Biosorptive recovery of platinum from platinum group metal refining wastewaters by immobilised Saccharomyces cerevisiae.

The process of platinum group metal (PGM) refining can be up to 99.99% efficient at best, and although it may seem small, the amount of valuable metal lost to waste streams is appreciable enough to warrant recovery. The method currently used to remove entrained metal ions from refinery wastewaters, chemical precipitation, is not effective for selective recovery of PGMs. The yeast Saccharomyces cerevisiae has been found capable of sorbing numerous precious and base metals, and is a cheap and abundant source of biomass. In this investigation, S. cerevisiae was immobilised using polyethyleneimine and glutaraldehyde to produce a suitable sorbent, capable of high platinum uptake (150-170 mg/g) at low pH (<2). The sorption mechanism was found to be a chemical reaction, which made effective desorption impossible. When applied to PGM refinery wastewater, two key wastewater characteristics limited the success of the sorption process; high inorganic ion content and complex speciation of the platinum ions. The results proved the concept principle of platinum recovery by immobilised yeast biosorption and indicated that a more detailed understanding of the platinum speciation within the wastewater is required before biosorption can be applied. Overall, the sorption of platinum by the S. cerevisiae sorbent was demonstrated to be highly effective in principle, but the complexity of the wastewater requires that pretreatment steps be taken before the successful application of this process to industrial wastewater.

Cardiopulmonary manifestations of portovenous shunts from congenital absence of the portal vein: pulmonary hypertension and pulmonary vascular dilatation.

HPS and PPHTN are unusual and challenging pulmonary manifestations of liver disease. We report two pediatric cases in association with heterotaxy polysplenia syndrome and congenital absence of the portal vein. Both patients were symptomatic and hemodynamically compromised and required aggressive medical therapy. One patient with PPHTN alone achieved a successful liver transplant. The second child presented with combined HPS and PPHTN and exhibited a different evolution of pulmonary vascular disease. These cases illustrate associations that must be entertained in the setting of heterotaxy syndrome, cyanosis, or pulmonary hypertension and how strategic medical combined with surgical management can provide a good outcome.

Living donor liver transplantation for children with liver failure and concurrent multiple organ system failure.

Liver transplantation for pediatric patients in liver failure and multiple organ system failure (MOSF) often results in poor patient survival. Progression of organ failure occurs while awaiting a cadaveric allograft. Therefore, we considered living donor liver transplantation (LDLT) in this critically ill group of children and report our initial results with comparison to a similar group who received cadaveric donation (CAD). A retrospective chart review was performed on all pediatric liver transplant recipients who met criteria for MOSF at the time of transplantation. Data collection involved pretransplantation patient profiles, as well as postoperative complications and patient survival. Eight patients in MOSF received living donor transplants and 11 patients received a cadaveric allograft. Mean wait time was 3.5 days in the LDLT group and 6.5 days in the CAD group. Pretransplantation patient profiles and postoperative complications were similar between groups. Mean cold ischemia times were 3.8 hours in the LDLT group and 7.9 hours in the CAD group (P = .0002). Thirty-day and 6-month survival rates of the LDLT group were 88% and 63% compared with 45% and 27% in the CAD group, respectively. Living donor transplant recipients in MOSF had decreased wait times to transplantation, as well as decreased cold ischemia times, compared with cadaveric transplant recipients. Patients in the LDLT group had markedly improved survival compared with the CAD group. Timely transplantation before worsening organ failure may account for these findings.

Pulmonary complications following liver transplantation in pediatric patients.

The purpose of this study was to define the incidence and type of pulmonary complications experienced by children after orthotopic liver transplantation (OLT). The radiological records of all patients receiving OLT during a 3-yr period were reviewed to identify evidence of a pulmonary abnormality. Medical records were then reviewed to determine type, duration, therapy and outcome of pulmonary disorders. Potential risk factors for the development of persistent pleural effusions were also analyzed. One hundred and fifty-one pediatric liver transplantations were performed on 113 patients during this period. Pneumonia developed in 27 patients, including 11 proven bacterial, six presumed bacterial, six viral and four fungal cases. All three deaths related to pulmonary complications were in this group. Three patients developed mild pulmonary hemorrhages, and three developed pulmonary calcifications, which did not impair lung function. Sixteen patients developed paralysis of the right hemidiaphragm, four required diaphragm plication. Pleural effusions developed in 86 patients, 38 persisted longer than 7 days. Patients with persistent effusions were more likely to develop allograft rejection than patients with no persistent effusion (p < 0.01) by chi2 analysis. Seven patients required tracheostomy placement. Of these, four were successfully decannulated, two died from non-pulmonary complications and one is receiving home ventilator support. In conclusion, the majority of children experience at least one pulmonary complication after OLT, but mortality due to pulmonary disease is low in this population. Persistent pleural effusions may be a heralding sign of allograft rejection. Viral, bacterial and fungal pneumonia were the only pulmonary causes of death and only one patient in this series has had significant chronic lung disease.

Inhibition of glutamine synthetase reduces ammonia-induced astrocyte swelling in rat.

Astrocyte hypertrophy and swelling occur in a variety of pathophysiological conditions, including diseases associated with hyperammonemia. Ammonia is rapidly incorporated into glutamine by glutamine synthetase localized in astrocytes. We tested the hypotheses that (1) 6 h of hyperammonemia (500-600 microM) is adequate for producing astrocyte enlargement, and (2) astrocyte enlargement is attenuated by inhibition of glutamine synthetase with methionine sulfoximine. Pentobarbital-anesthetized rats received an intravenous infusion of either sodium or ammonium acetate after intraperitoneal pretreatment with vehicle, methionine sulfoximine (0.8 mmol/kg) or buthionine sulfoximine (4 mmol/kg), an analogue that does not inhibit glutamine synthetase. Hyperammonemia produced enlarged cortical astrocytes characterized by (1) decreased electron density of cytoplasmic matrix in perikaryon, processes and perivascular endfeet, (2) increased circumference of nuclear membrane, (3) increased numbers of mitochondria and rough and smooth endoplasmic reticulum in perikarya and large processes, and (4) less compact bundles of intermediate filaments. Pretreatment with methionine sulfoximine, but not buthionine sulfoximine, attenuated the decrease in cytoplasmic density and the increase in nuclear circumference; most perivascular endfeet remained as dense as occurred with sodium acetate infusion. However, increased numbers of organelles in expanded perikarya and large processes occurred after methionine sulfoximine treatment with and without ammonium acetate infusion. In separate groups of rats, hyperammonemia produced an increase in cortical tissue water content which was inhibited by methionine sulfoximine, but not buthionine sulfoximine. We conclude that clinically-relevant levels of hyperammonemia can cause astrocyte enlargement within 6 h in vivo characterized by both watery cytoplasm and increased organelles indicative of a cellular metabolic stress and altered astrocyte function. The watery cytoplasm component of astrocyte enlargement depends on glutamine synthesis rather than on ammonium ions per se, and is possibly caused by the osmotic effect accumulated glutamine.