Estimation of the time since death in the early post-mortem period

Dental pulp tissue could be obtained in most cases from materials obtained under experimental conditions and from forensic casework (air accidents, burned and putrefied bodies). Teeth extracted during dental treatment (n = 30) were stored for 6 weeks and 4 years at room temperature. In addition teeth (n = 10) extracted from jaw fragments that had been stored for 15 years at room temperature, and teeth extracted post mortem from actual identification cases (n = 8) were investigated. Following extraction from dental pulp tissue the DNA concentration was measured by fluorometry. The amount of DNA obtained from the dental pulp tissue of a single tooth varied from 6 μg to 50 μg DNA. In most cases high molecular weight DNA was still present although the major portion consisted of degraded DNA. Genomic dot blot hybridization for sex determination using the biotinylated repetitive DNA probe pHY 2.1 was performed and sex was correctly classified in all cases using 50–100 ng target DNA. PCR typing of the HLA-DQα and ApoB 3′ VNTR systems from dental pulp tissue DNA was in agreement with the results obtained from blood, bloodstains, or lung tissue. In addition, Southern blot analysis of selected samples using the single locus VNTR probe pYNH24 was successfully performed. In all cases the DNA recovered from dental pulp was unsuitable for multilocus probe analysis.

Application of DNA techniques for identification using human dental pulp as a source of DNA

The combination of postmortem CT angiography and image-guided biopsy has the strong potential to act as a minimally invasive triage tool for diagnosis of suspected cardiovascular causes of death in forensic pathology and as a sufficient substitute to traditional autopsy in cases of refused autopsy.

Sudden Death after Chest Pain: Feasibility of Virtual Autopsy with Postmortem CT Angiography and Biopsy

The rate of sodium-lithium countertransport (SLC flux) across red cell membranes has been reported to be elevated in hypertensive persons and their relatives as compared to normotensive individuals without family histories of hypertension. We have investigated the inheritance of this trait in 434 persons from 10 kindreds. Relatives show positive correlation of SLC flux values, but there is no spouse-spouse correlation. Pedigree analysis favors a model of polygenic inheritance over models of major-gene inheritance. Major-gene index statistics and offspring-between-parent statistics provide similar results. The proportion of total pheno-typic variance that is attributable to polygenic differences between persons is estimated at 71%. The SLC flux values of hypertensive persons in this study population are lower than those reported from Boston, but are similar to those reported from Europe. We found a broad overlap of SLC flux values for hypertensive and normotensive persons. We conclude that SLC flux probably is not useful as a preclinical marker for essential hypertension.

Genetic analysis of sodium-lithium countertransport in 10 hypertension-prone kindreds.

Background: Hormonal responses to alcohol have been reported to differ in subjects with and without a family history of alcoholism which suggests that alcohol-induced hormonal changes might be used to identify individuals who are at elevated genetic risk for developing alcoholism. However, before a biological response can be used as a marker of genetic risk for disease, it must first be demonstrated that the response is, in fact, heritable. The present study was designed to determine whether hormonal responses to alcohol are heritable. Methods: The adrenocorticotropic hormone (ACTH), beta-endorphin (β-E), cortisol (CORT), and prolactin (PRL) responses to alcohol were examined in male and female identical (monozygotic or MZ) and fraternal (dizygotic or DZ) twin pairs. Male subjects consumed 0.35 g ethanol/kg body weight (BW) and females consumed 0.325 g ethanol/kg BW in each of two alcohol drinking sessions administered 1 hr apart (total dose of 0.7 g/kg BW in males and 0.65 g/kg BW in females). Plasma hormone content was analyzed in samples collected before (resting conditions) and at 15, 60, 75, 120, 180, and 240 min after onset of drinking. Hormonal responses to alcohol were examined with twin analyses using the TWINAN90 program. A separate analysis was performed for each of the four hormones. A subset of subjects from each zygosity was seen on two separate occasions to establish retest reliability. Heritability of hormonal responses to alcohol was estimated using the intraclass correlation approach before and after removing the contribution of covariates that have the potential of influencing the plasma levels of these hormones. Results: Resting plasma levels of all four hormones were within the expected range, and the β-E, ACTH, and PRL responses to the alcohol challenge evidenced good test-retest reliability. Of the four hormones examined, the only one that showed significant heritability after alcohol drinking was β-E. Heritability estimates were not altered for any of the four hormones after removal of the variance contributed by covariates, such as gender and age. Conclusions: Taken together with other recent findings, the results suggest that the β-E response to alcohol may represent a new biomarker that can be used to identify individuals who are at elevated genetic risk for developing alcoholism.

