Graphitic Armor: A Natural Molecular Sieve for Robust Hydrogen Electroxidation.

Carbon coating layers have been found to improve the catalytic performance of transition metals, which is usually explained as an outcome of electronic synergistic effect. Herein we reveal that the defective graphitic carbon, with a unique interlayer gap of 0.342 nm, can be a highly selective natural molecular sieve. It allows efficient diffusion of hydrogen molecules or radicals both along the in-plane and out-of-plane direction, but sterically hinders the diffusion of molecules with larger kinetic diameter (e.g., CO and O2) along the in-plane direction. As a result, poisonous species lager than 0.342 nm are sieved out, even when their adsorption on the metal is thermodynamically strong; at the same time, the interaction between H2 and the metal is not affected. This natural molecular sieve provides a very chance for constructing robust metal catalysts for hydrogen-relevant processes, which are more tolerant to chemical or electrochemical oxidation or CO-relevant poisoning.

[Effect of morphine on dorsal horn projection neurons in neuropathic pain rats].

OBJECTIVE: To explore the inhibitory effect of spinal topical morphine on the dorsal horn projection neurons in nerve-injured rats and its mechanism. METHODS: Single-unit activity of dorsal horn projection neurons was recorded in anesthetized L(5)/L(6) nerve-ligated rats. Allodynia was determined by a behavior test in nerve-injured rats. The evoked neuronal responses to mechanical stimuli applied to the receptive field were determined before and after the spinal topical application of morphine, bicuculline plus morphine, strychnine plus morphine, and both bicuculline and strychnine plus morphine in normal, sham operation, and nerve-injured rats. RESULTS: Spinal topical application of 10 micromol/L morphine significantly inhibited the evoked responses of dorsal horn projection neurons in normal, sham, operation and nerve-injured rats. However, the inhibitory effect of morphine was significantly reduced in nerve-injured rats compared with that in normal and sham operation rats. Furthermore, the topical application of 20 micromol/L bicuculline had little effect on the inhibitory effect of morphine in nerve-injured rats but it almost abolished the effect of morphine in normal and sham operation rats. The glycine receptor antagonist strychnine at 4 micromol/L significantly decreased the effect of morphine in nerve-injured, normal, and sham operation rats. CONCLUSION: The loss of tonic GABAergic inhibition contributes to the reduced inhibitory effect of morphine on dorsal horn projection neurons in nerve-injured rats.

[Effect of chloroquine on the apoptosis of intestinal mucosa epithelial cells and enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion in rats].

OBJECTIVE: To observe the effect of chloroquine on the apoptosis of intestinal mucosa epithelial cell and enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion in rats. METHODS: The rat total hepatic ischemia-reperfusion model was built by blocking the hepatic portal, suprahepatic and infrahepatic vena cava for 20 minutes. Ninety Sprague-Dawley rats were assigned randomly into the sham operation group (Group A, n = 30), total hepatic ischemia-reperfusion treatment group (Group B, n = 30), and chloroquine administrated group (Group C, n = 30). Each group was subdivided randomly into 3 subgroups (n = 10) according to different experiment time phases as follows: after 20 minutes of total hepatic vascular exclusion (T0), 4 hours after reperfusion (T1), and the 48 hours of survival. Group A and Group B were intravenously injected with normal saline 1 mL/kg while Group C received chloroquine 10 mg/kg which dissolved in 1 mL/kg normal saline intravenously. The levels of portal blood D-lactate, TNF-alpha, endotoxin, and the intestinal mucosa MDA concentration were measured at T0 and T1; the portal blood, mesenteric lymph node, and spleen tissues were cultured for bacteria; and the apoptotic index of intestinal mucosa epithelial cells at T0 and T1 and the survival rate after 48 hour reperfusion were obtained. RESULTS: Compared with Group A, the levels of portal blood D-lactate, TNF-alpha, endotoxin and the intestinal mucosa MDA in Group B and Group C were significantly higher (P < 0.05 or P < 0.01). These indexes of Group C were lower than those of Group B (P < 0.05). The portal vein blood, mesenteric lymph node and spleen tissues existed the bacterium translocation both in Group B and Group C, and the positive rate in Group C was lower than that in Group B (P < 0.05). Apoptotic index of the intestinal mucosa epithelial cell increased significantly in Group B (P < 0.01) and Group C (P < 0.05), but the apoptotic index in Group C was lower than that in Group B (P < 0.05); the 48 hour survival rate of the rats in Group C was higher than that in group B (P < 0.05). CONCLUSION: Chloroquine may decrease the intestinal mucosa epithelial cell apoptosis and the enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion and increase the survival rate of the rats.

