Multi-constraint spatial coupling for the body joint quadruped robot and the CPG control method on rough terrain.

Quadruped robots have frequently appeared in various situations, including wilderness rescue, planetary exploration, and nuclear power facility maintenance. The quadruped robot with an active body joint has better environmental adaptability than one without body joints. However, it is difficult to guarantee the stability of the body joint quadruped robot when walking on rough terrain. Given the above issues, this paper proposed a gait control method for the body joint quadruped robot based on multi-constraint spatial coupling (MCSC) algorithm. The body workspace of the robot is divided into three subspaces, which are solved for different gaits, and then coupled to obtain the stable workspace of the body. A multi-layer central pattern generator model based on the Hopf oscillator is built to realize the generation and switching of walk and trot gaits. Then, combined with the MCSC area of the body, the reflex adjustment strategy on different terrains is established to adjust the body's posture in real time and realize the robot's stable locomotion. Finally, the robot prototype is developed to verify the effectiveness of the control method. The simulation and experiment results show that the proposed method can reduce the offset of the swing legs and the fluctuation of the body attitude angle. Furthermore, the quadruped robot is ensured to maintain stability by dynamically modifying its body posture. The relevant result can offer a helpful reference for the control of quadruped robots in complex environments.

ILC2 influence the differentiation of alveolar type II epithelial cells in bronchopulmonary dysplasia mice.

Bronchopulmonary dysplasia, a common complication of premature infants, is mainly characterized by blocked alveolarization. Proverbially, the injury of alveolar type II epithelial cells is regarded as the pathologic basis of occurrence and development of bronchopulmonary dysplasia. In the case of alveolar epithelial damage, alveolar type II epithelial cells can also differentiate to alveolar type I epithelial cells as progenitor cells. During bronchopulmonary dysplasia, the differentiation of alveolar type II epithelial cells becomes abnormal. Group 2 innate lymphoid cells can produce type 2 cytokines in response to a variety of stimuli, including the epithelial cytokines IL-25, IL-33, and thymic stromal lymphopoietin. Previous studies have shown that group 2 innate lymphoid cells can inhibit the alveolarization process of bronchopulmonary dysplasia by secreting IL-13. However, whether group 2 innate lymphoid cells can affect the differentiation of alveolar type II epithelial cells in the pathologic process of bronchopulmonary dysplasia remains unclear. In this study, we have shown that IL-13 secreted by group 2 innate lymphoid cells increased during bronchopulmonary dysplasia, which was related to the release of large amounts of IL-33 by impaired alveolar type II epithelial cells. This led to abnormal differentiation of alveolar type II epithelial cells, reduced differentiation to alveolar type I epithelial cells, and increased transdifferentiation to mesenchymal cells through the epithelial-mesenchymal transition. Taken together, our study provides a complementary understanding of the development of bronchopulmonary dysplasia and highlights a novel immune mechanism in the pathogenesis of bronchopulmonary dysplasia.

[Isolation and culture of type 2 innate lymphoid cells (ILC2) in lungs of newborn mice].

Objective To investigate the isolation and culture of the type 2 innate lymphoid cell (ILC2) in the lungs of newborn mice. Methods Immunomagnetic bead enrichment and fluorescence activated cell sorting (FACS) were used to isolate ILC2s. Flow cytometry was used to identify the purity of ILC2s. Inverted microscope was used to observe the growth of cells. ELISA was used to detect the expression levels of interleukin 5 (IL-5) and IL-13. Results The purity of the isolated ILC2s reached more than 95%. The isolated ILC2s were round or oval, and suspended in cell culture medium. After stimulation with IL-2 and IL-7 combined with IL-33, the contents of IL-5 and IL-13 produced by ILC2s and the proliferation ability of ILC2s increased significantly. Conclusion A rapid and efficient method for isolation and culture of ILC2s in the lung of newborn mice has been found.

Group 2 innate lymphoid cells (ILC2s): The spotlight in asthma pathogenesis and lung tissue injury

Asthma is a heterogeneous disease with ranging etiology and severity. Asthma is a disease of chronic inflammation of the airways, with clinical symptoms of wheezing, breathlessness, cough, and chest tightness manifested as chronic fixed or variable airflow obstruction and airway hyperresponsiveness that predispose the airway epithelium to repeated injury, repair, and regeneration. In recent years, innate lymphoid cells (ILC1, ILC2, and ILC3) have been discovered. The predominant ILC type found in the lung tissue is group 2 innate lymphoid cells (ILC2s). Upon damage to the airway epithelium mediating the release of epithelial cytokines (TSLP, IL-33, and IL-25) ensued the activation of ILC2 in an antigen-independent manner. Activated ILC2 produces a significant amount of type 2 cytokines (IL-4, IL-5, IL-9, and IL-13), altogether contributing to type 2 inflammation in the airways. ILC2s are mediators of type 2 immunity for many type 2 inflammatory diseases such as asthma, since ILC2s were reported to play an important role in asthma pathogenesis. Here we discuss the role of ILC2 in the development of asthma and ILC2 effector cytokines (IL-4, IL-5, and IL-13) contributing to airway epithelial structural changes (AU)

Group 2 innate lymphoid cells (ILC2s): The spotlight in asthma pathogenesis and lung tissue injury.

