Death after anal "fisting"

A 45-year-old homeless woman was found dead at her usual sleeping place. Apart from traces of blood on the lower abdomen of the body, the police investigations did not produce any clues pointing to an unnatural death. At autopsy, it was found, however, that death had been caused by extensive disruptions of the intestine. After being confronted with the results, the sexual partner of the victim admitted manual anal penetration, but claimed that this had been done by mutual agreement. The court did not accept that statement and sentenced him to life imprisonment for murder. The frequency of such fatal outcomes of anal penetration, the relationship between the perpetrator and the victim and the special features at the scene are discussed.     

Histological examination of carotid artery tissue in cases of ligature strangulation and hanging

Violence against the neck can result in a range of macromorphological and micromorphological findings. However, the forensic relevance of the carotid sinus in cases of violence against the neck remains controversial. In this follow-up study of 22 cases of suicidal and accidental strangulations, carotid bifurcations were examined histologically for morphological changes implying direct trauma, including haemorrhage and immunohistochemical expression of heat-shock proteins 27, 60, and 70 and aquaporin-3. These cases were compared with a control group (82 cases) without neck compression or head trauma and with variable causes of death. No relevant histopathological findings implying direct trauma of the carotid bifurcation were found. No cases showed positive aquaporin-3 staining and only five cases showed positive heat-shock protein-27 staining, all of which were hangings. Without massive trauma of the carotid bifurcation, histological alterations cannot be expected. Without signs of rapid death, findings of acute circulatory failure, macromorphological and micromorphological findings of neck compression, and reliable markers indicating relevant impact on the carotid bifurcation the diagnosis of a lethal reflex cannot be verified.

Key points

• Among 22 cases of strangulation causing death, there were 16 cases of hanging and 6 cases of ligature strangulation
• Few cases showed small haemorrhages located predominantly in the surrounding fat and connective tissues; however, the haemorrhages did not have any effects on the tissues
• Neck compression had minimal effects on heat shock protein 27 expression in carotid artery tissue
• Aquaporin-3 staining suggested it is not a useful marker for relevant neck pressure, or that there had not been any relevant neck impact
• Our findings suggested no direct evidence for reflex cardiac death resulting from a brief force against the neck

     

Significant association of TH01 allele 9.3 and SIDS

Sudden infant death syndrome (SIDS) constitutes a considerable percentage of infant death of unknown etiology. Individual catecholamine response variation is suspected to play a role in SIDS. TH01 is a tetrameric short tandem repeat marker in the tyrosine hydroxylase gene, which regulates gene expression and catecholamine production with allele 9.3 exerting a particularly strong effect on noradrenaline production. We investigated in an age-controlled study the TH01 allele frequencies in 127 cases of SIDS and 406 control cases to assess whether in SIDS cases a distinct TH01 allele distribution could be determined as has been reported by a previous study. We found that genotypes containing one or two 9.3 alleles were significantly more frequent in SIDS patients (58.2%) than in control subjects (48.4%, p=0.038), whereas all other alleles were more frequent in the control subjects. Our findings support the notion that there exists a significant association between TH01 gene configuration and SIDS.     

Optimization and validation of CEDIA drugs of abuse immunoassay tests in serum on Hitachi 912

Due to sensitive limits of detection of chromatographic methods and low limit values regarding the screening of drugs under the terms of impairment in safe driving (§ 24a StVG, Street Traffic Law in Germany), preliminary immunoassay (IA) tests should be able to detect also low concentrations of legal and illegal drugs in serum in forensic cases. False-negatives should be avoided, the rate of false-positive samples should be low due to cost and time. An optimization of IA cutoff values and a validation of the assay is required for each laboratory. In a retrospective study results for serum samples containing amphetamine, methylenedioxy derivatives, cannabinoids, benzodiazepines, cocaine (metabolites), methadone and opiates obtained with CEDIA drugs of abuse reagents on a Hitachi 912 autoanalyzer were compared with quantitative results of chromatographic methods (gas or liquid chromatography coupled with mass spectrometry (GC/MS or LC/MS)). Firstly sensitivity, specificity, positive and negative predictive values and overall misclassification rates were evaluated by contingency tables and compared to ROC-analyses and Youden-Indices. Secondly ideal cutoffs were statistically calculated on the basis of sensitivity and specificity as decisive statistical criteria with focus on a high sensitivity (low rates of false-negatives), i.e. using the Youden-Index. Immunoassay (IA) and confirmatory results were available for 3014 blood samples. Sensitivity was 90% or more for nearly all analytes: amphetamines (IA cutoff 9.5 ng/ml), methylenedioxy derivatives (IA cutoff 5.5 ng/ml), cannabinoids (IA cutoff 14.5 ng/ml), benzodiazepines (IA cutoff >0 ng/ml). Test of opiates showed a sensitivity of 86% for a IA cutoff value of >0 ng/ml. Values for specificity ranged between 33% (methadone, IA cutoff 10 ng/ml) and 90% (cocaine, IA cutoff 20 ng/ml). Lower cutoff values as recommended by ROC analyses were chosen for most tests to decrease the rate of false-negatives. Analyses enabled the definition of cutoff values with good values for sensitivity. Small rates of false-positives can be accepted in forensic cases.     

No association of IL-10 promoter SNP −592 and −1082 and SIDS

Sudden infant death syndrome (SIDS) constitutes a considerable percentage of infant death of unknown etiology. The genetically controlled pathway of cytokine mediated response to inflammation is presumed to play a role in SIDS. The A allele of SNP ?592 of the promoter region of the anti-inflammatory cytokine IL-10 has been suggested to be associated with SIDS. Herein we investigated whether we could confirm this finding by SNP genotyping a series of 123 cases of SIDS and 406 control cases. We did not find a correlation between the A allele or an A allele containing genotype of IL-10 promoter SNP ?592 and SIDS which is in contrast to previous studies. Also, in concordance with previous work, no association of the A allele or A allele containing genotypes of IL-10 promoter SNP ?1082 and SIDS was found.     

Sarcomeric gene mutations in sudden infant death syndrome (SIDS)

In developed countries, sudden infant death syndrome (SIDS) represents the most prevalent cause of death in children between 1 month and 1 year of age. SIDS is a diagnosis of exclusion, a negative autopsy which requires the absence of structural organ disease. Although investigators have confirmed that a significant percentage of SIDS cases are actually channelopathies, no data have been made available as to whether other sudden cardiac death-associated diseases, such as hypertrophic cardiomyopathy (HCM), could be responsible for some cases of SIDS. The presence of a genetic mutation in the sarcomeric protein usually affects the force of contraction of the myocyte, whose weakness is compensated with progressive hypertrophy and disarray. However, it is unclear whether in the most incipient forms, that is, first years of life, the lack of these phenotypes still confers a risk of arrhythmogenesis. The main goal of the present study is to wonder whether genetic defects in the sarcomeric proteins, previously associated with HCM, could be responsible for SIDS. We have analysed 286 SIDS cases for the most common genes implicated in HCM in adults. A total of 680 mutations localised in 16 genes were analysed by semi-automated matrix-assisted laser desorption/ionisation time-of-flight mass spectrometry (MALDITOF-MS) using the Sequenom MassARRAY(?) System. Ten subjects with completely normal hearts showed mutated alleles at nine of the genetic variants analysed, and one additional novel mutation was detected by conventional sequencing. Therefore, a genetic mutation associated with HCM may cause sudden cardiac death in the absence of an identifiable phenotype.