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To improve the possibilities to delimitate the time of death after longer laytime, it was examined if this is possible by immunohistochemical insulin detection. The results show that in our examination material, the pancreatic beta-cells of up to 12-day-old corpses produce a positive immunoreaction towards insulin in all cases, whereas none of the corpses older than 30 days show such a reaction. This means that in case of a negative immunoreaction, the time of death can be assumed to lie more than 12 days before the autopsy. The fact that a negative immunoreaction occurs consistently after 30 days leads to the conclusion that when insulin has been stained in a specimen, the death of the respective person must lie a maximum of 29 days earlier, whereby these time-limits may change in considerably different surrounding conditions.

Human traumatic brain injury (TBI) is ideally suited for investigation of the kinetics of human microglial cell activation as the onset of lesion formation is precisely defined. The present study provides evidence of a distinct delay in macrophage/microglia response following TBI. Eighteen brains of patients who had survived TBI for 1 h to 6 months were analysed by immunohistology. Samples of contusional and non-contusional areas were studied using antibodies directed against antigens of microglia/ macrophages [major histocompatibility complex class II, CD4, interleukin (IL)-16, macrophage-related protein (MRP) 8 and MRP14]. IL-16, a natural ligand to CD4, was expressed constitutively by numerous microglial cells in all cases throughout the brain. CD4 could be detected regularly on perivascular cells. MRP8 and MRP14, which are only expressed on activated macrophages and microglial cells, could be detected only within brains with a survival time of more than 72 h post TBI. In addition, proliferation of microglia detected by MIB-1 was not present until 72 h. This delayed expression of the activation markers MRP8 and MRP14 and the proliferation marker MIB-1 is comparable to experimental closed head injuries but strictly different from acute activation found in ischemic brains. [ABSTRACT FROM AUTHOR]