Asthma is a heterogeneous disease with ranging etiology and severity. Asthma is a disease of chronic inflammation of the airways, with clinical symptoms of wheezing, breathlessness, cough, and chest tightness manifested as chronic fixed or variable airflow obstruction and airway hyperresponsiveness that predispose the airway epithelium to repeated injury, repair, and regeneration. In recent years, innate lymphoid cells (ILC1, ILC2, and ILC3) have been discovered. The predominant ILC type found in the lung tissue is group 2 innate lymphoid cells (ILC2s). Upon damage to the airway epithelium mediating the release of epithelial cytokines (TSLP, IL-33, and IL-25) ensued the activation of ILC2 in an antigen-independent manner. Activated ILC2 produces a significant amount of type 2 cytokines (IL-4, IL-5, IL-9, and IL-13), altogether contributing to type 2 inflammation in the airways. ILC2s are mediators of type 2 immunity for many type 2 inflammatory diseases such as asthma, since ILC2s were reported to play an important role in asthma pathogenesis. Here we discuss the role of ILC2 in the development of asthma and ILC2 effector cytokines (IL-4, IL-5, and IL-13) contributing to airway epithelial structural changes.

Tissue-Resident Type 2 Innate Lymphoid Cells Arrest Alveolarization in Bronchopulmonary Dysplasia.

Bronchopulmonary dysplasia (BPD) is a severe complication of the respiratory system associated with preterm birth. Type 2 innate lymphoid cells (ILC2s) play a major role in tissue homeostasis, inflammation, and wound healing. However, the role in BPD remains unclear. The present study showed that ILC2s, interleukin-4 (IL-4), IL-13, and anti-inflammatory (M2) macrophages increased significantly in BPD mice as compared to the control mice. Administration with recombinant mouse IL-33 amplified the above phenomena and aggravated the alveolar structural disorder and functional injury in mice subjected to BPD, and the opposite was true with anti-ST2 antibody. In addition, the depletion of ILC2s in BPD mice with anti-CD90.2 antibody substantially abolished the destructive effect on BPD. In the treatment of BPD with dexamethasone, the number of ILC2s and M2 macrophages and levels of IL-4 and IL-13 decreased with remission as compared to the control group. This study identified a major destructive role of the ILC2s in BPD that could be attenuated as a therapeutic strategy.

Carbocisteine attenuates TNF-α-induced inflammation in human alveolar epithelial cells in vitro through suppressing NF-κB and ERK1/2 MAPK signaling pathways.

AIM: We previously proven that carbocisteine, a conventional mucolytic drug, remarkably reduced the rate of acute exacerbations and improved the quality of life in the patients with chronic obstructive pulmonary disease. In this study we investigated the mechanisms underlying the anti-inflammatory effects of carbocisteine in human alveolar epithelial cells in vitro. METHODS: Human lung adenocarcinoma cell line A549 was treated with TNF-α (10 ng/mL). Carbocisteine was administered either 24 h prior to or after TNF-α exposure. The cytokine release and expression were measured using ELISA and qRT-PCR. Activation of NF-κB was analyzed with Western blotting, immunofluorescence assay and luciferase reporter gene assay. The expression of ERK1/2 MAPK signaling proteins was assessed with Western blotting. RESULTS: Carbocisteine (10, 100, 1000 µmol/L), administered either before or after TNF-α exposure, dose-dependently suppressed TNF-α-induced inflammation in A549 cells, as evidenced by diminished release of IL-6 and IL-8, and diminished mRNA expression of IL-6, IL-8, TNF-α, MCP-1 and MIP-1ß. Furthermore, pretreatment with carbocisteine significantly decreased TNF-α-induced phosphorylation of NF-κB p65 and ERK1/2 MAPK, and inhibited the nuclear translocation of p65 subunit in A549 cells. In an NF-κB luciferase reporter system, pretreatment with carbocisteine dose-dependently inhibited TNF-α-induced transcriptional activity of NF-κB. CONCLUSION: Carbocisteine effectively suppresses TNF-α-induced inflammation in A549 cells via suppressing NF-κB and ERK1/2 MAPK signaling pathways.

