Adaptive Guaranteed-Performance Consensus Control for Multiagent Systems With an Adjustable Convergence Speed

Adaptive guaranteed-performance consensus control problems for multi-agent systems are investigated, where the adjustable convergence speed is discussed. This paper firstly proposes a novel adaptive guaranteed-performance consensus protocol, where the communication weights can be adaptively regulated. By the state space decomposition method and the stability theory, sufficient conditions for guaranteed-performance consensus are obtained, as well as the guaranteed-performance cost. Moreover, since the convergence speed is usually adjusted by changing the algebraic connectivity in existing works, which increases the communication burden and the load of the controller, and the system topology is always given in practical applications, the lower bound of the convergence coefficient for multi-agent systems with the adaptive guaranteed-performance consensus protocol is deduced, which is linearly adjustable approximately by changing the adaptive control gain. Finally, simulation examples are introduced to demonstrate theoretical results

The Role of Deubiquitinases in DNA Double-Strand Break Repair

DNA double-strand break (DSB) is a type of the most critical DNA lesions, and if not repaired promptly, it can result in cell death or a wide variety of genetic alterations including genome instability, large- or small-scale deletions, chromosome loss, loss of heterozygosity, and translocations. DSBs are repaired by double-strand break repair (DSBR), including nonhomologous end-joining (NHEJ) and homologous recombination (HR) pathway, and defects in these pathways cause genome instability and promote tumorigenesis. Accumulating evidence has demonstrated that the superfamily of deubiquitinases (DUBs) can regulate the action and stability of DNA repair enzymes involving in DSBR via modifying ubiquitination levels, a reversible posttranslational modification pathway. In this review, we will discuss ubiquitination/deubiquitination modification involving in DSBR genes, the role of DUBs in DSBR and corresponding mechanisms, and the potential effects of this modification on human diseases

1-(2-Fluoro­benz­yl)-1-(2-fluoro­benz­yl­oxy)urea

In the title hydroxy­urea derivative, C15H14F2N2O2, the dihedral angle between the two benzene rings is 48.64 (19)°. The urea group forms dihedral angles of 48.1 (2) and 79.2 (2)° with the two benzene rings. In the crystal, inversion dimers linked by pairs of N—H⋯O hydrogen bonds occur, and further N—H⋯O links lead to chains of molecules

X-Ray Repair Cross Complementing 4 (XRCC4) Genetic Single Nucleotide Polymorphisms and the Liver Toxicity of AFB1 in Hepatocellular Carcinoma

Our previous reports have shown that the genetic single-nucleotide polymorphisms (GSNPs) in the DNA repair gene X-ray repair cross complementing 4 (XRCC4) are involved in the carcinogenesis of hepatocellular carcinoma (HCC) induced by aflatoxin B1 (AFB1). However, the effects of GSNPs in the coding regions of XRCC4 on hepatic toxicity of AFB1 have been less investigated. We conducted a hospital-based clinic tissue samples with pathologically diagnosed HCC (n = 380) in a high AFB1 exposure area to explore the possible roles of GSNPs in the coding regions of XRCC4 in AFB1-induced HCC using liver toxicity assays. A total of 143 GSNPs were included in the present study and genotyped using the SNaPshot method, whereas the liver toxicity of AFB1 was evaluated using AFB1-DNA adducts in the tissues with HCC. In the clinicopathological samples with HCC, the average adduct amount is 2.27 ± 1.09 μmol/mol DNA. Among 143 GSNPs of XRCC4, only rs1237462915, rs28383151, rs762419679, rs766287987, and rs3734091 significantly increased the levels of AFB1-DNA adducts. Furthermore, XRCC4 GSNPs (including rs28383151, rs766287987, and rs3734091) also increased cumulative hazard for patients with HCC. These results suggest that the liver toxicity of AFB1 may be modified by XRCC4 GSNPs

SC-TVP Green Practice Initiative in China’s Logistics Market Based on Case Analysis

In the era of circular economy, the concept of sustainable development has attracted more and more attention. With the development of cross-border e-commerce, the demand for logistics services has continued to surge, and the pressure on them to provide sustainable services has risen sharply. In 2020, China officially put forward the “double carbon” strategic goal, and green logistics has become the new direction of industry development, in line with the concept of sustainable development. However, the actual impact of green logistics practice on China’s sustainable logistics services is unknown. This paper aims to study the current situation and results of green logistics practice through data analysis and case analysis, including green design, green transportation, green management and other indicators. Based on the case analysis in this paper, the SC-TVP model is constructed to provide an effective green logistics practice framework, with a view to improving the management level of green logistics, promoting the development of enterprises, and providing some reference for the logistics development in the post-epidemic era

Production of copolyesters of 3-hydroxybutyrate and medium-chain-length 3-hydroxyalkanoates by E. coli containing an optimized PHA synthase gene

