Postmortem Phenomena Research Articles

Individual Identification from Skeletal Remains: Cases of Wild Chimpanzees of the Mahale Mountains National Park, Tanzania

The skeletal remains of five adult wild chimpanzees (Pan troglodytes schweinfurthii) stored at the Kansyana Research Camp in the Mahale Mountains National Park, Tanzania, were examined in order to identify the skeletons and to find pathological evidence on the bones. In Mahale, wild chimpanzees have been studied for nearly 40 years without interruption . Reference cards of chimpanzees for personal identification in life are now available at the camp. By contrasting morphological and pathological characteristics of the skeletons with the datum on the reference cards, two formerly unidentified skeletons could both be identified. Furthermore, the cause of death of a female chimpanzee was revealed from the skeletal evidence. Postmortem phenomenon of the body and what kinds of records in life are useful for the purpose of identification of the skeletons are discussed. Lastly, the prospect of such a study as a part of the long-term study of wild primates is discussed.

Heat-induced immunoreactivity of tau protein in neocortical neurons of fire fatalities.

Tau protein is the main component of neurofibrillary tangles of Alzheimer's disease (AD). Immunohistochemistry of tau protein is useful in the diagnosis of AD but produces diffuse staining of neocortical neurons in fire fatalities. To learn the cause of this phenomenon, we examined the temporal neocortex of 13 fire fatalities and 9 fatalities unrelated to fire. The diffuse tau immunoreactive neurons were observed in 10 fire fatalities with heat coagulation of the cerebrum. Diffuse staining was not found in the three fire fatalities without heat coagulation of the cerebrum or in fatalities unrelated to fire. The immunoreactivity progressively increased as a function of the degree of cerebral heat coagulation. These results demonstrate that diffuse tau immunoreactivity of neocortical neurons is a post-mortem phenomenon caused by prolonged exposure of the head to intense heat. Forensic pathologists should consider this phenomenon when they diagnose AD in fire fatalities.

Organ weight effects of drowning and asphyxiation on the lungs, liver, brain, heart, kidneys, and spleen

An examination of the organ weights associated with victims of drowning, asphyxiation and trauma was undertaken to determine (a) the effects of asphyxiation compared to a trauma group, and in turn, (b) the effects of drowning compared to an asphyxiation group. Included in the study were 217 drowning deaths, 166 pure asphyxiation deaths and 381 trauma deaths. The effects of asphyxiation (compared to trauma) resulted in elevated mean organ weights for the lungs, liver, kidneys and spleen (with mean increases of 17.8, 10.5, 10.3 and 23.4%, respectively). Effects of drowning (compared to asphyxiation) resulted in elevated mean organ weights only with the lungs and kidneys (with mean increases of 30.0 and 4.4%, respectively). Only the mean heart and brain weight remained constant across all experimental groups. A picture of drowning is suggested in which elevated lung and kidney weights are the result of both asphyxiation and the aspiration of water that occurs with drowning, whereas elevated spleen and liver weights in drowning victims are associated with only the effects of asphyxiation. In addition, the common autopsy finding of a small, anemic spleen in drowning, rather than caused by some pathophysiological mechanism of death, is hypothesized to be a postmortem phenomenon.

Application of restriction landmark genomic scanning for analysis of the postmortem phenomenon

The restriction landmark genomic scanning method modified by methylation (RLGS-M) was applied for analyses of the postmortem time interval (PMI) using the methylation sensitive enzyme Eco52I and methylation insensitive enzyme EagI as the landmarks. In the period between 4 and 8 h as a postmortem time interval, the methylation rate was slightly decreased and the gene activation seemed to be slightly increased. After that, the methylation rate was increased to the same level at the time of individual death. This fact suggested that the gene activation was decreased to the same level at the time of individual death. During the supra-vital period, which is defined as the period between the individual death and the cellular death in each organ, transient gene activation might occur even after the individual death.

Effects of acute "binge" cocaine on preprodynorphin, preproenkephalin, proopiomelanocortin, and corticotropin-releasing hormone receptor mRNA levels in the striatum and hypothalamic-pituitary-adrenal axis of mu-opioid receptor knockout mice.

