High-Transmittance Subwavelength Metal Grating with Relief Structure Composed of Multiple Steps

A new kind of subwavelength metal grating with relief structure is designed and analyzed, in which the shape of the grating lines is no longer a single rectangle, but a relief structure with multiple steps. GsolverV52 was used to determine the optimal values of the grating period, groove depth, and the number of steps. The optical performance of the novel structure is evaluated and compared in terms of the transmission efficiency and extinction ratio over the visible and near-infrared wavelength spectrum. It is shown that, in the near-infrared band, the maximum transmittance can be increased about 15% compared to the traditional metal grating under the same parameters. With the unique characteristics, the metal grating is expected to find applications in liquid crystal display fields, polarization imaging, optical communication, and so on

Calculation of the diffraction efficiency on concave gratings based on Fresnel–Kirchhoff’s diffraction formula

Fraunhofer diffraction formula cannot be applied to calculate the diffraction wave energy distribution of concave gratings like plane gratings because their grooves are distributed on a concave spherical surface. In this paper, a method based on the Kirchhoff diffraction theory is proposed to calculate the diffraction efficiency on concave gratings by considering the curvature of the whole concave spherical surface. According to this approach, each groove surface is divided into several limited small planes, on which the Kirchhoff diffraction field distribution is calculated, and then the diffraction field of whole concave grating can be obtained by superimposition. Formulas to calculate the diffraction efficiency of Rowland-type and flat-field concave gratings are deduced from practical applications. Experimental results showed strong agreement with theoretical computations. With the proposed method, light energy can be optimized to the expected diffraction wave range while implementing aberration-corrected design of concave gratings, particularly for the concave blazed gratings.Published versio

Minocycline protects against microgliopathy in a Csf1r haplo-insufficient mouse model of adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP)

Abstract Background Mutations in colony-stimulating factor 1 receptor (CSF1R) are known to cause adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP), which has been recently demonstrated as a primary microgliopathy characterized by cognitive impairment. Although the molecular mechanism underlying CSF1R-mediated microgliopathy remains unclear, therapeutic strategies have generally targeted modulation of microglial function. In particular, the microglial inhibitor, minocycline, has been shown to attenuate learning and memory deficits in several neurodegenerative diseases. The objectives of this study were to investigate the pathogenic mechanisms underlying ALSP and to explore the therapeutic effects of minocycline in an in vivo model of ALSP. We hypothesized that inhibiting microglial activation via minocycline could reverse the behavior and pathological defects in ALSP model mice. Methods We generated a Csf1r haploinsufficiency mouse model of ALSP using CRISPR/Cas9 genome editing and conducted electrophysiological recordings of long-term potentiation (LTP) and behavioral tests to validate the recapitulation of clinical ALSP characteristics in 8- to 11-month-old mice. RNA-sequencing was used to explore enriched gene expression in the molecular pathogenesis of ALSP. Microglial activation was assessed by immunofluorescent detection of Iba1 and CD68 in brain sections of male ALSP mice and pro-inflammatory activation and phagocytosis were assessed in Csf1r +/− microglia. Therapeutic effects were assessed by behavioral tests, histological analysis, and morphological examination after four weeks of intraperitoneal injection with minocycline or vehicle control in Csf1r +/− mice and wild-type control littermates. Results We found that synaptic function was reduced in LTP recordings of neurons in the hippocampal CA1 region, while behavioral tests showed impaired spatial and cognitive memory specifically in male Csf1r +/− mice. Increased activation, pro-inflammatory cytokine production, and enhanced phagocytic capacity were also observed in Csf1r +/− microglia. Treatment with minocycline could suppress the activation of Csf1r +/− microglia both in vitro and in vivo. Notably, the behavioral and pathological deficits in Csf1r +/− mice were partially rescued by minocycline administration, potentially due to inhibition of microglial inflammation and phagocytosis in Csf1r +/− mice. Conclusions Our study shows that CSF1R deficiency results in aberrant microglial activation, characterized by a pro-inflammatory phenotype and enhanced phagocytosis of myelin. Our results also indicate that microglial inhibition by minocycline can ameliorate behavioral impairment and ALSP pathogenesis in CSF1R-deficient male mice, suggesting a potential therapeutic target for CSF1R-related leukoencephalopathy. Collectively, these data support that minocycline confers protective effects against CSF1R-related microgliopathy in male ALSP model mice