BACKGROUND: Microbial polyhydroxyalkanoates (PHA) are biopolyesters consisting of diverse monomers. PHA synthase PhaC2(Ps) cloned from Pseudomonas stutzeri 1317 is able to polymerize short-chain-length (scl) 3-hydroxybutyrate (3HB) monomers and medium-chain-length (mcl) 3-hydroxyalkanoates (3HA) with carbon chain lengths ranging from C6 to C12. However, the scl and mcl PHA production in Escherichia coli expressing PhaC2(Ps) is limited with very low PHA yield. RESULTS: To improve the production of PHA with a wide range of monomer compositions in E. coli, a series of optimization strategies were applied on the PHA synthase PhaC2(Ps). Codon optimization of the gene and mRNA stabilization with a hairpin structure were conducted and the function of the optimized PHA synthase was tested in E. coli. The transcript was more stable after the hairpin structure was introduced, and western blot analysis showed that both codon optimization and hairpin introduction increased the protein expression level. Compared with the wild type PhaC2(Ps), the optimized PhaC2(Ps) increased poly-3-hydroxybutyrate (PHB) production by approximately 16-fold to 30% of the cell dry weight. When grown on dodecanoate, the recombinant E. coli harboring the optimized gene phaC2(Ps)O with a hairpin structure in the 5’ untranslated region was able to synthesize 4-fold more PHA consisting of 3HB and medium-chain-length 3HA compared to the recombinant harboring the wild type phaC2(Ps). CONCLUSIONS: The levels of both PHB and scl-mcl PHA in E. coli were significantly increased by series of optimization strategies applied on PHA synthase PhaC2(Ps). These results indicate that strategies including codon optimization and mRNA stabilization are useful for heterologous PHA synthase expression and therefore enhance PHA production

The correlation between the plasma concentration of gemcitabine and short-term efficacy and adverse reactions in patients with advanced squamous cell carcinoma of the lung using liquid chromatography-mass spectrometry

AbstractBackground: Worldwide, non-small cell lung cancers have the highest incidence and mortality rates of all cancers. Gemcitabine (2’,2’-difluoro-2’-deoxycytidine or dFdC, C9H11F2N304) is widely used as the first-line chemo-reagent for lung cancer patients whose tumors have been diagnosed to be at an advanced stage and are therefore unresectable. Objective: The objective of this systematic study was to establish the correlation between the plasma concentration of gemcitabine and short-term clinical efficacy and adverse reactions in patients with advanced squamous cell carcinoma of the lung using liquid chromatography-mass spectrometry. Material and methods: In total, 53 patients were given the chemotherapy medications, gemcitabine and cisplatin, every 3 weeks. Plasma concentrations of gemcitabine were determined using liquid chromatography-mass spectrometry. A modified methodology of the liquid chromatography-mass spectrometry system was verified and performed to detect plasma concentrations of gemcitabine. The clinical endpoints – short-term clinical efficacy and adverse reactions – were evaluated after two cycles. Results: The plasma concentration range of gemcitabine in 53 patients was 1.58-28.70μg/ml (mean 14.37±8.63μg/ml), with 28 patients in the >15μg/ml group (mean 21.76±3.45μg/ml), and 25 patients in the ≤15μg/ml group (mean 6.09±3.57μg/ml). The clinical benefit rate (CBR) of the >15μg/ml group was significantly higher than that of the 15μg/ml group (p<0.05). The incidences of leukopenia and neutropenia, thrombocytopenia and grade III-IV gastrointestinal reactions in the >15μg/ml group were significantly higher than in the ≤15μg/ml group (p<0.05). There was no statistical difference between the two groups in terms of the incidences of reduced hemoglobin, liver and kidney function damage, allergic reaction and rash (p>0.05). The analysis of the plasma concentration of gemcitabine and the percentage of reduction in neutrophil count (NEUT) (r2 = 0.3212; p<0.05) and platelet (PLT) (r2 = 0.6439; p<0.05) showed a significant positive correlation. Conclusions: In patients with advanced non-small cell lung cancer, a high plasma concentration of gemcitabine can improve the short-term clinical efficacy of treatment, but increase the incidence of grade III-IV adverse reactions. [Ethiop. J. Health Dev. 2021; 35(1):72-82] Key words: Non-small cell lung cancer, gemcitabine, plasma concentration, short-term efficacy, adverse reaction

Exendin-4 Protects MIN6 Cells from t-BHP-Induced Apoptosis via IRE1-JNK-Caspase-3 Signaling

Objectives. This study aimed to explore the effect of exendin-4 on t-BHP-induced apoptosis in pancreatic β cells and the mechanism of action. Methods. Murine MIN6 pancreatic β cells were treated with exendin-4 in the presence or absence of tert-butyl hydroperoxide (t-BHP). Cell survival was assessed by MTT staining. The percentage of apoptotic cells was determined by fluorescence microscopy analysis after Hoechst/PI staining and flow cytometric assay after Annexin V-FITC/PI staining. The activity of caspase-3 was determined using a caspase-3 activity kit. Expression of P-IRE1α, IRE1α, C-Jun N-terminal kinase (JNK), P-JNK, C-JUN, and P-C-JUN was detected by western blotting. Results. Exendin-4 was found to inhibit t-BHP-induced apoptosis in pancreatic β-cells by downregulating caspase-3 activity. Exendin-4 also inhibited the endoplasmic reticulum transmembrane protein IRE1, the apoptosis-related signaling molecule JNK, and c-Jun activation. Conclusions. Our findings suggest that exendin-4 ultimately reduces t-BHP-induced β-cell apoptosis. IRE1-JNK-c-Jun signaling is involved in the exendin-4-mediated modulation of β-cell apoptosis