Cocaine administration increases activity at dopamine receptors, increases preprodynorphin (ppDyn) gene expression in the caudate-putamen (CPu), and activates the stress responsive hypothalamic-pituitary-adrenal (HPA) axis. To examine the hypothesis that mu-opioid receptors (MOR) may play roles in these cocaine effects, we tested the effects of acute "binge" pattern cocaine administration in mice with targeted disruption of the MOR gene. Wild-type (+/+) and homozygous MOR-deficient (-/-) mice received three injections of 15 mg/kg cocaine at 1-h intervals. Mice were sacrificed 30 min after the last injection and mRNAs for ppDyn and preproenkephalin (ppEnk) in the CPu and nucleus accumbens (NAc), and for type I corticotropin-releasing hormone receptor (CRH(1) receptor) and pro-opiomelanocortin (POMC) in the hypothalamus and pituitary, were measured by solution hybridization RNase protection assays. Cocaine elevated ppDyn mRNA in the CPu, but not NAc, of both the MOR -/- and wild-type mice. ppEnk mRNA in the CPu, but not NAc, was lower in MOR -/- mice than in wild-type mice following cocaine administration. Hypothalamic CRH(1) receptor and POMC mRNAs were expressed at similar levels in untreated and in cocaine-treated mice of each genotype. However, there were lower basal levels of CRH(1) receptor mRNA in the anterior pituitary of the MOR -/- mice than in wild-type mice and the MOR -/- mice failed to show the cocaine-induced decreases in CRH(1) receptor mRNA found in the wild-type mice. Cocaine activated the HPA axis similarly in MOR -/- and wild-type mice, as reflected in similar increases in plasma corticosterone levels in both genotypes. These results support a specific role for MORs in acute cocaine effects on striatal ppEnk gene expression and fail to support critical roles for these receptors in acute cocaine's effects on either ppDyn gene expression or HPA activation. MOR -/- mice are useful models for studying cocaine effects on ppEnk gene expression that could aid interpretation of the similar postmortem phenomena found in human cocaine addicts.

A Scanning Transmission Microscopy and Energy-Dispersive X-ray Microanalysis of Idiopathic Ocular Calcification and Oxalosis in AIDS Patients

In a series of 98 consecutive eyeballs enucleated at postmortem from 86 patients dying with AIDS, the incidence of calcium deposits was 14 and 18.6%, respectively, for oxalates and calcium hydroxyapatite. The calcific eyes were examined by scanning electron microscopy (SEM) coupled with energy-dispersive X-ray microanalysis to confirm the elemental nature of the precipitates. Transmission electron microscopy was used in 2 of the cases with oxalosis. Oxalates with a free end exhibited a plate-like shape at SEM and appeared acicular at TEM, due to the reduced thickness of ultrathin sections. Crystals that were embedded in tissues such as the sclera or degenerate detached retinal tissue formed either spherules or plates at SEM. No clear relationship with intracellular structures could be found at TEM, possibly due to postmortem autolysis phenomena. Calcium hydroxyapatite deposits appeared at SEM as fine granules distributed over the collagen fibers of the corneal and conjunctival stroma and the scleral lamellae, but were also present intracellularly, both in the nucleus and cytoplasm of epithelial cells.

The postmortem activation status of platelets.

Platelets are activated by substances from the subendothelial matrix in endothelial lesions or by factors in the plasma coagulation cascade. Conversely, activated platelets are potent activators of this cascade. Only activated platelets express the adhesion molecules Gp53, GMP140 and thrombospondin on the plasma membrane. The postmortem activation status of platelets, therefore, can be determined immunoelectron microscopically by immunogold labeling of antibodies against these glycoproteins. Our studies revealed that the vast majority of these antigens were located within the granules postmortem, hence the platelets had not been activated. Thrombin-induced activation of platelets in vitro was only possible in the early postmortem interval, as demonstrated by labeling of the adhesion molecules on the plasma membrane. Later, such activation was no longer possible even though thrombin-induced fibrin formation gave the appearance of "coagulated blood". In forensic medicine, these findings can possibly be applied to distinguish intravital clotting from the postmortem coagulation phenomena and intravital hematomas from postmortem hematomas.

Geophysical Variables and Behavior: LXXI. Differential Contribution of Geomagnetic Activity to Paranormal Experiences concerning Death and Crisis: An Alternative to the Esp Hypothesis

A total of 621 reports (experienced over an approximately 70-year period) of putative psi experiences concerning death or crisis were differentiated according to traditional labels: telepathic, precognitive, and postmortem phenomena. The 232 telepathic experiences occurred during 24-hour periods in which the global geomagnetic activity was significantly less (quieter) than during the days before or after the experiences; this relationship was not displayed by the 186 precognitive or 203 postmortem cases. Key day differences in geomagnetic activity for the three classes of experiences were equivalent to a correlation of about 0.35. Although content analysis suggests that nocturnal psi experiences and temporal lobe epilepsy may share a similar mechanism, different classes of subjective psi experiences may not be affected by the same stimuli.

