Distortion measurement of a lithography projection lens based on multichannel grating lateral shearing interferometry.

The optical distortion of the lithographic projection lens can reduce imaging quality and cause overlay errors in lithography, thus preventing the miniaturization of printed patterns. In this paper, we propose a technique to measure the optical distortion of a lithographic projection lens by sensing the wavefront aberrations of the lens. A multichannel dual-grating lateral shearing interferometer is used to measure the wavefront aberrations at several field points in the pupil plane simultaneously. Then, the distortion at these field points is derived according to the proportional relationship between the Z 2 and Z 3 Zernike terms (the tilt terms) and the image position shifts. Without the need for additional devices, our approach can simultaneously retrieve both the wavefront aberrations and the image distortion information. Consequently, it improves not only measurement speed and accuracy but also enables accounting for displacement stage positioning error. Experiments were conducted on a lithographic projection lens with a numerical aperture of 0.57 to verify the feasibility of the proposed method.

Quality inspection of cube beam splitters by a white light interferometric approach.

Beam splitters have a wide range of applications as a key component in optical systems. Adopting beam splitters with geometric defects in an optical system, e.g., an interferometric measurement system, may cause additional optical path difference and degrade the measurement accuracy. The quality inspection of beam splitters is essential to meet the accuracy requirements for modern optical systems. Most of the current quality inspection methods rely on inefficient and inaccurate manual observation. Therefore, for commonly used cube beam splitters (CBSs), we propose a digital method to quantify the geometric quality based on the white light interferometric principle. A Fourier domain analysis is used to calculate the CBS misalignment error and perpendicularity error. This method is verified by inspecting six different CBS samples. The experimental results show that all samples have varying degrees of misalignment and perpendicularity errors. The maximum perpendicularity error is 0.93°, and three of the six samples have misalignment errors larger than 50 µm. Nanometer level precision of the misalignment measurement can be achieved.

The correlation between proteoglycan 2 and neuropsychiatric systemic lupus erythematosus.

The proposed pathogenesis of neuropsychiatric systemic lupus erythematosus (NPSLE) mainly includes ischemia and neuroinflammation mechanisms. Protein encoded by Proteoglycan 2 (PRG2) mRNA is involved in the immune process related to eosinophils, also being found in the placenta and peripheral blood of pregnant women. We evaluated the correlation between PRG2 and NPSLE for the first time and found that PRG2 protein was overexpressed in the serum of patients with NPSLE and correlated with the SLE disease activity index (SLEDAI) subset scores of psychosis. Moreover, we investigated the correlation between hippocampal PRG2 level and hippocampally dependent learning and memory ability in MRL/lpr mice, and discovered that the number of PRG2+GFAP+ astrocytes in the cortex and hypothalamus and the number of PRG2+IBA-1+ microglia in the hippocampus and cortex significantly increased in the MRL/lpr mice. These data provided a reference for the follow-up exploration of the role of PRG2 in SLE or other diseases.

Measurement and correction of lateral distortion in a Fizeau interferometer based on the self-calibration technique.

The lateral distortion of a surface measuring Fizeau interferometer may cause distorted image features in the lateral direction, as well as the surface form error in the axial direction (which is a source of the retrace error). Traditional method for lateral distortion measurement requires a high-accuracy calibration plate featuring a grid pattern. Such a calibration plate is not always available, especially when the required accuracy of the grid pattern comes to the order of sub-micrometer or even nanometer level. To remove the dependence on the plate accuracy, we propose a self-calibration method for the measurement and correction of lateral distortion in Fizeau interferometer. The self-calibration technique may separate the lateral distortion and the geometric error of the calibration plate. This method is verified using a 108-mm-aperture Fizeau interferometer. The experiments show that the form measurement error of a surface tilted at approximately 5° and 16° can be reduced from 92 nm to 43 nm and from 251 nm to 144 nm (peak-to-valley value), respectively, after the distortion correction.