Analysis of Heritability of Hormonal Responses to Alcohol in Twins: Beta-Endorphin as a Potential Biomarker of Genetic Risk for Alcoholism

A comprehensive survey is given of the most important theories of etiology, pathogenesis and pathophysiology of pulmonary fat embolism. Autopsy and microscopic examinations were performed on 26 corpses with different causes of death. The total contents of fat of the lungs was analyzed by chloroform extraction. Death due to pulmonary fat embolism was diagnosed in three cases. In those with whole fat contents of about 20 g or more the histological degree was equivalent to occlusion of half of all vessels. The histological feature resembled that of shock; hemorrhage and microthrombosis were regular findings. The functional and morphological relationships with shock are discussed. It is concluded that, at least in the initial stage, fat embolism is due to mechanical injury. This mechanism is possibly altered or enhanced by biochemical changes in later phases. Pulmonary fat embolism is a disease which may cause death if mechanical, toxic and shock-inducing effects lead to insufficiency of the cardio-respiratory system. In forensic cases death due to fat embolism should be diagnosed only after exclusion of other lethal factors. Posttraumatic cases often show competition with shock due to hemorrhage. It is important to relate the degree of fat embolism to preexisting diseases.

[Fat embolism of the lungs as the cause of death. Etiology, pathogenesis and reasoning (author's transl)].

Histomorphologische Lungenuntersuchungen bei 34 Todesfallen durch Strangulation. Diverse Farbungen einschlieslich Enzymhistochemie, Fettfarbung und Semidunnschnitt, z. T. fruhpostmortale Probenentnahmen. Die wichtigsten Befunde: In 9 Fallen fand sich eine meist geringgradige pulmonale Fettembolie. Fast alle Falle wiesen Zeichen der akuten hamodynamischen Dysregulation und erhohter Gefaspermeabilitat auf: z. T. hamorrhagisches alveolares, teilweise auch septales und perivaskulares Lungenodem. Gefaswandverquellungen. Bei fruher Probenentnahme auch hydropische Endothelzelldegeneration. Gefasinhaltsveranderungen folgender Qualitat: Knochenmarksembolie in drei Fallen. Disseminierte und aggregierte Zellembolien in allen Fallen, jedoch unterschiedlicher Zusammensetzung: Uberwiegend handelte es sich um unreife Knochenmarkszellen der myeloischen Reihe, daneben auch jugendliche und gelapptkernige Granulocyten sowie andere mononukleare Zellen. Weiterhin, meist in Kombination mit den aggregierten Zellen, Plattchenaggregate. Atiologisch wird an ein Zusammenwirken mehrerer Pathomechansimen gedacht: Erstickungskrampfe mit mechanischer Alteration des Knochenmarks; hypoxydotische Schadigung der Gefasendothelien der Knochenmarkssinusoide; humorale Mediatoren des fruhen Schocks mit direkter Knochenmarkswirkung. Die Befunde werden im Sinne einer vitalen Reaktion auf das Strangulationsgeschehen gedeutet.

Vitale Reaktionen in der Lungenstrombahn bei Tod durch Strangulation

A steam-tube of the main boiler exploded on a ship lying in the harbour of Hamburg. The steam temperature was 283‡ C. Cutaneous and severe inhalational scalding occured in the 27 fatalities, the men dying after different intervals.

Heat injuries to the respiratory system.

The pathophysiology of respiration and hemodynamics during the agonal period of death by obstructive asphyxia was investigated. Experiments were carried out on ten dogs that were strangulated by ligature (seven cases) or asphyxiated by occlusion of the intubation tube (three cases). The following parameters were registered: Blood pressure in the arteria femoralis and arteria pulmonalis, electrocardiogram, endotracheal pressure, respiratory frequency, electroencephalogram. These were the most important findings: (a) An excessive and distinctly biphasic hypertonic reaction takes place after strangulation by ligature whereas occlusion of the intubation tube results in a slight increase of arterial blood pressure. (b) After occlusion of the tube more than after strangulation the endotracheal pressure becomes deeply negative during the inspiration trials. (c) After cessation of respiration a distinct pulmonary arterial hypertension develops in both forms of obstructive asphyxia. (d) The paralysis of the respiratory center takes place after about 4 min at the same time when the circulatory breakdown develops. The final cardiac failure occurs after about 9-10 min. The dysregulation of respiration and hemodynamics in the agony of obstructive asphyxia can be differentiated from other shock models. This results in special morphological alterations of the lung tissue which have been described elsewhere.

[Death by obstructive asphyxia: the pathophysiology of respiration and hemodynamics (author's transl)].

Die Literatur uber die Behinderung der arteriellen Kopfdurchblutung bei Strangulation wird referiert. In eigenen Experimenten werden die isolierten Halsarterien von zehn Leichen unter verschiedenen Drucken perfundiert. Die experimentelle Strangulation erfolgt mit verschiedenen Strangwerkzeugen und in unterschiedlicher Lokalisation. Dabei werden die zum Gefasverschlus erforderlichen Krafte bestimmt. Weiterhin werden verschiedene atypische supracervicale Erhangungsformen simuliert und der Einflus verschiedener Kopfhaltungen untersucht. Die wesentlichen Ergebnisse sind:
 Individuelle Parameter wie Halsumfang, Arteriosklerose und Leichenstarre sind ohne erkennbaren Einflus auf die zum Verschlus der Carotiden erforderlichen Krafte.

[Compression of the neck and arterial obstruction (author's transl)].

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