Death caused by a signal rocket--not an isolated case*.

Fatalities related to sporting events are predominantly caused by blunt force injuries especially due to the emotional involvement of crowd, but occasionally other types of trauma are reported as well. A case of very rare trauma caused by shooting with a hand-held parachute signal rocket during a football match is presented. A 17-year-old football fan sustained fatal injuries, a combination of mechanical trauma caused by rocket penetration, as well as extensive thermal burning of the thoracic viscera. Analysis of the event was based on autopsy findings and evidence produced by medicolegal and ballistic experts. Improper use of a hand-held signal rocket, designed for marine distress signals, may cause serious injuries either mechanically, due to explosion, or as a result of thermal discharge. In the reported case, pattern of injuries is discussed, and medical finding corroborated to other available evidence. The presented case is a reminder that the forensic pathologist should be informed accordingly on the type and features of weapon suspected to produce injury, to be able to understand traumatic changes, and look for potential presence of foreign bodies at postmortem examination.

[Influence of the myocardial bridging phenomenon on the myocardial structure and the coronary arteries wall structure changes].

BACKGROUND/AIM: Our research was performed to evaluate the influences of the myocardial bridgings of coronary arteries on the myocardial and coronary arteries wall structure chages, that could be a reason for multiple heart malfunctions. METHODS: We analyzed the autopsy material, collected during a five-years period, and especially the group of 575 cases with the major aim to diagnose mors naturalis. In all cases with the presence of myocardial bridge over the arterial coronary wall revealed at autopsy, samples were taken for microscopic verification and examination. RESULTS: We found myocardial bridges over the coronary arteries or their major branches in 27 of the cases (4.70%). We believe that myocardial bridges compromise coronary perfusion by cyclic compression of the overbridged vessels, and that it could be the initial factor in the pathogenesis of arteriosclerotic degeneration processes on the coronary artery wall. We found different grades of arteriosclerotic changes in 88.89% of the cases, as well as fibrosis of myocardium in 88.89% and lipomatosis in 66.67% of the cases with the present myocardial bridges. CONCLUSION: Our results suggested that myocardial bridging of coronary arteries and/or their branches was the pathological and even lethal phenomenon that de serves more intensive clinical evaluation.

Morphological differences among cavum septi pellucidi obtained in patients with schizophrenia and healthy individuals: forensic implications. A post-mortem study.

Cavum septi pellucidi (CSP), especially when longer than 6 mm, has been recognized as a neurodevelopmental anomaly associated with schizophrenia. The present post-mortem study was designed to determine the importance of linear parameters of CSP and to evaluate the possible differences of CSP in schizophrenic patients (n=25 out of 110 CSP+ brains) and normal persons (n=40 out of 110 CSP+ brains). According to our results, schizophrenia patients had significantly longer and wider CSP than normal individuals. Also, statistical analysis revealed a higher suicide rate in CSP-positive patients with schizophrenia.

Regulation of the major isoform of human endothelin-converting enzyme-1 by a strong housekeeping promoter modulated by polymorphic microsatellites.

BACKGROUND: Human endothelin-converting enzyme (ECE)-1, the key enzyme in endothelin biosynthesis, shows broad cell and tissue expression within the cardiovascular system. Expression of ECE-1c, which represents the major ECE-1 isoform, is directed by an alternative promoter, but the mechanisms of ECE-1c promoter regulation are largely unknown. As ECE-1c transcription is initiated from several start sites, we hypothesized that the ECE-1c promoter functions as a housekeeping promoter. OBJECTIVE: To investigate the putative housekeeping function of the ECE-1c promoter in vascular endothelial cells, which represent a main site of its expression. RESULTS: Using promoter reporter assays, gel shift and supershift assays, we have demonstrated, in human endothelial EA.hy926 cells, functionality of cis-acting elements for binding of the CAAT-box binding protein NF-YB, GATA-2) E2F-2, and a GC-box binding factor, which are spatially associated with transcriptional start sites of ECE-1c. In the more upstream promoter region we have identified three highly polymorphic dinucleotide repeats, 5'-(CA)n, (CG)n and 3'-(CA)n, which strongly affected promoter function in endothelial EA.hy926 cells (2.7-fold activation comparing the most active to the least active allele) and, in a similar manner, in human neuronal KELLY cells. Finally, by in-vitro methylation, we were able to achieve strong suppression of the ECE-1c promoter activity in endothelial cells. CONCLUSION: Our results provide a molecular explanation for constitutive expression of ECE-1c mRNA. Modulation by genetic and epigenetic mechanisms as revealed in our study may account for interindividual variation of the constitutive endothelin system activity in humans and thus influence individual predisposition to cardiovascular disease.