[Effects of aminoguanidine on the lung injury induced by the total hepatic ischemia-reperfusion in rats].

OBJECTIVE: To investigate the effects of aminoguanidine on the lung injury induced by the total hepatic ischemia-reperfusion in rats. METHODS: The total hepatic ischemia-reperfusion model was built after blocking of the hepatic porta, suprahepatic and infrahepatic vena cava. Ninety Sprague-Dawley rats were assigned randomly into 3 groups: Sham operation group (Group A, n=30); total hepatic ischemia group (Group B, n=30); and aminoguanidine treatment group (Group C, n=30). Each group was subdivided randomly into 3 subgroups (n=10) according to different time phases: 20 minutes after the total hepatic vascular exclusion (T0), 4 hours after the reperfusion (T1), and 48 hours after the survival Group A and Group B were intravenously injected with normal saline ( mL/kg) while Group C was injected with aminoguanidine (20 mg/kg) dissolved in normal saline (1 mL/kg) 10 minutes before the open of the abdomin. The levels of portal blood nitric oxide ( O) endotoxin ( ET), tumor necrosis factor-alpha (TNF-alpha at T0 and T1 were detected; 48 hours survival rates and the lung wet/dry weight ratio were counted; and the histological changes of the lung tissues were observed. RESULTS: Compared with Group A, the levels of portal vein NO, ET, and TNF-alpha T0 and T1 in Group B and Group C were significantly higher (P < 0.05 or P < 0.01). But those indexes of Group C were lower than those of Group B (P < 0.05). The 48-hour survival rate in Group C was higher than that in Group B (P < 0.05). The lung wet/dry weight ratio in Group C was lower than in Group B (P < 0.05) and the histological change of Group C was slighter than that in Group B. CONCLUSION: Aminoguanidine has the protective effects on the lungs against the total hepatic ischemia-reperfusion induced injury.

[Treatment with total hepatic vascular exclusion and reperfusion for the intestinal barrier in rats].

OBJECTIVE: To investigate the influence of treatment with total hepatic vascular exclusion and reperfusion on the intestinal barrier in rats. METHODS: The total hepatic vascular exclusion and reperfusion model was built after the block of hepatic portal, suprahepatic and infraheptic vena cava for 20 minutes. Sixty Sprague-Dawley rats were divided randomly into 2 groups: sham operation group (Group A, n=30) and total hepatic vascular exclusion and reperfusion treatment group (Group B, n=30). Each group was subdivided randomly into 3 subgroups (n=10) according to different experiment time points as follows: at the end of the total hepatic vascular exclusion (T0), 4 reperfusion after total hepatic vascular exclusion (T1) and the 48 h survival. Portal vein blood gas was analysed at T0. At T0 and T1 the following items were detected: the level of portal vein blood D-lactate, tumor necrosis factor-alpha (TNF-alpha), the MDA concentration and pathologic morphology change of intestinal mucosa. RESULTS: Compared with Group A, the PCO2 at T0 in Group B increased while pH, P02, and HCO3- decreased significantly (P < 0.05). The level of portal blood D-lactate, TNF-alpha and intestinal mucosa MDA at T0 and T1 was significantly higher (P < 0.05, or P < 0.01). The histologic damage in the intestinal mucosa was observed in Group B, and the rat survival in Group B was lower than that in Group A (P < 0.05). CONCLUSION: The treatment with total hepatic vascular exclusion and reperfusion can damage the intestinal barrier in rats.