Frequency tuning and automatic frequency tracking of shunted piezoelectric transducers.

Piezoelectric ultrasonic transducers, vital in medical devices and aerospace, often face challenges like resonant frequency shifts and impedance variations affecting their operational efficiency. This paper introduces a shunted piezoelectric transducer which could tune itself by digitally programmable inductance. A transformer and inductance-capacitance matching network ensures enhanced compatibility and impedance management. Proposing a fuzzy PI-based phase control method achieves resonant frequency tracking, synchronizing operational frequency with the transducer. In contrast to traditional methods, our approach enables faster and more precise fine-tuning, detecting and rectifying real-world deviations for optimal performance. A comprehensive experimental validation, based on fundamental knowledge analysis, confirms the feasibility and superiority of our proposed method, and the commonly encountered issues of resonance frequency deviation and impedance variation in high-power piezoelectric transducer applications can be effectively mitigated.

Phosphorylation of RGS16 at Tyr168 promote HBeAg-mediated macrophage activation by ERK pathway to accelerate liver injury.

Liver injury is closely associated with macrophage activation following HBV infection. Our previous study showed that only HBeAg, but not HBsAg and HBcAg, stably enhances inflammatory cytokine production in macrophages. And we also indicated that HBeAg could induce macrophage activation via TLR2 and thus aggravate the progression of liver fibrosis. However, the specific molecular mechanism of HBeAg in macrophage activation is not clear. We screened significantly overexpressed RGS16 from RNASeq results of HBeAg-stimulated macrophages and validated them with cellular assays, GSE83148 microarray dataset, and in clinical samples. Meanwhile, small interference, plasmid, and lentivirus transfection assays were used to establish cell models for knockdown and overexpression of RGS16, and q-PCR, ELISA, Transwell, and CCK-8 assays were used to analyze the role of RGS16 in HBeAg-induced macrophage activation. In addition, the upstream and downstream mechanisms of RGS16 in HBeAg-treated macrophage activation were explored using inhibitors, phostag gels, and RGS16 phosphorylation mutant plasmids. Finally, the effect of RGS16 on hepatic inflammation in murine tissues was evaluated by H&E staining, liver enzyme assay and immunofluorescence. RGS16 was significantly upregulated in HBeAg-induced macrophage activation, and its expression was enhanced with increasing HBeAg content and treatment time. Functional experiments showed that overexpression of RGS16 promoted the production of inflammatory factors TNF-α and IL-6 and boosted macrophage proliferation and migration, while knockdown of RGS16 exhibited the opposite effect. Mechanistically, we discovered that RGS16 is regulated by the TLR2/P38/STAT5 signaling pathway. Meanwhile, RGS16 enhanced ERK phosphorylation via its own Tyr168 phosphorylation to contribute to macrophage activation, thereby accelerating liver injury. Finally, in mice, overexpression of RGS16 markedly strengthened liver inflammation. HBeAg upregulates RGS16 expression through the TLR2-P38-STAT5 axis, and the upregulated expression of RGS16 enhances macrophage activation and accelerates liver injury by promoting ERK phosphorylation. In this process, phosphorylation of Tyr168 is necessary for RGS16 to function. KEY MESSAGES: RGS16 boosted HBeAg-induced macrophage inflammation, proliferation, and migration. Tyr168 phosphorylation of RGS16 affected by ERK promoted macrophage activation. HBeAg upregulated the expression of RGS16 through TLR2/P38/STAT5 signal pathway. RGS16 promoted liver injury by regulating macrophage functions in mouse model.

Albumin, an interesting and functionally diverse protein, varies from 'native' to 'effective' (Review).

