[ Recommendations for the forensic and age determination from the skeleton].
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Biomedical subjects
Publications and source records attributed to S Ritz-Timme.
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The yellow ligaments of the spine are characterized by an exceptionally high content of elastin, a protein with a proved longevity in several human tissues. This unique biochemical composition suggested a suitability of yellow ligaments for age estimation based on aspartic acid racemization (AAR), which was tested by determination of AAR in total tissue specimens and in purified elastin from yellow ligaments of individuals of known age. AAR was found to increase with age in both sample sets. The purified elastin samples exhibited a much faster kinetics than the total tissue, with ca. 3.7-4.6-fold higher apparent rates. The relationship between AAR and age was much closer in the purified elastin samples ( r=0.96-0.99) and it can therefore be used as a basis for biochemical age estimation. The analysis of total tissue samples cannot be recommended since the AAR values can be strongly influenced even by slight, histologically non-detectable variations in the collagen content. Age estimation based on AAR in purified elastin from yellow ligaments may be a valuable additional tool in the identification of unidentified cadavers, especially in cases where other methods cannot be applied (e.g. no available teeth, body parts).
BACKGROUND: So far in Germany, no legally binding standards for blood alcohol concentration exist that prove an impairment of navigability. The aim of our interdisciplinary project was to obtain data in order to identify critical blood alcohol limits. In this context the visual system seems to be of decisive importance. MATERIALS AND METHODS: 21 professional skippers underwent realistic navigational demands soberly and alcoholized in a sea traffic simulator. The following parameters were considered: visual acuity, stereopsis, color vision, and accommodation. RESULTS: Under the influence of alcohol (average blood alcohol concentration: 1.08 per thousand ) each skipper considered himself to be completely capable of navigating. While simulations were running, all of the skippers made nautical mistakes or underestimated dangerous situations. Severe impairment in visual acuity or binocular function were not observed. Accommodation decreased by an average of 18% ( p=0.0001). In the test of color vision skippers made more mistakes ( p=0.017) and the time needed for this test was prolonged ( p=0.004). CONCLUSIONS: Changes in visual function as well as vegetative and psychological reactions could be the cause of mistakes and alcohol should therefore be regarded as a severe risk factor for security in sea navigation.
OBJECTIVE: To evaluate data in an interdisciplinary project (ophthalmology, forensic medicine, internal medicine, psychology,and nautical science) in order to identify critical blood alcohol limits in sea navigation. METHODS: A sea traffic simulator was employed for realistic nautical demands on 21 professional experienced skippers under sober and alcoholized conditions (target blood alcohol concentration: 1.0 per thousand ). After simulated navigation, pupil light reflex, spontaneous pupil movements,nystagmus,and saccades were evaluated by pupillography. Modification of the pupillograph enabled us also to measure optokinetic nystagmus. RESULTS: Evaluation of the pupil light reflex revealed obvious changes in the extent of relative contraction and in redilatation time under the influence of alcohol. Diminished vigilance could be observed in all of the skippers when optokinetic nystagmus was tested. CONCLUSION: The pupillograph represents a suitable device for measuring functions of the visual and vegetative systems. Thus, the impact of these functions on nautical capability can be demonstrated. If further investigations such as ophthalmological, medical, psychological, and nautical evaluations are taken into account, it could be determined that blood alcohol levels of 1.0 per thousand may exclude safe navigation.
BACKGROUND: In extracellular proteins, aspartic acid racemization (AAR) has the potential to identify long-lived or permanent proteins. OBJECTIVES: We present data to show an age-dependent increase in AAR in chronologically aged skin elastin. METHODS: Elastin was purified in a multistep procedure designed to remove contaminating proteins and to avoid induced racemization. As a control experiment, elastin was also purified from the richest elastin bearing tissue, the yellow ligaments of the spine. RESULTS: In total skin, specimens displayed a slight age-dependent increase in d-aspartyl residues, but in purified elastin the rate of increase was rapid and highly correlated with age (r = 0.98). Similar rates were observed in the control data from the yellow ligaments. The AAR rates were found to be higher in elastin from skin (and yellow ligaments) than previous studies of lung parenchyma and from aorta had shown. These differences appear to be related to the purity of the extracted elastin product, and to a significant in vivo degradation of elastin in skin. CONCLUSIONS: The age-dependent accumulation of modified aspartic acid residues appears to be a common feature in ageing elastin, independent of the tissue source. This indicates a lack of turnover and an accumulation of elastin damage in diverse ageing tissues, possibly as part of programmed ageing.