The complete mitochondrial genome of the Plectorhinchus cinctus (Teleostei, Haemulidae).

We present the complete mitochondrial genome of the Plectorhinchus cinctus in this study. The mitochondrial genome is 16,523 bp in length and consists of 13 protein-coding genes, 2 rRNA genes, 22 tRNA genes and a control region. The nucleotide compositions of the light strand are 31.30% of C, 27.66% of A, 24.54% of T, and 16.50% of G. With the exception of ND6 and eight tRNA genes, all other mitochondrial genes are encoded on the heavy strand. All the protein-coding genes begin with an ATG initiation codon except for COX1 with GTG. Five types of termination codons revealed are TAA (ND1, ND2, ATP8, ND4L, ND5), T (COXП, ND3, ND4, CYTB), TA (ATP6, COXШ), AGG (COXІ) and TAG (ND6).

Synthesis and biological evaluation of levofloxacin core-based derivatives with potent antibacterial activity against resistant Gram-positive pathogens.

A series of C10 non-basic building block-substituted, levofloxacin core-based derivatives were synthesized in 43-86% yield. The antibacterial activity of these new fluoroquinolones was evaluated using a standard broth microdilution technique. The quinolone (S)-9-fluoro-10-(4-hydroxypiperidin-1-yl)-3-methyl-7-oxo-3,7-dihydro-2H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid L-arginine tetrahydrate exhibited superior antibacterial activity against quinolone-susceptible and resistant strains compared with the clinically used fluoroquinolones ciprofloxacin, levofloxacin, moxifloxacin, penicillin, and vancomycin, especially to the methicillin-resistant Staphylococcus aureus clinical isolates, penicillin-resistant Streptococcus pneumoniae clinical isolates, and Streptococcus pyogenes.

Carbocisteine attenuates hydrogen peroxide-induced inflammatory injury in A549 cells via NF-κB and ERK1/2 MAPK pathways.

Carbocisteine is a mucolytic drug with anti-oxidative effect, we had previously proved that carbocisteine remarkably reduced the rate of acute exacerbations and improved the quality of life in patients with chronic obstructive pulmonary disease (COPD), however, very little is known about its mechanisms. In this study, we aimed to investigate the anti-inflammatory effects of carbocisteine against hydrogen peroxide (H2O2). A549 cells were cultured in vitro and treated with H2O2 as damaged cell models, carbocisteine was administered 24h prior to or after H2O2 exposure, and the protective effects of carbocisteine were determined by MTT, qRT-PCR, ELISA, western blot and immunofluorescence assays. The results showed that carbocisteine could increase cell viability and decrease LDH, IL-6 and IL-8 levels in the supernatant. Additionally, carbocisteine decreased IL-6, IL-8, TNF-α, IP-10 and MIP-1ß mRNA in a dose-dependent manner. Moreover, carbocisteine could attenuate phosphorylation of NF-κB p65 and ERK1/2 and inhibit the nuclear translocation of pNF-κB p65 induced by H2O2. In conclusion, carbocisteine inhibited H2O2-induced inflammatory injury in A549 cells, NF-κB and ERK1/2 MAPK were the target pathways.

[Research on active part of Sambucus chinensis against hepatitis mice induced by CCl4].

OBJECTIVE: To investigate the best extraction process of Sambucus chinensis against hepatitis and research on its active part. METHODS: We studied the protective effects of different extracts of Sambucus chinensis distilled by different extraction process on mice acute hepatic injury induced by CCl4, and searched for the active part of Sambucus chinensis against hepatitis from the best extract by extraction with different solvent and purification with macroporous adsorption resin, then studied their protective effects on mice acute hepatic injury induced by CCl4. RESULTS: The extraction of Sambucus chinensis by 75% alcohol showed very significantly protective effects on mice acute hepatic injury induced by CCl4 and the effects were better than that of other extraction process. The extraction eluted by 30% alcohol after purification with macroporous adsorption resin and extracted by EtOAc in the extraction of Sambucus chinensis by 75% alcohol all showed significantly protective effects on mice acute hepatic injury induced by CCl4, and the effects of the extraction eluted by 30% alcohol after purification with macroporous adsoption resin were better than extraction with EtOAc. CONCLUSIONS: The best extraction solvent is 75% alcohol. The active part of Sambucus chinensis against hepatitis is the extraction eluted by 30% alcohol after purification with macroporous adsorption resin and extraction with EtOAc.