Human serum albumins (HSAs) are synthesized in the liver and are the most abundant proteins in plasma of healthy human. They play an important role in the pathophysiological processes of the liver and even the whole organism. Previous studies have mainly focused on the regulation of HSAs' expression. However, with the progress of research in recent years, it has been found that the content of circulating albumin cannot fully reflect the biological function of albumin itself. Given the aforementioned fact, the concept of serum 'effective albumin concentration' has been proposed. It refers to the content of albumin that is structurally and functionally intact. Alterations in the molecular structure and function of albumin have been reported in a variety of diseases, including liver disease. Moreover, these changes have been verified to affect the progression of oxidative stress­related diseases. However, the link between albumin structure and function has not been fully elaborated, and the mechanisms by which different forms of albumin affect disease also need to be further investigated. In this context, the present review mainly expounded the biological characteristics and functions of albumin, summarized the different types of post­translational modification of albumin, and discussed their functional changes and possible mechanisms in non­alcoholic fatty liver disease, alcoholic hepatitis, viral hepatitis and different stages of cirrhosis. This will help to improve understanding of the role of albumin in disease development and provide a more comprehensive physiological basis for it in disease treatment.

RNF144A promotes antiviral responses by modulating STING ubiquitination.

Stimulator of interferon (IFN) genes (STING, also named MITA, ERIS, MPYS, or TMEM173) plays an essential role in DNA virus- or cytosolic DNA-triggered innate immune responses. Here, we demonstrate that the RING-in-between RING (RBR) E3 ubiquitin ligase family member RING-finger protein (RNF) 144A interacts with STING and promotes its K6-linked ubiquitination at K236, thereby enhancing STING translocation from the ER to the Golgi and downstream signaling pathways. The K236R mutant of STING displays reduced activity in promoting innate immune signal transduction. Overexpression of RNF144A upregulates HSV-1- or cytosolic DNA-induced immune responses, while knockdown of RNF144A expression has the opposite effect. In addition, Rnf144a-deficient cells exhibit impaired DNA virus- or cytosolic DNA-triggered signaling, and RNF144A protects mice from DNA virus infection. In contrast, RNF144A does not affect RNA virus- or cytosolic RNA-triggered innate immune responses. Taken together, our findings identify a new positive regulator of DNA virus- or cytosolic DNA-triggered signaling pathways and a critical ubiquitination site important for fully functional STING during antiviral responses.

Epithelial TIPE1 Protein Guards against Colitis by Inhibiting TNF-α-Mediated Inflammation.

Intestinal epithelial cells (IECs) at the internal/external interface orchestrate the mucosal immune response, and IEC dysfunction has been linked to multiple inflammatory diseases, including inflammatory bowel disease. In this study, we found that a member of the TNF-α-induced protein 8 (TNFAIP8 or TIPE) family called TIPE1 is indispensable for maintaining epithelial cell barrier integrity and homeostasis under inflammatory conditions. TIPE1-deficient mice, or chimeric mice that were deficient in TIPE1 in their nonhematopoietic cells, were more sensitive to dextran sulfate sodium-induced experimental colitis; however, TIPE1 deficiency had no impact on the development of inflammation-associated and sporadic colorectal cancers. Mechanistically, TIPE1 prevented experimental colitis through modulation of TNF-α-dependent inflammatory response in IECs. Importantly, genetic deletion of both TIPE1 and its related protein TNFAIP8 in mice led to the development of spontaneous chronic colitis, indicating that both of these two TIPE family members play crucial roles in maintaining intestinal homeostasis. Collectively, our findings highlight an important mechanism by which TIPE family proteins maintain intestinal homeostasis and prevent inflammatory disorders in the gut.

Race between virus and inflammasomes: inhibition or escape, intervention and therapy.

The inflammasome is a multiprotein complex that further regulates cell pyroptosis and inflammation by activating caspase-1. The assembly and activation of inflammasome are associated with a variety of diseases. Accumulative studies have shown that inflammasome is a key modulator of the host's defense response to viral infection. Indeed, it has been established that activation of inflammasome occurs during viral infection. At the same time, the host has evolved a variety of corresponding mechanisms to inhibit unnecessary inflammasome activation. Therefore, here, we review and summarize the latest research progress on the interaction between inflammosomes and viruses, highlight the assembly and activation of inflammosome in related cells after viral infection, as well as the corresponding molecular regulatory mechanisms, and elucidate the effects of this activation on virus immune escape and host innate and adaptive immune defenses. Finally, we also discuss the potential therapeutic strategies to prevent and/or ameliorate viral infection-related diseases via targeting inflammasomes and its products.

