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A study of the eye-ground during the first three days after death revealed regular sequence of changes manifested in a characteristic dynamics of colour, level and relief of the visual nerve disk surface, clarity of its borders, state of arterial and venous vessels. It is suggested that evaluation of the dynamics of postmortal changes of the eye-ground may be used in determining the time of death.
The programme design is based on the process of changes in dead body temperature. Specific features of the process of changes in temperature values of a dead body are characterized by a parameter which involves process sample obtained by temperature measurements in diagnostical area of a cadaver at the accident scene during 1 hour. Programme provides for estimation of postmortem interval within the first 60 h after death occurrence. Diagnostical deviations don't exceed +/- 3% as compared to the real time of death.
Significant post-mortem changes in peptide concentration occur within the previously unstudied timeframe, i.e. within 1 h, for the proenkephalin A, proopiomelanoccortin, and tachykinin neuropeptidergic systems in the pituitary. These data differ from data obtained in other studies that concluded that peptides are stable for up to 72 h post-mortem. The post-mortem stability of the three neuropeptides, methionine enkephalin, substance P, and beta-endorphin, was studied in the rat pituitary to test the hypothesis that significant post-mortem concentration changes of those three neuropeptides occur in the immediate post-mortem time period.
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We studied the spin-echo signal of muscle water in a large time domain and found that the motion of the nuclear magnetic moment of tissue water cannot be characterized by a single spin-lattice relaxation time (T1). The relaxation time T1B, which is the T1 characterized by those protons with a slower relaxation rate, is influenced by the early post mortem changes in skeletal muscle. T1B increased with time after the tissue was taken from the animal and reached a maximum at 3 h. However, the weighted average of T1 of all water protons (T1A) did not change throughout the time course of the experiments.
OBJECTIVE: To determine whether changes in brain biometals in Alzheimer disease (AD) and in normal brain tissue are tandemly associated with amyloid beta-peptide (Abeta) burden and dementia severity. METHODS: The authors measured zinc, copper, iron, manganese, and aluminum and Abeta levels in postmortem neocortical tissue from patients with AD (n = 10), normal age-matched control subjects (n = 14), patients with schizophrenia (n = 26), and patients with schizophrenia with amyloid (n = 8). Severity of cognitive impairment was assessed with the Clinical Dementia Rating Scale (CDR). RESULTS: There was a significant, more than twofold, increase of tissue zinc in the AD-affected cortex compared with the other groups. Zinc levels increased with tissue amyloid levels. Zinc levels were significantly elevated in the most severely demented cases (CDR 4 to 5) and in cases that had an amyloid burden greater than 8 plaques/mm(2). Levels of other metals did not differ between groups. CONCLUSIONS: Brain zinc accumulation is a prominent feature of advanced Alzheimer disease (AD) and is biochemically linked to brain amyloid beta-peptide accumulation and dementia severity in AD.
Samples of thoracic fluid were obtained at regular intervals from the putrefying bodies of dead dogs. For quantitative estimation of the proteins two-dimensional immunoelectrophoresis was employed and for the amino acids and amines two-dimensional thin-layer chromatography. The results lead to speculation that the initially lagging proteolytic changes are due to catalysis of autoenzymes, whereas bacteriological processes are responsible for a distinct acceleration from the 20th day after death. At this time the amino-acid concentrations showed a marked increase, which is followed by a maximum of bacterial growth, that ultimately leads to a sudden regression of amino acids. Simultaneously amines appear. The drying up of the thoracic cavity after 35 to 45 days marks the change from liquefaction to the terminal decay.
Identification using lip prints was first performed in the 1950s and was the subject of much research in the 1960s and 70s, leading to the acceptance of this technique as evidence in the criminal justice system. Previous research has focused on identifying lip print types or on methods of obtaining hidden lip prints left at the crime scene. The present study aimed to clarify characteristics of lip prints from cadavers with various causes of death (including drowning and hanging) and to determine the effects of fixation on post mortem changes in lip impressions.
