Recovery of high purity phosphorus from municipal wastewater secondary effluent by a high-speed adsorbent.

High purity phosphorus was recovered from municipal wastewater secondary effluent as phosphate, using a newly developed phosphorus adsorption and recovery system. A high-speed adsorbent having a unique porous structure was used in this system. The secondary effluent, showing total phosphorus (TP) of 0.1-2.1 mg P/L, was passed through an adsorbent packed column at high space velocity (SV) of 15 h(-1). The TP of the treated water was as low as 0.02-0.04 mg P/L, indicating that 97% of phosphorus in the secondary effluent was removed. The removed phosphorus was desorbed from the adsorbent by passing a sodium hydroxide aqueous solution through the column. Calcium hydroxide was added to this solution to precipitate the phosphorus as calcium phosphate. This precipitate was neutralized with hydrochloric acid aqueous solution, washed with water, and then solid-liquid separation was performed for the phosphorus recovery. The main constituent of the recovered phosphorus was apatite-type calcium phosphate, with 16% phosphorus content, which matched that of high-grade phosphorus ore. The hazardous elements content of the recovered phosphorus was exceedingly low. Therefore the recovered phosphorus can be applied to an alternative for phosphorus ore, or to a phosphate fertilizer.

A new mechanism for anti-inflammatory actions of proton pump inhibitors--inhibitory effects on neutrophil-endothelial cell interactions.

BACKGROUND: Neutrophil-endothelial cell interactions mediated by adhesion molecules may be involved in gastric mucosal inflammation associated with Helicobacter pylori or nonsteroidal anti-inflammatory drugs. AIM: To investigate the effects of proton pump inhibitors and histamine-2 receptor antagonists (HRA) on neutrophil-endothelial cell adhesive interactions induced by H. pylori water extract (HPE) or interleukin-1beta (IL-1beta). METHODS: Human peripheral neutrophils and umbilical vein endothelial cells were incubated with either proton pump inhibitors (lansoprazole and omeprazole) or HRA (famotidine and ranitidine). Neutrophil surface expression of CD11b and CD18 and endothelial cell intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) were assessed by flow cytometry and an enzyme immunoassay, respectively. Neutrophil adherence was defined as the ratio of exogenous neutrophils that adhered to the endothelial monolayers. RESULTS: The expression of CD11b and CD18 on neutrophils and neutrophil-dependent adhesion to endothelial cells elicited by HPE were inhibited by lansoprazole and omeprazole at clinical relevant doses, and the expression of ICAM-1 and VCAM-1 on endothelial cells and endothelial-dependent neutrophil adherence induced by IL-1beta were also inhibited by lansoprazole and omeprazole at similar doses. Famotidine and ranitidine had no effect on neutrophil-endothelial cell interactions. CONCLUSIONS: These results indicate that proton pump inhibitors can attenuate neutrophil adherence to endothelial cells via inhibiting the expression of adhesion molecules, suggesting that proton pump inhibitors may have anti-inflammatory activity.

Helicobacter pylori water extract induces interleukin-8 production by gastric epithelial cells.

In Helicobacter pylori-associated gastric mucosal injury, interleukin (IL) -8, a potent leukocyte chemoattractant, is produced by epithelial cells infected by H. pylori and directs neutrophils to the gastric mucosa. According to previous studies, the IL-8 production requires direct contact between the bacteria and epithelial cells. The aims of the present study were to determine whether an H. pylori water extract (HPE) induces IL-8 production by gastric epithelial cells and to characterize IL-8-inducing substances in HPE. Extracts were prepared from a standard strain and from strains obtained from patients with gastric ulcers. After addition of HPE to MKN 45 cells, a gastric cancer cell line, IL-8 in supernatants and IL-8 mRNA were measured by immunoassay and reverse transcription-polymerase chain reaction, respectively. For characterization, active fractions obtained by gel filtration of standard-strain HPE were treated by heating or trypsinization. To study the signal pathway leading to IL-8 production, inhibitors for protein kinase A (PKA), protein kinase C (PKC), or protein tyrosine kinase (PTK) were incubated with MKN45 cells before HPE stimulation. HPE from the standard strain and one of these clinical strains induced IL-8 production. Lipopolysaccharide or cagA in the strains showed no correlation with IL-8 concentration. Standard-strain HPE induced IL-8 mRNA expression in MKN 45 cells. Gel filtration localized activity to a low-molecular-weight fraction of about 7 kDa, which was resistant to heat and trypsin digestion. PKC inhibitors significantly blocked HPE-induced IL-8 production by MKN 45 cells; however, the PKA inhibitor or PTK inhibitors showed a partial inhibitory effect. HPE contains a nonprotein substance of low molecular weight that is responsible for IL-8 induction in gastric epithelial cells. This induction is mainly dependent on the activation of PKC but partially also dependent on PKA or PTK.

Interactions of neutrophils and endothelial cells under low flow conditions in vitro.

The interactions of polymorphonuclear leukocytes (PMN) and endothelial cells are modulated by adhesion molecules, inflammatory cytokines, and shear stress. We investigated the changes in PMN-endothelial cell interactions induced by interleukin (IL)-1 beta under low flow conditions. PMN were isolated from the venous blood of healthy adults, and endothelial cells were obtained from human umbilical veins. The number of PMN that adhered to the endothelial cells monolayer that was treated with IL-1 increased significantly at shear stresses from .5 to 4.0 dyn/cm2 as compared with untreated endothelial cells. Anti-intercellular adhesion molecule (ICAM)-1 monoclonal antibody (mAb), anti-E-selectin mAb, and anti-CD18 mAb each significantly inhibited the increase in PMN adherence induced by IL-1 at a low shear stress (1.0 dyn/cm2). Anti-CD18 mAb significantly reduced the number of PMN that migrated through the endothelial monolayer by blocking the adherence of PMN to the luminal surface of the endothelial cells, as well as their transendothelial migration. In contrast, anti-ICAM-1 and anti-E-selectin mAb each reduced the number of PMN that migrated by reducing the number of PMN that adhered to the luminal surface without significantly influencing the percent of the adherent PMN that had migrated. Although anti-L-selectin mAb reduced the adherence and migration of PMN, these effects were not statistically significant. These results indicated that under low flow conditions, as well as in the nonflow state, PMN-endothelial cell interactions were elicited via CD11/CD18 and ICAM-1 without the involvement of selectins.

Release of cytotoxin by macrophages on treatment with human placenta lectin.

Human lectin purified from placenta induced release of cytotoxin from a murine macrophage cell line and human peritoneal monocytes. This activity was not due to contamination of the lectin preparation with lipopolysaccharide.