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To improve the effectiveness of spatial spectrum sampling for the photonic-integrated interferometric imaging, an array forming scheme is proposed with evenly distributed interferometric baselines, which is referred to as the even sampling photonic-integrated interferometric array (ESPIA). The subaperture array of ESPIA is configured as equi-spaced concentric rings. The subaperture beams are coupled and transmitted to the photonic integrated circuit through fiber optic channels and paired into baselines by the interferometric beam combination. The characteristics of ESPIA are analyzed with the discrete modulation transfer function (D-MTF) and multi-resolution mutual information (MR-MI). The simulation results show that it can realize the even sampling coverage of spatial spectrum effectively. With the same scale of synthetic aperture and subaperture array, it can also improve the capabilities of information acquisition for the interferometric array.

Inappropriate synaptic development has been proposed as a potential mechanism of neurodevelopmental disorders, including attention-deficit hyperactivity disorder (ADHD). Major histocompatibility complex class I (MHCI), an immunity-associated molecule expressed by neurons in the brain, regulates synaptic development; however, the involvement of MHCI in these disorders remains elusive. We evaluated whether functional MHCI deficiency induced by β2m -/- Tap1 -/- double-knockout in mice leads to abnormalities akin to those seen in neurodevelopmental disorders. We found that functional MHCI deficiency induced locomotor hyperactivity, motor impulsivity, and attention deficits, three major symptoms of ADHD. In contrast, these mice showed normal spatial learning, behavioral flexibility, social behavior, and sensorimotor integration. In the analysis of the dopamine system, upregulation of dopamine D1 receptor (D1R) expression in the nucleus accumbens and a greater locomotor response to D1R agonist SKF 81297 were found in the functional MHCI-deficient mice. Low-dose methylphenidate, used for the treatment of ADHD patients, alleviated the three behavioral symptoms and suppressed c-Fos expression in the D1R-expressing medium spiny neurons of the mice. These findings reveal an unexpected role of MHCI in three major symptoms of ADHD and may provide a novel landmark in the pathogenesis of ADHD., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Objective: To study the association between apparent temperature (AT) and the incidence of hand,foot, and mouth disease (HFMD) and its spatial heterogeneity in 46 cities in Guangdong, Anhui and Jilin provinces, and provide scientific evidence for the early warning of HFMD. Methods: The data of HFMD incidence and meteorological factors from 2009 to 2018 in Guangdong province, 2009 to 2015 in Anhui province, and 2013 to 2018 in Jilin province were collected. Distributed lag non-linear models were constructed to investigate the association between AT and the incidence of HFMD in 46 cities from three provinces in China. Meta-analysis was used to pool the city-specific estimates, and Meta-regression was applied to analyze the factors that may cause spatial heterogeneity. Results: The relationship between daily AT and the incidence of HFMD in 46 cities appeared nonlinear. The association in Guangdong was similar to that in Jilin, and the risk of HFMD increased with the increase of AT. While the risk of HFMD in Anhui first increased with the increase of AT, and peaked at 18.1 ℃ and then went down. AT on different levels showed different lag impacts and the higher AT showed greater and longer lag impact. The spatial heterogeneity of associations may have been caused by latitude, longitude, average temperature, and average sunshine hours. Conclusions: AT is a comprehensive index to evaluate the association between temperature, relative humidity and wind speed and the incidence of HFMD. Higher AT may increase the risk of HFMD. The AT and HFMD relationship across spatial heterogeneity varies depending on geographic location and meteorological conditions.

Objective: To investigate the possible function and mechanism of lncRNA SNHG8 in the pathogenesis of endometrial carcinoma., Patients and Methods: We utilized qRT-PCR to detect the expression of SNHG8 in 60 cases of endometrial carcinoma and 25 cases of normal endometrium; after that, the endometrial carcinoma cell lines were screened. SNHG8 was transfected into endometrial carcinoma cells by Lipofectamine and the proliferative activity of cells was detected by cell counting kit-8 (CCK-8) assay. Bioinformatics methods were used to detect the target microRNA. miR-152 is predicted to bind to SNHG8 and target genes of c-MET. Luciferase reporter assay was performed to detect the relative luciferase activity between miR-152 and c-MET, SNHG8. The interactions between SNHG8, miR-152, and c-MET were further verified by transfection of miR-152 mimics, miR-152 mimics + OE-SNHG8, SNHG8 siRNA, and SNHG8 siRNA + miR-152 inhibitor., Results: SNHG8 expression in endometrial carcinoma tissue was significantly higher than that in normal endometrium. After transfection with SNHG8 siRNA, the cell viability of AN3CA cells decreased, whereas the activity of Ishikawa was increased after transfection with SNHG8 overexpression plasmid. Bioinformatics predictions and dual luciferase reporter assay illustrated that SNHG8 was bound to miR-152 and miR-152 targeted on c-MET. In addition, miR-152 mimics inhibited the expression of c-MET, and the inhibitory effect was reversed after SNHG8 overexpression. Silencing SNHG8 reduced c-MET expression, and c-MET expression was reversed after addition of miR-152 inhibitor., Conclusions: SNHG8 is highly expressed in endometrial carcinoma, and SNHG8 targets c-MET through miR-152 to regulate the proliferation of endometrial cancer cells.

Protective immunity against murine malaria infection depends largely on the establishment of effective Th1 immune response during the early stages of infection. Experimental data suggest that the death of Plasmodium yoelii 17XL (Py 17XL) susceptible BALB/c mice results from the suppression of Th1 immune response mediated by CD4+CD25+Foxp3+ regulatory T cells (Tregs). However, the mechanism by which Tregs regulate Th1 immune response is poorly understood. Since immunity is initiated by dendritic cells (DCs), we analysed DC responses to Py 17XL in control and Treg-depleted BALB/c mice. Myeloid DC proliferation, phenotypic maturation and interleukin-12 (IL-12) production were strongly inhibited in control BALB/c mice. In contrast, plasmacytoid DC proliferation and IL-10 production were strongly enhanced in control BALB/c mice. In-vivo depletion of Tregs resulted in significantly reversed inhibition of DC response, which may contribute to the establishment of Th1 immune response, indicating that Tregs contribute to the suppression of Th1 immune response during malaria. These findings suggest Tregs contribute to prevent Th1 immune response establishment during the early stage of Py 17XL infection by inhibiting DC response.

Restin, a homologous protein of endostatin, was found by Ramchandran et al. It was the C-terminal fragment of type XV collagen. To analysis the inhibition activity of mouse restin on the proliferation of endothelial cells, the cDNA of restin was amplified from the total RNA of the mouse muscle and cloned into the prokaryotic expression plasmid pQE32. The recombinant protein was expressed in inclusion body with a yield about 60%--70% of total protein. After refolding, the purified recombinant protein specifically inhibits bovine aortic endothelial (BAE) cell proliferation stimulated by basic fibroblast growth factor (bFGF) in a dose-dependent manner, but the activity of restin was weaker than that of endostatin. Treatment of BAE cell with recombinant restin caused G(1) arrest and apoptosis in BAE cells.