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Gear involute artifact (GIA) is a kind of calibration standard used for traceability of involute metrology. To machine GIAs with sub-micron profile form deviations, the effect on the involute profile deviations caused by the geometric deviations and 6-DoF errors of the machining tool based on the double roller-guide involute rolling generation mechanismwas analysed.At the same time, a double roller-guide involute lapping instrument and a lapping method for GIAs was proposed for lapping and in-situ measuring the gear involute artifacts. Moreover, a new GIA with three design base radii (50 mm, 100 mm, and 131 mm) was proposed for more efficient calibration and was machined with profile form deviations of 0.3 μm (within evaluation length of 38 mm, 68 mm, 80 mm, respectively, measured by the Chinese National Institute of Metrology), and the surface roughness Ra of the involute flanks was less than 0.05 μm. The research supports small-batch manufacturing for high-precision GIAs.

Abstract Biomimetic mechanosensors have profound implications for various areas, including health care, prosthetics, human‒machine interfaces, and robotics. As one of the most important parameters, the sensitivity of mechanosensors is intrinsically determined by the detection resolution to mechanical force. In this manuscript, we expand the force detection resolution of current biomimetic mechanosensors from the micronewton to nanonewton scale. We develop a nanocrack-based electronic whisker-type mechanosensor that has a detection resolution of 72.2 nN. We achieve the perception of subtle mechanical stimuli, such as tiny objects and airflow, and the recognition of surface morphology down to a 30 nm height, which is the finest resolution ever reported in biomimetic mechanosensors. More importantly, we explore the use of this mechanosensor in wearable devices for sensing gravity field orientation with respect to the body, which has not been previously achieved by these types of sensors. We develop a wearable smart system for sensing the body’s posture and movements, which can be used for remote monitoring of falls in elderly people. In summary, the proposed device offers great advantages for not only improving sensing ability but also expanding functions and thus can be used in many fields not currently served by mechanosensors.

Abstract White organic light-emitting diodes (WOLEDs) is a new generation of lighting technology and has stimulated wide-ranging studies. Despite the advantage of simple device structure, single-emitting-layer WOLEDs (SEL-WOLEDs) still face the challenges of difficult material screening and fine energy level regulation. Herein, we report efficient SEL-WOLEDs with a sky-blue emitting cerium(III) complex Ce-TBO2Et and an orange-red emitting europium(II) complex Eu(Tp2Et)2 as the emitters, showing a maximum external quantum efficiency of 15.9% and Commission Internationale de l’Eclairage coordinates of (0.33, 0.39) at various luminances. Most importantly, the electroluminescence mechanism of direct hole capture and hindered energy transfer between the two emitters facilitate a manageable weight doping concentration of 5% for Eu(Tp2Et)2, avoiding the low concentration (

ABSTRACT Epstein-Barr virus (EBV) infects host cells and establishes a latent infection that requires evasion of host innate immunity. A variety of EBV-encoded proteins that manipulate the innate immune system have been reported, but whether other EBV proteins participate in this process is unclear. EBV-encoded envelope glycoprotein gp110 is a late protein involved in virus entry into target cells and enhancement of infectivity. Here, we reported that gp110 inhibits RIG-I-like receptor pathway-mediated promoter activity of interferon-β (IFN-β) as well as the transcription of downstream antiviral genes to promote viral proliferation. Mechanistically, gp110 interacts with the inhibitor of NF-κB kinase (IKKi) and restrains its K63-linked polyubiquitination, leading to attenuation of IKKi-mediated activation of NF-κB and repression of the phosphorylation and nuclear translocation of p65. Additionally, gp110 interacts with an important regulator of the Wnt signaling pathway, β-catenin, and induces its K48-linked polyubiquitination degradation via the proteasome system, resulting in the suppression of β-catenin-mediated IFN-β production. Taken together, these results suggest that gp110 is a negative regulator of antiviral immunity, revealing a novel mechanism of EBV immune evasion during lytic infection. IMPORTANCE Epstein-Barr virus (EBV) is a ubiquitous pathogen that infects almost all human beings, and the persistence of EBV in the host is largely due to immune escape mediated by its encoded products. Thus, elucidation of EBV’s immune escape mechanisms will provide a new direction for the design of novel antiviral strategies and vaccine development. Here, we report that EBV-encoded gp110 serves as a novel viral immune evasion factor, which inhibits RIG-I-like receptor pathway-mediated interferon-β (IFN-β) production. Furthermore, we found that gp110 targeted two key proteins, inhibitor of NF-κB kinase (IKKi) and β-catenin, which mediate antiviral activity and the production of IFN-β. gp110 inhibited K63-linked polyubiquitination of IKKi and induced β-catenin degradation via the proteasome, resulting in decreased IFN-β production. In summary, our data provide new insights into the EBV-mediated immune evasion surveillance strategy.

