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Submerged biofilm systems, such as integrated fixed-film activated sludge (IFAS) and moving bed bioreactors (MBBRs), are increasingly being used for domestic wastewater treatment, often to improve nitrification. Little is known about whether and how biofilm attachment surface chemical properties affect treatment performance, although surface chemistry is known to affect attachment in other systems, and work with pure strains has suggested that attachment of nitrifying bacteria may be enhanced on high surface energy surfaces. The objective of this research was to systematically evaluate the effects of surface chemistry on biofilm quantity and rates of nitrification and estrogen removal. Biofilms were grown on four plastic attachment surfaces with a range of hydrophobicity and surface energy values (nylon, melamine, high-density-polyethylene [HDPE], and acetal polymeric plastic) by immersing them in a full scale nitrifying activated sludge wastewater treatment system, followed by batch test experiments. The attachment surface water contact angles ranged from 53° to 98° and surface energies ranged from 48.9 to 20.9 mJ/m(2). Attachment surface hydrophilicity and surface energy were positively correlated with total biomass attachment, with more than twice as much biomass on the highest surface energy, most hydrophilic surface (nylon) than on the lowest surface energy, least hydrophilic surface (acetal plastic). Absolute and specific nitrification rates were also correlated with hydrophilicity and surface energy (varying by factors of 5 and 2, respectively), as were absolute and specific removal first order rate constants of the hormones estrone (E1), β-estradiol (E2) and 17α-ethynylestradiol (EE2). These results suggested that attachment surface chemistry may be a useful design parameter for improving biofilm performance for removal of ammonia and endocrine disrupting hormones from wastewater. Further research is required to verify these results at longer time scales and with typical media geometries.

Background— Induction of profound hypothermia for emergency preservation and resuscitation (EPR) of trauma victims who experience exsanguination cardiac arrest may allow survival from otherwise-lethal injuries. Previously, we achieved intact survival of dogs from 2 hours of EPR after rapid hemorrhage. We tested the hypothesis that EPR would achieve good outcome if prolonged hemorrhage preceded cardiac arrest. Methods and Results— Two minutes after cardiac arrest from prolonged hemorrhage and splenic transection, dogs were randomized into 3 groups (n=7 each): (1) the cardiopulmonary resuscitation (CPR) group, resuscitated with conventional CPR, and the (2) EPR-I and (3) EPR-II groups, both of which received 20 L of a 2°C saline aortic flush to achieve a brain temperature of 10°C to 15°C. CPR or EPR lasted 60 minutes and was followed in all groups by a 2-hour resuscitation by cardiopulmonary bypass. Splenectomy was then performed. The CPR dogs were maintained at 38.0°C. In the EPR groups, mild hypothermia (34°C) was maintained for either 12 (EPR-I) or 36 (EPR-II) hours. Function and brain histology were evaluated 60 hours after rewarming in all dogs. Cardiac arrest occurred after 124±16 minutes of hemorrhage. In the CPR group, spontaneous circulation could not be restored without cardiopulmonary bypass; none survived. Twelve of 14 EPR dogs survived. Compared with the EPR-I group, the EPR-II group had better overall performance, final neurological deficit scores, and histological damage scores. Conclusions— EPR is superior to conventional CPR in facilitating normal recovery after cardiac arrest from trauma and prolonged hemorrhage. Prolonged mild hypothermia after EPR was critical for achieving intact neurological outcomes.

Clinical studies have demonstrated improved survival after cardiac arrest with induction of mild hypothermia (34 degrees C). Infusion of ice-cold saline seems beneficial. The American Heart Association recommends therapeutic hypothermia for comatose survivors of cardiac arrest. For hemorrhagic shock (HS), laboratory studies suggest that mild hypothermia prolongs the golden hour for resuscitation. Yet, the effects of hypothermia during HS are unclear since retrospective clinical studies suggest that hypothermia is associated with increased mortality. Using a clinically relevant, large animal model with trauma and intensive care, we tested the hypothesis that mild hypothermia, induced with intravenous cold saline (ice cold or room temperature) and surface cooling, would improve survival after HS in pigs.Pigs were prepared under isoflurane anesthesia. After laparotomy, venous blood (75 mL/kg) was continuously withdrawn over 3 hours (no systemic heparin). At HS 35 minutes, the spleen was transected. At HS 40 minutes, pigs were divided into three groups (n = 8, each): 1) Normothermia (Norm)(38 degrees C), induced with warmed saline; 2) Mild hypothermia (34 degrees C) induced with i.v. infusion of 2 degrees C saline (Hypo-Ice) and surface cooling; and 3) Mild hypothermia (34 degrees C), induced with room temperature (24 degrees C) i.v. saline (Hypo-Rm) and surface cooling. Fluids were given when mean arterial pressure (MAP) was30 mmHg. At HS 3 hours, shed blood was returned and splenectomy was performed. Intensive care was continued to 24 hours.At 24 hours, there were two survivors in the Norm group, four in the Hypo-Ice group and seven in the Hypo-Rm group (p0.05 versus the Norm group, Log Rank). Time required to achieve 34 degrees C was 17 +/- 9 minutes in the Hypo-Ice group and 15 +/- 4 minutes in the Hypo-Rm group (NS). Compared with the Hypo-Rm group, the Hypo-Ice group required less saline during early HS (321 +/- 122 versus 571 +/- 184 mL, p0.05). The Hypo-Ice group also had higher lactate levels than the Hypo-Rm group (p0.05). Hypothermia did not cause any increase in bleeding compared with normothermia.Mild hypothermia during HS, induced by infusion of room temperature saline and surface cooling, improves survival in a clinically relevant model of HS and trauma. However, the use of iced saline in this model had detrimental effects and did not cool the animal more quickly than room temperature fluids. These findings suggest that optimal methods for induction of hypothermia need to be addressed for each potential indication, e.g. cardiac arrest versus HS.