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A 25-year-old, emaciated man without medical treatment was found to have died suddenly at home by his mother. At autopsy, there were no injuries to his body, but significant circulatory insufficiency was observed. Electron microscopy revealed abnormal mitochondria in cells of the cardiac conduction system. The conduction system was filled with mitochondrial size abnormalities and mitochondrial cristae abnormalities. No notable abnormal findings were observed in other organs. Genetic examination of the blood revealed the mitochondrial pathogenetic variant m.3243AG. Epileptic seizures, diabetic ketoacidosis, and hyperosmolar hyperglycemic state were unlikely to be the cause of sudden death. The cause of death was diagnosed as arrhythmia possibly induced by the failure of the cardiac conduction system due to mitochondrial disease. This is a rare case of sudden death caused by an accumulation of abnormal mitochondria in the cardiac conduction system.

A man and a woman were rescued from a room that had exploded. Many empty cassette gas cylinders were found in the room. The man and woman were hospitalized immediately for the treatment of burns. The woman died 6 days later, and the man died 31 days later without regaining consciousness. Carbonization and hardening of the frontal facial skin and parts of the left and right fingers were observed on the man's body. In both cases, systemic burns had led to progressive systemic edema and markedly suppressed circulation. Analytical samples for butanes obtained from their bodies at autopsy were stored at −20 °C for 14 and 25 days, respectively, before analysis. Normal butane and isobutane were quantified in the brain and subcutaneous adipose tissue of the woman. Only the isobutane was quantified in the adipose tissue of the man. The evidence suggests that the man lit a cigarette while breathing gas and the entire room exploded. Our results also suggest that butane can be detected in the adipose tissue of autopsy cases long after inhalation even under the present storage conditions, and isobutane may remain in adipose tissue longer than n-butane.

The efficacy of DRIVEN-FLOW® M7-II(DFM7II) for seven drug groups was compared with Triage DOA® (Triage) using 340 autopsy urine samples taken from bodies within 1 month of death based on mass screening analysis of GC/MS and LC-MS/MS. The sensitivity to benzodiazepines was 0.56 in Triage and 0.53 in DFM7II with few false positives, and their accuracy was 0.88. Triage detected triazolo diazepine derivatives more easily than DFM7II. DFM7II detected diazepam and nitro benzodiazepines more easily than Triage. There were nine amphetamine false-positive cases of more than 10 days after death in Triage, but these were absent in DFM7II during this period. The accuracy of amphetamines for Triage was 0.96 and for DFM7II was 1. Tricyclic antidepressant (TCA) was detected in five cases by mass analysis, while there were four false-positive cases using Triage and eight cases using DFM7II. In the TCA false-positive cases of both kits, tricyclic psychotics such as chlorpromazine, carbamazepine, and quetiapine were included as well as the drug poisoning cases. There were no samples containing cocaine or THC. The accuracy of DFM7II for opiate and barbiturates was 1, but those of Triage was less than 1. Based on the above, DFM7II is a more accurate kit with fewer false-positives for target drug groups, other than TCA, than Triage.

An experimental DNA extraction kit (new kit) was recently developed to extract DNA from degraded skeletal remains without the need for powdering the samples. We compared the utility of the new kit with the conventional phenol/chloroform method using real-time quantitative PCR and multiplex STR analysis. The new kit yielded large amounts of DNA from a compact bone fragment compared with the conventional phenol/chloroform method. We were able to extract sufficient DNA for STR analysis from 75% (3 of 4) and 60% (3 of 5) of the un-powdered tooth and bone samples, respectively, using the new kit. We were able to perform mini-STR analysis of the remaining samples using DNA extracted with the new kit. Furthermore, we successfully performed mitochondrial DNA sequencing of every sample. The new kit simplifies the DNA extraction procedure as it does not require powdering samples. Decreasing the number of procedural steps in DNA extraction will be beneficial in controlling DNA contamination in laboratories. Our results suggest that the new kit may be used for the simple, simultaneous extraction of DNA from multiple samples.

A total of 3046 males of Chinese, Malay, Thai, Japanese, and Indian population affinity were previously typed for the Y STR loci DYS19, DYS385 (counted as two loci), DYS389I, DYS389II, DYS390, DYS391, DYS392, DYS393, DYS437, DYS438, DYS439, DYS456, DYS458, DYS635, DYS448, and Y GATA H4 using the AmpFlSTR Yfiler kit. These samples were assessed for population genetic parameters that impact forensic statistical calculations. All population samples were highly polymorphic for the 16 Y STR markers with the marker DYS385 being the most polymorphic, because it is comprised of two loci. Most (2677 out of a total of 2806 distinct haplotypes) of the 16 marker haplotypes observed in the sample populations were represented only once in the data set. Haplotype diversities were greater than 99.57% for the Chinese, Malay, Thai, Japanese, and Indian sample populations. For the Y STR markers, population substructure correction was considered when calculating the rarity of a Y STR profile. An F(ST) value, rather than a R(ST) value, is more appropriate under a forensic model. Because the F(ST) values are very small within the Asian populations, the estimate of the rarity of a haplotype comprised of 10-16 markers does not need substructure correction. However haplotypes with fewer markers may require F(ST) corrections when calculating the rarity of the profile.

Hemorrhagic shock has often been cited as a cause of death in forensic practical cases, but it is usually difficult to prove by autopsy findings alone. Our experimental studies demonstrated that hemorrhagic shock has promoted the endovascular recruitment of activated neutrophils and finally led to dysfunction of the shock organs. In this study, activated neutrophils were studied as a marker of death from hemorrhagic shock in the organs of autopsy cases in our department. Morphological changes in the heart, lung, liver, and kidney were examined in cases of death from hemorrhagic shock. The frequency of appearance of activated neutrophils was measured by immunohistochemical staining in the organs. The commonly observed morphological changes of hemorrhagic shock, which were not always expressed in any cases, could not account well for the cause of death. However, the expression of activated neutrophils in the organs elevated significantly at a middle and long antemortem interval. The appearance of activated neutrophils in the shock organs might be useful as a morphological marker of the cause of death from hemorrhagic shock in forensic practice cases.