ABSTRACT Virus infection triggers intricate signal cascade reactions to activate the host innate immunity, which leads to the production of type I interferon (IFN-I). Herpes simplex virus 1 (HSV-1), a human-restricted pathogen, is capable of encoding over 80 viral proteins, and several of them are involved in immune evasion to resist the host antiviral response through the IFN-I signaling pathway. Here, we determined that HSV-1 UL31, which is associated with nuclear matrix and is essential for the formation of viral nuclear egress complex, could inhibit retinoic acid-inducible gene I (RIG-I)-like receptor pathway-mediated interferon beta (IFN-β)–luciferase (Luc) and (PRDIII-I)4-Luc (an expression plasmid of IFN-β positive regulatory elements III and I) promoter activation, as well as the mRNA transcription of IFN-β and downstream interferon-stimulated genes (ISGs), such as ISG15, ISG54, ISG56, etc., to promote viral infection. UL31 was shown to restrain IFN-β activation at the interferon regulatory factor 3 (IRF3)/IRF7 level. Mechanically, UL31 was demonstrated to interact with TANK binding kinase 1 (TBK1), inducible IκB kinase (IKKi), and IRF3 to impede the formation of the IKKi-IRF3 complex but not the formation of the IRF7-related complex. UL31 could constrain the dimerization and nuclear translocation of IRF3. Although UL31 was associated with the CREB binding protein (CBP)/p300 coactivators, it could not efficiently hamper the formation of the CBP/p300-IRF3 complex. In addition, UL31 could facilitate the degradation of IKKi and IRF3 by mediating their K48-linked polyubiquitination. Taken together, these results illustrated that UL31 was able to suppress IFN-β activity by inhibiting the activation of IKKi and IRF3, which may contribute to the knowledge of a new immune evasion mechanism during HSV-1 infection. IMPORTANCE The innate immune system is the first line of host defense against the invasion of pathogens. Among its mechanisms, IFN-I is an essential cytokine in the antiviral response, which can help the host eliminate a virus. HSV-1 is a double-stranded DNA virus that can cause herpes and establish a lifelong latent infection, due to its possession of multiple mechanisms to escape host innate immunity. In this study, we illustrate for the first time that the HSV-1-encoded UL31 protein has a negative regulatory effect on IFN-β production by blocking the dimerization and nuclear translocation of IRF3, as well as promoting the K48-linked polyubiquitination and degradation of both IKKi and IRF3. This study may be helpful for fully understanding the pathogenesis of HSV-1.

Taking Binhu New Area (BNA) as a case study, based on multi-period (2005, 2012, 2020) Landsat remote sensing images, the landscape pattern index and grey relational analysis (GRA) were chosen to quantitatively examine the dynamic change process and driving mechanism of green space landscape patterns. The results showed: (1) From 2005 to 2020, the green space area in BNA showed increases at first and decreases later with the highest degree of dynamic change found in regional green space. (2) Urban green space showed increased diversity and good connectivity, but its green patch was simple with a decreased degree of sprawl. The green patch also showed a tendency towards homogenization, aggregation, and simplification. The patch shapes of park green space, attached green space, and protective green space are relatively simple and there are blind spots in the distribution. (3) Population growth and industrial structure changes are the main driving forces of the changes in green space landscape patterns in BNA. Besides, urban planning and policies also play a big part in these changes. The research results can provide a reference for green space planning and construction in BNA. [ABSTRACT FROM AUTHOR]

Epstein-Barr virus (EBV) is a member of the lymphotropic virus family and is highly correlated with some human malignant tumors. It has been reported that envelope glycoprotein 110 (gp110) plays an essential role in viral fusion, DNA replication, and nucleocapsid assembly of EBV. However, it has not been established whether gp110 is involved in regulating the host's innate immunity. In this study, we found that gp110 inhibits tumor necrosis factor α-mediated NF-κB promoter activity and the downstream production of NF-κB-regulated cytokines under physiological conditions. Using dual-luciferase reporter assays, we showed that gp110 might impede the NF-κB promoter activation downstream of NF-κB transactivational subunit p65. Subsequently, we used coimmunoprecipitation assays to demonstrate that gp110 interacts with p65 during EBV lytic infection, and that the C-terminal cytoplasmic region of gp110 is the key interaction domain with p65. Furthermore, we determined that gp110 can bind to the N-terminal Rel homologous and C-terminal domains of p65. Alternatively, gp110 might not disturb the association of p65 with nontransactivational subunit p50, but we showed it restrains activational phosphorylation (at Ser536) and nuclear translocation of p65, which we also found to be executed by the C-terminal cytoplasmic region of gp110. Altogether, these data suggest that the surface protein gp110 may be a vital component for EBV to antagonize the host's innate immune response, which is also helpful for revealing the infectivity and pathogenesis of EBV. [ABSTRACT FROM AUTHOR]