In our cornea bank, it was noticed that corneas from donors with alcoholism seemed to be of lower quality than corneas from other donors. High blood ethanol concentrations can induce high alcohol concentrations in aqueous and vitreous humor. This could be demonstrated in the case of a lethal alcohol intoxication. We conducted in vitro experiments to clarify the question of alcohol-induced changes of corneas. The corneas were stored in a standardized culture medium including ethanol, formic acid, methanol, and acetaldehyde in concentrations to be expected in chronic alcoholism. During cultivation over 4 weeks, endothelial morphology and extent of aspartic acid racemization in stromal proteins were evaluated. The extent of aspartic acid racemization served as a biochemical parameter of alcohol-induced protein changes of the corneas. In the in vitro experiments, a drop in the endothelial cell counts could be seen in corneas stored in culture medium with acetaldehyde. The extent of aspartic acid racemization increases in corneas stored in medium containing ethanol, which obviously is the result of alcohol-induced protein degradation. High concentrations of ethanol and its metabolics can be detected in vitreous and aqueous humor in chronic alcoholism. Clearly, these concentrations have a direct toxic effect on the corneal endothelium (acetaldehyde) and on the stromal proteins (ethanol).
During their life span, human proteins may undergo post-translational modifications that can be interpreted as manifestations of protein aging. The most frequently discussed modifications in that context are oxidation, glycation, deamidation, isomerization and racemization. Their pathophysiological relevance depends on the availability of repair mechanisms and on the protein turnover. Proteins with high turnover will be exchanged before molecular modifications become relevant. The most affected proteins are long-living and permanent proteins. Such proteins can be identified by the determination of their D-aspartic content (as a measure of an in vivo racemization and isomerization of aspartyl and asparaginyl residues). Using this method it could be demonstrated that numerous proteins in diverse human tissues are long-living or permanent and cannot escape post-translational modification by turnover. The human organism is confronted with an accumulation of "abnormal", post-translationally modified proteins during aging, especially in the extracellular space, but also at a cellular level. The exact pathophysiological dimension of post-translational modifications as manifestations of protein aging has to be further elucidated. However, they have been already discussed as relevant factors in the pathogenesis of diseases of old age.
A fatality caused by ingestion of a decalcifying agent containing formic acid is reported. Quantitative analysis of formic acid in the form of its methyl ester was performed in different body fluids and organ samples using head-space gas chromatography with flame ionization detection. The blood taken at the time of admission to hospital had a concentration of 370.3 microg/ml, which declined to 13.9 microg/ml after 6.5 h of haemodialysis. Post-mortem concentrations were 855.4 microg/ml (heart blood), 2,712 microg/ml (gastric contents), 1128 microg/ml (haemorrhagic fluid from abdominal cavity), 3,051 microg/ml (bile), 2,664 microg/ml (contents of small intestine), 442.7 microg/g (liver) and 542.3 microg/g (kidney). The most important morphological findings for differentiating between oral and respiratory ingestion were ulceration of the oropharynx and the oesophagus as well as extensive necrotic lesions in the stomach and the duodenum without perforation. Death was caused by massive acidosis, haemolysis, bleeding complications, hepatic and renal failure. Toxicological and morphological findings revealed that a considerable amount of formic acid had been ingested orally with a suicidal intention.
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Estimates of the age of living and dead individuals, obtained in order to answer legal or social questions, require minimum quality standards in order to guarantee data quality. We present an outline strategy (with recommendations) for the attainment of quality assurance in age estimation based on aspartic acid racemisation. The strategy is based on a definition of minimum standards for laboratories, including documentation of procedures, methodology and levels of expertise, and the formulation of guidelines for intralaboratory and interlaboratory quality control.
