Key technology of HX-NGS adsorption for treating organic matter in orchid carbon wastewater.

In this article, COD, volatile phenol and ammonia nitrogen concentrations of the wastewater from semicarbon are reported as 38,000; 6,400 and 5,700 mg/L, respectively. According to the field test, when the pH of the wastewater is 9, the field test temperature is 20 °C, the adsorption time is 30 min and the optimal dosing ratio of nitrogen-doped gasification slag (HX-NGS) to the wastewater is 1:4, HX-NGS has the best removal effect on COD, volatile phenol and ammonia nitrogen in the wastewater from the semicarbon. The removal rates of COD, volatile phenol and ammonia nitrogen are 94, 91 and 85%, respectively, and the concentrations of the remaining COD, volatile phenol and ammonia nitrogen are 2,280, 576 and 855 mg/L, respectively, after regeneration, the material HX-NGS has a good effect on the treatment of the wastewater from the semicarbon. The reuse rate of the adsorption material is at least eight times. The adsorption effect of the material HX-NGS conforms to the mechanism law of dynamics and thermodynamics.

Mitochondrial energy metabolism plays a critical role in the cardioprotection afforded by intermittent hypobaric hypoxia.

Intermittent hypobaric hypoxia (IHH) is an effective protective strategy against myocardial ischaemia-reperfusion (I/R) injury, but the precise mechanisms are far from clear. To understand the overall effects of IHH on the myocardial proteins during I/R, we analysed functional performance and the protein expression profile in isolated hearts from normoxic rats and from rats adapted to IHH (5000 m, 4 h day(-1), 4 weeks) following I/R injury (30 min/45 min). Intermittent hypobaric hypoxia significantly improved the postischaemic recovery of left ventricular function compared with the recovery in time-matched normoxic control hearts. Two-dimensional electrophoresis with matrix-assisted laser desorption/ionization and time-of-flight mass spectrometric analysis was then used to assess protein alterations in left ventricles from normoxic and IHH groups, with or without I/R. The expressions of 16 proteins changed by over fivefold; nine of these proteins are involved in energy metabolism. Immunoblot and real-time PCR analysis confirmed the IHH-increased expressions of the ATP synthase subunit ß, mitochondrial aldehyde dehydrogenase and heat shock protein 27 in left ventricles. Furthermore, IHH significantly attenuated the reduction of myocardial ATP content, mitochondrial ATP synthase activity, membrane potential and respiratory control ratios due to I/R. In addition, inhibition of mitochondrial ATP synthase by oligomycin (1 µmol l(-1)) abolished the IHH-induced improvements in three parameters: postischaemic recovery of left ventricular function, mitochondrial membrane potential and respiratory control ratios. These results suggest that an improvement in mitochondrial energy metabolism makes an important contribution to the cardioprotection afforded by IHH against postischaemic myocardial dysfunction.

[Research on variable selection of wheat near-infrared spectroscopy based on latent projective graph].

To simplify the model and improve the precision of prediction model, latent projective graph (LPG) was used for variable selection. The original spectrum was processed by continuous wavelet transform (CWT), LPG was obtained by principal component analysis (PCA), and based on the assumption that collinear wavelengths might have the same contribution to the modeling, a few latent spectral variables were selected for establishing prediction model. The root mean square error of prediction (RMSEP) model was 0. 3454, better than other modeling methods. This work proved that variable selection with LPG could simplify the near-infrared spectral model effectively, and improve the precision of prediction model.

Intermittent hypobaric hypoxia improves postischemic recovery of myocardial contractile function via redox signaling during early reperfusion.

Intermittent hypobaric hypoxia (IHH) protects hearts against ischemia-reperfusion (I/R) injury, but the underlying mechanisms are far from clear. ROS are paradoxically regarded as a major cause of myocardial I/R injury and a trigger of cardioprotection. In the present study, we investigated whether the ROS generated during early reperfusion contribute to IHH-induced cardioprotection. Using isolated perfused rat hearts, we found that IHH significantly improved the postischemic recovery of left ventricular (LV) contractile function with a concurrent reduction of lactate dehydrogenase release and myocardial infarct size (20.5 ± 5.3% in IHH vs. 42.1 ± 3.8% in the normoxic control, P < 0.01) after I/R. Meanwhile, IHH enhanced the production of protein carbonyls and malondialdehyde, respective products of protein oxidation and lipid peroxidation, in the reperfused myocardium and ROS generation in reperfused cardiomyocytes. Such effects were blocked by the mitochondrial ATP-sensitive K(+) channel inhibitor 5-hydroxydecanoate. Moreover, the IHH-improved postischemic LV performance, enhanced phosphorylation of PKB (Akt), PKC-ε, and glycogen synthase kinase-3ß, as well as translocation of PKC-ε were not affected by applying H(2)O(2) (20 µmol/l) during early reperfusion but were abolished by the ROS scavengers N-(2-mercaptopropionyl)glycine (MPG) and manganese (III) tetrakis (1-methyl-4-pyridyl)porphyrin. Furthermore, IHH-reduced lactate dehydrogenase release and infarct size were reversed by MPG. Consistently, inhibition of Akt with wortmannin and PKC-ε with εV1-2 abrogated the IHH-improved postischemic LV performance. These findings suggest that IHH-induced cardioprotection depends on elevated ROS production during early reperfusion.

Overexpression of heat shock protein 27 protects against ischaemia/reperfusion-induced cardiac dysfunction via stabilization of troponin I and T.

AIMS: Heat shock protein 27 (Hsp27) renders cardioprotection from ischaemia/reperfusion (I/R) injury, but little is known about its role in myofilaments. We proposed that increased expression of Hsp27 may improve post-ischaemic contractile dysfunction by preventing I/R-induced cardiac troponin I (cTnI) and troponin T (cTnT) degradation. METHODS AND RESULTS: Adenovirus-mediated Hsp27 overexpression improved contractile function in perfused rat hearts subjected to global no-flow I/R (30-min/30-min). Such improvement was further confirmed in Hsp27-overexpressing cardiomyocytes subjected to simulated I/R (20-min/30-min). Moreover, these cells showed restored myofilament response to Ca(2+) but not intracellular Ca(2+) transients. The protection correlated with attenuation of I/R-induced cTnI and cTnT degradation. Confocal microscopy revealed co-localization of Hsp27 with these proteins. Co-immunoprecipitation and pull-down assays further confirmed that Hsp27 interacted with the COOH-terminus of cTnI and the NH(2)-terminus of cTnT and that Hsp27 overexpression decreased the interaction between mu-calpain (a protease mediating proteolysis of cTnI and cTnT) and cTnI or cTnT under I/R. CONCLUSION: The findings reveal a novel role of Hsp27 in the protection of cTnI and cTnT from I/R-induced degradation by preventing their proteolytic cleavage via interacting with these proteins. Such protection may result in restored post-ischaemic myofilament response to Ca(2+) and improved post-ischaemic contractile function.