Sirt1 Negatively Regulates Cellular Antiviral Responses by Preventing the Cytoplasmic Translocation of Interferon-Inducible Protein 16 in Human Cells.

Interferon-inducible protein 16 (IFI16) plays a critical role in antiviral innate immune responses against DNA viruses. Although the acetylation of IFI16 is crucial to its cytoplasmic translocation and downstream signal transduction, the regulation of IFI16 acetylation remains unclear. In this study, we demonstrated that the NAD-dependent deacetylase silent information regulatory 1 (Sirtuin1, Sirt1) interacted with IFI16 and decreased the acetylation of IFI16, resulting in the inhibition of IFI16 cytoplasmic localization and antiviral responses against DNA virus and viral DNA in human cells. Meantime, Sirt1 could not inhibit RNA virus-triggered signal transduction. Interestingly, even p204, the murine ortholog of human IFI16, barely interacted with Sirt1. Thus, Sirt1 could not negatively regulate the acetylation of p204 and subsequent signal transduction upon herpes simplex virus 1 (HSV-1) infection in mouse cells. Taken together, our research work showed a new mechanism by which Sirt1 manipulated IFI16-mediated host defense. Our study also demonstrated a difference in the regulation of antiviral host defense between humans and mice, which might be considered in preclinical studies for antiviral treatment. IMPORTANCE DNA viruses, such as hepatitis B virus (HBV), human papillomavirus (HPV), human cytomegalovirus (HCMV), Epstein-Barr virus (EBV), and herpes simplex virus (HSV), can cause a wide range of diseases and are considered a global threat to human health. Interferon-inducible protein 16 (IFI16) binds virus DNA and triggers antiviral innate immune responses to restrict viral infection. In this study, we identified that silent information regulatory 1 (Sirtuin1, Sirt1) interacted with IFI16 and regulated IFI16-mediated innate host defense. Therefore, the activator or inhibitor of Sirt1 may have the potential to be used as a novel strategy to treat DNA virus-associated diseases. We also found that Sirt1 barely interacted with p204, the murine ortholog of human IFI16, and could not negatively regulate innate immune responses upon HSV-1 infection in mouse cells. This difference between humans and mice in the regulation of antiviral host defense might be considered in preclinical studies for antiviral treatment.

TRIM7/RNF90 promotes autophagy via regulation of ATG7 ubiquitination during L. monocytogenes infection.

