Hydrogen production and phosphorus recovery via supercritical water gasification of sewage sludge in a batch reactor.

In this study, gasification of sewage sludge in supercritical water using a batch reactor was investigated. The effects of temperature, retention time, and the oxidation coefficient on gas composition, gas yield, total organic carbon removal efficiency (XTOC), gasification efficiency (GE), carbon gasification efficiency (CE), and phosphorus release rate (Xp) were investigated. The experimental results indicated that the yields for hydrogen, methane, and carbon dioxide increased with the increase in temperature from 380 °C to 460 °C. A maximum hydrogen molar fraction of 55.72% and a yield of 19.86 mol/kg were obtained at 460 °C and 27 MPa after 6 min. The GE, CE, XTOC, and Xp also increased with the increase in temperature. An extension of the retention time promoted the gasification of sludge, thereby resulting in an increase in the hydrogen and methane molar fraction, yield, GE, CE, XTOC, and Xp. Under the conditions of 420 °C and 27 MPa after 6 min, with an increase in the oxidation coefficient from 1.5 to 2.5, the oxidation reaction became dominant in the supercritical water. Hydrogen and methane were converted to carbon dioxide and water with an excess of hydrogen peroxide, which resulted in a lower hydrogen yield. However, the decomposition of organic compounds in the sludge was promoted with the addition of hydrogen peroxide, thereby resulting in an increase in the GE, CE, XTOC, and Xp. When the oxidation coefficient reached 2.5, a maximum GE of 131.6% and Xp of 98.74% were obtained.

Effects of moxibustion pretreatment on extracellular signal-regulated kinase signaling transduction pathway in the gastric tissues of rats with gastric mucosal damage / 针灸推拿医学（英文版）

Objective: To observe the effects of moxibustion pretreatment on the protein expressions of epidermal growth factor receptor (EGFR), phosphorylation extracellular signal-regulated kinase 1/2 (p-ERK1/2) and activated protein-1 (AP-1), the key factors of extracellular signal-regulated kinase signaling transduction pathway in gastric tissue of rats with stress-induced gastric mucosal damage, and to discuss the mechanisms of moxibustion therapy in promoting the restoration of damaged gastric mucosa. Methods: Thirty Sprague-Dawley (SD) rats were randomly divided into a normal group, a model group, and a moxibustion group using the random digits table, 10 in each group. Except the rats in the normal group, rats in the other two groups were used to make stress-induced gastric mucosal damage model using restraint and cold stress. Before modeling, rats in the moxibustion group were alternately treated with moxibustion at Zusanli (ST 36) and Zhongwan (CV 12), or Pishu (BL 20) and Weishu (BL 21), once a day, for a total of 8 d. Histological changes of gastric mucosa were observed under the light microscopy, the expression of gastric tissue p-ERK1/2 was detected by immunohistochemistry assay, and the protein levels of EGFR and AP-1 were measured by Western blots. Results: Compared with rats in the normal group, gastric mucosal damage was more serious, and protein expressions of gastric tissue EGFR, p-ERK1/2 and AP-1 increased in the model group (P Conclusion:Moxibustion at Zusanli (ST 36), Zhongwan (CV 12), Pishu (BL 20) and Weishu (BL 21) couldincrease EGFR, p-ERK1/2 and AP-1 expression levels in gastric tissue of stress-induced gastric mucosal damage rats, maintain the information transfer function of ERK signaling transduction pathway, and promote restoration of gastric mucosal damage.

Effect of Pretreatment with Electroacupuncture at Point Neiguan(PC6) on CK and Myocardial Cell Activity in Rabbit Myocardial Ischemia and Reperfusion / 上海针灸杂志

Objective To investigate the effect of pretreatment with electroacupuncture at point Neiguan(PC6) on CK and myocardial cell activity in rabbit myocardial ischemia-reperfusion injury and provide an experimental basis for a relatively specific relationship between pericardium meridian points and the heart. Methods Forty New Zealand big ear rabbits were randomly allocated to groups A, B, C, D and E, eight rabbits each. Group A was a sham operation group. Group B was an ischemia-reperfusion model group, in which the left anterior descending coronary artery was occlude for 30 min and reperfused for 60 min. In groups C, D and E, points Neiguan(PC6), Lieque(LU7) and Hegu(LI4) were separately given electroacupuncture stimulation, 20 min every day, at seven days before model making. Creatine kinase (CK) and myocardial formazan contents were compared between the groups. Results There were statistically significant differences in serum CK and myocardial formazan contents between group B, C, D or E and group A (P＜0.01, P＜0.05). There was a statistically significant differences in serum CK content between group C, D or E and group B (P＜0.01). There was a statistically significant differences in myocardial formazan content between groups C and B (P＜0.05). There were statistically significant differences in serum CK and myocardial formazan contents between group D or E and group C (P＜0.01, P＜0.05). Conclusion Electroacupuncture at point Neiguan(PC6) can reduce myocardial ischemia-reperfusion induced injury to myocardial cells to produce a protective effect on the heart.

Resolvin D1 attenuates lipopolysaccharide induced acute lung injury through CXCL-12/CXCR4 pathway.

BACKGROUND: The recruitment of neutrophils plays an important role in the progress of acute lung injury (ALI). Excessive neutrophils released from bone marrow accumulate in lung, release proinflammatory factors, and cause tissue damage. CXCL-12/CXCR4 is an important signaling pathway, which regulates the migration of bone marrow hematopoietic cells out of bone marrow and involves in neutrophil accumulation and retention in the inflammatory site. Resolvin D1 (RvD1) is a kind of lipid mediators, which can alleviate many inflammatory diseases. We hypothesized that RvD1 can alleviate lipopolysaccharide (LPS)-induced ALI through regulating CXCL-12/CXCR4 pathway. METHODS: We randomized mice into five groups: control group, RvD1 group, LPS group, LPS plus RvD1 group, and LPS plus AMD3100 group. ALI was established by intratracheal instillation of LPS. After 24 and 72 h, mice were sacrificed, and lung tissues were harvested for histologic analysis, wet-to-dry ratio, myeloperoxidase activity, and CXCL-12 expression. Bronchoalveolar fluid was collected for protein analysis, cytokines assay, and flow cytometry analysis. RESULTS: Histologic findings as well as wet-to-dry ratio, protein concentration, cytokines assay, neutrophil number, and myeloperoxidase activity confirmed that RvD1 and AMD3100 alleviated LPS-induced ALI. RvD1 decreased CXCL-12 messenger RNA expression in lung. However, RvD1 promoted CXCR4 expression in neutrophils in the initial stage of inflammation and reduced its level in the later stage. CONCLUSIONS: RvD1 protects LPS-induced ALI partially through regulating CXCL-12/CXCR4 pathway.