Quaternary vegetation history in Hungary

Detailed information of SSR markers used for genotyping the RIL population. (XLSX 49 kb

Core-in-Shell, Cellulose-Templated CaO-Based Sorbent Pellets for CO₂ Capture at Elevated Temperatures

Calcium looping is a promising postcombustion CO2 capture technology due to its low cost and widespread applicability. However, CaO-based sorbents are prone to encounter severe sintering and elutriation during practical carbonation/calcination cycles. To overcome the above issues, core-in-shell CaO-based pellets composed of a highly reactive CaO-based core and a hard cement-based outer shell were prepared. The highly reactive core contains 80 wt % Ca­(OH)2 and 20 wt % cellulose, which was prepared via an extrusion–spheronization method. The cement-based outer shells were prepared via an approach of coating, and different amounts of cellulose (varying from 0 to 40 wt %) were added as a pore-forming template. It is found that the mechanical properties of the fresh, core-in-shell, cellulose-templated CaO-based pellets are gradually improved with the increased addition ratio of cellulose in the outer shell. It is mainly attributed to the adequately dispersed cellulose fibers reinforcing the cement-based outer shell. Although the high-temperature calcination causes the internal structure of the CaO-based pellets to become loose, they still exhibit relatively desirable compression strengths (0.95–1.80 MPa). Moreover, the porous outer shell contributes to promoting the accessibility of CO2 to the highly reactive core pellet, consequently obtaining superior CO2 capture performance. After 15 cycles, the core-in-shell, cellulose-templated CaO-based pellets containing 40 wt % of cellulose in the outer shell exhibit the highest CO2 capture capacity of 0.144 g/g, which is nearly 6.8 times that of the core-in-shell pellets with pure cement shell

A Facile Solvent-Manipulated Mesh for Reversible Oil/Water Separation

A controllable oil/water separation mesh has been successfully developed and easily manipulated by immersion in a stearic acid ethanol solution and tetrahydrofuran with a very short period of time. The superhydrophilic and underwater superoleophobic mesh is first obtained via a one-step chemical oxidation and subsequently converts to superhydrophobic after it is immersed in an ethanol solution of stearic acid for 5 min. The surface wettability is regained to superhydrophilic quickly by immersion in tetrahydrofuran for 5 min. More importantly, the reversible superhydrophobic-and-superhydrophilic switching can be repeated multiple times with almost no visible morphology variation. Therefore, this approach provides potential application in controllable oil/water separation and opens up new perspectives in manipulation of various metallic oxide substrates

A Facile Solvent-Manipulated Mesh for Reversible Oil/Water Separation

A controllable oil/water separation mesh has been successfully developed and easily manipulated by immersion in a stearic acid ethanol solution and tetrahydrofuran with a very short period of time. The superhydrophilic and underwater superoleophobic mesh is first obtained via a one-step chemical oxidation and subsequently converts to superhydrophobic after it is immersed in an ethanol solution of stearic acid for 5 min. The surface wettability is regained to superhydrophilic quickly by immersion in tetrahydrofuran for 5 min. More importantly, the reversible superhydrophobic-and-superhydrophilic switching can be repeated multiple times with almost no visible morphology variation. Therefore, this approach provides potential application in controllable oil/water separation and opens up new perspectives in manipulation of various metallic oxide substrates

Primers used for real-time quantitative PCR.