L. monocytogenes is a widely used infection model for the research on pathogenesis and host defense against gram-positive intracellular bacteria. Emerging evidence indicates that posttranslational modifications play a critical role in the regulation of macroautophagy/autophagy. However, little is known about the posttranslational modifications of ATG7, the essential protein in the autophagy process. In this study, we demonstrated that the RING-type E3 ligase TRIM7/RNF90 positively regulated autophagosome accumulation by promoting the ubiquitination of ATG7 at K413, thereby affecting L. monocytogenes infection. TRIM7 expression was induced by a variety range of conditions, including starvation, rapamycin stimulation, and L. monocytogenes infection. TRIM7 deficiency in mice or cells resulted in elevated innate immune responses and increased L. monocytogenes infection. ATG7 was associated with TRIM7 and the positive regulatory role of TRIM7 in L. monocytogenes infection-, starvation- or rapamycin-induced autophagosome accumulation was suggested by TRIM7 deficiency, TRIM7 overexpression, and TRIM7 knockdown. Further mechanistic investigation indicated that TRIM7 promoted the K63-linked ubiquitination of ATG7 at K413 and ubiquitination at this site was required for the function of ATG7 in autophagy and L. monocytogenes infection. Thus, our findings suggested a new regulator in intracellular bacterial infection and autophagy, with a novel posttranslational modification targeting ATG7. This research may expand our understanding of host anti-bacterial defense and the role of autophagy in intracellular bacterial infection.Abbreviations: ATG3: autophagy related 3; ATG5: autophagy related 5; ATG7: autophagy related 7; ATG10: autophagy related 10; ATG12: autophagy related 12; ATG16L1: autophagy related 16 like 1; Baf A1: bafilomycin A1; CQ: chloroquine; BMDC: bone marrow-derived dendritic cell; BMDM: bone marrow-derived macrophage; CFUs: colony-forming units; CXCL10/IP-10: C-X-C motif chemokine ligand 10; EBSS: Earle's balanced salt solution; ELISA: enzyme-linked immunosorbent assay; IFIT1/ISG56: interferon induced protein with tetratricopeptide repeats 1; IFNB/IFN-ß: interferon beta; IL6: interleukin 6; IRF3, interferon regulatory factor 3; Lm: L. monocytogenes; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MEF: mouse embryonic fibroblast; MOI: multiplicity of infection; PLA: proximity ligation assay; PMA: phorbol myristate acetate; PMA-THP1, PMA-differentiated THP1; PMs: peritoneal macrophages; PTMs: posttranslational modifications; STING1, stimulator of interferon response cGAMP interactor 1; TBK1, TANK binding kinase 1; TNF/TNF-α: tumor necrosis factor; TRIM7/RNF90: tripartite motif containing; Hainan Provincial Natural Science Foundation of China.

Research on Factors and Influencing Correlation of Coal Core Temperature during Coring.

The core-tube method is a common method to measure the coal seam gas content (CSGC). However, cutting heat and friction heat will be generated in the core-tube coring process, which will increase the coal core temperature and the coal core gas loss, thus resulting in a large error in the determination of the gas content. The accuracy of the gas content determination is closely related to the temperature variation of coal core during core-taking. Based on this, the team developed the "thermal effect simulation device of coal core in the core-taking process" and carried out the temperature change test experiment of the coal core in the core-taking process under different conditions. The results show that the temperature variation of the coal core during the core-taking process shows four stages: constant temperature, rapid temperature rise, slow temperature rise, and temperature drop. The temperature rise rate, temperature rise duration, and temperature rise peak of the coal core increase with the increase in rotate speed, coal strength, friction area, and frictional load. In the axial direction, the closer to the upper end of the core pipe, the higher the core temperature. In the radial direction, the closer the core is to the wall of the core pipe, the higher the core temperature is. Under the influence of cutting heat and friction heat in the process of core-taking, the maximum heating rate of the core-taking tube wall within 8 min is 20 °C/min, the peak temperature is 158.4 °C, the average temperature of the wall is above 100 °C, and the average temperature rise of the coal core reaches 55.7 °C. Within 60 min, the average temperature of the coal core remained above 50 °C. The order of influence of coal core temperature from large to small is as follows: rotate speed, frictional load, friction area, and coal strength. It can provide a reference for accurately determining CSGC using the core-tube method or designing a coring device to eliminate or reduce the thermal effect during coring.

Quantitative phase imaging in digital holographic microscopy based on image inpainting using a two-stage generative adversarial network.

Based on the hologram inpainting via a two-stage Generative Adversarial Network (GAN), we present a precise phase aberration compensation method in digital holographic microscopy (DHM). In the proposed methodology, the interference fringes of the sample area in the hologram are firstly removed by the background segmentation via edge detection and morphological image processing. The vacancy area is then inpainted with the fringes generated by a deep learning algorithm. The image inpainting finally results in a sample-free reference hologram containing the total aberration of the system. The phase aberrations could be deleted by subtracting the unwrapped phase of the sample-free hologram from our inpainting network results, in no need of any complex spectrum centering procedure, prior knowledge of the system, or manual intervention. With a full and proper training of the two-stage GAN, our approach can robustly realize a distinct phase mapping, which overcomes the drawbacks of multiple iterations, noise interference or limited field of view in the recent methods using self-extension, Zernike polynomials fitting (ZPF) or geometrical transformations. The validity of the proposed procedure is confirmed by measuring the surface of preprocessed silicon wafer with a Michelson interferometer digital holographic inspection platform. The results of our experiment indicate the viability and accuracy of the presented method. Additionally, this work can pave the way for the evaluation of new applications of GAN in DHM.

