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A Nonlinear Proportional-Derivative (NPD) controller with gravity compensation is proposed and applied to robot manipulators in this paper. The proportional and derivative gains are changed by the nonlinear function of errors in the NPD controller. The closed-loop system, composed of nonlinear robot dynamics and NPD controllers, is globally asymptotically stable in position control of robot manipulators. The comparison of the simulation experiments in the position control (the step response) of a robot manipulator with two degrees of freedom is also presented to illustrate that the NPD controller is superior to the conventional PD controller in a position control system. The experimental results show that the NPD controller can obtain a faster response velocity and higher position accuracy than the conventional PD controller in the position control of robot manipulators because the proportional and derivative gains of the NPD controller can be changed by the nonlinear function of errors. The NPD controller provides a novel approach for robot control systems.

aimed to bibliometrically analyse the main features of the 100 top-cited articles on the midwifery index on the Web of Science. Methods: Academic articles on midwifery' research published from 1985 to 2020 were included. VOSviewer 1.6.15, SPSS 22.0 software and a homemade applet were used to identify, analyse and visualise the citation ranking, publication year, journal, country and organisation of origin, authorship, journal impact factor and keywords along with the total link strength of countries, organisations and keywords. Results: Among the 100 top-cited articles, the highest number of citations of the retrieved articles was 484. The median number of citations per year was 5.16 (interquartile range: 3.74– 8.38). Almost two-thirds of the included articles (n = 61) centred on nursing and obstetrics/gynaecology. The top-cited articles were published in 38 different journals, the highest number of which was published by Midwifery (15%). Australia was the most productive country (24%). According to the total link strength, the sequence ran from the United States (28) to England (28) to Australia (19). The University of Technology Sydney and La Trobe University in Australia topped the list with four papers each. Hunter B was the most productive author (n = 4), and the average citations were positively related to the number of authors (r = 0.336, p < 0.05). Conclusion: This study identified the most influential articles on midwifery and documented the core journals and the most productive countries, organisations and authors along with future research hotspots for this field; the findings may be beneficial to researchers in their publication and scientific cooperation endeavours. [ABSTRACT FROM AUTHOR]

In this article, novel molecularly imprinted polymers based on 3D reduced graphene oxide aerogel (3D RGO‐GBMIPs) were successfully fabricated and applied as adsorbents for dispersed solid‐phase extraction (DSPE) of ginkgolide B (GB). After being prepared by surface molecular imprinted technology, 3D RGO‐GBMIPs were successively characterized by fourier transform infrared spectroscopy, thermogravimetric analysis, Raman spectroscopy, and scanning electron microscope. The results of adsorption experiments revealed that 3D RGO‐GBMIPs presented highly selective recognition properties and well reusability. The main variables influencing DSPE efficiency, including extraction solvent, 3D RGO‐GBMIPs dosage, category, and volume of eluent, as well as elution time were investigated. The DSPE results showed that 3D RGO‐GBMIPs had an obvious effect on the improvement of GB purity in ginkgo biloba extract, with a satisfactory recovery rate and yield. Therefore, 3D RGO‐GBMIPs are expected to be applied for the enrichment of GB from complex matrices. [ABSTRACT FROM AUTHOR]

Limited by ecological conditions, in order to improve the innovation efficiency concerning energy, a change from "extensive" to "green" is required. The development of sustainable technology is the most important productive force. Economic development is centered on finance. Only by mutual penetration and interaction can China's energy innovation be effectively promoted. "Green GDP (Gross Domestic Product)" is the main direction of China's current economic development. A sustainable green digital economy is the primary condition for promoting energy efficiency, and it is the key to improving energy efficiency in China to achieve a green transition. Green finance for sustainable development refers to economic finance centered on energy conservation, environmental protection and technological innovation. Attention is constantly paid to the financial industry in China, and we are trying to combine the concept of environmental protection with financial development to promote the continuous development of China's environmental protection economy. A company's economic and environmental benefits will be improved from the point of view of improving resource conservation and reducing the environmental impact of equipment and processes. To achieve this goal, the "efficiency effect" of the financial system needs to be fully exploited to maximize energy efficiency. An empirical study about the relationship of financial performance and energy efficiency in the green sector is carried out while considering the environmental constraints. The results show that the expansion of the financial scale and the adjustment of the financial structure have increased the energy utilization efficiency by more than 15% from the past to the present and reduced the pollution of the ecological environment by more than 10% nationwide, realizing the effective allocation of resources. Digital finance is a new generation of financial services that combines the Internet and information technology with traditional financial service formats. Including Internet payment, mobile payment, online banking, financial service outsourcing and online loans, online insurance, online funds and other financial services. Therefore, the sustainable development of all aspects of finance has a huge catalytic effect on the doubling of energy utilization efficiency. [ABSTRACT FROM AUTHOR]