Pyruvate kinase isoform M2 impairs cognition in systemic lupus erythematosus by promoting microglial synaptic pruning via the ß-catenin signaling pathway.

BACKGROUND: Neuropsychiatric systemic lupus erythematosus (NPSLE) is a severe complication, which involves pathological damage to the brain and cognitive function. However, its exact mechanism of action still remains unclear. In this study, we explored the role of microglia in the cognitive dysfunction of NPSLE mice. We also analyzed and compared the metabolites in the hippocampal tissues of the lupus model and control mice. METHODS: MRL/MpJ-Faslpr (MRL/lpr) female mice were used as the NPSLE mouse model. Metabolomics was used to assess hippocampal glycolysis levels. Glucose, lactic acid, IL-6, and IL-1ß of the hippocampus were detected by ELISA. Based on the glycolysis pathway, we found that pyruvate kinase isoform M2 (PKM2) in the hippocampus was significantly increased. Thus, the expression of PKM2 was detected by qRT-PCR and Western blotting, and the localization of PKM2 in microglia (IBA-1+) or neurons (NeuN+) was assessed by immunofluorescence staining. Flow cytometry was used to detect the number and phenotype of microglia; the changes in microglial phagocytosis and the ß-catenin signaling pathway were detected in BV2 cells overexpressing PKM2. For in vivo experiments, MRL/lpr mice were treated with AAV9-shPKM2. After 2 months, Morris water maze and conditional fear tests were applied to investigate the cognitive ability of mice; H&E and immunofluorescence staining were used to evaluate brain damage; flow cytometry was used to detect the phenotype and function of microglia; neuronal synapse damage was monitored by qRT-PCR, Western blotting, and immunofluorescence staining. RESULTS: Glycolysis was elevated in the hippocampus of MRL/lpr lupus mice, accompanied by increased glucose consumption and lactate production. Furthermore, the activation of PKM2 in hippocampal microglia was observed in lupus mice. Cell experiments showed that PKM2 facilitated microglial activation and over-activated microglial phagocytosis via the ß-catenin signaling pathway. In vivo, AAV9-shPKM2-treated mice showed decreased microglial activation and reduced neuronal synapses loss by blocking the ß-catenin signaling pathway. Furthermore, the cognitive impairment and brain damage of MRL/lpr mice were significantly relieved after microglial PKM2 inhibition. CONCLUSION: These data indicate that microglial PKM2 have potential to become a novel therapeutic target for treating lupus encephalopathy.

Hippocampal microglia CD40 mediates NPSLE cognitive dysfunction in mice.

Neuropsychiatric systemic lupus erythematosus (NPSLE) is the most serious and complicated clinical manifestation of lupus erythematosus. Cognitive dysfunction is the most common symptom of NPSLE. A variety of potential mechanisms or mediators related to the pathogenesis of NPSLE cognitive dysfunction have been proposed. However, the involvement of microglia CD40 has not been reported yet. This study aimed to investigate whether hippocampal microglia CD40 of MRL/MpJ-Faslpr (MRL/lpr) mice was involved in NPSLE cognitive dysfunction. This study found, using quantitative polymerase chain reaction, western blotting and immunohistochemistry, that hippocampal CD40 was aberrantly overexpressed in the MRL/lpr lupus mice. It also determined using flow cytometry and immunofluorescence that the aberrantly overexpressed CD40 was mainly derived from hippocampal microglia. The adeno-associated virus was used to inhibit microglia CD40 expression, and the brain damage and cognitive dysfunction of MRL/lpr mice improved. Also, imiquimod (IMQ)-induced lupus mice had the same NPSLE cognitive dysfunction, brain damage, and overexpressed hippocampal microglia CD40 as MRL/lpr mice. Therefore, IMQ-induced lupus mouse was proposed as one of the mouse models for studying NPSLE cognitive dysfunction for the first time in this study. The findings indicated that hippocampal microglia CD40 was involved in the development of NPSLE cognitive dysfunction, thus providing a novel research direction for the study of the pathogenesis of NPSLE.