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The influence of oxidation on the production of high-porosity carbons from phenol−formaldehyde resins with KOH activation were examined under various preparation conditions. The activation process principally consisted of KOH impregnation followed by carbonization. Experimental results showed that prior to carbonization treating the resins with oxygen at 120 °C, either before or after KOH impregnation, enabled the enhancement of the yield of the carbon products. The porosity development was found to be hindered by conducting oxidation prior to the impregnation. For oxidation performed after the impregnation, at a low KOH/resin ratio the porosity was found to decrease upon oxidation, whereas the oxidation enhanced porosity development for activation performed at higher ratios. Varying the carbonization temperature and time did not show obvious influence on the effects of the oxidation.

The high-temperature oxidation behaviour of Si-bearing cobalt-base superalloys has been investigated. Isothermal oxidation tests conducted at 900, 1000, and 1150°C indicated that silicon addition can improve oxidation resistance. Furthermore, the alloy content of tungsten can have profound impact on the oxidation behaviour; low content of tungsten can promote the formation of protective alumina at temperatures at and above 1000°C, while high tungsten content can slow down oxidation at 900°C. Graphical Abstract

Myocardial ischemia/reperfusion (I/R) injury can stimulate mitochondrial reactive oxygen species production. Optic atrophy 1- (OPA1-) induced mitochondrial fusion is an endogenous antioxidative mechanism that preserves the mitochondrial function. In our study, we investigated whether melatonin augments OPA1-dependent mitochondrial fusion and thus maintains redox balance during myocardial I/R injury. In hypoxia/reoxygenation- (H/R-) treated H9C2 cardiomyocytes, melatonin treatment upregulated OPA1 mRNA and protein expression, thereby enhancing mitochondrial fusion. Melatonin also suppressed apoptosis in H/R-treated cardiomyocytes, as evidenced by increased cell viability, diminished caspase-3 activity, and reduced Troponin T secretion; however, silencing OPA1 abolished these effects. H/R treatment augmented mitochondrial ROS production and repressed antioxidative molecule levels, while melatonin reversed these changes in an OPA1-dependent manner. Melatonin also inhibited mitochondrial permeability transition pore opening and maintained the mitochondrial membrane potential, but OPA1 silencing prevented these outcomes. These results illustrate that melatonin administration alleviates cardiomyocyte I/R injury by activating OPA1-induced mitochondrial fusion and inhibiting mitochondrial oxidative stress.

This study demonstrates that elevations of discharge cTn I and NT-proBNP are associated with increased 1-year mortality and HF-related readmission. Patients with increasing serial cTnI and NT-proBNP had increased risk for 60-day HF-related events. The two markers can act as independent predicators, and complete each other in prognostic utility of HF patients.

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The present study aimed to evaluate the prognostic value of venous-arterial CO 2 to arterial-venous O 2 (Cv-aCO 2 /Da-vO 2) for patients with septic shock treated by fluid resuscitation. A total of 108 cases who received fluid resuscitation for septic shock at the Intensive Care Unit were retrospectively screened according to the 2012 surviving sepsis campaign guidelines. Patients were divided into 2 groups according to the Cv-aCO 2 /Da-vO 2 ratio at 6 h after fluid resuscitation: Group A, Cv-aCO 2 /Da-vO 2 >1; group B, Cv-aCO 2 /Da-vO 2 ≤1. The resuscitation target rate and transfused resuscitation volume at 6 h exhibited no significant difference between the 2 groups. The cardiac output at 6 and 24 h, as well as the ratio of patients who reached the target of resuscitation within 24 h, the 24-h lactic acid clearance rate and the number of cases with central venous oxygen saturation >70% were significantly decreased in group A compared with those in group B (all P<0.05). The Sequential Organ Failure Assessment score at day 3 in group A was higher compared with that in group B (7.94±1.6 vs. 6.82±1.9; P= 0.0013). The mortality rate at day 7 and 35 was higher in group A compared with that in group B (29/52 vs. 6/56, P<0.001; 48/52 vs. 36/56; P<0.001). In conclusion, the Cv-aCO 2 /Da-vO 2 was able to effectively evaluate the success rate of resuscitation and, regarding prognosis, it was able to identify patients at high risk of adverse outcomes.