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China is a big agricultural country, and China's agricultural development is related to the development of the country. Especially in poor rural areas, the development of agriculture still stays at low-level manual farming. Therefore, with the help of the developed Internet of Things technology, it is necessary for digital technology to develop and reform the rural areas in poverty-stricken areas. This paper aims to promote the supply-side structural revolution of agriculture in poverty-stricken areas by digital technology based on intelligent environment of Internet of Things. Firstly, the KNN intelligent algorithm is improved to improve the accuracy and reduce the time complexity. Then, based on the data support of Internet of Things technology, a prediction model is built, and the parameters are optimized by particle swarm optimization, and finally the best prediction model with high prediction accuracy, good stability and reduced prediction time complexity is obtained. Taking the source area of the Danjiang River in the South-to-North Water Transfer Project as the research object, the total grain output and soybean production demand in this area from 2010 to 2018 were selected, and the change trend of soybean production and demand in this area from 2019 to 2021 was predicted. The experimental data show that the soybean output in this region has increased year by year, with a cumulative increase of 6,985.4 tons from 2010 to 2018. Soybean output sometimes exceeds demand, and sometimes it is less than demand. There will be an oversupply situation in 2019 and 2021, and an oversupply situation in 2020. Therefore, the prediction model of Internet of Things can effectively predict the supply and demand situation of soybean with an accuracy rate of over 90%, which can provide data support for the decision-making of structural change of agricultural supply side in poverty-stricken areas. [ABSTRACT FROM AUTHOR]

BACKGROUND: Protecting the intestinal mucosa from being destroyed helps reduce the inflammation caused by acute pancreatitis (AP). In this study, whether okra pectin (OP) could attenuate the inflammation of AP through protecting the intestinal barrier was investigated. RESULTS: OP was obtained from crude okra pectin (COP) through the purification by DEAE cellulose 52 column. Supplementation with OP or COP in advance reduced the severity of AP, as revealed by lower serum amylase and lipase levels, abated pancreatic edema, attenuated myeloperoxidase activity and pancreas histology. OP or COP inhibited the production of pancreatic proinflammatory cytokines, including tumor necrosis factor‐α and interleukin‐6. In addition, the upregulation of AP‐related proteins including ZO‐1, occludin, the antibacterial peptide‐defensin‐1 (DEFB1) and cathelicidin‐related antimicrobial peptide (CRAMP), as well as the histological examination of colon injuries, demonstrated that OP or COP provision could effectively maintain intestinal barrier function. Ultimately, dietary OP or COP supplementation could inhibit AP‐induced intestinal inflammation. For the above, the effect of OP was better than COP. CONCLUSION: Dietary OP supplementation could be considered as a preventive method that effectively interferes with intestinal damage and attenuates inflammatory responses trigged by AP. © 2020 Society of Chemical Industry [ABSTRACT FROM AUTHOR]

Viral fulminant hepatitis (FH) is a severe disease with high mortality resulting from excessive inflammation in the infected liver. Clinical interventions have been inefficient due to the lack of knowledge for inflammatory pathogenesis in the virus-infected liver. We show that wild-type mice infected with murine hepatitis virus strain-3 (MHV-3), a model for viral FH, manifest with severe disease and high mortality in association with a significant elevation in IL-1β expression in the serum and liver. Whereas, the viral infection in IL-1β receptor-I deficient (IL-1R1-/-) or IL-1R antagonist (IL-1Ra) treated mice, show reductions in virus replication, disease progress and mortality. IL-1R1 deficiency appears to debilitate the virus-induced fibrinogen-like protein-2 (FGL2) production in macrophages and CD45+Gr-1high neutrophil infiltration in the liver. The quick release of reactive oxygen species (ROS) by the infected macrophages suggests a plausible viral initiation of NLRP3 inflammasome activation. Further experiments show that mice deficient of p47phox, a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit that controls acute ROS production, present with reductions in NLRP3 inflammasome activation and subsequent IL-1β secretion during viral infection, which appears to be responsible for acquiring resilience to viral FH. Moreover, viral infected animals in deficiencies of NLRP3 and Caspase-1, two essential components of the inflammasome complex, also have reduced IL-1β induction along with ameliorated hepatitis. Our results demonstrate that the ROS/NLRP3/IL-1β axis institutes an essential signaling pathway, which is over activated and directly causes the severe liver disease during viral infection, which sheds light on development of efficient treatments for human viral FH and other severe inflammatory diseases. [ABSTRACT FROM AUTHOR]