Dermal surface in electric and thermal injuries. Observations by scanning electron microscopy.

The dermal surface (after enzymatic digestion of the dermo-epidermal junction) in electric and heat lesions is described. There do not appear to be elements that help in forming a precise differential diagnosis. It is possible, however, to differentiate these lesions from all traumatic cutaneous injuries and some limited nontraumatic lesions (e.g., verrucae). Remarkably good preservation of the dermal surface even in an advanced state of decomposition does suggest the possibility of certain diagnosis of electric and heat lesions even when postmortem phenomena have greatly damaged or even totally removed the epithelial part of the skin.

Mode of death and post-mortem time effects on 3, 3', 5-triiodothyronine levels -- relevance to elevated post-mortem T3 levels in SIDS

Post-mortem T3 levels have been reported to be increased in victims of SIDS. Recent animal studies suggest, however, that elevated T3 in SIDS may be a non-specific post-mortem phenomenon. Therefore, we studied the possible effects of post-mortem time on T3 levels in 10− and 20-day-old rats killed by various methods including: Sodium pentobarbital overdose, injection of KCl, cervical dislocation or asphyxia with 100% N, 95% N-5% CO 2 or 100% CO 2. In both age groups T3 remained unchanged or increased slightly when the animals were killed with Na Pentobarbital or KCl. Greater increases were observed when rats were killed by cervical dislocation or asphyxia (100% N, 95% N–5% CO 2 or 100% CO 2). T3 levels did not become elevated in asphyxiated adult rats in which the inferior vena cava was ligated immediately following death. By extension to the human infant, the results of this study support the possibility that elevated T3 levels in SIDS victims may result from post-mortem processes. However, these results also suggest that the post-mortem elevation in T3 levels may be directly related to the mode of death.

EFFECTS OF POSTMORTEM AGING ON CHICKEN BREAST MUSCLE SARCOPLASMIC RETICULUM LIPIDS

Polar lipids of chicken breast muscle sarcoplasmic reticulum have been extracted and quantitated from preparations at various times of postmortem aging. Neutral lipids and fatty acid composition of selected polar lipids were determined in at-death preparations. While phospholipase activity against endogenous membrane lipids was not demonstrated, exogenous phosphatidyl choline was hydrolyzed when incubated with the fragmented sarcoplasmic reticulum. Electron micrographs of negatively stained sarcoplasmic reticulum, showing different vesicle types and selective uptake of calcium oxalate, are also presented. The significance of the results is discussed in light of postmortem aging phenomena.

Pink Teeth Appearing as a Post-Mortem Phenomenon

Biochemical investigations into the nature of the post-mortem occurrence of pink teeth are described. Spectral studies and iso-electric focusing indicated the presence of haemoglobin or other haem derivatives. The presence of carbon monoxide was also observed. It is suggested this unstable pink colouration results from the formation of a complex, possibly a haem-carbon monoxide complex, which differs from the more stable carbon-monoxy-haemoglobin.

Infraglomerular Epithelial Reflux as a Postmortem Phenomenon in the Kidneys of Dog and Rat.

The significance of postmortem renal changes for the pathogenesis of infraglomerular epithelial reflux (IER) was examined in a number of experiments with kidneys of the dog and rat. The reflux can develop after death in both species. Intravital circumstances (e.g., ischemia) may stimulate the postmortem development of IER. The development of IER was accompanied by swelling of tubular epithelial cells and could be provoked by palpation at autopsy. The type of fixative can also influence the degree of the phenomenon, which was more pronounced in ethanol-fixed than in formalin-fixed kidney. IER has to be considered primarily a postmortem phenomenon and a correct evaluation of IER is only possible if the postmortem treatment of the kidney be exactly known and, in appropriate investigations, has been very well standardized for control and experimental animals.

