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BACKGROUND: Diaphragmatic electromyographic (EMGdi) is a helpful method to reflect the respiratory center's activity visually. However, the electrocardiogram (ECG) severely affected its weakness, limiting its use. OBJECTIVE: To remove the ECG artifact from the EMGdi, we designed a Morphological ECG subtraction method (MES) based on three steps: 1) ECG localization, 2) morphological tracking, and 3) ECG subtractor. METHODS: We evaluated the MES method against the wavelet-based dual-threshold and stationary wavelet filters using visual and frequency-domain characteristics (median frequency and power ratio). RESULTS: The results show that the MES method can preserve the features of the original diaphragm signal for both surface diaphragm signal (SEMGdi) and clinical collection of diaphragm signal (EMGdi_clinic), and it is more effective than the wavelet-based dual-threshold and stationary wavelet filtering methods. CONCLUSION: The MES method is more effective than other methods. This technique may improve respiratory monitoring and assisted ventilation in patients with respiratory diseases.

Asunto(s)

Diafragma , Procesamiento de Señales Asistido por Computador , Humanos , Electromiografía/métodos , Tórax , Electrocardiografía/métodos

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The crystal structures, mechanical properties, and electrical properties of Cu doped SnO2, F doped SnO2, and Cu F co-doped SnO2 were studied by using the first-principles method. Meanwhile, AgSnO2, AgSnO2-F, AgSnO2-Cu, and AgSnO2-Cu-F contacts were prepared by using the sol-gel method for a series of experiments to verify the theoretical analysis. According to the XRD patterns, the doping does not change the structure of SnO2, but increases its lattice constant and volume. Compared with the single-doped system, the doping formation energy of Cu F co-doped system is the smallest and the structure is more stable. Among the three groups of doping systems, the Cu F co-doped system has the highest shear modulus, Young's modulus, hardness, and Debye temperature, and its mechanical properties and wear resistance are relatively best, and the melting point is also the highest. Cu F co-doping can further narrow the band gap of SnO2, reduce the electron effective mass and donor ionization energy, increase the electron mobility, and further enhance the conductivity of SnO2. The wetting angle of SnO2-Cu-F sample with Ag liquid is 1.15°, which indicates that Cu and F co-doping can significantly improve the wettability of SnO2 and Ag liquid. AgSnO2-Cu-F contact has a hardness of 82.03 HV, an electrical conductivity of 31.20 mS⋅m-1, and a contact resistance of 1.048 mΩ. Cu F co-doping can improve the shortcomings of AgSnO2 contact properties.

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Objective The aim of this study was to explore the regulatory effects and mechanism of autophagy on epithelial-to-mesenchymal transition(EMT) in idiopathic pulmonary fibrosis(IPF). Methods The experiment was divided into two group: control group and experimental group(IPF group, autophagy induction group, autophagy inhibition group). A549 cells were cultivated by the conventional method in control group. The A549 cells of the experimental group were induced by TGF-β1(5 ng/mL). Then, no further treatment was given to IPF group. Rapamycin(10 μg/L) or 3-Methyladenine(10mmol/L) was given to autophagy induction group or autophagy inhibition group respectively. The hydroxyproline content of lung tissue was measured, and the mRNA and protein levels of α-SMA, LC3-Ⅱ or LC3-Ⅱ/LC3-Ⅰ, Beclin1, E-cadherin and Vimentin were tested by Realtime PCR and Western blot. Results At each time point, the hydroxyproline content of lung tissue and the mRNA and protein levels of α-SMA and Vimentin in the experimental group were significantly higher than those in the control group（all P<0.05）. The above detections in autophagy induction group or autophagy inhibition group were significantly lower or higher than those in the IPF group（all P<0.05）. The mRNA and protein levels of LC3-Ⅱor LC3-Ⅱ/LC3-Ⅰ, Beclin1 and E-cadherin in the experimental group were significantly lower than those in the control group（all P<0.05）. Moreover, the same detections in autophagy induction group or autophagy inhibition group were significantly higher or lower than those in the IPF group（all P<0.05）. Conclusion The autophagy and EMT played an important role in IPF. Induction of autophagy might inhibit the development of IPF by inhibiting EMT, and Inhibition of autophagy could promote the development of IPF by activating EMT.