The cross-talk between the hepatitis B virus X protein (HBx) and B7-H1 in hepatocarcinoma (HCC) is unclear. This study analyzed the potential relationships between HBx and B7-H1 in hepatocarcinogenesis. One of human HCC cell lines, HepG2 cells, was transfected to stably express HBx protein (HBx+-HepG2). The transcription of B7-H1 mRNA was increased significantly in these cells compared to cells transfected with control vector (HBx--HepG2), as confirmed by a comparative genome-wide microarray analysis (Capitalbio) and real time quantitative PCR (qPCR). Flow cytometry and western-blot further demonstrated that B7-H1 protein synthesis was enhanced in HBx+-HepG2 cells. Site-directed mutagenesis of promoter constructs revealed that the transcription factor (NF)-κB binding site between 128 and 137 bp upstream of B7-H1 gene transcriptional start site is primarily responsible for HBx-mediated B7-H1 expression. Co-culture experiments with HBx+-HepG2/T cells showed that the number of apoptotic T cells increased profoundly, and this effect could be partially prevented when a neutralizing mAb against B7-H1 was added to the culture, demonstrating that B7-H1 signaling can promote T cell apoptosis. Our results suggest that the expression of B7-H1 in hepatocarcimona cells can be initiated by HBx antigen, thus inducing T cell apoptosis and finally potentially facilitates the genesis of HCC. [ABSTRACT FROM AUTHOR]

Abstract: Co-inhibitory signals from the B7 superfamily have been demonstrated to induce T cell dysfunction in chronic HBV infection (CHB). However, the expression and function of Z39Ig, a new inhibitor of the B7 superfamily, is still unclear in CHB. Here immunohistochemical staining showed that Z39Ig was restricted to macrophages and that its level was decreased significantly in CHB patients compared to healthy controls. Moreover, reduced Z39Ig expression was positively correlated with plasma HBV load but was inversely related to serum alanine aminotransaminase levels. Further, Z39Ig mRNA had a negative relation to IFN-γ in vivo, and IFN-γ also down-regulated Z39Ig expression on monocyte-derived macrophages (MDMs) in a time- and dose-dependent manner in vitro. Interestingly, Z39Ig expression on MDMs was restored when IFN-γ neutralizing antibodies were added to the T cell/MDM co-culture system, indicating that the IFN-γ derived from activated-T cells may contribute to the reduction of Z39Ig in the CHB environment. Our results suggest that T cells can opposite T cell hyporesponsiveness through dampening Z39Ig inhibitory signals from macrophages and thus maintain their anti-viral function in CHB. Therefore, decreasing Z39Ig signals from macrophages could contribute to CHB clinical therapy. [Copyright &y& Elsevier]

Chronic hepatitis B was characterized by fluctuant immune response to infected hepatocytes resulting in hepatic inflammation and virus persistence. Recently, Programmed Death-1 (PD-1) and its ligand PD-L1 have been demonstrated to play an essential role in balancing antiviral immunity and inflammation in the livers of acute hepatitis B patients, significantly influencing disease outcome. PD-1 up-regulation in peripheral T cells is associated with immune dysfunction in chronic hepatitis B patients. However, the effect of PD-1/PD-L1 on hepatic damage and chronic infective status is still unknown in patients with chronic HBV infection. Here, we report up-regulation of PD-1 and PD-L1 in liver biopsies from 32 chronic HBV patients compared to 4 healthy donors. PD-1/PD-L1 up-regulation was significantly associated with hepatic inflammation and ALT elevation. Moreover, appropriate up-regulation but not overexpression of PD-L1 in the active phase of chronic hepatitis B as well as lower expression of PD-L1 in the inactive phase in liver residential antigen presenting cells (including Kupffer cells and sinusoidal endothelial cells) may contribute to viral inhibition. Our data suggest that the intrahepatic interaction of PD-1 and PD-L1 might play an important role in balancing the immune response to HBV and immune-mediated liver damage in chronic HBV infection. [ABSTRACT FROM AUTHOR]