The Diagnosis of Intra-Auricular Thrombosis in the Living

In Chronic Disease of the heart, prognosis and therapy depend not only upon the anatomical and etiological diagnosis of the damage but also on the proper assessment of the repair, the work demanded of the damaged organ, and the reserve left to deal with the load thrown upon the defective mechanism. Even the most careful calculations, however, may be overthrown by unforeseen accidents, and the outlook may suddenly be completely changed. Among such accidents is the occurrence of thrombi within the chambers of the heart, with consequent interference with the peripheral circulation and embolism. The frequent occurrence of thrombi within the ventricles and auricles, particularly in mitral stenosis, is proved by numerous autopsy reports. Among 178 rheumatic hearts examined by Graef et al., 24 showed mural thrombi, which in 14 cases were lodged in the left auricle, in 5 in the right, and in 5 in both auricles. Among 60 patients with auricular fibrillation and rheumatic heart disease, Garvin found 26 cases of mural thrombosis at autopsy (43.3 per cent). In a series of 771 patients with all types of heart disease, including coronary artery disease, hypertensive heart disease, and syphilitic heart lesions, the incidence was 34.4 per cent. In sharp contrast to their frequency in autopsy series is the small number of intra-auricular thrombi diagnosed during life. Few have been recognized clinically, and still fewer roentgenographically. These thrombi are not an agonal or post-mortem phenomenon; they are not the terminal outcome of auricular fibrillation; they are, according to Levine, an important cause of an appreciable number of deaths (20 per cent), and they might well be amenable to modem anticoagulant treatment. That there is sufficient time for the application of such treatment if the diagnosis is made early is evident from a report by Schwartz and Biloon in which signs of embolism occurred in 1919 and death ensued seven years later (1926) from proved auricular thrombosis. Similarly one of our own patients who now shows roentgenologic evidence of auricular thrombosis and electrocardiographic evidence of auricular fibrillation had the first signs of cerebral embolism, leading to temporary hemiplegia, in 1931 and signs of pulmonary infarction in 1946. Auricular thrombi are of two kinds, the non-occluding and the occluding. The non-occluding thrombi are those which do not impinge on the auriculo-ventricular orifice and therefore do not impede the flow of blood from auricle to ventricle. By far the great majority of auricular thrombi are of this type. The occluding thrombi are those which, because of their size and position, impinge on the valve orifice and hinder the flow of blood through it. They may be pedunculated or completely free as loose bodies in the auricular cavity. The spherical free clots are the so-called ball thrombi.

Cystitis emphysematosa: V. A case in a woman in which trauma appeared to be an etiologic factor

Another case of cystitis emphysematosa is reported, with clinical and pathologic details. This case represents a very early lesion, which probably was initiated by the slight trauma produced by a catheter abrading the mucosa of the bladder. There are two lesions, one older than the other, corresponding to catheterization on two successive days, the latter on the day preceding death. The injuries must have been trivial and did not cause the loss of an appreciable amount of blood, as the control specimens of urine were free from erythrocytes. Perhaps any form of injury to the mucosa, whether by a catheter, instrument or spontaneous hemorrhage, may initiate the lesion if other conditions be fulfilled.Cystitis appears to be necessary as a background on which cystitis emphysematosa may develop. Evidence is accumulating that the lesion results from some form of infection.The lymphatics are capable of transporting the gas to a certain extent beyond the point of its production. They are at first distended and then degenerate. There is no evidence that giant cells arise by multiplication of the cells of their endothelial lining.It is now certain that cystitis emphysematosa develops during life, and is not a postmortem phenomenon. Lowered resistance, at least of the bladder, seems to be necessary for its development, but whether this condition is limited to the last few days of life of a patient practically moribund, or whether it may occur in a patient with only serious disease of the bladder, has not been determined.

GRANULAR DEGENERATION OF RED BLOOD CELLS.

The so-called granular degeneration of the red blood corpuscles of Grawitz has been a subject for much discussion. It is characterized by the presence in the red blood corpuscles of basophilic granules. Some investigators consider the bodies to be fragments of broken-down nuclei (karyorhexis), others believe them to be artefacts or postmortem phenomena, while most authors agree with Grawitz in recognizing the basophilic granules, sometimes seen in red blood corpuscles, as due to degenerative changes in the cells, and having no connection with a process of karyolysis. This form of degeneration has been observed in a variety of diseased conditions, such as pernicious anemia, malaria, carcinoma of the stomach, various suppurative diseases, leukemia, lead poisoning, etc. It is especially prominent in cases of poisoning by lead, and may be found in the blood of persons working with lead when all other signs of poisoning by the metal are wanting. Moritz