ABSTRACT
The radiolytic degradation of three N,N-dialkyl amide ligands relevant to nuclear fuel reprocessing was studied. The degradation of these ligands: N,N di-2-ethyhexylbutyramide (DEHBA), N,N di-2-ethyhexylisobutyramide (DEHiBA) and N,N di-2-ethyhexyl-3-dimethylbutanamide (DEHDMBA) was examined to evaluate the effect of the structure on the formation of degradation products as well as to compare alpha induced degradation to gamma induced degradation. In situ alpha radiolysis by introduction of plutonium(iv) as the alpha source in the solution and ex situ gamma radiolysis with 60Co as the gamma source were compared. Upon identification of the main degradation products, a degradation scheme was proposed. The effects of radiation on the stability of Pu-monoamide complexes were discussed. Theoretical calculations were also performed to determine bond dissociation energy and estimate the relative strength of the bond in the molecule. The results show that neither the type of radiation (alpha vs. gamma) nor the structure modification (introduction of branching on the alkyl chain off the carbonyl carbon) of the molecule significantly impact the formation of degradation products under the conditions studied. Moreover, it was observed that the overall stability of the monoamide remains good and that Pu complexation is not greatly affected by either alpha or gamma irradiation.
ABSTRACT
An acute or fulminant adenovirus hepatitis developed in 5 of 224 pediatric patients who were recipients of orthotopic liver transplants. All had received prednisolone, azathioprine, and cyclosporine as basal immunosuppression, and four received monoclonal (OKT3) or polyclonal (antithymocyte globulin) antibodies for steroid-resistant rejection episodes. These patients initially had high fever and a worsening condition for a mean of 73 days after transplantation (range 44 to 140 days). Results of biochemical tests showed very high serum levels of lactate dehydrogenase. Aspartate aminotransferase values were always markedly more elevated than those of alanine aminotransferase. Two patients had severe leukopenia. Results of histologic studies of the liver showed extensive areas of confluent necrosis and targetlike hepatocyte nuclei. Typical intranuclear viral inclusions were observed on electron microscopy. Adenovirus was cultured in all patients and in two relatives. Two patients died of liver failure; others recovered after cessation of immunosuppression. We conclude that adenovirus hepatitis can be fatal in liver transplant recipients. There is no specific treatment, and immunosuppression must be discontinued.