Negative Regulation of RNF90 on RNA Virus-Triggered Antiviral Immune Responses Targeting MAVS.

The antiviral innate immunity is the first line of host defense against viral infection. Mitochondrial antiviral signaling protein (MAVS, also named Cardif/IPS-1/VISA) is a critical protein in RNA virus-induced antiviral signaling pathways. Our previous research suggested that E3 ubiquitin-protein ligases RING-finger protein (RNF90) negatively regulate cellular antiviral responses by targeting STING for degradation, though its role in RNA virus infection remains unknown. This study demonstrated that RNF90 negatively regulated RNA virus-triggered antiviral innate immune responses in RNF90-silenced PMA-THP1 cells, RNF90-deficient cells (including HaCaTs, MEFs, and BMDMs), and RNF90-deficient mice. However, RNF90 regulated RNA virus-triggered antiviral innate immune responses independent of STING. RNF90 promoted K48-linked ubiquitination of MAVS and its proteasome-dependent degradation, leading to the inhibition of innate immune responses. Altogether, our findings suggested a novel function and mechanism of RNF90 in antiviral innate immunity.

E3 ligase c-Cbl regulates intestinal inflammation through suppressing fungi-induced noncanonical NF-κB activation.

Intestinal fungi are critical for modulating host immune homeostasis and underlying mechanisms remain unclear. We show that dendritic cell (DC)-specific deficiency of casitas B-lineage lymphoma (c-Cbl) renders mice susceptible to dextran sodium sulfate (DSS)-induced colitis. Mechanistically, we identify that c-Cbl functions downstream of Dectin-2 and Dectin-3 to mediate the ubiquitination and degradation of noncanonical nuclear factor κB subunit RelB. Thus, c-Cbl deficiency in DCs promotes α-mannan-induced activation of RelB, which suppresses p65-mediated transcription of an anti-inflammatory cytokine gene, il10, thereby aggravating DSS-induced colitis. Moreover, suppressing fungal growth with fluconazole or inhibition of RelB activation in vivo attenuates colitis in mice with DC-specific deletion of c-Cbl. We also demonstrate an interaction between c-Cbl and c-Abl tyrosine kinase and find that treatment with DPH, a c-Abl agonist, synergistically increases fungi-induced c-Cbl activation to restrict colitis. Together, these findings unravel a previously unidentified fungi-induced c-Cbl/RelB axis that sustains intestinal homeostasis and protects against intestinal inflammation.

Identification of the first Alu-mediated gross deletion involving the BCKDHA gene in a compound heterozygous patient with maple syrup urine disease.

AIMS: To investigate a family with clinical symptoms of maple syrup urine disease and reveal a genetic cause underlying this disease. METHODS: Targeted capture sequencing was used to screen for mutations in the patient. Real-Time PCR was carried out to perform exon 1, 5, 9 CNV analysis of samples from the patient's father, mother and sister. Whole genome sequencing was performed to map the approximate location of the break points of the gross deletion. Long-range PCR and Sanger sequencing were performed to identify the length of the deletion and to locate the break points. RESULTS: The patient is a compound heterozygous mutation including a small deletion mutation (c.1227_1229del chr19: 41930402) and a gross novel deletion including exon1-9 in BCKDHA. The junction site of the gross deletion was localized within a microhomologous sequence in two Alu elements. CONCLUSIONS: This study is the first time report on rearrangement sequences in BCKDHA mediated by Alu element, which resulted in MSUD. Our results may also offer new insights into the formation and pathogenicity of MSUD, and may be useful to genetic counseling and genetic testing.

RNF90 negatively regulates cellular antiviral responses by targeting MITA for degradation.