Primers used for real-time quantitative PCR.</p

Attenuating Oxidative Stress by Paeonol Protected against Acetaminophen-Induced Hepatotoxicity in Mice

<div><p>Acetaminophen (APAP) overdose is the most frequent cause of drug-induced acute liver failure. The purpose of this study was to investigate whether paeonol protected against APAP-induced hepatotoxicity. Mice treated with paeonol (25, 50, 100 mg/kg) received 400 mg/kg acetaminophen intraperitoneally (i.p.) and hepatotoxicity was assessed. Pre-treatment with paeonol for 6 and 24 h ameliorated APAP-induced hepatic necrosis and significantly reduced the serum alanine aminotransferase (ALT) and aspartate transaminase (AST) levels in a dose-dependent manner. Post-treatment with 100 mg/kg paeonol ameliorated APAP-induced hepatic necrosis and reduced AST and ALT levels in the serum after APAP administration for 24 h. Western blot revealed that paeonol inhibited APAP-induced phosphorylated JNK protein expression but not p38 and Erk1/2. Moreover, paeonol showed anti-oxidant activities with reducing hepatic MDA contents and increasing hepatic SOD, GSH-PX and GSH levels. Paeonol dose-dependently prevented against H₂O₂ or APAP-induced LDH releasing and ROS production in primary mouse hepatocytes. In addition, the mRNA levels of pro-inflammatory genes such as TNF-α, MCP-1, IL-1β and IL-6 in the liver were dose-dependently reduced by paeonol pre-treatment. Pre-treatment with paeonol significantly inhibited IKKα/β, IκBα and p65 phosphorylation which contributed to ameliorating APAP-induced hepatic inflammation. Collectively, the present study demonstrates paeonol has a protective ability against APAP-induced hepatotoxicity and might be an effective candidate compound against drug-induced acute liver failure.</p></div

Post-treatment with paeonol protected against APAP-induced liver injury.

<p>Mice were intraperitoneally injected with either 400 mg/kg APAP or an equal volume of PBS. After 30 min, mice were administered with either vehicle (0.5% CMC-Na) or paeonol (25, 50, 100 mg/kg) by gavage. Liver tissue and blood were collected after paeonol treatment for 24 h. (A) Liver sections were stained with H&E. Magnification: 200X. (B) The levels of ALT and AST in the serum were determined by a commercially available kit. Data are shown as means ± S.E.M. *<i>P</i><0.05, **<i>P</i><0.01 v.s. APAP treatment (n = 8).</p

Paeonol inhibited APAP-induced MAPK pathway activation.

<p>The protein levels of total and phosphorylated p38, JNK and Erk1/2 in the liver were determined by western blot. β-actin was used as the endogenous control. The representative data are shown and bands were analyzed by densitometry. Data are shown as means ± S.E.M. *<i>P</i><0.05, **<i>P</i><0.01 v.s. APAP treatment.</p

Paeonol reduced APAP-induced hepatic oxidative stress.

<p>(A) Mice were administered with either vehicle (0.5% CMC-Na) or paeonol (25, 50, 100 mg/kg) by gavage for three days. At day 3, mice were intraperitoneally injected with either 400 mg/kg APAP or an equal volume of PBS. Liver was collected and hepatic homogenates were used for the determination of MDA, SOD, GSH and GSH-PX levels by using commercial kits. (B) Mice were administered with either vehicle (0.5% CMC-Na) or paeonol (25, 50, 100 mg/kg) by gavage for three days. At day 3, mice were co-treated with either 400 mg/kg APAP and 300 mg/kg NAC by intraperitoneal injection. The levels of ALT and AST in the serum were determined by a commercially available kit. (C) The protein levels of total and phosphorylated JNK in the liver were determined by western blot. β-actin was used as the endogenous control. The representative data are shown and bands were analyzed by densitometry. Data are shown as means ± S.E.M. *<i>P</i><0.05, **<i>P</i><0.01 v.s. APAP treatment (n = 8).</p

Paeonol prevented against H₂O₂ or APAP-induced LDH releasing and ROS production in primary mouse hepatocytes.

<p>Primary mouse hepatocytes were treated with paeonol (20, 40, 80 μM) in the absence or presence of 5 mM APAP or 250 μM H₂O₂ for 6 h. (A) LDH leakage percentage were determined by a commercial kit. (B) ROS formation was measured using a fluorescence microplate reader. Data are shown as means ± S.E.M. *<i>P</i><0.05, **<i>P</i><0.01 v.s. APAP treatment.</p