A review of NAPL source zone remediation efficiency and the mass flux approach.

A number of previous studies are reviewed to examine the actual reduction of NAPL from source zones and the effectiveness of the specific technique of remediation used at sites under study. It has been shown that complete removal of the NAPL in free phase or residual is not possible due to the complex entrapment architecture of NAPLs at field sites. Consequently, the assessment of remediation efficiency should not be solely based on the reduction of entrapped NAPL mass from source zone. Instead, it should be based on the reduction of risk achieved through the lowering of the concentration of the dissolved constituents emanating from the entrapped NAPL during source zone clean-up. The prediction of the concentration in the plume requires a knowledge of the dissolution of NAPLs in the source zone. Attention is directed to the need for the understanding the mass transfer from entrapped NAPLs in the source zone before and after remediation. In this paper, the current knowledge of mass transfer processes from the non-aqueous phase to the aqueous phase is summarised and the use of mass flux measurements (monitoring the concentration of contaminants in aqueous phase due to source zone NAPL-groundwater mass transfer) is introduced as a potential tool to assess the efficiency of technologies used in source zone remediation. Preliminary results of numerical simulations reveal that factors such as source zone morphology as determined by the heterogeneity of the formation control the post-remediation dissolution behaviour, than the local mass transfer. Thus, accurate site characterization is essential for predicting NAPL dissolution and mass flux relationships as well as for assigning site-specific remediation target values.

Aging of the chromatic onset visual evoked potential.

PURPOSE: To examine changes in the chromatic onset visual evoked potential (VEP) as a function of aging. METHODS: VEP's were measured in response to chromatic sinusoidal gratings (1.0 and 0.5 cpd), selectively chosen to modulate the L-M channel and S - (L+M) channel and presented in onset-offset mode. Responses to achromatic gratings presented in a reversal mode were also measured. Twenty subjects were tested, ranging in age from 21 to 93 years. RESULTS: Unlike changes observed earlier in life, the general shape of the chromatic onset wave-form changed little with age; however, latencies increased significantly as a function of age. Amplitude changes revealed a decreasing trend that was not statistically significant. There was little change in the achromatic responses with age. CONCLUSIONS: Our results demonstrate a systematic slowing of the chromatic onset VEP with age. The gradual nature of the latency changes and the lack of dramatic and complex wave-form shape changes may allow development of age-based normative data for use in clinical settings.

Kinetic and physical studies of beta-lactamase inhibition by a novel penem, BRL 42715.

The interactions of Staphylococcus aureus, Bacillus cereus I, TEM, Klebsiella pneumoniae K1 and Enterobacter cloacae P99 beta-lactamases with the novel penem inhibitor BRL 42715 were investigated kinetically and, in some cases, by electrospray mass spectrometry (e.s.m.s.). All the beta-lactamases were rapidly inactivated by BRL 42715, with second-order rate constants ranging from 0.17 to 6.4 microM-1.s-1. The initial stoichiometry of beta-lactamase inhibition was essentially 1:1, with the exception of the K1 enzyme. In this instance about 20 molecules of BRL 42715 were hydrolysed before the enzyme was completely inhibited. Inhibited beta-lactamases did not readily regain activity in the absence of BRL 42715, the half-lives for regeneration of free enzyme ranging from 5 min for the K1 beta-lactamase to over 2 days for the staphylococcal enzyme. Recovery of activity was incomplete for TEM-1, K1 and P99 beta-lactamases, suggesting partitioning of the inhibited enzymes to give a permanently (or at least very stable) inactivated species. Examination of the interactions of the penem with TEM, B. cereus I and P99 beta-lactamases by e.s.m.s. also showed rapid and stoichiometric binding of the inhibitor. In all cases a mass increase of 264 Da over the native enzyme was observed, corresponding to the molecular mass of BRL 42715, showing that no fragmentation of the penem occurred on reaction with the beta-lactamases.

In vitro evaluation of BRL 42715, a novel beta-lactamase inhibitor.

The penem BRL 42715, C6-(N1-methyl-1,2,3-triazolylmethylene)penem, is a potent inhibitor of a broad range of bacterial beta-lactamases, including the plasmid-mediated TEM, SHV, OXA, and staphylococcal enzymes, as well as the chromosomally mediated enzymes of Bacteroides, Enterobacter, Citrobacter, Serratia, Morganella, Escherichia, Klebsiella, and Proteus species. The concentration of BRL 42715 needed to reduce the initial rate of hydrolysis of most beta-lactamase enzymes by 50% was less than 0.01 micrograms/ml, which was 10- to 100-fold lower than for other beta-lactamase inhibitors. These potent inhibitory activities were reflected in the low concentrations of BRL 42715 needed to potentiate the antibacterial activity of beta-lactamase-susceptible beta-lactams. Concentrations of 0.25 micrograms/ml or less considerably enhanced the activity of amoxicillin against many beta-lactamase-producing strains. The MIC50 (MIC for 50% of strains tested) of amoxicillin for 412 beta-lactamase-producing members of the family Enterobacteriaceae fell from greater than 128 to 2 micrograms/ml in the presence of 1 microgram of BRL 42715 per ml, whereas 5 micrograms of clavulanic acid per ml brought the MIC50 down to 8 micrograms/ml. Among these 412 strains were 73 Citrobacter and Enterobacter strains, and 1 microgram of BRL 42715 per ml reduced the MIC50 of amoxicillin from greater than 128 to 2 micrograms/ml for the 48 cefotaxime-susceptible strains and from greater than 128 to 8 micrograms/ml for the 25 cefotaxime-resistant strains.

Gross and histological signs of dietary deficiencies of biotin and pantothenic acid in lake trout, Salvelinus namaycush.

We describe the pathologic changes of single or simultaneous dietary deprivations of biotin (B) and pantothenic acid (PA) in lake trout, Salvelinus namaycush. A deficiency of PA produced gross signs of anorexia, inanition, emaciation, gill abnormalities and high mortality. In B-deficient fish, growth retardation reached statistically significant levels (P less than 0.05) after week 10, but gill and liver lesions were observed earlier. Anorexia and reduced weight gain were observed earlier in fish deprived of both nutrients than in those deficient in B alone. All B-deficient trout fed PA survived the study, and were less anorexic, anemic and emaciated than were those fed B without PA. Deposition of glycogen was greater in kidney tubules of B-deficient fish than in those lacking both vitamins. However, lesions interpreted to be mitochondrial conglutination and cellular necrosis of renal tubules and pancreatic acini were more exaggerated in fish fed neither nutrient than in those deprived of only one. Both vitamins are needed for energy transfer metabolism and their absence in metabolically active tissues causes lesions that resemble those reported for cellular anoxia.

Supplementation of a semipurified casein diet for catfish with free amino acids and gelatin.

Semipurified diets with casein as the sole protein source were supplemented with gelatin, arginine, cystine, methionine or tryptophan, and fed to channel catfish (Ictalurus punctatus) fingerlings. Increasing the arginine level from 1.1% to 1.7% of diet by the isonitrogenous substitution of gelatin for casein resulted in a significant enhancement of growth. However, the addition of free arginine, cystine, tryptophan or methionine to casein had little effect on growth or food conversion. These data substantiate a previous report that suggested catfish were similar to carp in their inability to utilize free amino acids.