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Experimental results show that nanoscale pores in coal are affected by coal rank and deformation structures. In terms of pore volume, the transitional pores occupy the largest proportion, and in terms of specific surface area, the sub-micropores take up the largest proportion. For weak brittle deformed coal (including normal structured coal), when the coal rank increases, the volume and specific surface area of pores in different sizes firstly decrease and then increase. The volume and specific surface area of transitional pores and micropores in coal reach the minimum at about R O,ran = 2.0 %. After that, a slow increasing trend is observed. The volume of sub-micropores reaches the minimum at about R O,ran = 1.5 % and then shows a trend of rapid growth as coal rank increases. As the degree of coal deformation increases, both pore volume and specific surface area have a significant increase. Under strong tectonic deformation, both the volume and total specific surface area of the nanoscale pores and of sub-micropores increase significantly; the volume of transitional pores increases moderately, and their specific surface area shows a decreasing trend; the volume and specific surface area increments of micropores decline rapidly as the degree of metamorphism increases.

Visible–ultraviolet upconversion carbon quantum dots (CQDs) are synthesized with a hydrothermal method using l -glutamic acid ( l -Glu) and m -phenylenediamine (MPD) and then combined with commercial nano-TiO 2 to prepare CQDs/TiO 2 composites. The fluorescence spectra prove that the prepared CQDs can convert approximately 600 nm visible light into 350 nm ultraviolet light. In photocatalysis experiments, CT-1, a CQDs/TiO 2 composite with 1:1 molar ratio of l -Glu to TiO 2 , has the best degradation efficiency for methyl orange (MO). Transmission electron microscopy (TEM) and X-ray photoelectron spectroscopy (XPS) experiments confirm that CT-1 is composed of quasi-spherical nano-TiO 2 and CQDs with a crystal plane of graphitic carbon. CT-1 can degrade 70.56% of MO (40 ppm) within 6 h under the irradiation of a 600 nm light source, which is close to its degradation rate of 78.75% under 365 nm ultraviolet light. The apparent rate constant of CT-1 degradation equation is 12.7 times that of TiO 2 . Free radical scavenging experiments and electron spin resonance (ESR) tests show that the degradation ability should be attributed to the existence of h + and • OH under visible light. Therefore, we provide a simple and low-cost solution with heavy-metal-free products to improve the photocatalytic performance of TiO 2 .

Ginsenoside Rg1 is the primary active substance in ginseng, and it has multiple pharmacological actions. Investigations on the pharmacologic action of ginsenoside Rg1 have developed, with a particular focus on the regulation of metabolism. The present study hypothesized that the neuroprotective effects of ginsenoside Rg1 prevent cognitive impairment induced by isoflurane anesthesia via antioxidant, anti‑inflammatory and anti‑apoptotic effects, mediated by the phosphoinositide 3‑kinase (PI3K)/AKT/glycogen synthase kinase‑3β (GSK‑3β) pathway in aged rats. Sprague‑Dawley rats were divided into isoflurane and ginsenoside Rg1 groups and were treated with 20 mg/kg ginsenoside Rg1 for 7 days. Morris water maze was performed to analyze the cognitive function of the rats. Enzyme‑linked immunosorbent assays were used to analyze the levels of malondialdehyde, glutathione, interleukin (IL)‑1β, IL‑6 and caspase 3. The protein expression levels of AKT, GSK 3β, p21WAF1/CIP1 and p53 were measured using western blot analysis. Ginsenoside Rg1 significantly improved cognitive function, and exhibited antioxidant and anti‑inflammatory effects, demonstrating the neuroprotective effects of ginsenoside Rg1 against the effect of isoflurane anesthesia in the rats. In addition, ginsenoside Rg1 significantly reduced caspase‑3 activity, upregulated the expression of PI3K/AKT/GSK‑3β and downregulated the mRNA expression levels of p21WAF1/CIP1 and p53 in the aged rats exposed to isoflurane anesthesia. The data obtained in the present study provided evidence that the neuroprotective effects of ginsenoside Rg1 prevented the cognitive impairment induced by isoflurane anesthesia via antioxidant, anti‑inflammatory and anti‑apoptotic effects, mediated by the PI3K/AKT/GSK‑3β pathway.