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Objective: To study the chemical constituents of the methanol extract from the aerial parts of the mangrove plant Sonneratia paracaseolaris. Methods: The methanol extract was isolated and purified with various chromatographic methods, including silica gel, ODS, Sephadex LH-20 columns, TLC, and HPLC. The compounds were identified by their physical chemical properties and 1H-NMR and 13C-NMR data. Results: Seventeen compounds were obtained from the methanol extract of Sonneratia paracaseolaris and identified as phytol (1), stigmasta-4-ene-3,6-dione (2), stigmata-4,22-diene-3,6-dione (3), cholesterol (4), (22E)-cholesterol-5,22-diene-3β-alcohol (5), diosmetin (6), tricin (7), 5,3′,5′-trihydroxy-7,4′-dimethoxyflavone (8), 5-hydroxy- 7,4′-dimethoxyflavone (9), 5-hydroxyl-7,3′,4′-trimethoxydihydroflavone (10), vanillin (11), p-hydroxy benzaldehyde (12), salicylic acid (13), trans-p-hydroxyl ethyl cinnamate (14), 4-hydroxy-2,6-dimethoxy-benzaldehyde (15), 3,4,5-trimethoxybenzoic acid (16), and 3,3′,4-trimethoxyellagic acid (17). Conclusion: All the compounds except 4, 11, 15, and 17 are obtained from genus Sonneratia. All compounds are isolated from S. paracaseolaris for the first time.

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Objective Idiopathic pulmonary fibrosis ( IPF) is a chronic inflammatory disease with unknown etiology and is lack of effective therapy. The aim of this study is to explore the function of Ca2+ and PI3K/AKT/mTOR pathway in the pathogenesis of IPF, and the impact of 1,25?( OH) 2 D3 on Ca2+ and PI3K/AKT/mTOR pathway in type Ⅱalveolar epithelial cells of rat with IPF. Methods 150 male SD rats were randomly divided into 2 groups: prevention group ( control groupⅠ, model groupⅠ, medication groupⅠ) and treatment group ( control groupⅡ, model groupⅡ, medication groupⅡ) . The tracheal exposure surgery was operated in control groupⅠ/Ⅱ, and then 200μL sterile physiological saline was administered by intraperitoneal injection of each rats 2 days and 14 days after surgery, separately. Bleomycin(BLM)(5 mg/kg) was in?jected into the trachea of model groupⅠ/Ⅱ, and then vitamin D3 solvent(0.1%ethanol and 99.9%glycol propylene, 1μL/g) was ad?ministered by intraperitoneal injection 2 days and 14 days after surger?y, separately. Bleomycin( BLM) ( 5 mg/kg) was injected into the tra?chea of medication groupⅠ/Ⅱ, and then 1,25?( OH) 2 D3( 2μg/kg) was administered by intraperitoneal injection 2 days and 14 days after surgery, separately. IPF model was built by injecting Bleomycin into the trachea of rats, 1,25?(OH)2D3(2μg/kg) was used to prevent and treat IPF by intraperitoneal injection in medication group. The hydroxyproline content of lung tissue in each group was measured, type Ⅱalveolar epithelial cells were separated from lung tissue and labeled with Fluo?3AM, then concentration of Ca2+ was detected by Laser scanning confocal microscope. The mRNA levels of PI3K, AKT and mTOR in the typeⅡalveolar epithelial cells were tested by RT?PCR. Results Compared with control groupⅠ/Ⅱ at each time point, hydroxyproline content of lung tissue, Ca2+ concentration and expression of PI3K, AKT and mTOR in typeⅡalveolar epithelial cells in model groupⅠ/Ⅱand medication groupⅠ/Ⅱwere sig?nificantly raised( P<0.05 or P<0.01) , but these were significantly reduced in medication groupⅠ/Ⅱcompared with model groupⅠ/Ⅱ( P<0.05 or P<0.01) . Correlation analysis showed that there is significant positive correlation between Ca2+ concentration and mRNA expression levels of PI3K, AKT and mTOR in model groupⅠ/Ⅱ(r=0.5988, r=0.6230, r=0.6603,P<0.01)and medication groupⅠ/Ⅱ( r=0.701 2, r=0.632 3,r=0.740 3,P<0.01) . Conclusion The PI3K/AKT/mTOR pathway plays an important role in devel?opment of IPF. 1,25?( OH) 2 D3 is able to reduce Ca2+concentration in typeⅡalveolar epithelial cells and inhibit the PI3K/AKT/mTOR pathway, and then inhibit the development of IPF.