Nineteen human cadaver corneas with few damaged endothelial cells were incubated under tissue culture conditions for time periods ranging from five min to 48 h. Morphological alterations of the endothelial cells were studied in whole wet mounts stained by alizarine red-alkohol-trypane blue and by scanning electron microscopy. Joint meetings of three cells are characteristic for normal corneal endothelium. After 15--60 min of incubation, damaged cells were expelled from the coherent cell sheet by expanding neighbouring cells. Joint meetings of 5--8 expanding cells were formed. After 24 h of incubation, joint meetings of four cells were the dominating morphological abnormality. Morphological changes during reduction of the numbers of cells in joint meetings are described.
Morphological changes found during post-mortem examination of victim dying from accidental hypothermia were collected and disputed in this paper. The practical usefulness of these changes in the diagnosis of sudden death was estimated.
Electron-microscope studies of experimental models of myocardial ischaemia have provided basic information on the pathogenesis of hypoxic heart injury. Correlation of ultrastructural changes with biochemical data confirms the importance of catecholamine release and ionic shifts in the early evolution of ischaemic injury. An altered cellular metabolism induced by ischaemia causes rapid depletion of glycogen and is followed quickly by alterations in the nucleus, the mitochondria and the sarcotubular system; the myofibril is the organelle most resistant to hypoxia.Postmortem autolysis mimics early ischaemic change very closely and it probably has an initial hypoxic basis. Significant hypoxic-autolytic changes may begin during the agonal state. The time elapsing and the techniques of tissue preservation are critical in determining the amount of artefact. At present it is unrealistic to expect to obtain acutely ischaemic human myocardium soon enough after death to be of value in the estimation of the degree or duration of ischaemia by electron-microscope techniques. Rapidly progressive autolytic changes preclude the meaningful morphological assessment of hypoxic change at the ultrastructural level.
High concentrations of histamine and serotonin were found in the blood, cerebral and cortical substance of the kidney from 8 patients who had died of HFRS. These elevated levels may be responsible for renal edema and loss of function. Underlying causes of the above changes are considered.
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The brains of 232 patients with a case-note diagnosis of schizophrenia or affective disorder who died in one mental hospital over a period of 22 years were weighed, and were assessed in a coronal section at the level of the interventricular foramina. From this sample were eliminated the brains of patients whose illnesses did not meet the Washington University criteria for a diagnosis of definite schizophrenia or primary affective disorder and those brains that showed significant histopathologic evidence of Alzheimer's-type change or cerebrovascular disease. This left a sample of 41 patients with schizophrenia and 29 patients with affective disorder. With age, sex, and year of birth controlled for, the brains of the patients with schizophrenia were 6% lighter, had lateral ventricles that were larger in the anterior (by 19%), and particularly in the temporal, (by 97%) horn cross section, and had significantly thinner parahippocampal cortices (by 11%). The findings provide postmortem confirmation of reports of ventricular enlargement in radiological studies and suggest that such enlargement is associated with tissue loss in the temporal lobe. The changes in schizophrenia were of a lesser degree than those seen in a sample of brains of patients with Alzheimer's-type dementia and Huntington's chorea.
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The problems of testing patients or the deceased using classical blood group systems for identity or paternity purposes after multiple transfusions are well known. In a paternity case where the putative father received multiple transfusions it was possible to determine some classical blood group systems. The investigation showed no incompatibility between the putative father and the child and led to a probability of paternity of 72.33%. Using the DNA technique (single locus probes) it could be demonstrated that the DNA patterns were not influenced by the transfusion and the possibility of paternity reached 99.9%. For a further consideration of this problem classical blood group systems and DNA systems were investigated in 12 patients before and after multiple transfusions. It was possible to determine the changes due to transfusion in the classical systems but changes in the DNA pattern were not observed.
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