The interpretation of mixed DNA stains is explained in the context of likelihood ratios. The probabilities for the mixedstain profile are evaluated under alternative explanations that specify the numbers of contributors and the profiles of any known contributors. Interpretations based simply on the frequencies with which random members of a population would not be excluded from a mixed-stain profile do not make use of all the information, and may overstate the strength of the evidence against included people. The effects of the numbers of contributors depends on whether all the alleles at a locus are present in the mixed stain. A general equation is given to allow likelihood ratios to be calculated, and includes the "2p" modification suggested by the 1996 NRC report. This modification is not always conservative. A computer program to perform calculations is available.

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Requests for estimates of blood alcohol concentrations (BACs) are often made when blood samples are taken some hours after the time of interest. Many believe that such estimates are not reliable because the subject's alcohol clearance rate is never known and often there is uncertainty as to whether the subject was postabsorptive at the time in question. In order to evaluate the potential errors associated with BAC estimates under these non-ideal conditions, BAC estimates were compared with empirical data obtained from 24 healthy males, ranging in age from 22 to 56 years, who took part in a three hour social drinking session. One blood sample for alcohol analysis was taken from each subject approximately 1 hour after drinking stopped and another was taken approximately 3.5 hours after drinking stopped. Estimations of BACs at the blood sampling time points were made assuming each person had a constant blood alcohol clearance rate in the range of 10 to 20 mg/dL/h (0.01 to 0.02 g/dL/h) over the whole of the experimental period. A variety of methods were used to estimate the volume of distribution for alcohol. All BAC estimations were made assuming complete absorption and full equilibration of the total alcohol dose. The results showed that actual BACs were usually within or very close to the range of “forward” estimates based on the known alcohol doses. Furthermore, most BACs measured about an hour after cessation of drinking were within or very close to the predicted range based on back extrapolation from the actual 3.5 hour BAC result.

1. With two different methods for assaying the tryptophan oxygenase activity in rat liver homogenates, the effects of some methodological factors on the activity of the enzyme were studied. 2. In fed, but not in starved, rats a compound(s) absorbing at 365 nm, interfering with the reading of kynurenine absorbance, disappeared gradually during incubation. 3. A correction for this tryptophan-independent reaction was necessary in order to determine correct tryptophan oxygenase activity. 4. Blood remaining in liver tissue post mortem can serve as a source of cofactor haem for tryptophan oxygenase, causing spuriously high values for the activity of the holoenzyme form of tryptophan oxygenase. 5. A rapid and progressive activation of tryptophan oxygenase post mortem occurs in undisrupted liver tissue, and this activation is temperature-dependent.

We have compared beta-hexosaminidase (beta-Hex) activity, carbohydrate-deficient transferrin (CDT), mean corpuscular volume (MCV), gamma-glutamyltransferase (GGT), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) values in serum from male alcoholic patients with the corresponding values in moderate and non-drinking subjects. The total beta-Hex activity was 2.5 times higher in the alcoholics than in the moderate drinkers and this increase was mainly due to a 5-fold increase in the activity of the B-isoform of the enzyme. This was expressed as a percentage of the total beta-Hex activity and called 'beta-Hex B%'. Strong correlations were found between alcohol consumption (g/ day) and beta-Hex B% (r = 0.757, P < 0.001, n = 42), alcohol consumption and CDT (r = 0.671, P < 0.001, n = 42), and beta-Hex B% and CDT (r = 0.628, P < 0.001, n = 57). Serum beta-Hex B% had a sensitivity of 94% and a specificity of 91% in detecting alcoholic drinking of > 60 g/day. As a single marker of alcoholic drinking, it was markedly more sensitive than MCV and the liver enzymes GGT, AST and ALT, and slightly more sensitive than serum CDT (94 vs 83%). At the CDT cut-off level of 20 U/l, 17% of the moderate and non-drinkers would have been classified as alcoholic drinkers and 17% of the alcoholics would have been classified as moderate drinkers. Some of these misclassifications were eliminated if the beta-Hex B% results were taken into account. We suggest that serum beta-Hex B% can be a useful and inexpensive laboratory test for alcohol abuse.