Age estimation in cadavers, human remains and living individuals may clarify issues with significant legal and social ramifications for individuals as well as for the community. In such cases methods for estimating age should fulfil the following specific demands: (1) they must have been presented to the scientific community, as a rule by publication in peer-reviewed journals, (2) clear information concerning accuracy of age estimation by the method should be available, (3) the methods need to be sufficiently accurate and (4) in cases of age estimation in living individuals principles of medical ethics and legal regulations have to be considered. We have identified and summarized the methods that essentially fulfil these specific demands. In childhood and adolescence morphological methods based on the radiological examination of dental and skeletal development are to be recommended. In adulthood, the accuracy of most morphological methods is much reduced. Here a biochemical method based on aspartic acid racemization in dentine provides the most accurate estimates of age, followed by special morphological dental and skeletal methods. The choice of method has to take account of the individual circumstances of each case. Most methods require either the consultation of specialised and trained scientists or an adequate calibration by the "user". Very few attempts have been made to find common standardisation, calibration and evaluation procedures or to develop means of quality assurance for methods of age estimation. Efforts in these directions are necessary to guarantee quality standards and adequate answers to the important legal and social issue of age estimation in forensic medicine.
Intraarterial angiography was performed on a patient with peripheral arterial occlusive disease (Fontaine IIb). No relevant risk factors were known, and a previous angiography had been undertaken without incident. After administration of contrast medium, the patient complained of acute pain in the lower abdomen and both legs, and a sudden rise in blood pressure was observed. The patient subsequently lost consciousness and died within 1.5 h. Postmortem examination showed that death was due to peripheral atheromatous microembolism of lipids, and not cholesterol as is usual in these cases. The differential diagnosis is discussed and a review of the literature is presented.
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Accurate age determination of adult cadavers and human remains is a key requirement in forensic practice. The current morphological methods lack accuracy and precision, require specialist training and are costly. The use of aspartic acid racemization (AAR) in human dentine provides a simple, cost-effective solution and the method can achieve accuracies of +/- 3 years at best. Currently, there are differences in AAR methodology between laboratories which produce different results on the rate of racemization in teeth. These inconsistencies must be resolved if the technique is to be successfully applied to age determinations in forensic cases. This paper reviews the differences in protocol which have been used, discusses how each method will affect the results obtained from AAR analysis and gives recommendations for optimization of the methological protocol as a first step towards international standardization.
A chimera is an organism whose cells derive from two or more distinct zygote lineages. and therefore two different blood cell populations circulate in one individual. To point out the potential pitfalls in forensic analysis, a set of triplets (a girl and two boys) who revealed blood chimerism was investigated with four STR systems using PCR. The results indicated that a DNA profile based on DNA extracted from blood can lead to a false determination because the band pattern of each triplet contained a mixture of the original genotype and the genotype of the siblings. Additional investigations on biological materials other than blood must be made in order to find out the real genetic characteristics of each child.
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Leukocyte and platelet accumulations around apparently empty spaces ("air bubbles") in the blood of the right heart or branches of the pulmonary artery should constitute histomorphological evidence of a venous air embolism prior to death. Such findings have been evaluated as the result of active cellular reactions to air bubbles and as a vital reaction. This interpretation was reviewed by injecting a frothy mixture of blood and air into the pulmonary artery of six human lungs 12-110 h post mortem. The lungs were fixed and (immuno)histologically prepared (haematoxylin-eosin staining, immunohistological visualization of platelets, fibrinogen and fibrin). Leukocyte and platelet accumulations around "air bubbles" in blood were provoked late post mortem by injection of the frothy blood-air mixture and are thus possibly not the result of vital cellular reactions. The case is rather that attachment of particles (cells) to flowing air bubbles in an aqueous medium (blood) could correspond physicochemically to a flotation process such as those used in industry for separation techniques. A flotation process would, however, require an intensive dynamic blood-air bubble contact, which would only be obtainable if cardiac action is maintained for a sufficient length of time after air embolism. Leukocyte and platelet accumulations around "air bubbles" in the blood would then indeed be properly interpreted as a vital reaction (albeit possibly not resulting from vital cellular reactions) and could be used as evidence of an air embolism prior to death.