Confirmation of death.

A working party set up to study the problems surrounding the confirmation of death investigated current practice by means of a questionnaire sent to a random sample of accident and emergency departments in district general hospitals. Of the 38 replying, 24 said that bodies were examined in the ambulance, four in the accident and emergency department, and 10 in both. Answers to the other questions also suggest that the present procedures are in general unsatisfactory, and some dissatisfaction was expressed by departments. The individuals and organisations consulted were unanimous that confirmation of death should not be carried out in the ambulance. A change of practice would, however, create practical problems. The working party recommends therefore that the standard practice should be for all bodies to be properly examined by a doctor in the accident and emergency department, and that funds should be made available for any building alterations and increase in staff made necessary by such changes.     

Excitotoxic cell death.

Excitotoxicity refers to the ability of glutamate or related excitatory amino acids to mediate the death of central neurons under certain conditions, for example, after intense exposure. Such excitotoxic neuronal death may contribute to the pathogenesis of brain or spinal cord injury associated with several human disease states. Excitotoxicity has substantial cellular specificity and, in most cases, is mediated by glutamate receptors. On average, NMDA receptors activation may be able to trigger lethal injury more rapidly than AMPA or kainate receptor activation, perhaps reflecting a greater ability to induce calcium influx and subsequent cellular calcium overload. It is possible that excitotoxic death may share some mechanisms with other forms of neuronal death.     

The dNTP imbalance death.

The mechanism of intracellular deoxyribonucleoside-triphosphates (dNTP) pool imbalance-induced cell death in mouse FM3A (F28-7) cells was studied. When the cells were treated with 5-fluorodeoxyuridine (FdUrd), deoxyadenosine, 2-chlorodeoxyadenosine, or alpha,alpha-bis(2-hydroxy-6-isopropyltropon-3-yl)-4-methoxytolu ene, an imbalance in the cellular dNTP pool was induced. The imbalance was followed by DNA double-strand breaks and subsequent cell death. Fragmented DNA appeared to be approximately 100-200 kbp in size. The base of 5'-termini in the DNA were adenine and thymine. The endonuclease toward double stranded DNA has been found in a fraction of FdUrd treated cell lysate, and isolated using column chromatography. We propose the new mechanism dNTP pool imbalance induced cell death named; dNTP Imbalance Death.