A statistical approach to identifying the batch of origin of mixed-meat products using DNA profiles.

Comparison of DNA samples at different points of a supply chain offers a powerful means of verifying tracing systems for primal cuts of meat. However, this approach is problematic for products made from ground (or mixed) meat because such products are typically made from an unknown (and random) number of unidentified animals. We present a statistical method that uses DNA profiles to verify or refute the contention that a particular mixed-meat product came from a particular manufacturing batch. This method involves randomly isolating a number of individual DNA samples (comprising an unknown number of individual genotypes) from the end product and comparing them with a set of DNA samples (also comprising an unknown number of individuals) that had been collected randomly before preparation of a manufacturing batch. Confidence levels are given for refuting spurious claims, and the development of optimum sampling strategies is discussed. The results are discussed in relation to batch verification of mixed-meat products in the food industry, with an emphasis on traceability issues.

Modeling the effect of energy status on mammary gland growth and lactation.

The impact of nutrition on lactation can be separated into acute effects, affecting day-to-day yield, and chronic effects, which govern the persistency of lactation and rate of decline of the lactation curve. A mathematical model of the mammary gland was constructed to investigate both acute and chronic effects. Mammary growth is expressed in terms of the dynamics of populations of active (secreting) and quiescent (engorged) alveoli. The secretion rate of active alveoli is expressed in terms of the energy status of the dam. The model was fitted to data from a 2 x 2 factorial trial in which lactation curves were measured for heifers of two different genotypes (North American and New Zealand Holstein-Friesians) fed two different diets [grass and total mixed rations (TMR)]. Total formation of alveoli during pregnancy and lactation was statistically the same across all groups despite differences between diets, in the rate of formation of alveoli at parturition. The senescence rate of alveoli was significantly higher for heifers fed grass compared with heifers fed TMR, which corresponds to better persistency for heifers fed TMR. Heifers fed TMR had a higher rate of reactivation of quiescent alveoli than heifers fed grass, which also contributes to increased persistence for heifers fed TMR. There was a genotype x diet interaction in the rate of quiescence of active alveoli: the North American-Grass group had a higher rate of quiescence than the other three groups, perhaps reflecting differences in selection pressures between the New Zealand and North American genotypes.

Onset of insensibility at slaughter in calves: effects of electroplectic seizure and exsanguination on spontaneous electrocortical activity and indices of cerebral metabolism.

Cerebral venous and femoral arterial blood samples were collected from 21 young calves either during electrical stunning and recovery or electrical stunning and slaughter by carotid severance or slaughter without stunning. The blood samples were analysed for PO2, PCO2, pH, glucose and lactate. The results were compared with simultaneous recordings of spontaneous electrocortical (ECOG) activity. Calves subjected to head-only electrical stunning and slaughter became permanently insensible at the time of the stun. The six calves slaughtered without stunning lost sensibility within 10 seconds. One calf, in which a clot formed in the carotid arteries inhibiting bleeding, maintained some evidence of cortical activity beyond 52 seconds; this was high amplitude low frequency activity and analysis by Fast Fourier Transform showed sensibility was not regained. In the remaining calves the ECOG activity was lost on average within 49 +/- 3.5 (SEM) seconds after slaughter. The cerebral extraction of metabolites increased after carotid severance, indicating inadequacy of cerebral bloodflow after slaughter. No correlations were found between indices of cerebral metabolism and the time of loss of cortical function.

Alcohol and other discriminants between cases of sudden death and myocardial infarction.

A register of acute coronary events in Auckland, New Zealand collected data on both cases of definite myocardial infarction not dying suddenly, and cases of sudden cardiac death. This paper compares these two syndromes with respect to several clinical and pathologic variables. The following variables discriminated between these two syndromes significantly: season of the year, painful prodromal symptoms, use of digoxin and/or furosemide, age, race, alcohol consumption over the previous one year. Possible biases and sources of confounding are discussed. Heavy alcohol consumers have a higher proportion of coronary events as sudden deaths. This proportionate increase is probably due, in part at least, to an absolute increase in the frequency of sudden death. The data are supportive of the idea that persons with a high alcohol consumption who also suffer myocardial infarction are more likely to die suddenly with the infarction. The rather conflicting data from many other studies are discussed. A model is proposed, based on reported data that could explain the present findings and those previously reported by others.

The incidence of juvenile diabetes mellitus in New Zealand.

The incidence of juvenile diabetes in New Zealand over a five year period (1968--1972) was determined from hospital admission data stored at the Department of Health, National Statistics Centre. The average annual incidence for persons under 20 years was 10.4 persons/100,000. There was no sex difference below 16 years, and the increased incidence among females 16--19 years could be attributed to pregnancy. There was a 1.4-fold higher incidence in the South Island than in the North Island. There were no regular seasonal trends. The incidence was constant between 1--9 years increasing to a sustained 2.2-fold higher level from 11 years. The absence of childhood peaks and the sustained higher incidence in adolescence is in contrast to European studies.

The proliferative activity of leukaemic myeloblasts following the intravenous infusion of cytarabine.

Serial bone marrow aspirates were obtained from 16 adults with acute myeloid leukaemia (AML) before and after a single infusion of cytarabine (5.0 mg/kg i.v. over 30 min). Changes in the proliferative activity of the leukaemic myeloblasts were monitored by determination of the labelling index (LI) and the mitotic index (MI). There was a significant fall in both LI and MI within a few hours of the administration of cytarabine (P = 0.005). In 14 of the 16 cases the LI subsequently rose to observed maxima 0.3% to 14.1% (mean 5.0%) above the preinfusion LI, 11 to 77 hours (mean 40.8 h) after the infusion (P less than 0.05). The MI returned to the mean pretreatment level within the period of observation in 11 of the 16 cases. In general, the changes in MI followed those in LI; the results are consistent with cytarabine-induced arrest or death of leukaemic blast cells in S phase. Because of the variability in timing of kinetic changes in leukaemic myeloblasts following cytarabine, it is not possible to institute remission induction therapy consistently at the time of maximum synchronization with any fixed chemotherapeutic schedule. Furthermore, the degree of synchronization attained is, in general, small, limiting the prospect of exploiting synchronization with cytarabine as a means of improving the remission rate for AML.