Ostrich chick mortality was studied in 2522 chicks that were hatched artificially during the 1999/2000 breeding season. High levels of mortality were observed, with 1978 (78.4 %) of these chicks dying before 90 days after hatching. Atotal of 46.7 %(1177) of these chicks died before 28 days of age, and a further 30.7 %(801) died between 28 and 90 days post-hatching. Chick mortality to 28 days of age could not be conclusively related to sex, day of external pipping or breeder diet. Mortality rates were higher (P < 0.05) at the beginning and end of the breeding season than in the middle months. Differences in mortality levels of chicks incubated in different incubators could be related to the time of the breeding season during which the incubator was mostly used. The regression of chick mortality to 28 days of age on day-old chick mass followed a 2nd-degree polynomial. Chicks with day-old masses below 762.5 g were particularly at risk of dying before 28 days after hatching. Chicks hatching from eggs where excessive water loss to 35 days of incubation (>18 %) was recorded were also at risk of succumbing before 28 days of age. Chick mortality percentages for the period from 28 to 90 days of age exceeded 80 %in chicks weighing an average of 1050 g at 28 days. Mortaliy percentages declined sharply at higher live masses, to between 20 and 30 % in chicks weighing ?1950 g. This 'core' level of mortality remained throughout, even in the heaviest chicks. It was concluded that the high levels of chick mortality could be related to stress in chicks, resulting from an inability to adapt to the rearing environment. The high subsequent mortality percentages of low live mass chicks that survived to 28 days after hatching could probably be attributed to residual setbacks suffered earlier. Abetter understanding of the underlying principles involved in ostrich chick mortality in intensive rearing environments is required for progress in this field, resulting in more predictable survival rates under these conditions.

Background. In a group of patients with metastatic melanoma treated with high dose immunotherapy, there was an unexpectedly high incidence of severe cardiac adverse effects. Methods. Sixteen patients with metastatic melanoma were treated with high dose interleukin‐2 (IL‐2) and alpha‐interferon (α‐IFN). Each treatment cycle consisted of IL‐2 at a dose of 12 MIU/m2 and α‐IFN at a dose of 3 MIU/m2, given as intravenous bolus injections every ß hours on Days 1‐5, every 3 weeks for a total of three cycles. Before treatment, careful cardiologic screening was performed, including electrocardiogram (ECG), stress test, cardiac multiple uptake‐gated acquisition (MUGA) scan, and echocardiography. During therapy, patients were monitored with daily ECG and creatine phospokinase measurements. Once cardiac damage was suspected, IL‐2 and α‐IFN were discontinued, and echocardiography, stress test and MUGA‐scan were repeated. If indicated, cardiac catheterization with endomyocardial biopsies was performed. Results. Despite pretreatment cardiac screening, seven patients (44%) exhibited myocardial injury. Acute myocardial infarction occurred in one patient, cardiomyopathy developed in four, asymptomatic ECG changes appeared in one, and 1 patient died of acute cardiac arrest. Echocardiography showed hypokinesis and decreased left ventricular ejection fraction. These abnormalities disappeared within 6 months. Cardiac catheterization in four affected patients revealed normal coronary arteries, but endomyocardial biopsies showed interstitial edema, vacuolation, and degeneration of myocytes. Electron‐microscopic examination showed fragmentation of myofibrils, swelling of mitochondria and loss of mitochondrial cristae. Conclusions. This intensive treatment schedule of IL‐2 and α‐IFN is prohibited by severe and life‐threatening cardiac toxicity.

Myelodysplastic syndromes (MDS) are acquired bone-marrow disorders, characterized by a decreased ability of the haemopoietic cell to differentiate, resulting in peripheral cytopenias. The majority of patients will die either from acute myeloid leukaemia or from infection and/or haemorrhage. Thirty-eight courses of low dose Ara C were administered in 26 MDS patients. Nineteen courses (50%) were associated with good (12) or partial (7) response. Three complete remissions were observed. The median duration of response overall was 19.5 weeks, 26 weeks for the good and 10 weeks for the partial responders. A high incidence of treatment failure was seen in patients treated after transition to AML. Major complications were observed during 14 courses and mortality was directly related to therapy in five patients. Platelet transfusions were required during 26 courses. Aggravation of peripheral-blood cytopenia during the first weeks and hypocellularity of bone-marrow aspirates at the end of therapy suggest that low-dose Ara C exerts its main activity by suppression of leukaemic growth, rather than by induction of differentiation in malignant cells. Our results in MDS patients demonstrate that low-dose Ara C can be of value in severe cytopenia and can decrease the proportion of leukaemic cells in the bone marrow, but the danger of treatment should not be underestimated.

IRON overload is characterized by an increase of reserve iron in the body. As a screening test for the presence of such increased iron reserves the determination of the serum iron concentration and the percentage saturation of the iron-binding protein ( s i d e r o p b , transferrin) is

FFPE tissue-derived DNA can be used as a valid proxy for germline DNA for a selection of SNPs in (retrospective) pharmacogenetic association studies in colorectal cancer. However, for future studies, genotyping of blood-derived DNA is preferred.