Mediator of IRF3 activation (MITA, also named as STING/ERIS/MPYS/TMEM173), is essential to DNA virus- or cytosolic DNA-triggered innate immune responses. In this study, we demonstrated the negative regulatory role of RING-finger protein (RNF) 90 in innate immune responses targeting MITA. RNF90 promoted K48-linked ubiquitination of MITA and its proteasome-dependent degradation. Overexpression of RNF90 inhibited HSV-1- or cytosolic DNA-induced immune responses whereas RNF90 knockdown had the opposite effects. Moreover, RNF90-deficient bone marrow-derived dendritic cells (BMDCs), bone marrow-derived macrophages (BMMs) and mouse embryonic fibroblasts (MEFs) exhibited increased DNA virus- or cytosolic DNA-triggered signaling and RNF90 deficiency protected mice from DNA virus infection. Taken together, our findings suggested a novel function of RNF90 in innate immunity.

Expanded newborn screening for inborn errors of metabolism by tandem mass spectrometry in newborns from Xinxiang city in China.

BACKGROUND: Tandem mass spectrometry is a powerful technology available in China over the last 15 years. The development of tandem mass spectrometry had made it possible to rapidly screen newborns for inborn errors of metabolism. The aim of this study was to determine the birth incidence of inborn errors of metabolism through expanded screening of newborns by tandem mass spectrometry in Xinxiang area. METHODS: Dried blood spots from 50 112 newborns were assessed for inborn errors of metabolism by tandem mass spectrometry. The diagnoses were confirmed based on the clinical features, conventional laboratory tests, and the organic acid levels tested in urine by gas chromatography-mass spectrometry. RESULTS: The study findings revealed that 31 newborns were diagnosed with inborn errors of metabolism. The total incidence rate of inborn errors of metabolism was 1/1617, and these included 16 cases of amino acid disorders (51.6%), nine cases of organic acid disorders (29.0%), and 6 (19.4%) cases of fatty acid beta-oxidation disorders. CONCLUSIONS: The screening for the incidence of inborn errors of metabolism in Xinxiang area showed that the rate was higher than previously reported. This study provides valuable data which may be useful in facilitating improvements in the expansion of screening to enable early diagnosis and treatment of inborn errors of metabolism before the onset of symptoms.

Robust Stereo Visual-Inertial Odometry Using Nonlinear Optimization.

The fusion of visual and inertial odometry has matured greatly due to the complementarity of the two sensors. However, the use of high-quality sensors and powerful processors in some applications is difficult due to size and cost limitations, and there are also many challenges in terms of robustness of the algorithm and computational efficiency. In this work, we present VIO-Stereo, a stereo visual-inertial odometry (VIO), which jointly combines the measurements of the stereo cameras and an inexpensive inertial measurement unit (IMU). We use nonlinear optimization to integrate visual measurements with IMU readings in VIO tightly. To decrease the cost of computation, we use the FAST feature detector to improve its efficiency and track features by the KLT sparse optical flow algorithm. We also incorporate accelerometer bias into the measurement model and optimize it together with other variables. Additionally, we perform circular matching between the previous and current stereo image pairs in order to remove outliers in the stereo matching and feature tracking steps, thus reducing the mismatch of feature points and improving the robustness and accuracy of the system. Finally, this work contributes to the experimental comparison of monocular visual-inertial odometry and stereo visual-inertial odometry by evaluating our method using the public EuRoC dataset. Experimental results demonstrate that our method exhibits competitive performance with the most advanced techniques.

Down-regulation of mitogen-activated protein kinases and nuclear factor-κB signaling is involved in rapamycin suppression of TLR2-induced inflammatory response in monocytic THP-1 cells.