Sublytic C5b-9 has been described as a pro-inflammatory mediator that triggers cell activation rather than inducing cell death. Dendritic cells (DC) play a critical role in controlling antigen-specific immune responses. Although DC maturation induced by various stimuli has been well characterized, the role of C5b-9 in DC function has not been described. In this report, we use in vitro assembled functional C5b-9 based on purified distal complement protein to show that DC maturation is promoted by sublytic C5b-9. This was demonstrated by up-regulation of CD83, HLA-antigens and costimulatory molecules, including CD80, D86, B7-H1, B7-H3, B7-H4 and BTLA. In addition, secretion of cytokines such as interleukin (IL)-12 and tumor necrosis factor-α was increased while the capacity for antigen uptake (FITC-Dextran and Lucifer Yellow) was reduced in C5b-9-treated DC. Mixed lymphocyte reactions indicated that C5b-9-activated DC acted as stimulators that significantly promoted CD4 T cell activation and elicited production of cytokines, including interferon-γ and IL-2. Interestingly, C5b-9-treated DC also orient CD4CD45RA naïve T cells toward Th1 polarization. Our results are the first to report that DC are potential immunoregulatory targets of C5b-9, suggesting that C5b-9 bridges innate and acquired immunity by inducing DC maturation. [ABSTRACT FROM AUTHOR]

Objective. To systematically evaluate the effect of collaborative nursing on self-care ability of postcolostomy patients with colorectal cancer (CRC). Methods. PubMed, Web of Science, Embase, China National Knowledge Infrastructure, and Wanfang databases were searched to collect relevant literatures on randomized controlled trials of postcolostomy patients with CRC. The search period was started from 2010 to 2021. Statistical analysis was performed on the data extracted from the comprehensive meta-analysis with STATA 16.0 analysis software. Results. As a result, it was found that the incidence of adverse reactions in the control group was higher than that in the treatment group. Seven studies included the preintervention self-care concept and preintervention self-care skills. Six studies included preintervention self-care responsibility and preintervention exercise of self-care agency (ESCA) scale. In the comparison among the concept of self-care after intervention, self-care skills, self-care responsibility, and ESCA scale, all of them had higher scores in the treatment group than in the control group (P < 0.05). It fully explains that collaborative nursing can significantly improve the evaluation indicators of patients' self-care ability and reduce patient complications. Conclusion. The application of collaborative nursing in the nursing work of patients with CRC after colostomy can significantly reduce the incidence of adverse nursing reactions. [ABSTRACT FROM AUTHOR]

Currently, there are few studies on acid-soluble pectin from okra, especially in biological activity for antioxidant and anti-inflammatory. In this study, the antioxidant properties of acid-soluble okra pectin components and their anti-inflammatory were explored. Firstly, two acid-soluble okra pectic fractions, namely crude acid-soluble okra pectin (CAOP) and acid-soluble okra pectin (AOP), were obtained and exhibited structural and compositional variation. The two pectic fractions contained a low degree of esterification (42.0–46.5%) and a relatively high uronic acid content (31.6–37.3%). AOP was composed of galacturonic acid (79.1 mol/%), galactose (4.3 mol/%), rhamnose (14.5 mol/%) and xylose (2.1 mol/%), and the molecular weight was 92.8 kDa. Morphological and thermal properties of acid-soluble okra pectin components were also investigated. Compared to CAOP, AOP expressed better antioxidant activity, and suppressed the NO production in LPS-induced RAW 264.7 macrophages. All the above results indicated that AOP had the potential to act as a natural antioxidant or a functional anti-inflammatory food, which would broaden the development and utilization of okra resources. • The physicochemical properties of acid-soluble pectin from okra were studied. • The structure of acid-soluble pectin from okra was analyzed. • The pectin exhibited a protective effect against LPS-induced cell toxicity. • The pectin possessed antioxidant properties and anti-inflammatory potential. [ABSTRACT FROM AUTHOR]

Abstract: Increased lymphocyte apoptosis has been suggested to contribute to the development of systemic lupus erythematosus (SLE), but the critical factors involved in the apoptotic pathways are still unknown. By long serial analysis of gene expression (LongSAGE) profiles and microarray analyses, a novel apoptosis-related gene BclGL expression was found significantly increased in peripheral blood CD4+ T cells of SLE patients, which was correlated with the enhanced CD4+ T cells apoptosis, anti-nuclear antibody (ANA) titer and proteinuria. In vitro, BclGL expression could be specially upregulated by SLE serum stimulation and positively correlated with induced CD4+ T cell apoptosis. Enforcing BclGL overexpression by lentivirus could directly enhance CD4+ T cell apoptosis, but these apoptosis-inducing effects could be partially inhibited by knockdown of BclGL expression. Collectively, these results indicate that increased BclGL expression may contribute to the aberrant CD4+ T cell apoptosis which causes an inappropriate immune response and impaired homeostasis in SLE. [Copyright &y& Elsevier]