Reaction Mechanism of Wollastonite In Situ Mineral Carbonation for CO2 Sequestration: Effects of Saline Conditions, Temperature, and Pressure.

The research presented here investigates the reaction mechanism of wollastonite in situ mineral carbonation for carbon dioxide (CO2) sequestration. Because wollastonite contains high calcium (Ca) content, it was considered as a suitable feedstock in the mineral carbonation process. To evaluate the reaction mechanism of wollastonite for geological CO2 sequestration (GCS), a series of carbonation experiments were performed at a range of temperatures from 35 to 90 °C, pressures from 1500 to 4000 psi, and salinities from 0 to 90,000 mg/L NaCl. The kinetics batch modeling results were validated with carbonation experiments at the specific pressure and temperature of 1500 psi and 65 °C, respectively. The results showed that the dissolution of calcium increases with increment in pressure and salinity from 1500 to 4000 psi and 0 to 90000 mg/L NaCl, respectively. However, the calcium concentration decreases by 49%, as the reaction temperature increases from 35 to 90 °C. Besides, it is clear from the findings that the carbonation efficiency only shows a small difference (i.e., ±2%) for changing the pressure and salinity, whereas the carbonation efficiency was shown to be enhanced by 62% with increment in the reaction temperature. These findings can provide information about CO2 mineralization of calcium silicate at the GCS condition, which may enable us to predict the fate of the injected CO2, and its subsurface geochemical evolution during the CO2-fluid-rock interaction.

Collagen-embedded hydroxylapatite-beta-tricalcium phosphate-silicon dioxide bone substitute granules assist rapid vascularization and promote cell growth.

In the present study we assessed the biocompatibility in vitro and in vivo of a low-temperature sol-gel-manufactured SiO(2)-based bone graft substitute. Human primary osteoblasts and the osteoblastic cell line, MG63, cultured on the SiO(2) biomatrix in monoculture retained their osteoblastic morphology and cellular functionality in vitro. The effect of the biomaterial in vivo and its vascularization potential was tested subcutaneously in Wistar rats and demonstrated both rapid vascularization and good integration within the peri-implant tissue. Scaffold degradation was progressive during the first month after implantation, with tartrate-resistant acid phosphatase-positive macrophages being present and promoting scaffold degradation from an early stage. This manuscript describes successful osteoblastic growth promotion in vitro and a promising biomaterial integration and vasculogenesis in vivo for a possible therapeutic application of this biomatrix in future clinical studies.

Effects of nucleoside transport inhibition on hepatosplanchnic perfusion, oxygen extraction capabilities, and TNF release during acute endotoxic shock.

We explored the effects of the nucleoside transport inhibitor draflazine on regional blood flow, O2 extraction capabilities, and tumor necrosis factor (TNF) release in acute endotoxic shock. Fourteen anesthetized and mechanically ventilated dogs received 2 mg/kg of Escherichia coli endotoxin and were divided into two groups. Seven dogs received 0.1 mg/kg of draflazine 30 min before endotoxin, and 7 dogs served as a control group. Draflazine decreased arterial pressure without influencing cardiac index. Mesenteric and portal blood flow and ileum mucosal perfusion increased, but renal blood flow dramatically decreased. After endotoxemia, the draflazine-treated dogs had a lesser fall in cardiac index, filling pressures, and left ventricular stroke work index, and a lesser increase in pulmonary vascular resistance. After fluid resuscitation, they had a consistently lower renal blood flow and ileum mucosal perfusion, but a higher mixed venous and hepatic oxygen saturation and arterial pH than the control group. When cardiac index was reduced by tamponade to study the O2 extraction capabilities, renal blood flow and ileum mucosal perfusion remained lower in the draflazine group. Draflazine did not influence whole-body O2 extraction capabilities, but it delayed the occurrence of liver O2 supply dependency as indicated by a significantly lower liver DO2crit (27.7 +/- 3.9 vs. 43.3 +/- 10.8 mL/min) and a higher O2ERcrit (62.7 +/- 9.5 vs. 42.5 +/- 7.1%) than controls (both P< 0.05). On the other hand, draflazine increased intestinal DO2crit (42.4 +/- 15.4 vs. 27.7 +/- 6.5 mL/min, P < 0.05) compared to the control group. TNF levels remained higher in the draflazine group than in the control group, particularly 3 and 4 h after endotoxin administration. We conclude that nucleoside transport inhibition with draflazine does not alter global and hepatosplanchnic hemodynamics but may decrease gut mucosal perfusion and renal blood flow. However, this intervention can improve liver O2 extraction capabilities in acute endotoxic shock.