Tripalmitoyl-S-glycero-Cys-(Lys) 4 (Pam3CSK4) interacted with TLR2 induces inflammatory responses through the mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB) signal pathway. Rapamycin can suppress TLR-induced inflammatory responses; however, the detailed molecular mechanism is not fully understood. Here, the mechanism by which rapamycin suppresses TLR2-induced inflammatory responses was investigated. It was found that Pam3CSK4-induced pro-inflammatory cytokines were significantly down-regulated at both the mRNA and protein levels in THP-1 cells pre-treated with various concentrations of rapamycin. Inhibition of phosphatidylinositol 3-kinase/protein kinase-B (PI3K/AKT) signaling did not suppress the expression of pro-inflammatory cytokines, indicating that the immunosuppression mediated by rapamycin in THP1 cells is independent of the PI3K/AKT pathway. RT-PCR showed that Erk and NF-κB signal pathways are related to the production of pro-inflammatory cytokines. Inhibition of Erk or NF-κB signaling significantly down-regulated production of pro-inflammatory cytokines. Additionally, western blot showed that pre-treatment of THP-1 cells with rapamycin down-regulates MAPKs and NF-κB signaling induced by Pam3CSK4 stimulation, suggesting that rapamycin suppresses Pam3CSK4-induced pro-inflammatory cytokines via inhibition of TLR2 signaling. It was concluded that rapamycin suppresses TLR2-induced inflammatory responses by down-regulation of Erk and NF-κB signaling.

Real-time EEG-based detection of fatigue driving danger for accident prediction.

This paper proposes a real-time electroencephalogram (EEG)-based detection method of the potential danger during fatigue driving. To determine driver fatigue in real time, wavelet entropy with a sliding window and pulse coupled neural network (PCNN) were used to process the EEG signals in the visual area (the main information input route). To detect the fatigue danger, the neural mechanism of driver fatigue was analyzed. The functional brain networks were employed to track the fatigue impact on processing capacity of brain. The results show the overall functional connectivity of the subjects is weakened after long time driving tasks. The regularity is summarized as the fatigue convergence phenomenon. Based on the fatigue convergence phenomenon, we combined both the input and global synchronizations of brain together to calculate the residual amount of the information processing capacity of brain to obtain the dangerous points in real time. Finally, the danger detection system of the driver fatigue based on the neural mechanism was validated using accident EEG. The time distributions of the output danger points of the system have a good agreement with those of the real accident points.

Development of a sandwich ELISA for the quantification of enterovirus 71.

Since 2008, enterovirus 71 (EV71) has been responsible for high-mortality seasonal epidemics of hand, foot and mouth disease in China. Currently many groups in the world are in the process of developing EV71 vaccines to combat this deadly disease. We have developed three EV71-specific monoclonal antibodies, and in this study we report the establishment of a fast and cost-effective sandwich ELISA kit for measurement of virus concentration in EV71 vaccines using a pair of mouse anti-EV71 monoclonal antibodies. The system is specific for EV71 virus, with no cross-reactivity to coxsackievirus A16, H1N1, rabies, and hepatitis A. Using a reference EV71 vaccine standard, the sensitivity of the assay kit was determined to be 0.82 U/ml, with a linear range between 3.75 and 120 U/ml.

Vapor-phase synthesis, growth mechanism and thickness-independent elastic modulus of single-crystal tungsten nanobelts.

Single-crystal tungsten nanobelts with thicknesses from tens to hundreds of nanometers, widths of several micrometers and lengths of tens of micrometers were synthesized using chemical vapor deposition. Surface energy minimization was believed to have played a crucial role in the growth of the synthesized nanobelts enclosed by the low-energy {110} crystal planes of body-centered-cubic structure. The anisotropic growth of the crystallographically equivalent {110} crystal planes could be attributable to the asymmetric concentration distribution of the tungsten atom vapor around the nanobelts during the growth process. The elastic moduli of the synthesized tungsten nanobelts with thicknesses ranging from 65 to 306 nm were accurately measured using a newly developed thermal vibration method. The measured modulus values of the tungsten nanobelts were thickness-dependent. After eliminating the effect of surface oxidization using a core-shell model, the elastic modulus of tungsten nanobelts became constant, which is close to that of the bulk tungsten value of 410 GPa.