectropolarimeters (CMMSPs) have gained increasing popularity in recent years due to no moving parts. However, in order to obtain more accurate measurements, thorough studies on the influence and correction of their systematic errors are still needed. This paper presents a novel perspective for CMMSPs based on a signal processing technique, and propose a coherence demodulation method to extract channel signals in the modulated intensity. From theoretical analysis, the influence of phase deviation resulting from the imperfection of retarders is pinpointed. Meanwhile, the mechanism of phase deviation is described in theory and visually displayed by simulation. To mitigate the interference of retarder phase deviation, this work proposes a way for correction utilizing a vacuum and polarizer as determinant samples. Noticeably, the phase deviations are treated as a whole and represented by polynomials during correction. The reverse process of error mechanism is used to correct the influence. Finally, this means is proved by a series of simulation validations with a detector noise of 30 dB and retarder misalignment errors of 0.5°.
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Waveguide coupling design is one of the most challenging topics in augmented reality (AR) near-eye displays (NED). The primary challenge stems from the necessity to simultaneously address two competing factors: the overall volume of the AR system and the occurrence of chromatic aberration. To address this issue, what we believe to be a novel tandem trilayer achromatic metasurface is specifically designed for waveguide coupling in AR NEDs, capable of achieving an achromatic effect in a nanometer-thin layer.
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View Article and Find Full Text PDFCytokine
January 2025
Department of Molecular Biology and Bioinformatics, Tripura University, Agartala, India. Electronic address:
Transforming growth factor-beta (TGF-β), displaying a dual role in immunosuppression and pathogenesis, has emerged as a key regulator of anti-leishmanial immune responses. In Leishmania infections, TGF-β drives immune deviation by enhancing regulatory T-cell (T-reg) differentiation and inhibiting macrophage activation, suppressing critical antiparasitic responses. This cytokine simultaneously promotes fibroblast proliferation, extracellular matrix production, and fibrosis in infected tissues, which aids in wound healing but impedes immune cell infiltration, particularly in visceral leishmaniasis, where splenic disorganization and compromised immune access are notable.
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